980 resultados para Consumer risk
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For a hundred years, since Federation, Australian consumers have suffered the indignity and the tragedy of price discrimination. From the time of imperial publishing networks, Australia has been suffered from cultural colonialism. In respect of pricing of copyright works, Australian consumers have been gouged; ripped-off; and exploited. Digital technologies have not necessarily brought an end to such price discrimination. Australian consumers have been locked out by technological protection measures; subject to surveillance, privacy intrusions and security breaches; locked into walled gardens by digital rights management systems; and geo-blocked.
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Background: Body mass index (BMI) is widely used as a measure of adiposity. However, currently used cut-off values are not sensitive in diagnosing obesity in South Asian populations. Aim: To define BMI and waist circumference (WC), cut-off values representing percentage fat mass (%FM) associated with adverse health outcomes. Subjects and methods: A cross-sectional descriptive study of 285 5–14 year old Sri Lankan children (56% boys) was carried out. Fat mass (FM) was assessed using the isotope (D2O) dilution technique based on 2C body composition model. BMI and WC cut-off values were defined based on %FM associated with adverse health outcomes. Results: Sri Lankan children had a low fat free mass index (FFMI) and a high fat mass index (FMI). Individuals with the same BMI had %FM distributed over a wide range. Lean body tissue grew very little with advancing age and weight gain was mainly due to increases in body fat. BMI corresponding to 25% in males and 35% in females at 18 years was 19.2 kg/m2 and 19.7 kg/m2, respectively. WC cut-off values for males and females were 68.4 cm and 70.4 cm, respectively. Conclusion: This chart analysis clearly confirms that Sri Lankan children have a high %FM from a young age. With age, more changes occur in FM than in fat free mass (FFM). Although the newly defined BMI and WC cut-off values appear to be quite low, they are comparable to some recent data obtained in similar populations.
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Our aim is to examine evidence-based strategies to motivate appropriate action and increase informed decision-making during the response and recovery phases of disasters. We combine expertise in communication, consumer psychology and marketing, disaster and emergency management, and law. This poster presents findings from a social media work package, and preliminary findings from the focus group work package on emergency warning message comprehension.
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BACKGROUND Hamstring strain injuries (HSIs) represent the most common cause of lost playing time in rugby union. Eccentric knee-flexor weakness and between-limb imbalance in eccentric knee-flexor strength are associated with a heightened risk of hamstring injury in other sports; however these variables have not been explored in rugby union. PURPOSE To determine if lower levels of eccentric knee-flexor strength or greater between-limb imbalance in this parameter during the Nordic hamstring exercise are risk-factors for hamstring strain injury in rugby union. STUDY DESIGN Cohort study; level of evidence, 3. METHODS This prospective study was conducted over the 2014 Super Rugby and Queensland Rugby Union seasons. In total, 178 rugby union players (age, 22.6 ± 3.8 years; height, 185 ± 6.8 cm; mass, 96.5 ± 13.1 kg) had their eccentric knee-flexor strength assessed using a custom-made device during the pre-season. Reports of previous hamstring, quadriceps, groin, calf and anterior cruciate ligament injury were also obtained. The main outcome measure was prospective occurrence of hamstring strain injury. RESULTS Twenty players suffered at least one hamstring strain during the study period. Players with a history of hamstring strain injury had 4.1 fold (RR = 4.1, 95% CI = 1.9 to 8.9, p = 0.001) greater risk of subsequent hamstring injury than players without such history. Between-limb imbalance in eccentric knee-flexor strength of ≥ 15% and ≥ 20% increased the risk of hamstring strain injury 2.4 fold (RR = 2.4, 95% CI = 1.1 to 5.5, p = 0.033) and 3.4 fold (RR = 3.4, 95% CI = 1.5 to 7.6, p = 0.003), respectively. Lower eccentric knee flexor strength and other prior injuries were not associated with increased risk of future hamstring strain. Multivariate logistic regression revealed that the risk of re-injury was augmented in players with strength imbalances. CONCLUSION Previous hamstring strain injury and between-limb imbalance in eccentric knee-flexor strength were associated with an increased risk of future hamstring strain injury in rugby union. These results support the rationale for reducing imbalance, particularly in players who have suffered a prior hamstring injury, to mitigate the risk of future injury.
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Hamstring strain injuries are the predominant injury in many sports, costing athletes and clubs a significant financial and performance burden. Therefore the ability to identify and intervene with individuals who are considered at a high risk of injury is important. One measure which has grown in popularity as an outcome variable following hamstring intervention/prevention studies and rehabilitation is the angle of peak knee flexor torque. This current opinion article will firstly introduce the measure and the processes behind it. Secondly, this article will summarise how the angle of peak knee flexor torque has been suggested to measure hamstring strain injury risk. Finally various limitations will be presented and outlined as to how they may influence the measure. These include the lack of muscle specificity, the common concentric contraction mode of assessment, reliability of the measure, various neural contributions (such as rate of force development and neuromuscular inhibition) as well as the lack of prospective data showing any predictive value in the measure.
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"The Australian Consumer Law came into operation on 1 January 2011 as a single national law. It replaced 17 different pieces of Commonwealth, State and Territory legislation relating to consumer protection. Its introduction meant that for the first time, consumers throughout Australia had the same rights and remedies and correspondingly, businesses had the same obligations and responsibilities towards consumers without the barrier of confusing and expensive local variations in the law. Australian Consumer Law: Commentary and Materials contains up-to-date material on the Australian Consumer Law, and in particular the fifth edition incorporates: a revised treatment of unconscionability, taking account of the changes to Part 2-2 of the ACL that became effective in 2012; other State and Federal provisions relating to unfair terms and cases such as Kakavas v Crown Melbourne, ACCC v Lux Distributors, Director of Consumer Affairs v Scully and PT Ltd v Spuds Surf; a comprehensive treatment of the impact of Google v ACCC, Forrest v ASIC and ACCC v TPG – the trilogy of decisions that provide the most recent insights into the High Court’s thinking on aspects of the prohibitions of misleading conduct in the ACL and the Corporations Act 2001; numerous decisions of note; and the possible impact of the Harper Review."--publisher website
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Osteoporotic fracture is a major cause of morbidity and mortality worldwide. Low bone mineral density (BMD) is a major predisposing factor to fracture and is known to be highly heritable. Site-, gender-, and age-specific genetic effects on BMD are thought to be significant, but have largely not been considered in the design of genome-wide association studies (GWAS) of BMD to date. We report here a GWAS using a novel study design focusing on women of a specific age (postmenopausal women, age 55-85 years), with either extreme high or low hip BMD (age- and gender-adjusted BMD z-scores of +1.5 to +4.0, n = 1055, or -4.0 to -1.5, n = 900), with replication in cohorts of women drawn from the general population (n = 20,898). The study replicates 21 of 26 known BMD-associated genes. Additionally, we report suggestive association of a further six new genetic associations in or around the genes CLCN7, GALNT3, IBSP, LTBP3, RSPO3, and SOX4, with replication in two independent datasets. A novel mouse model with a loss-of-function mutation in GALNT3 is also reported, which has high bone mass, supporting the involvement of this gene in BMD determination. In addition to identifying further genes associated with BMD, this study confirms the efficiency of extreme-truncate selection designs for quantitative trait association studies. © 2011 Duncan et al.
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We aimed to identify genetic variants associated with cortical bone thickness (CBT) and bone mineral density (BMD) by performing two separate genome-wide association study (GWAS) meta-analyses for CBT in 3 cohorts comprising 5,878 European subjects and for BMD in 5 cohorts comprising 5,672 individuals. We then assessed selected single-nucleotide polymorphisms (SNPs) for osteoporotic fracture in 2,023 cases and 3,740 controls. Association with CBT and forearm BMD was tested for ~2.5 million SNPs in each cohort separately, and results were meta-analyzed using fixed effect meta-analysis. We identified a missense SNP (Thr>Ile; rs2707466) located in the WNT16 gene (7q31), associated with CBT (effect size of -0.11 standard deviations [SD] per C allele, P = 6.2×10-9). This SNP, as well as another nonsynonymous SNP rs2908004 (Gly>Arg), also had genome-wide significant association with forearm BMD (-0.14 SD per C allele, P = 2.3×10-12, and -0.16 SD per G allele, P = 1.2×10-15, respectively). Four genome-wide significant SNPs arising from BMD meta-analysis were tested for association with forearm fracture. SNP rs7776725 in FAM3C, a gene adjacent to WNT16, was associated with a genome-wide significant increased risk of forearm fracture (OR = 1.33, P = 7.3×10-9), with genome-wide suggestive signals from the two missense variants in WNT16 (rs2908004: OR = 1.22, P = 4.9×10-6 and rs2707466: OR = 1.22, P = 7.2×10-6). We next generated a homozygous mouse with targeted disruption of Wnt16. Female Wnt16-/- mice had 27% (P<0.001) thinner cortical bones at the femur midshaft, and bone strength measures were reduced between 43%-61% (6.5×10-13<P<5.9×10-4) at both femur and tibia, compared with their wild-type littermates. Natural variation in humans and targeted disruption in mice demonstrate that WNT16 is an important determinant of CBT, BMD, bone strength, and risk of fracture. © 2012 Zheng et al.
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Human genetic and animal studies have implicated the costimulatory molecule CD40 in the development of multiple sclerosis (MS). We investigated the cell specific gene and protein expression variation controlled by the CD40 genetic variant(s) associated with MS, i.e. the T-allele at rs1883832. Previously we had shown that the risk allele is expressed at a lower level in whole blood, especially in people with MS. Here, we have defined the immune cell subsets responsible for genotype and disease effects on CD40 expression at the mRNA and protein level. In cell subsets in which CD40 is most highly expressed, B lymphocytes and dendritic cells, the MS-associated risk variant is associated with reduced CD40 cell-surface protein expression. In monocytes and dendritic cells, the risk allele additionally reduces the ratio of expression of full-length versus truncated CD40 mRNA, the latter encoding secreted CD40. We additionally show that MS patients, regardless of genotype, express significantly lower levels of CD40 cell-surface protein compared to unaffected controls in B lymphocytes. Thus, both genotype-dependent and independent down-regulation of cell-surface CD40 is a feature of MS. Lower expression of a co-stimulator of T cell activation, CD40, is therefore associated with increased MS risk despite the same CD40 variant being associated with reduced risk of other inflammatory autoimmune diseases. Our results highlight the complexity and likely individuality of autoimmune pathogenesis, and could be consistent with antiviral and/or immunoregulatory functions of CD40 playing an important role in protection from MS. © 2015 Field et al.
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Introduction Canadian C spine rule and NEXUS criteria have identified risk factors for cervical spine injury in adults but not for children. PECARN has developed an 8 variable model for cervical spine injury in children. We sought to identify the mechanism, prevalence of PECARN risk factors, injury patterns, and management of severe Paediatric cervical spine injuries presenting to the major children’s hospitals in Brisbane, Australia. Methods This a retrospective study of the children with cervical spine injuries who presented directly or were referred to the major children’s hospitals in Brisbane over 5 years. Results There were 38 patients with 18 male and 20 female.The mean age was 8.6 years. They were divided into two groups according to their age, (Group 1 < =8 years had 18 (47%) patients, while group 2 (9-15 years) had 20 (53%) patients. Motor vehicle related injuries were the most common (61%) in Group 1 while it was sporting injuries (50%) in group 2. All patients in group 1 had upper cervical injury (C0-C2) while subaxial injuries were most common in group 2 (66.6%). 82% of the patients had 2 or more PECARN risk factors. 18 children (47%) had normal neurological assessment at presentation, 6 (16%) had radicular symptoms, 11 (29%) could not be assessed as they had already been intubated due to the severity of the injury, 3 (8%) had incomplete cord injury. 29 (69%) patients had normal neurological assessment at final follow up and 2 children died from their injuries. Conclusion Our study confirms that younger children sustain upper cervical injuries most commonly secondary to motor vehicle accidents, while the older sustain subaxial injuries from sporting activities. The significant prevalence of the PECARN risk factors among this cohort of patients have led to them being incorporated into a protocol at these hospitals used to assess patients with suspected cervical spinal injury.
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Migraine has been defined as a common disabling primary headache disorder. Epidemiology studies have provided with the undeniable evidence of genetic components as active players in the development of the disease under a polygenic model in which multiple risk alleles exert modest individual effects. Our objective was to test the contribution of a polygenic effect to migraine risk in the Norfolk Island population using a panel of SNPs reported to be disease associated in published migraine GWAS. We also investigated whether individual SNPs were associated with gene expression levels measured in whole-blood. Polygenic scores were calculated in a total of 285 related individuals (74 cases, 211 controls) from the Norfolk Island using 51 SNPs previously reported to be associated with migraine in published GWAS. The association between polygenic score and migraine case-control status was tested using logistic regression. Results indicate that a migraine polygenic risk score was associated with migraine case-control status in this population (P=0.016). This supports the hypothesis that multiple SNPs with weak effects collectively contribute to migraine risk in this population. Amongst the SNPs included in the polygenic model, 4 were associated with the expression of the USMG5 gene, including rs171251 (P = 0.012). Results from this study provide evidence for a polygenic contribution to migraine risk in an isolated population and highlight specific SNPs that regulate the expression of USMG5, a gene critical for mitochondrial function.
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Objectives - It has long been suspected that susceptibility to ankylosing spondylitis (AS) is influenced by genes lying distant to the major histocompatibility complex. This study compares genetic models of AS to assess the most likely mode of inheritance, using recurrence risk ratios in relatives of affected subjects. Methods - Recurrence risk ratios in different degrees of relatives were determined using published data from studies specifically designed to address the question. The methods of Risch were used to determine the expected recurrence risk ratios in different degrees of relatives, assuming equal first degree relative recurrence risk between models. Goodness of fit was determined by χ2 comparison of the expected number of affected subjects with the observed number, given equal numbers of each type of relative studied. Results - The recurrence risks in different degrees of relatives were: monozygotic (MZ) twins 63% (17/27), first degree relatives 8.2% (441/5390), second degree relatives 1.0% (8/834), and third degree relatives 0.7% (7/997). Parent-child recurrence risk (7.9%, 37/466) was not significantly different from the sibling recurrence risk (8.2%, 404/4924), excluding a significant dominance genetic component to susceptibility. Poor fitting models included single gene, genetic heterogeneity, additive, two locus multiplicative, and one locus and residual polygenes (χ2 > 32 (two degrees of freedom), p < 10-6 for all models). The best fitting model studied was a five locus model with multiplicative interaction between loci (χ2 = 1.4 (two degrees of freedom), p = 0.5). Oligogenic multiplicative models were the best fitting over a range of population prevalences and first degree recurrence risk rates. Conclusions - This study suggests that of the genetic models tested, the most likely model operating in AS is an oligogenic model with predominantly multiplicative interaction between loci.