11 resultados para Noël, Francine

em Deakin Research Online - Australia


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Background: Asthma is one of the most common reasons for paediatric admissions to hospital, with substantial cost to the community. There is some evidence to suggest that many hospital admissions could be prevented with effective education about asthma and its management.
Objectives: To conduct a systematic review of the literature in order to identify whether asthma education leads to improved health outcomes in children who have attended the emergency department for asthma.
Search strategy
: We searched the Cochrane Airways Group trials register, including MEDLINE, EMBASE, and CINAHL databases, and reference lists of trials and review articles.
Selection criteria
: Randomised controlled trials or controlled clinical trials of asthma education for children who had attended the emergency department for asthma, with or without hospitalisation, within the previous 12 months. Data collection and analysis:Two reviewers independently assessed trial quality and extracted data. Study authors were contacted for additional information.
Main results: Eight trials involving 1407 patients were included, in all the education was provided by nurses or researchers. Compared to control (usual care or lower intensity education) education did not reduce subsequent emergency department (ED) visits [4 trials; relative risk (RR)= 0.87, 95% confidence interval (CI) 0.37 to 2.08], hospital admissions [5 trials; RR=0.74, 95% CI 0.38 to 1.46] and unscheduled doctor visits [5 trials; RR= 0.74, 95% CI 0.49 to 1.12). Each analysis showed evidence of heterogeneity among the studies (P<0.01). Subgroup analyses by the overall difference in scale of intervention between treatment and control groups (comprehensive programme versus information only) or the timing of the intervention/recruitment (early versus delayed) gave similar results to the main analysis and still revealed significant heterogeneity between trials. Authors' conclusions: On the basis of the published trials, there is no firm evidence to support the use of asthma education for children who have attended the emergency department for asthma as a means of reducing subsequent ED visits, hospital admissions or unscheduled doctor visits. Some trials appeared to show clear evidence of benefit, but reasons for differences between these and the negative studies is not clear. More research is required.

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The Spotted Bowerbird, Chlamydera maculata, appears to be sexually monomorphic. We caught and marked 118 birds in central Queensland, and sexed 88 using molecular methods. We found that our catch was strongly male-biased, both at bower sites and at non-bower feeding sites. We continued to observe the bird's behaviour after their release and so sub-divided males into sexual status groups as either bower-owners or non-owners. We searched for morphological measures, subjectively judged colour differences and quantitatively collected spectral measures of the visual properties of the crest feathers that would allow us to separate birds of differing sex and status. We found that bower owners had larger crests than non-owner males or females and that crest area provided the most accurate predictor of a bird's sex and status in a discriminant function analysis. We studied a cohort of seven males who went from non-owners to bower owners over three years, and found that their change in status was accompanied by a change in crest size – the only significant change in their morphology. Crest size did not relate to the mating success of a bower-owner. Instead, we suggest why the crest may differ between status groups and the implications that this may have for the sexual behaviour of male and female Spotted Bowerbirds.

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The article focuses on the public–private divide in law and which organizes principles for and governance. It analyzes the governance model of public–private divide regarding for climate change adaptation in context to a case study of water governance and flood risk. It compares the relationship between state and individual laws which helps in policy setting.

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Short telomeres are associated with increased risk of cardiovascular disease. Here we studied cardiomyocyte telomere length at key ages during the ontogeny of cardiac hypertrophy and failure in the hypertrophic heart rat (HHR), and compared these with the normal heart rat (NHR) control strain. Key ages corresponded with the pathophysiological sequence beginning with fewer cardiomyocytes (2-days), leading to left ventricular hypertrophy (LVH) (13-weeks) and subsequently progression to heart failure (38-weeks). We measured telomere length, tissue activity of telomerase, mRNA levels of telomerase reverse transcriptase (Tert) and telomerase RNA component (Terc), and expression of the telomeric regulator microRNA miR-34a. Cardiac telomere length was longer in the HHR compared to the control strain at 2-days and 38-weeks, but shorter at 13-weeks. Neonatal HHR had higher cardiac telomerase activity and expression of Tert and miR-34a. Telomerase activity was not different at 13- or 38-weeks. Tert mRNA and Terc RNA were over-expressed at 38-weeks, while miR-34a was over-expressed at 13-weeks but down-regulated at 38-weeks. Circulating leukocytes were strongly correlated with cardiac telomere length in the HHR only. The longer neonatal telomeres in HHR are likely to reflect fewer foetal and early postnatal cardiomyocyte cell divisions and explain the reduced total cardiomyocyte complement that predisposes to later hypertrophy and failure. Although shorter telomeres were a feature of cardiac hypertrophy at 13-weeks, they were not present at the progression to heart failure at 38-weeks.

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BACKGROUND: Left ventricular (LV) hypertrophy is a risk factor for cardiovascular death, but the genetic factors determining LV size and predisposition to hypertrophy are not well understood. We have previously linked the quantitative trait locus cardiac mass 22 (Cm22) on chromosome 2 with cardiac hypertrophy independent of blood pressure in the spontaneously hypertensive rat. From an original cross of spontaneously hypertensive rat with F344 rats, we derived a normotensive polygenic model of spontaneous cardiac hypertrophy, the hypertrophic heart rat (HHR) and its control strain, the normal heart rat (NHR).

METHODS AND RESULTS: To identify the genes and molecular mechanisms underlying spontaneous LV hypertrophy we sequenced the HHR genome with special focus on quantitative trait locus Cm22. For correlative analyses of function, we measured global RNA transcripts in LV of neonatal HHR and NHR and 198 neonatal rats of an HHR × NHR F2 crossbred population. Only one gene within locus Cm22 was differentially expressed in the parental generation: tripartite motif-containing 55 (Trim55), with mRNA downregulation in HHR (P < 0.05) and reduced protein expression. Trim55 mRNA levels were negatively correlated with LV mass in the F2 cross (r = -0.16, P = 0.025). In exon nine of Trim55 in HHR, we found one missense mutation that functionally alters protein structure. This mutation was strongly associated with Trim55 mRNA expression in F2 rats (F = 10.35, P < 0.0001). Similarly, in humans, we found reduced Trim55 expression in hearts of subjects with idiopathic dilated cardiomyopathy.

CONCLUSION: Our study suggests that the Trim55 gene, located in Cm22, is a novel candidate gene for polygenic LV hypertrophy independent of blood pressure.