The tales we tell : exploring the legal stories of Queensland women who kill

The bulk of the homicide research to date has focused on male offending, with little consideration given to women's offending and in particular, their constructions within the courtroom following a homicide-related charge. This thesis examines, in detail, nineteen homicide cases finalised in the Queensland Supreme Courts between 01/01/1997 and 31/12/2002, in order to document and discuss the various legal stories available to women who kill. Predominantly, two “stock stories” are available within the court. The first, presented by the defence, offers the accused woman a victimised position to occupy. Evidence of victimisation is made available through previous abuse, expert testimony from psychologists and psychiatrists, challenges to her mental health, or appeals to her emotional nature. The second stock story, presented by the prosecution, positions the accused woman as angry, full of revenge, calculating and self serving. Such a script is usually supported by witnesses, police evidence, and family members. This thesis examines these competing and contradictory scripts using thematic discourse analysis to examine the court transcripts in detail. It argues that the "truth" of the fatal incident is based on one of these two prevailing scripts. This research destabilises the dominant script of violent female offending in the feminist literature. Most research to date has focussed on explaining the circumstances in which women kill, concentrating attention on the victimisation of the violent offending woman and negating or de-prioritising any volition on her part. By analysing all transcripts of women whose trials were held within the specified period, this research is able to demonstrate the stories used to describe their complex offending, and draw attention to the anger and intent that can occur alongside the victimisation.

The beliefs which motivate young male and female drivers to speed : a comparison of low and high intenders

In Australia, young drivers aged 17 to 24 years, and particularly males, have the highest risk of being involved in a fatal crash. Investigation of young drivers’ beliefs allows for a greater understanding of their involvement in risky behaviours, such as speeding, as beliefs are associated with intentions, the antecedent to behaviour. The theory of planned behaviour (TPB) was used to conceptualise beliefs using a scenario based questionnaire distributed to licensed drivers (N = 398). The questionnaire measured individual’s beliefs and intentions to speed in a particular situation. Consistent with a TPB-based approach, the beliefs of those with low intentions to speed (‘low intenders’) were compared with the beliefs of those with high intentions (‘high intenders’) with such comparisons conducted separately for males and females. Overall, significant differences in the beliefs held by low and high intenders and for both females and males were found. Specifically, for females, it was found that high intenders were significantly more likely to perceive advantages of speeding, less likely to perceive disadvantages, and more likely to be encouraged to speed on familiar and inappropriately signed roads than female low intenders. Females, however, did not differ in their perceptions of support from friends, with all females reporting some level of disapproval from most friends and all females (i.e., low and high intenders) reporting approval to speed from their male friends. The results for males revealed that high intenders were significantly more likely to speed on familiar and inappropriately signed roads as well as having greater perceptions of support from all friends, except from those friends with whom they worked. Low and high intending males did not differ in their perceptions of the advantages and disadvantages of speeding, with the exception of feelings of excitement whereby high intenders reported speeding to be more exciting than low intenders. The findings are discussed in terms of how they may directly inform the content of mass media and public education campaigns aimed at encouraging young drivers to slow down.

Evidence for u.v. induction of CDKN2 mutations in melanoma cell lines

The CDKN2 gene, encoding the cyclin dependent kinase inhibitor p16, is a tumour suppressor gene involved in melanoma and maps to chromosome band 9p22. Mutations or interstitial deletions of this gene have been found both in the germline of familial melanoma cases and somatically in melanoma cell lines. Previous mutation analyses of melanoma cell lines have indicated a high frequency of C:G to T:A transitions, with all of these mutations occurring at dipyrimidine sites. Including three melanoma cell lines carrying tandem CC to TT mutations, the spectrum of mutations so far reported indicates a possible role for u.v. radiation in the mutagenesis of this gene in some tumours. To further examine this hypothesis we have characterised mutations of the CDKN2 gene in 30 melanoma cell lines. Nineteen lines carried complete or partial homozygous deletions of the gene. Of the remaining cell lines, eight were shown by direct sequencing of PCR products from exon 1 and exon 2 to carry a total of nine different mutations of CDKN2. Two cell lines carried tandem CC to TT mutations and a high rate of C:G to T:A transitions was observed. This study provides further evidence for the role of u.v. light in the genesis of melanoma, with one target being the CDKN2 tumour suppressor gene.

The CDKN2A (p16) gene and human cancer

CDKN2A, the gene encoding the cell-cycle inhibitor p16CDKN2A, was first identified in 1994. Since then, somatic mutations have been observed in many cancers and germline alterations have been found in kindreds with familial atypical multiple mole/melanoma (FAMMM), also known as atypical mole syndrome. In this review we tabulate the known mutations in this gene and discuss specific aspects, particularly with respect to germline mutations and cancer predisposition.

CDKN2A mutation in a non-FAMMM kindred with cancers at multiple sites results in a functionally abnormal protein

The CDKN2A gene encodes p16 (CDKN2A), a cell-cycle inhibitor protein which prevents inappropriate cell cycling and, hence, proliferation. Germ-line mutations in CDKN2A predispose to the familial atypical multiple-mole melanoma (FAMMM) syndrome but also have been seen in rare families in which only 1 or 2 individuals are affected by cutaneous malignant melanoma (CMM). We therefore sequenced exons 1alpha and 2 of CDKN2A using lymphocyte DNA isolated from index cases from 67 families with cancers at multiple sites, where the patterns of cancer did not resemble those attributable to known genes such as hMLH1, hMLH2, BRCA1, BRCA2, TP53 or other cancer susceptibility genes. We found one mutation, a mis-sense mutation resulting in a methionine to isoleucine change at codon 53 (M531) of exon 2. The individual tested had developed 2 CMMs but had no dysplastic nevi and lacked a family history of dysplastic nevi or CMM. Other family members had been diagnosed with oral cancer (2 persons), bladder cancer (1 person) and possibly gall-bladder cancer. While this mutation has been reported in Australian and North American melanoma kindreds, we did not observe it in 618 chromosomes from Scottish and Canadian controls. Functional studies revealed that the CDKN2A variant carrying the M531 change was unable to bind effectively to CDK4, showing that this mutation is of pathological significance. Our results have confirmed that CDKN2A mutations are not limited to FAMMM kindreds but also demonstrate that multi-site cancer families without melanoma are very unlikely to contain CDKN2A mutations.

Deletion mapping suggests that the 1p22 melanoma susceptibility gene is a tumor suppressor localized to a 9-Mb interval

Loss of the short arm of chromosome 1 is frequently observed in many tumor types, including melanoma. We recently localized a third melanoma susceptibility locus to chromosome band 1p22. Critical recombinants in linked families localized the gene to a 15-Mb region between D1S430 and D1S2664. To map the locus more finely we have performed studies to assess allelic loss across the region in a panel of melanomas from 1p22-linked families, sporadic melanomas, and melanoma cell lines. Eighty percent of familial melanomas exhibited loss of heterozygosity (LOH) within the region, with a smallest region of overlapping deletions (SRO) of 9 Mb between D1S207 and D1S435. This high frequency of LOH makes it very likely that the susceptibility locus is a tumor suppressor. In sporadic tumors, four SROs were defined. SRO1 and SRO2 map within the critical recombinant and familial tumor region, indicating that one or the other is likely to harbor the susceptibility gene. However, SRO3 may also be significant because it overlaps with the markers with the highest 2-point LOD score (D1S2776), part of the linkage recombinant region, and the critical region defined in mesothelioma. The candidate genes PRKCL2 and GTF2B, within SRO2, and TGFBR3, CDC7, and EVI5, in a broad region encompassing SRO3, were screened in 1p22-linked melanoma kindreds, but no coding mutations were detected. Allelic loss in melanoma cell lines was significantly less frequent than in fresh tumors, indicating that this gene may not be involved late in progression, such as in overriding cellular senescence, necessary for the propagation of melanoma cells in culture.

Drink driving after the first offence: Characteristics of offenders who continue to drink and drive

Drink driving remains a significant problem on Australian roads, with about a quarter to a third of fatal crashes involving drivers or riders who have a BAC of 0.05 or greater. Last available data in the state of Queensland (2003) of the major factors involved in road fatalities and injuries indicated that alcohol and drugs were noted as one of the contributing factors in 38% of fatalities and 11% of all crashes, making it the highest single contributing factor to road fatalities. Until this point, there has been little information about first time offenders as a group, but it is known that offenders typically are not first time drink drivers but rather ‘first time apprehended’, in that most have engaged in drink driving in the years leading to the first offence. This paper follows 89 first time drink driving offenders who were interviewed at the time of court mention and followed up around 6 months following the court hearing. Of the offenders, 27% reported to have driven over the limit in the time between initial contact and follow up. The paper demonstrates the characteristics and offending patterns of first offenders who engaged in drink driving following conviction and those who didn’t, providing suggestions on how to target those at high risk for the behaviour and subsequent offending.

Refusal of medical treatment : a child's prerogative?

Society has a need for children to be able to make health care decisions. Homeless children need access to health care. Parents may not be accessible or competent to consent to their child’s health care. The familial relationship may have broken down. Children may not want their parents to know about drug, alcohol or pregnancy related issues. There is legal and academic support for the right of children to make autonomous decisions with respect to their health care. However what these decisions cover and who can make them is not clear. Whether or not a minor has capacity and is therefore competent to consent to medical treatment is a question of law. Some states of Australia have enacted legislation, while others rely on the common law to determine this issue. At common law a minor is capable of giving consent to medical treatment when he or she achieves a sufficient understanding and intelligence to be able to understand fully what is proposed. Known as ‘Gillick competence’ this is a well known principle of law. The question posed by this paper is whether the decision of a ‘Gillick competent’ child can and should be overridden by the court?

Tragic tale of Surachai

The Tragic Tale of Surachai tells the story of a young man in Thailand who suffers a near fatal motorcycle accident and the impact this event has upon his life after he is left a quadriplegic. This film was developed to raise discussion amongst students studying social work and human services at Queensland University of Technology.

Winds of Change

Winds of Change is a short film that contrasts the Tragic Tale of Surachai by tracing the life of a rural Australian man who is left a quadriplegic after a near fatal motorcycle accident. The film highlights issues confronting people living with a disability and its impact on family. This film was developed to raise discussion amongst students studying social work and human services at Queensland University of Technology.

An exploration of the reasons why adolescents engage in traditional and cyber bullying

This study explored the reasons underlying adolescents’ perceptions of why their peers engage in bullying in the real and the cyber world. While there has been much research on why bullies engage in such behaviour, ranging from personality characteristics to social or familial reasons, the perceptions of young people on the motives of cyberbullies has not been researched. A new instrument, based on interviews and a literature review was piloted to measure young people’s perceptions of why their peers engage in both traditional and cyberbullying behaviour, according to their role in bullying. Four hundred students were surveyed in three co-educational independent secondary schools. A comparison between perceptions of bullies’ motives in traditional and cyberbullying was made. Implications for interventions with bullies are discussed.

A comparison of the psychological, social, and legal factors contributing to speeding and drink driving behaviour

Within Australia, motor vehicle injury is the leading cause of hospital admissions and fatalities. Road crash data reveals that among the factors contributing to crashes in Queensland, speed and alcohol continue to be overrepresented. While alcohol is the number one contributing factor to fatal crashes, speeding also contributes to a high proportion of crashes. Research indicates that risky driving is an important contributor to road crashes. However, it has been debated whether all risky driving behaviours are similar enough to be explained by the same combination of factors. Further, road safety authorities have traditionally relied upon deterrence based countermeasures to reduce the incidence of illegal driving behaviours such as speeding and drink driving. However, more recent research has focussed on social factors to explain illegal driving behaviours. The purpose of this research was to examine and compare the psychological, legal, and social factors contributing to two illegal driving behaviours: exceeding the posted speed limit and driving when over the legal blood alcohol concentration (BAC) for the drivers licence type. Complementary theoretical perspectives were chosen to comprehensively examine these two behaviours including Akers’ social learning theory, Stafford and Warr’s expanded deterrence theory, and personality perspectives encompassing alcohol misuse, sensation seeking, and Type-A behaviour pattern. The program of research consisted of two phases: a preliminary pilot study, and the main quantitative phase. The preliminary pilot study was undertaken to inform the development of the quantitative study and to ensure the clarity of the theoretical constructs operationalised in this research. Semi-structured interviews were conducted with 11 Queensland drivers recruited from Queensland Transport Licensing Centres and Queensland University of Technology (QUT). These interviews demonstrated that the majority of participants had engaged in at least one of the behaviours, or knew of someone who had. It was also found among these drivers that the social environment in which both behaviours operated, including family and friends, and the social rewards and punishments associated with the behaviours, are important in their decision making. The main quantitative phase of the research involved a cross-sectional survey of 547 Queensland licensed drivers. The aim of this study was to determine the relationship between speeding and drink driving and whether there were any similarities or differences in the factors that contribute to a driver’s decision to engage in one or the other. A comparison of the participants self-reported speeding and self-reported drink driving behaviour demonstrated that there was a weak positive association between these two behaviours. Further, participants reported engaging in more frequent speeding at both low (i.e., up to 10 kilometres per hour) and high (i.e., 10 kilometres per hour or more) levels, than engaging in drink driving behaviour. It was noted that those who indicated they drove when they may be over the legal limit for their licence type, more frequently exceeded the posted speed limit by 10 kilometres per hour or more than those who complied with the regulatory limits for drink driving. A series of regression analyses were conducted to investigate the factors that predict self-reported speeding, self-reported drink driving, and the preparedness to engage in both behaviours. In relation to self-reported speeding (n = 465), it was found that among the sociodemographic and person-related factors, younger drivers and those who score high on measures of sensation seeking were more likely to report exceeding the posted speed limit. In addition, among the legal and psychosocial factors it was observed that direct exposure to punishment (i.e., being detected by police), direct punishment avoidance (i.e., engaging in an illegal driving behaviour and not being detected by police), personal definitions (i.e., personal orientation or attitudes toward the behaviour), both the normative and behavioural dimensions of differential association (i.e., refers to both the orientation or attitude of their friends and family, as well as the behaviour of these individuals), and anticipated punishments were significant predictors of self-reported speeding. It was interesting to note that associating with significant others who held unfavourable definitions towards speeding (the normative dimension of differential association) and anticipating punishments from others were both significant predictors of a reduction in self-reported speeding. In relation to self-reported drink driving (n = 462), a logistic regression analysis indicated that there were a number of significant predictors which increased the likelihood of whether participants had driven in the last six months when they thought they may have been over the legal alcohol limit. These included: experiences of direct punishment avoidance; having a family member convicted of drink driving; higher levels of Type-A behaviour pattern; greater alcohol misuse (as measured by the AUDIT); and the normative dimension of differential association (i.e., associating with others who held favourable attitudes to drink driving). A final logistic regression analysis examined the predictors of whether the participants reported engaging in both drink driving and speeding versus those who reported engaging in only speeding (the more common of the two behaviours) (n = 465). It was found that experiences of punishment avoidance for speeding decreased the likelihood of engaging in both speeding and drink driving; whereas in the case of drink driving, direct punishment avoidance increased the likelihood of engaging in both behaviours. It was also noted that holding favourable personal definitions toward speeding and drink driving, as well as higher levels of on Type-A behaviour pattern, and greater alcohol misuse significantly increased the likelihood of engaging in both speeding and drink driving. This research has demonstrated that the compliance with the regulatory limits was much higher for drink driving than it was for speeding. It is acknowledged that while speed limits are a fundamental component of speed management practices in Australia, the countermeasures applied to both speeding and drink driving do not appear to elicit the same level of compliance across the driving population. Further, the findings suggest that while the principles underpinning the current regime of deterrence based countermeasures are sound, current enforcement practices are insufficient to force compliance among the driving population, particularly in the case of speeding. Future research should further examine the degree of overlap between speeding and drink driving behaviour and whether punishment avoidance experiences for a specific illegal driving behaviour serve to undermine the deterrent effect of countermeasures aimed at reducing the incidence of another illegal driving behaviour. Furthermore, future work should seek to understand the factors which predict engaging in speeding and drink driving behaviours at the same time. Speeding has shown itself to be a pervasive and persistent behaviour, hence it would be useful to examine why road safety authorities have been successful in convincing the majority of drivers of the dangers of drink driving, but not those associated with speeding. In conclusion, the challenge for road safety practitioners will be to convince drivers that speeding and drink driving are equally risky behaviours, with the ultimate goal to reduce the prevalence of both behaviours.

The role of insulin and IGF2 signalling on metabolic pathways in prostate cancer progression

Prostate cancer (CaP) is the most commonly diagnosed cancer in males in Australia, North America, and Europe. If found early and locally confined, CaP can be treated with radical prostatectomy or radiation therapy; however, 25-40% patients will relapse and go on to advanced disease. The most common therapy in these cases is androgen deprivation therapy (ADT), which suppresses androgen production from the testis. Lack of the testicular androgen supply causes cells of the prostate to undergo apoptosis. However, in some cases the regression initially seen with ADT eventually gives way to a growth of a population of cancerous cells that no longer require testicular androgens. This phenotype is essentially fatal and is termed castrate resistant prostate cancer (CRPC). In addition to eventual regression, there are many undesirable side effects which accompany ADT, including development of a metabolic syndrome, which is defined by the U.S. National Library of Medicine as “a combination of medical disorders that increase the risk of developing cardiovascular disease and diabetes.” This project will focus on the effect of ADT induced hyperinsulinemia, as mimicked by treating androgen receptor positive CaP cells with insulin in a serum (hormone) deprived environment. While this side effect is not widely explored, in this thesis it is demonstrated for the first time that insulin upregulates pathways important to CaP progression. Our group has previously shown that during CaP progression, the enzymes necessary for de novo steroidogenesis are upregulated in the LNCaP xenograft model, total steroid levels are increased in tumours compared to pre castrate levels, and de novo steroidogenesis from radio-labelled acetate has been demonstrated. Because of the CaP dependence on AR for survival, we and other groups believe that CaP cells carry out de novo steroidogenesis to survive in androgen deprived conditions. Because (a) men on ADT often develop metabolic syndrome, and (b) men with lifestyle-induced obesity and hyperinsulinemia have worse prognosis and faster disease progression, and because (c) insulin causes steroidogenesis in other cell lines, the hypothesis that insulin may contribute to CaP progression through upregulation of steroidogenesis was explored. Insulin upregulates steroidogenesis enzymes at the mRNA level in three AR positive cell lines, as well as upregulating these enzymes at the protein level in two cell lines. It has also been demonstrated that insulin increases mitochondrial (functional) levels of steroid acute regulatory protein (StAR). Furthermore, insulin causes increased levels of total steroids in and induction of de novo steroid synthesis by insulin has been demonstrated at levels induced sufficient to activate AR. The effect of insulin analogs on CaP steroidogenesis in LNCaP and VCaP cells has also been investigated because epidemiological studies suggest that some of the analogs developed may have more cancer stimulatory effects than normal insulin. In this project, despite the signalling differences between glargine, X10, and insulin, these analogs did not appear to induce steroidogenesis any more potently that normal insulin. The effect of insulin of MCF7breast cancer cells was also investigated with results suggesting that breast cancer cells may be capable of de novo steroidogenesis, and that increase in estradiol production may be exacerbated by insulin. Insulin has also been long known to stimulate lipogenesis in the liver and adipocytes, and has been demonstrated to increase lipogenesis in breast cancer cells; therefore, investigation of the effect of insulin on lipogenesis, which is a hallmark of aggressive cancers, was investigated. In CaP progression sterol regulatory element binding protein (SREBP) is dysregulated and upregulates fatty acid synthase (FASN), acetyl CoA-carboxylase, and other lipogenesis genes. SREBP is important for steroidogenesis and in this project has been shown to be upregulated by insulin in CaP cells. Fatty acid synthesis provides building blocks of membrane growth, provides substrates for acid oxidation, the main energy source for CaP cells, provides building blocks for anti-apoptotic and proinflammatory molecules, and provides molecules that stimulate steroidogenesis. In this project it has been shown that insulin upregulates FASN and ACC, which synthesize fatty acids, as well as upregulating hormone sensitive lipase (HSL), diazepam-binding inhibitor (DBI), and long-chain acyl-CoA synthetase 3 (ACSL3), which contribute to lipid activation of steroidogenesis. Insulin also upregulates total lipid levels and de novo lipogenesis, which can be suppressed by inhibition of the insulin receptor (INSR). The fatty acids synthesized after insulin treatment are those that have been associated with CaP; furthermore, microarray data suggests insulin may upregulate fatty acid biosynthesis, metabolism and arachidonic acid metabolism pathways, which have been implicated in CaP growth and survival. Pharmacological agents used to treat patients with hyperinsulinemia/ hyperlipidemia have gained much interest in regards to CaP risk and treatment; however, the scientific rationale behind these clinical applications has not been examined. This thesis explores whether the use of metformin or simvastatin would decrease either lipogenesis or steroidogenesis or both in CaP cells. Simvastatin is a 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) inhibitor, which blocks synthesis of cholesterol, the building block of steroids/ androgens. It has also been postulated to down regulate SREBP in other metabolic disorders. It has been shown in this thesis, in LNCaP cells, that simvastatin inhibited and decreased insulin induced steroidogenesis and lipogenesis, respectively, but increased these pathways in the absence of insulin. Conversely, metformin, which activates AMP-activated protein kinase (AMPK) to shut down lipogenesis, cholesterol synthesis, and protein synthesis, highly suppresses both steroidogenesis and lipogenesis in the presence and absence of insulin. Lastly, because it has been demonstrated to increase steroidogenesis in other cell lines, and because the elucidation of any factors affecting steroidogenesis is important to understanding CaP, the effect of IGF2 on steroidogenesis in CaP cells was investigated. In patient samples, as men progress to CRPC, IGF2 mRNA and the protein levels of the receptors it may signal through are upregulated. It has also been demonstrated that IGF2 upregulates steroidogenic enzymes at both the mRNA and protein levels in LNCaP cells, increases intracellular and secreted steroid/androgen levels in LNCaPs to levels sufficient to stimulate the AR, and upregulated de novo steroidogenesis in LNCaPs and VCaPs. As well, inhibition of INSR and insulin-like growth factor 1 receptor (IGF1R), which IGF2 signals through, suggests that induction of steroidogenesis may be occurring predominantly through IGF1R. In summary, this project has illuminated for the first time that insulin is likely to play a large role in cancer progression, through upregulation of the steroidogenesis and lipogenesis pathways at the mRNA and protein levels, and production levels, and demonstrates a novel role for IGF-II in CaP progression through stimulation of steroidogenesis. It has also been demonstrated that metformin and simvastatin drugs may be useful in suppressing the insulin induction of these pathways. This project affirms the pathways by which ADT- induced metabolic syndrome may exacerbate CaP progression and strongly suggests that the monitoring and modulation of the metabolic state of CaP patients could have a strong impact on their therapeutic outcomes.

Cardiac ARIA Index: Measuring Accessibility to Cardiovascular Services in Rural and Remote Australia via Applied Geographic Spatial Technology

Cardiovascular disease (CVD) continues to impose a heavy burden in terms of cost, disability and death in Australia. Evidence suggests that increasing remoteness, where cardiac services are scarce, is linked to an increased risk of dying from CVD. Fatal CVD events are reported to be between 20% and 50% higher in rural areas compared to major cities. The Cardiac ARIA project, with its extensive use of geographic Information Systems (GIS), ranks each of Australia’s 20,387 urban, rural and remote population centres by accessibility to essential services or resources for the management of a cardiac event. This unique, innovative and highly collaborative project delivers a powerful tool to highlight and combat the burden imposed by cardiovascular disease (CVD) in Australia. Cardiac ARIA is innovative. It is a model that could be applied internationally and to other acute and chronic conditions such as mental health, midwifery, cancer, respiratory, diabetes and burns services. Cardiac ARIA was designed to: 1. Determine by expert panel, what were the minimal services and resources required for the management of a cardiac event in any urban, rural or remote population locations in Australia using a single patient pathway to access care. 2. Derive a classification using GIS accessibility modelling for each of Australia’s 20,387 urban, rural and remote population locations. 3. Compare the Cardiac ARIA categories and population locations with census derived population characteristics. Key findings are as follows: • In the event of a cardiac emergency, the majority of Australians had very good access to cardiac services. Approximately 71% or 13.9 million people lived within one hour of a category one hospital. • 68% of older Australians lived within one hour of a category one hospital (Principal Referral Hospital with access to Cardiac Catheterisation). • Only 40% of indigenous people lived within one hour of the category one hospital. • 16% (74000) of indigenous people lived more than one hour from a hospital. • 3% (91,000) of people 65 years of age or older lived more than one hour from any hospital or clinic. • Approximately 96%, or 19 million, of people lived within one hour of the four key services to support cardiac rehabilitation and secondary prevention. • 75% of indigenous people lived within one hour of the four cardiac rehabilitation services to support cardiac rehabilitation and secondary prevention. Fourteen percent (64,000 persons) indigenous people had poor access to the four key services to support cardiac rehabilitation and secondary prevention. • 12% (56,000) of indigenous people were more than one hour from a hospital and only had access one the four key services (usually a medical service) to support cardiac rehabilitation and secondary prevention.