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Dataset results
412 results for “genetic risk”
Understanding Genetic Risk for Alcohol Use Disorder
ClinicalTrials.gov study NCT05143073. IPD Sharing: NO. Countries: 1. Publications: 2.
Relating Genetic and Environmental Risk Scores to Multiple Sclerosis Susceptibility
ClinicalTrials.gov study NCT01617395. IPD Sharing: NO. Countries: 1. Publications: 3.
Preliminary Evaluation of Screening for Pancreatic Cancer in Patients With Inherited Genetic Risk
ClinicalTrials.gov study NCT02478892. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Understanding of Genetic Risk Information for Type 2 Diabetes
ClinicalTrials.gov study NCT01186354. IPD Sharing: Not stated. Countries: 1. Publications: 4.
The Genetics and Vascular Health Check Study (GENVASC) Aims to Help Determine Whether Gathering Genetic Information Can Improve the Prediction of Risk of Coronary Artery Disease (CAD)
ClinicalTrials.gov study NCT04417387. IPD Sharing: YES. Countries: 1. Publications: 1.
Data from: A study on genetic variants of Fibroblast Growth Factor Receptor 2 (FGFR2) and the risk of breast cancer from North India
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Data from: At risk of population decline? An ecological and genetic approach to the threatened palm species Butia eriospatha (Arecaceae) of southern Brazil
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Data from: Genetic variation and risks of introgression in the wild Coffea arabica gene pool in south-western Ethiopian montane rainforests
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Data from: Managing the risk of genetic swamping of a rare and restricted tree
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Data from: The effect of sex-biased dispersal on opposite-sexed spatial genetic structure and inbreeding risk
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Data from: White matter lesions: spatial heterogeneity, links to risk factors, cognition, genetics, atrophy
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Insight into the genetic population structure of wild red foxes in Poland reveals low risk of genetic introgression from escaped farm red foxes
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Data from: Association mapping of genetic risk factors for chronic wasting disease in wild deer
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Data from: Populations at risk: conservation genetics of kangaroo mice (Microdipodops) of the Great Basin Desert
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Genetically determined blood pressure, antihypertensive drug classes and risk of stroke subtypes
<p><b>Objective: </b>We employed Mendelian Randomization to explore whether the effects of blood pressure (BP) and BP lowering through different antihypertensive drug classes on stroke risk vary by stroke etiology.</p> <p><b>Methods: </b>We selected genetic variants associated with systolic and diastolic BP and BP-lowering variants in genes encoding antihypertensive drug targets from a GWAS on 757,601 individuals. Applying two-sample Mendelian randomization, we examined associations with any stroke (67,162 cases; 454,450 controls), ischemic stroke and its subtypes (large artery, cardioembolic, small vessel stroke), intracerebral hemorrhage (ICH, deep and lobar), and the related small vessel disease phenotype of WMH.</p> <p><b>Results</b>: Genetic predisposition to higher systolic and diastolic BP was associated with higher risk of any stroke, ischemic stroke, and ICH. We found associations between genetically determined BP and all ischemic stroke subtypes with a higher risk of large artery and small vessel stroke compared to cardioembolic stroke, as well as associations with deep, but not lobar ICH. Genetic proxies for calcium channel blockers, but not beta blockers, were associated with lower risk of any stroke and ischemic stroke. Proxies for CCBs showed particularly strong associations with small vessel stroke and the related radiological phenotype of WMH.</p> <p><b>Conclusions: </b>This study supports a causal role of hypertension in all major stroke subtypes except lobar ICH. We find differences in the effects of BP and BP lowering through antihypertensive drug classes between stroke subtypes and identify calcium channel blockade as a promising strategy for preventing manifestations of cerebral small vessel disease.</p>
Genetic variation in parental effects contributes to the evolutionary potential of prey responses to predation risk
<p class="CxSpFirst">Despite the ubiquity of parental effects and their potential impact on evolutionary dynamics, their contribution to the evolution of predator-prey interactions remains poorly understood. Using quantitative genetics, here we demonstrate that parental effects substantially contribute to the evolutionary potential of larval antipredator responses in a leaf<i> </i>beetle (<em>Leptinotarsa</em> <i>decemlineata</i>). Previous research showed that larger <em>L.</em> <i>decemlineata</i> larvae elicit stronger antipredator responses, and mothers perceiving predators improved offspring responses by increasing intraclutch cannibalism –an extreme form of offspring provisioning. We now report substantial additive genetic variation underlying maternal ability to induce intraclutch cannibalism, indicating the potential of this adaptive maternal effect to evolve by natural selection. We also show that paternal size, a heritable trait, impacted larval responses to predation risk, but that larval responses themselves had little additive genetic variation. Together, these results demonstrate how larval responses to predation risk can evolve via two types of parental effects, both of which provide indirect sources of genetic variation for offspring traits.<b> </b></p>
Data from: Non-consumptive effects of predation: does perceived risk strengthen the genetic integration of behaviour and morphology in stickleback?
<p>Predators can shape genetic correlations in prey by altering prey perception of risk. We manipulated perceived risk to test whether such non-consumptive effects tightened behavioural trait correlations in wild-caught stickleback from high- compared to low-risk environments due to genetic variation in plasticity. We expected tighter genetic correlations within perceived risk treatments than across them, and tighter genetic correlations in high-risk than in low-risk treatments. We identified genetic variation in plasticity, with genetic correlations between boldness, sociality and antipredator morphology, as expected, being tighter within treatments than across them, for both of two populations. By contrast, genetic correlations did not tighten with exposure to risk. Tighter phenotypic correlations in wild stickleback may thus arise because predators induce correlational selection on environmental components of these traits, or because predators tighten residual correlations by causing environmental heterogeneity that is controlled in the laboratory. Our study places phenotypic integration firmly into an ecological context.</p>
Data from: Sexual traits are sensitive to genetic stress and predict extinction risk in the stalk-eyed fly, Diasemopsis meigenii
The handicap principle predicts that sexual traits are more susceptible to inbreeding depression than nonsexual traits. However, this hypothesis has received little testing and results are inconsistent. We used 11 generations of full-sibling mating to test the effect of inbreeding on sexual and nonsexual traits in the stalk-eyed fly Diasemopsis meigenii. Consistent with the theoretical predictions, the male sexual trait (eyespan) decreased more than nonsexual traits (female eyespan and male wing length), even after controlling for body size variation. In addition, male eyespan was a reliable predictor of line extinction, unlike other nonsexual traits. After 11 generations, inbred lines were crossed to generate inbred and outbred families. All morphological traits were larger in outbred individuals than inbred individuals. This heterosis was greater in male eyespan than in male wing length, but not female eyespan. The elevated response in male eyespan to genetic stress mirrored the result found using environmental stress during larval development and suggests that common mechanisms underlie the patterns observed. Overall, these results support the hypothesis that male sexual traits suffer more from inbreeding depression than nonsexual traits and are in line with predictions based on the handicap principle.
Data from: Genetic and lifestyle risk factors for MRI-defined brain infarcts in a population-based setting
Objective: We explored genetic and lifestyle risk factors of MRI-defined brain infarcts (BI) in large population-based cohorts. Methods: We performed meta-analyses of genome-wide association studies (GWAS) and examined associations of vascular risk factors and their genetic risk scores (GRS) with MRI-defined BI and a subset of BI, namely small sub-cortical BI (SSBI), in eighteen population-based cohorts (N=20,949) from five ethnicities (3,726 with BI, 2,021 with SSBI). Top loci were followed up in seven population-based cohorts (N=6,862, 1,483 with BI, 630 with SBBI), and tested associations with related phenotypes including ischemic stroke and pathologically-defined BI. Results: The mean prevalence was 17.7% for BI and 10.5% for SSBI, steeply rising after age 65. Two loci showed genome-wide significant association with BI: FBN2, P=1.77×10-8 and LINC00539/ZDHHC20, P=5.82×10-9. Both have been associated with blood pressure (BP) related phenotypes, but did not replicate in the smaller follow-up sample nor show associations with related phenotypes. Age and sex-adjusted associations with BI and SSBI were observed for BP traits (P-value for BI, P[BI]=9.38×10-25; P[SSBI]=5.23×10-14 for hypertension), smoking (P[BI]=4.4×10-10; P[SSBI]=1.2×10-4), diabetes (P[BI]=1.7×10-8; P[SSBI]=2.8×10-3), previous cardiovascular disease (P[BI]=1.0×10-18; P[SSBI]=2.3×10-7), stroke (P[BI]=3.9×10-69; P[SSBI]=3.2×10-24), and MRI-defined white matter hyperintensity burden (P[BI]=1.43×10-157; P[SSBI]=3.16×10-106), but not with body-mass-index or cholesterol. GRS of BP traits were associated with BI and SSBI (P≤0.0022), without indication of directional pleiotropy. Conclusions: In this multi-ethnic GWAS meta-analysis, including over 20,000 population-based participants, we identified genetic risk loci for BI requiring validation once additional large datasets become available. High BP, including genetically determined, was the most significant modifiable, causal risk factor for BI.
Data from: Linking genetic and environmental factors in amphibian disease risk
A central question in evolutionary biology is how interactions between organisms and the environment shape genetic differentiation. The pathogen Batrachochytrium dendrobatidis (Bd) has caused variable population declines in the lowland leopard frog (Lithobates yavapaiensis); thus, disease has potentially shaped, or been shaped by, host genetic diversity. Environmental factors can also influence both amphibian immunity and Bd virulence, confounding our ability to assess the genetic effects on disease dynamics. Here, we used genetics, pathogen dynamics, and environmental data to characterize L. yavapaiensis populations, estimate migration, and determine relative contributions of genetic and environmental factors in predicting Bd dynamics. We found that the two uninfected populations belonged to a single genetic deme, whereas each infected population was genetically unique. We detected an outlier locus that deviated from neutral expectations and was significantly correlated with mortality within populations. Across populations, only environmental variables predicted infection intensity, whereas environment and genetics predicted infection prevalence, and genetic diversity alone predicted mortality. At one locality with geothermally elevated water temperatures, migration estimates revealed source–sink dynamics that have likely prevented local adaptation. We conclude that integrating genetic and environmental variation among populations provides a better understanding of Bd spatial epidemiology, generating more effective conservation management strategies for mitigating amphibian declines.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.