631 resultados para at risk populations
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This essay examines the possibilities for practices that appeal to the primitive in the contemporary cultural context. The idea of the primitive is driven by a desire to challenge the limitations of Western culture, while at the same time attracting the charge of promoting Eurocentrism. This essay investigates this double risk and how artists have sought to evade it, confound it, or accentuate it.
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The future on-road safety of drivers affected by Whiplash Associated Disorder (WAD), the most common soft-tissue injury suffered in a traffic crash, has not been extensively explored. We obtained an anonymised file of 4280 insurance claimants with WAD and, as controls, 1116 claimants with comparably severe soft-tissue injuries who are considered to be at no increased risk than the general population. Their demographic information, road user type and traffic crash records both prior and subsequent to the traffic incident in which the injury occurred, the index crash, were obtained. Rates of subsequent crash involvement in these two groups were then compared, adjusting for age, sex, road user type and prior crash experience. The risk of a subsequent crash in the WAD group relative to controls was 1.14 (95% confidence interval, 0.87–1.48). To allow for differentially altered driving exposure after index crash we distributed a brief survey asking about changes in driving habits after a traffic crash involving injury via physiotherapy clinics and online through the electronic newsletter of a local motoring organisation. The survey yielded responses from 113 drivers who had experienced WAD in a traffic crash and 53 with other soft tissue injuries. There were no differences on average between the groups in their prior driving levels or their percentage change therein at one, three or six months after injury. There was thus no evidence that drivers with WAD are at any higher safety risk than drivers with other types of relatively minor post-crash soft tissue injury.
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BACKGROUND Mosquito-borne diseases are climate sensitive and there has been increasing concern over the impact of climate change on future disease risk. This paper projected the potential future risk of Barmah Forest virus (BFV) disease under climate change scenarios in Queensland, Australia. METHODS/PRINCIPAL FINDINGS We obtained data on notified BFV cases, climate (maximum and minimum temperature and rainfall), socio-economic and tidal conditions for current period 2000-2008 for coastal regions in Queensland. Grid-data on future climate projections for 2025, 2050 and 2100 were also obtained. Logistic regression models were built to forecast the otential risk of BFV disease distribution under existing climatic, socio-economic and tidal conditions. The model was applied to estimate the potential geographic distribution of BFV outbreaks under climate change scenarios. The predictive model had good model accuracy, sensitivity and specificity. Maps on potential risk of future BFV disease indicated that disease would vary significantly across coastal regions in Queensland by 2100 due to marked differences in future rainfall and temperature projections. CONCLUSIONS/SIGNIFICANCE We conclude that the results of this study demonstrate that the future risk of BFV disease would vary across coastal regions in Queensland. These results may be helpful for public health decision making towards developing effective risk management strategies for BFV disease control and prevention programs in Queensland.
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Fibrogenic stresses promote progression of renal tubulointerstitial fibrosis, disparately affecting survival, proliferation and trans-differentiation of intrinsic renal cell populations through ill-defined biomolecular pathways. We investigated the effect of fibrogenic stresses on the activation of cell-specific mitogen-activated protein kinase (MAPK) in renal fibroblast, epithelial and endothelial cell populations. The relative outcomes (cell death, proliferation, trans-differentiation) associated with activation or inhibition of extracellular-regulated protein kinase (ERK) or stress activated/c-Jun N terminal kinase (JNK) were analysed in each renal cell population after challenge with oxidative stress (1 mmol/L H2O2), transforming growth factor-beta1 (TGF-beta1, 10 ng/mL) or tumour necrosis factor-alpha (TNF-alpha, 50 ng/mL) over 0-20 h. Apoptosis increased significantly in all cell types after oxidative stress (P < 0.05). In fibroblasts, oxidative stress caused the activation of ERK (pERK) but not JNK (pJNK). Inhibition of ERK by PD98059 supported its role in a fibroblast death pathway. In epithelial and endothelial cells, oxidative stress-induced apoptosis was preceded by early induction of pERK, but its inhibition did not support a pro-apoptotic role. Early ERK activity may be conducive to their survival or promote the trans-differentiation of epithelial cells. In epithelial and endothelial cells, oxidative stress induced pJNK acutely. Pretreatment with SP600125 (JNK inhibitor) verified its pro-apoptotic activity only in epithelial cells. Transforming growth factor-beta1 did not significantly alter mitosis or apoptosis in any of the cell types, nor did it alter MAPK activity. Tumor necrosis factor-alpha caused increased apoptosis with no associated change in MAPK activity. Our results demonstrate renal cell-specific differences in the activation of ERK and JNK following fibrotic insult, which may be useful for targeting excessive fibroblast proliferation in chronic fibrosis.
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OBJECTIVES To investigate and describe the relationship between indigenous Australian populations, residential aged care services, and community-onset Staphylococcus aureus bacteremia (SAB) among patients admitted to public hospitals in Queensland, Australia. DESIGN Ecological study. METHODS We used administrative healthcare data linked to microbiology results from patients with SAB admitted to Queensland public hospitals from 2005 through 2010 to identify community-onset infections. Data about indigenous Australian population and residential aged care services at the local government area level were obtained from the Queensland Office of Economic and Statistical Research. Associations between community-onset SAB and indigenous Australian population and residential aged care services were calculated using Poisson regression models in a Bayesian framework. Choropleth maps were used to describe the spatial patterns of SAB risk. RESULTS We observed a 21% increase in relative risk (RR) of bacteremia with methicillin-susceptible S. aureus (MSSA; RR, 1.21 [95% credible interval, 1.15-1.26]) and a 24% increase in RR with nonmultiresistant methicillin-resistant S. aureus (nmMRSA; RR, 1.24 [95% credible interval, 1.13-1.34]) with a 10% increase in the indigenous Australian population proportion. There was no significant association between RR of SAB and the number of residential aged care services. Areas with the highest RR for nmMRSA and MSSA bacteremia were identified in the northern and western regions of Queensland. CONCLUSIONS The RR of community-onset SAB varied spatially across Queensland. There was increased RR of community-onset SAB with nmMRSA and MSSA in areas of Queensland with increased indigenous population proportions. Additional research should be undertaken to understand other factors that increase the risk of infection due to this organism.
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Australian multicultural society consists of culturally and linguistically diverse (CALD) migrants, refugees and international students from different parts of the world. Despite hardships, these individuals show resilience and adapt successfully. However, there is a dearth of scales measuring these positive developments and personal strengths. The study describes the development and evaluation of a scale measuring resilience and acculturation of CALD people. Items were generated for the Acculturation and Resilience Scale (AARS).The AARS and other acculturation and psychological distress scales were administered to 225 CALD community members. Exploratory factor analyses resulted in a 27-item AARS with three subscales: Acculturation, Resilience, and Spirituality. The three-factor structure was subjected to a confirmatory factor analysis on a sample of 515 international students. The factor structure stability was upheld by the second sample. The psychometric properties were investigated using the two samples and demonstrated satisfactory internal consistency, test-retest reliability, and divergent validity. The scale addresses a major gap in the literature and can be used to measure the positive acculturation and resilience of the newly arrived and relocated individuals. Further research is warranted to examine the scale’s psychometric properties with migrants and refugees from a range of ethnic communities.
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Malaria has been a heavy social and health burden in the remote and poor areas in southern China. Analyses of malaria epidemic patterns can uncover important features of malaria transmission. This study identified spatial clusters, seasonal patterns, and geographic variations of malaria deaths at a county level in Yunnan, China, during 1991–2010. A discrete Poisson model was used to identify purely spatial clusters of malaria deaths. Logistic regression analysis was performed to detect changes in geographic patterns. The results show that malaria mortality had declined in Yunnan over the study period and the most likely spatial clusters (relative risk [RR] = 23.03–32.06, P < 0.001) of malaria deaths were identified in western Yunnan along the China–Myanmar border. The highest risk of malaria deaths occurred in autumn (RR = 58.91, P < 0.001) and summer (RR = 31.91, P < 0.001). The results suggested that the geographic distribution of malaria deaths was significantly changed with longitude, which indicated there was decreased mortality of malaria in eastern areas over the last two decades, although there was no significant change in latitude during the same period. Public health interventions should target populations in western Yunnan along border areas, especially focusing on floating populations crossing international borders.
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Background: Appropriate disposition of emergency department (ED) patients with chest pain is dependent on clinical evaluation of risk. A number of chest pain risk stratification tools have been proposed. The aim of this study was to compare the predictive performance for major adverse cardiac events (MACE) using risk assessment tools from the National Heart Foundation of Australia (HFA), the Goldman risk score and the Thrombolysis in Myocardial Infarction risk score (TIMI RS). Methods: This prospective observational study evaluated ED patients aged ≥30 years with non-traumatic chest pain for which no definitive non-ischemic cause was found. Data collected included demographic and clinical information, investigation findings and occurrence of MACE by 30 days. The outcome of interest was the comparative predictive performance of the risk tools for MACE at 30 days, as analyzed by receiver operator curves (ROC). Results: Two hundred eighty-one patients were studied; the rate of MACE was 14.1%. Area under the curve (AUC) of the HFA, TIMI RS and Goldman tools for the endpoint of MACE was 0.54, 0.71 and 0.67, respectively, with the difference between the tools in predictive ability for MACE being highly significant [chi2 (3) = 67.21, N = 276, p < 0.0001]. Conclusion: The TIMI RS and Goldman tools performed better than the HFA in this undifferentiated ED chest pain population, but selection of cutoffs balancing sensitivity and specificity was problematic. There is an urgent need for validated risk stratification tools specific for the ED chest pain population.
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OBJECTIVES: Four randomized phase II/III trials investigated the addition of cetuximab to platinum-based, first-line chemotherapy in patients with advanced non-small cell lung cancer (NSCLC). A meta-analysis was performed to examine the benefit/risk ratio for the addition of cetuximab to chemotherapy. MATERIALS AND METHODS: The meta-analysis included individual patient efficacy data from 2018 patients and individual patient safety data from 1970 patients comprising respectively the combined intention-to-treat and safety populations of the four trials. The effect of adding cetuximab to chemotherapy was measured by hazard ratios (HRs) obtained using a Cox proportional hazards model and odds ratios calculated by logistic regression. Survival rates at 1 year were calculated. All applied models were stratified by trial. Tests on heterogeneity of treatment effects across the trials and sensitivity analyses were performed for all endpoints. RESULTS: The meta-analysis demonstrated that the addition of cetuximab to chemotherapy significantly improved overall survival (HR 0.88, p=0.009, median 10.3 vs 9.4 months), progression-free survival (HR 0.90, p=0.045, median 4.7 vs 4.5 months) and response (odds ratio 1.46, p<0.001, overall response rate 32.2% vs 24.4%) compared with chemotherapy alone. The safety profile of chemotherapy plus cetuximab in the meta-analysis population was confirmed as manageable. Neither trials nor patient subgroups defined by key baseline characteristics showed significant heterogeneity for any endpoint. CONCLUSION: The addition of cetuximab to platinum-based, first-line chemotherapy for advanced NSCLC significantly improved outcome for all efficacy endpoints with an acceptable safety profile, indicating a favorable benefit/risk ratio.
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Indigenous Australians are among the most unhealthy populations in the world and yet they reside in a country where the non-Indigenous population enjoys high standards of well-being. Education has been identified as the key mechanism for closing this equity gap. At school commencement many Indigenous children are already at risk of disengagement. This four-year longitudinal study of two Indigenous boys from a socially marginalised community examined key factors affecting transitional trajectories into school. While child characteristics affected level of achievement the critical factors in sustaining positive educational engagement were social support, school practices, inclusion of family and positive expectation.
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Purpose To evaluate the association between retinal nerve fibre layer (RNFL) thickness and diabetic peripheral neuropathy in people with type 2 diabetes, and specifically those at higher risk of foot ulceration. Methods RNFL thicknesses was measured globally and in four quadrants (temporal, superior, nasal and inferior) at 3.45 mm diameter around the optic nerve head using optical coherence tomography (OCT). Severity of neuropathy was assessed using the Neuropathy Disability Score (NDS). Eighty-two participants with type 2 diabetes were stratified according to NDS scores (0-10) as: none, mild, moderate, and severe neuropathy. A control group was additionally included (n=17). Individuals with NDS≥ 6 (moderate and severe neuropathy) have been shown to be at higher risk of foot ulceration. A linear regression model was used to determine the association between RNFL and severity of neuropathy. Age, disease duration and diabetic retinopathy levels were fitted in the models. Independent t-test was employed for comparison between controls and the group without neuropathy, as well as for comparison between groups with higher and lower risk of foot ulceration. Analysis of variance was used to compare across all NDS groups. Results RNFL thickness was significantly associated with NDS in the inferior quadrant (b= -1.46, p=0.03). RNFL thicknesses globally and in superior, temporal and nasal quadrants did not show significant associations with NDS (all p>0.51). These findings were independent of the effect of age, disease duration and retinopathy. RNFL was thinner for the group with NDS ≥ 6 in all quadrants but was significant only inferiorly (p<0.005). RNFL for control participants was not significantly different from the group with diabetes and no neuropathy (superior p=0.07, global and all other quadrants: p>0.23). Mean RNFL thickness was not significantly different between the four NDS groups globally and in all quadrants (p=0.08 for inferior, P>0.14 for all other comparisons). Conclusions Retinal nerve fibre layer thinning is associated with neuropathy in people with type 2 diabetes. This relationship is strongest in the inferior retina and in individuals at higher risk of foot ulceration.
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Risk taking is central to human activity. Consequently, it lies at the focal point of behavioral sciences such as neuroscience, economics, and finance. Many influential models from these sciences assume that financial risk preferences form a stable trait. Is this assumption justified and, if not, what causes the appetite for risk to fluctuate? We have previously found that traders experience a sustained increase in the stress hormone cortisol when the amount of uncertainty, in the form of market volatility, increases. Here we ask whether these elevated cortisol levels shift risk preferences. Using a double-blind, placebo-controlled, cross-over protocol we raised cortisol levels in volunteers over eight days to the same extent previously observed in traders. We then tested for the utility and probability weighting functions underlying their risk taking, and found that participants became more risk averse. We also observed that the weighting of probabilities became more distorted among men relative to women. These results suggest that risk preferences are highly dynamic. Specifically, the stress response calibrates risk taking to our circumstances, reducing it in times of prolonged uncertainty, such as a financial crisis. Physiology-induced shifts in risk preferences may thus be an under-appreciated cause of market instability.
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Recent literature suggests that mesenchymal stem/stromal cells (MSC) could be used as Trojan Horses to deliver “death-signals” to cancer cells. Herein, we describe the development of a novel multichannel cell migration device, and use it to investigate the relative migration rates of bone marrow-derived MSC and breast cancer cells (MCF-7) towards each other. Confluent monolayers of MSC and MCF-7 were established in adjacent chambers separated by an array of 14 microchannels. Initially, culture chambers were isolated by air bubbles (air-valves) contained within each microchannel, and then bubbles were displaced to initiate the assay. The MCF-7 cells migrated preferentially towards MSC, whilst the MSC did not migrate preferentially towards the MCF-7 cells. Our results corroborate previous literature that suggests MSC migration towards cancer cells in vivo is in response to the associated inflammation rather than directly to signals secreted by the cancer cells themselves.
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BACKGROUND Experimental and epidemiologic evidence have suggested that chronic inflammation may play a critical role in endometrial carcinogenesis. METHODS To investigate this hypothesis, a two-stage study was carried out to evaluate single-nucleotide polymorphisms (SNP) in inflammatory pathway genes in association with endometrial cancer risk. In stage I, 64 candidate pathway genes were identified and 4,542 directly genotyped or imputed SNPs were analyzed among 832 endometrial cancer cases and 2,049 controls, using data from the Shanghai Endometrial Cancer Genetics Study. Linkage disequilibrium of stage I SNPs significantly associated with endometrial cancer (P < 0.05) indicated that the majority of associations could be linked to one of 24 distinct loci. One SNP from each of the 24 loci was then selected for follow-up genotyping. Of these, 21 SNPs were successfully designed and genotyped in stage II, which consisted of 10 additional studies including 6,604 endometrial cancer cases and 8,511 controls. RESULTS Five of the 21 SNPs had significant allelic odds ratios (ORs) and 95% confidence intervals (CI) as follows: FABP1, 0.92 (0.85-0.99); CXCL3, 1.16 (1.05-1.29); IL6, 1.08 (1.00-1.17); MSR1, 0.90 (0.82-0.98); and MMP9, 0.91 (0.87-0.97). Two of these polymorphisms were independently significant in the replication sample (rs352038 in CXCL3 and rs3918249 in MMP9). The association for the MMP9 polymorphism remained significant after Bonferroni correction and showed a significant association with endometrial cancer in both Asian- and European-ancestry samples. CONCLUSIONS These findings lend support to the hypothesis that genetic polymorphisms in genes involved in the inflammatory pathway may contribute to genetic susceptibility to endometrial cancer. Impact statement: This study adds to the growing evidence that inflammation plays an important role in endometrial carcinogenesis.