36 research outputs found

    Disasters as Ambivalent Multipliers: Influencing the Pathways from Disaster to Conflict Risk and Peace Potential Through Disaster Risk Reduction

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    Disasters, including disaster-related activities, have been shown to precipitate, intensify, and lengthen violent conflicts, yet disasters have also demonstrated the potential to reduce violent conflict, encourage cooperation, and build peace. Disaster-conflict and disaster-peace literature has sought to establish causal and linear relationships, but research has not explored with the same rigour the causal mechanisms linking these phenomena in long-term processes of social-political change and how they are influenced by human actions and inactions. This research fills this gap by drawing on in-depth interviews with disaster risk reduction (DRR) professionals in 25 disaster- and conflict-affected countries in South Asia, the Middle East, and Africa to analyse the pathways leading from disasters and disaster-related activities to violent conflict and peace. The findings highlight how these pathways can be deliberately swayed toward peace potential through DRR

    Building blocks of community positive health: the contribution of Kenyan communities

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    BACKGROUND: Beyond the health system, people draw on a complex system of everyday community resources to strengthen human and environmental health. These resources, and the community members who use them, are often overlooked by traditional approaches to planetary health. We aimed to apply a resourcefulness approach to define community positive health and the systems of resources that support this, and to define ways in which communities can pursue and sustain health agendas driven by local priorities. METHODS: Through a multi-site, mixed-methods research project, we worked with different groups of community members across three diverse field sites in Kenya, in the Baringo, Siaya, and Nakuru counties. We used a mixture of qualitative (78 focus discussion groups), participatory (67 activities, such as cognitive mapping, community timelines and mapping, tree diagrams, patient journeys, and walking interviews), and data-driven approaches to understand community concepts of positive health and collaboratively define the building blocks that shape community positive health. FINDINGS: Preliminary research findings indicated that community positive health was defined by building blocks that included nutrition, clean water, education, and adequate local infrastructure. Crucially, these building blocks were underpinned by intangible community resources, such as culture, knowledge, and social cohesion. With cognitive mapping, we understood how communities leveraged these building blocks into a functioning community-level system. However, one of the greatest challenges felt by each community was the detrimental effects of climate change, contributing alongside human action and inaction to droughts, floods, and natural resource degradation. INTERPRETATION: This initial stage of research defined community positive health and uncovered systems of local resources. Findings will be refined in a further stage of research to co-produce a pilot-tested, validated toolkit to enable resourcefulness-based approaches to community positive health. This output will be supported by an inclusive knowledge-building process that will set the stage to support communities to make more effective decisions about the use of local resources. FUNDING: Belmont Forum by the UK Natural Environment Research Council

    Think global, act local: using a translocal approach to understand community-based organisations’ responses to planetary health crises during COVID-19

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    Little is known on how community-based responses to planetary health crises, such as the COVID-19 pandemic, can integrate concerns about livelihoods, equity, health, wellbeing, and the environment. We used a translocal learning approach to co-develop insights on community-based responses to complex health and environmental and economic crises with leaders from five organisations working with communities at the front line of intersecting planetary health challenges in Finland, India, Kenya, Peru, and the USA. Translocal learning supports collective knowledge production across different localities in ways that value local perspectives but transcend national boundaries. There were three main findings from the translocal learning process. First, thanks to their proximity to the communities they served, community-based organisations (CBOs) can quickly identify the ways in which COVID-19 might worsen existing social and health inequities. Second, localised CBO actions are key to supporting communities with unique challenges in the face of systemic planetary health crises. Third, CBOs can develop rights-based, ecologically-minded actions responding to local priorities and mobilising available resources. Our findings show how solutions to planetary health might come from small-scale community initiatives that are well connected within and across contexts. Locally-focused globally-aware actions should be harnessed through greater recognition, funding, and networking opportunities. Globally, planetary health initiatives should be supported by applying the principles of subsidiarity and translocalism

    Hundreds of variants clustered in genomic loci and biological pathways affect human height

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    Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.

    Gene expression in the prefrontal cortex during adolescence: implications for the onset of schizophrenia

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    <p>Abstract</p> <p>Background</p> <p>Many critical maturational processes take place in the human brain during postnatal development. In particular, the prefrontal cortex does not reach maturation until late adolescence and this stage is associated with substantial white matter volume increases. Patients with schizophrenia and other major psychiatric disorders tend to first present with overt symptoms during late adolescence/early adulthood and it has been proposed that this developmental stage represents a "window of vulnerability".</p> <p>Methods</p> <p>In this study we used whole genome microarrays to measure gene expression in post mortem prefrontal cortex tissue from human individuals ranging in age from 0 to 49 years. To identify genes specifically altered in the late adolescent period, we applied a template matching procedure. Genes were identified which showed a significant correlation to a template showing a peak of expression between ages 15 and 25.</p> <p>Results</p> <p>Approximately 2000 genes displayed an expression pattern that was significantly correlated (positively or negatively) with the template. In the majority of cases, these genes in fact reached a plateau during adolescence with only subtle changes thereafter. These include a number of genes previously associated with schizophrenia including the susceptibility gene neuregulin 1 (NRG1). Functional profiling revealed peak expression in late adolescence for genes associated with energy metabolism and protein and lipid synthesis, together with decreases for genes involved in glutamate and neuropeptide signalling and neuronal development/plasticity. Strikingly, eight myelin-related genes previously found decreased in schizophrenia brain tissue showed a peak in their expression levels in late adolescence, while the single myelin gene reported increased in patients with schizophrenia was decreased in late adolescence.</p> <p>Conclusion</p> <p>The observed changes imply that molecular mechanisms critical for adolescent brain development are disturbed in schizophrenia patients.</p

    Profiling Trait Anxiety: Transcriptome Analysis Reveals Cathepsin B (Ctsb) as a Novel Candidate Gene for Emotionality in Mice

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    Behavioral endophenotypes are determined by a multitude of counteracting but precisely balanced molecular and physiological mechanisms. In this study, we aim to identify potential novel molecular targets that contribute to the multigenic trait “anxiety”. We used microarrays to investigate the gene expression profiles of different brain regions within the limbic system of mice which were selectively bred for either high (HAB) or low (LAB) anxiety-related behavior, and also show signs of comorbid depression-like behavior

    Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk.

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    Blood pressure is a heritable trait influenced by several biological pathways and responsive to environmental stimuli. Over one billion people worldwide have hypertension (≥140 mm Hg systolic blood pressure or  ≥90 mm Hg diastolic blood pressure). Even small increments in blood pressure are associated with an increased risk of cardiovascular events. This genome-wide association study of systolic and diastolic blood pressure, which used a multi-stage design in 200,000 individuals of European descent, identified sixteen novel loci: six of these loci contain genes previously known or suspected to regulate blood pressure (GUCY1A3-GUCY1B3, NPR3-C5orf23, ADM, FURIN-FES, GOSR2, GNAS-EDN3); the other ten provide new clues to blood pressure physiology. A genetic risk score based on 29 genome-wide significant variants was associated with hypertension, left ventricular wall thickness, stroke and coronary artery disease, but not kidney disease or kidney function. We also observed associations with blood pressure in East Asian, South Asian and African ancestry individuals. Our findings provide new insights into the genetics and biology of blood pressure, and suggest potential novel therapeutic pathways for cardiovascular disease prevention

    Measurements of top-quark pair differential cross-sections in the eμe\mu channel in pppp collisions at s=13\sqrt{s} = 13 TeV using the ATLAS detector

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    Measurement of the W boson polarisation in ttˉt\bar{t} events from pp collisions at s\sqrt{s} = 8 TeV in the lepton + jets channel with ATLAS

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