35 research outputs found

    Results from the Scottish report card on physical activity for children and youth

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    The Active Healthy Kids Scotland Report Card aims to consolidate existing evidence, facilitate international comparisons, encourage more evidence-informed physical activity and health policy, and improve surveillance of physical activity. Application of the Active Healthy Kids Canada Report Card process and methodology to Scotland, adapted to Scottish circumstances and availability of data. The Active Healthy Kids Scotland Report Card 2013 consists of indicators of 7 Health Behaviors and Outcomes and 3 Influences on Health Behaviors and Outcomes. Grades of F were assigned to Overall Physical Activity, Sedentary Behavior (recreational screen time), and Obesity Prevalence. A C was assigned to Active Transportation and a D- was assigned to Diet. Two indicators, Active and Outdoor Play and Organized Sport Participation, could not be graded. Among the Influences, Family Influence received a D, while Perceived Safety, Access, and Availability of Spaces for Physical Activity and the National Policy Environment graded more favorably with a B. The Active Healthy Kids Canada process and methodology was readily generalizable to Scotland. The report card illustrated low habitual physical activity and extremely high levels of screen-based sedentary behavior, and highlighted several opportunities for improved physical activity surveillance and promotion strategies

    The influence of the food environment on overweight and obesity in young children : a systematic review

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    The increasing prevalence of childhood obesity has led to interest in its prevention, particularly through school-based and family-based interventions in the early years. Most evidence reviews, to date, have focused on individual behaviour change rather than the ‘obesogenic environment’. This paper reviews the evidence on the influence of the food environment on overweight and obesity in children up to 8 years. Electronic databases (including MEDLINE, EMBASE, Cochrane Controlled Trials Register (CCTR), DARE, CINAHL and Psycho-Info) and reference lists of original studies and reviews were searched for all papers published up to 31 August 2011. Study designs included were either population-based intervention studies or a longitudinal study. Studies were included if the majority of the children studied were under 9 years, if they related to diet and if they focused on prevention rather than treatment in clinical settings. Data included in the tables were characteristics of participants, aim, and key outcome results. Quality assessment of the selected studies was carried out to identify potential bias and an evidence ranking exercise carried out to prioritise areas for future public health interventions. Thirty-five studies (twenty-five intervention studies and ten longitudinal studies) were selected for the review. There was moderately strong evidence to support interventions on food promotion, large portion sizes and sugar-sweetened soft drinks. Reducing food promotion to young children, increasing the availability of smaller portions and providing alternatives to sugar-sweetened soft drinks should be considered in obesity prevention programmes aimed at younger children. These environment-level interventions would support individual and family-level behaviour change

    Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

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    IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

    Coupling of autism genes to tissue-wide expression and dysfunction of synapse, calcium signalling and transcriptional regulation.

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    Autism Spectrum Disorder (ASD) is a heterogeneous disorder that is often accompanied with many co-morbidities. Recent genetic studies have identified various pathways from hundreds of candidate risk genes with varying levels of association to ASD. However, it is unknown which pathways are specific to the core symptoms or which are shared by the co-morbidities. We hypothesised that critical ASD candidates should appear widely across different scoring systems, and that comorbidity pathways should be constituted by genes expressed in the relevant tissues. We analysed the Simons Foundation for Autism Research Initiative (SFARI) database and four independently published scoring systems and identified 292 overlapping genes. We examined their mRNA expression using the Genotype-Tissue Expression (GTEx) database and validated protein expression levels using the human protein atlas (HPA) dataset. This led to clustering of the overlapping ASD genes into 2 groups; one with 91 genes primarily expressed in the central nervous system (CNS geneset) and another with 201 genes expressed in both CNS and peripheral tissues (CNS+PT geneset). Bioinformatic analyses showed a high enrichment of CNS development and synaptic transmission in the CNS geneset, and an enrichment of synapse, chromatin remodelling, gene regulation and endocrine signalling in the CNS+PT geneset. Calcium signalling and the glutamatergic synapse were found to be highly interconnected among pathways in the combined geneset. Our analyses demonstrate that 2/3 of ASD genes are expressed beyond the brain, which may impact peripheral function and involve in ASD co-morbidities, and relevant pathways may be explored for the treatment of ASD co-morbidities.Funding was provided by Science Foundation Ireland (Grant 13/IA/1787 to S.S. and L.G., 16/RC/3948 to FutureNeuro), and National University of Ireland Galway (Grant RSU002 to S.S.) for funding the research.peer-reviewe

    Coupling of autism genes to tissue-wide expression and dysfunction of synapse, calcium signalling and transcriptional regulation.

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    Autism Spectrum Disorder (ASD) is a heterogeneous disorder that is often accompanied with many co-morbidities. Recent genetic studies have identified various pathways from hundreds of candidate risk genes with varying levels of association to ASD. However, it is unknown which pathways are specific to the core symptoms or which are shared by the co-morbidities. We hypothesised that critical ASD candidates should appear widely across different scoring systems, and that comorbidity pathways should be constituted by genes expressed in the relevant tissues. We analysed the Simons Foundation for Autism Research Initiative (SFARI) database and four independently published scoring systems and identified 292 overlapping genes. We examined their mRNA expression using the Genotype-Tissue Expression (GTEx) database and validated protein expression levels using the human protein atlas (HPA) dataset. This led to clustering of the overlapping ASD genes into 2 groups; one with 91 genes primarily expressed in the central nervous system (CNS geneset) and another with 201 genes expressed in both CNS and peripheral tissues (CNS+PT geneset). Bioinformatic analyses showed a high enrichment of CNS development and synaptic transmission in the CNS geneset, and an enrichment of synapse, chromatin remodelling, gene regulation and endocrine signalling in the CNS+PT geneset. Calcium signalling and the glutamatergic synapse were found to be highly interconnected among pathways in the combined geneset. Our analyses demonstrate that 2/3 of ASD genes are expressed beyond the brain, which may impact peripheral function and involve in ASD co-morbidities, and relevant pathways may be explored for the treatment of ASD co-morbidities.Funding was provided by Science Foundation Ireland (Grant 13/IA/1787 to S.S. and L.G., 16/RC/3948 to FutureNeuro), and National University of Ireland Galway (Grant RSU002 to S.S.) for funding the research.peer-reviewe

    Coupling of autism genes to tissue-wide expression and dysfunction of synapse, calcium signalling and transcriptional regulation.

    Get PDF
    Autism Spectrum Disorder (ASD) is a heterogeneous disorder that is often accompanied with many co-morbidities. Recent genetic studies have identified various pathways from hundreds of candidate risk genes with varying levels of association to ASD. However, it is unknown which pathways are specific to the core symptoms or which are shared by the co-morbidities. We hypothesised that critical ASD candidates should appear widely across different scoring systems, and that comorbidity pathways should be constituted by genes expressed in the relevant tissues. We analysed the Simons Foundation for Autism Research Initiative (SFARI) database and four independently published scoring systems and identified 292 overlapping genes. We examined their mRNA expression using the Genotype-Tissue Expression (GTEx) database and validated protein expression levels using the human protein atlas (HPA) dataset. This led to clustering of the overlapping ASD genes into 2 groups; one with 91 genes primarily expressed in the central nervous system (CNS geneset) and another with 201 genes expressed in both CNS and peripheral tissues (CNS+PT geneset). Bioinformatic analyses showed a high enrichment of CNS development and synaptic transmission in the CNS geneset, and an enrichment of synapse, chromatin remodelling, gene regulation and endocrine signalling in the CNS+PT geneset. Calcium signalling and the glutamatergic synapse were found to be highly interconnected among pathways in the combined geneset. Our analyses demonstrate that 2/3 of ASD genes are expressed beyond the brain, which may impact peripheral function and involve in ASD co-morbidities, and relevant pathways may be explored for the treatment of ASD co-morbidities.Funding was provided by Science Foundation Ireland (Grant 13/IA/1787 to S.S. and L.G., 16/RC/3948 to FutureNeuro), and National University of Ireland Galway (Grant RSU002 to S.S.) for funding the research

    Results from Scotland’s 2016 report card on physical activity for children and youth

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    Background: The 2016 Active Healthy Kids Scotland Report Card aims to improve surveillance of physical activity (PA), facilitate international comparisons, and encourage evidence-informed PA and health policy. Methods: Active Healthy Kids Canada Report Card methodology was used: a search for data on child and adolescent PA and health published after the 2013 Scottish Report Card was carried out. Data sources were considered for grading if based on representative samples with prevalence estimates made using methods with low bias. Ten health behaviors/outcomes were graded on an A to F scale based on quintiles (prevalence meeting recommendations ≥80% graded A down to <20% graded F). Results: Three of the seven Health Behaviors and Outcomes received F or F- grades: Overall PA, Sedentary Behavior, and Obesity. Active and Outdoor Play and Organized Sport Participation could not be graded. Active Commuting to School was graded C, and Diet was graded D-. Family and Peer Influence was graded D-; Perceived Safety and Availability of Space for PA as well as the National Policy Environment were more favorable (both B). Conclusions: Grades were identical to those in 2013. Scotland has a generally favorable environment for PA, but children and adolescents have low PA and high sedentary behavior. Gaps in surveillance included lack of objectively measured PA, no surveillance of moderate-to-vigorous PA in children, summary surveillance data not expressed in ways which match recommendations (eg, for PA in young children; for screen-time), and no surveillance of Sport Participation, Active and Outdoor Play, or Sitting. Scottish policy does not include sedentary behavior at present
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