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94 results for “Mendelian”
Data from: Childhood adiposity and type 1 diabetes: a Mendelian randomization study
BACKGROUND: The incidence of type 1 diabetes (T1D) is increasing globally. One hypothesis is that increasing childhood obesity rates may explain part of this increase, but, as T1D is rare, intervention studies are challenging to perform. The aim of this study was to assess this hypothesis with a Mendelian randomization approach that uses genetic variants as instrumental variables to test for causal associations. METHODS AND FINDINGS: We created a genetic instrument of 23 single nucleotide polymorphisms (SNPs) associated with childhood adiposity in children aged 2-10 years. Summary-level association results for these 23 SNPs with childhood-onset (<17 years) T1D were extracted from a meta-analysis of genome-wide association study with 5,913 T1D cases and 8,828 reference samples. Using inverse-variance weighted Mendelian randomization analysis, we found support for an effect of childhood adiposity on T1D risk (odds ratio 1.32, 95% CI 1.06-1.64 per standard deviation score in body mass index [SDS-BMI]). A sensitivity analysis provided evidence of horizontal pleiotropy bias (p = 0.04) diluting the estimates towards the null. We therefore applied Egger regression and multivariable Mendelian randomization methods to control for this type of bias and found evidence in support of a role of childhood adiposity in T1D (odds ratio in Egger regression, 2.76, 95% CI 1.40-5.44). Limitations of our study include that underlying genes and their mechanisms for most of the genetic variants included in the score are not known. Mendelian randomization requires large sample sizes, and power was limited to provide precise estimates. This research has been conducted using data from the Early Growth Genetics (EGG) Consortium, the Genetic Investigation of Anthropometric Traits (GIANT) Consortium, the Tobacco and Genetics (TAG) Consortium, and the Social Science Genetic Association Consortium (SSGAC), as well as meta-analysis results from a T1D genome-wide association study. CONCLUSIONS: This study provides genetic support for a link between childhood adiposity and T1D risk. Together with evidence from observational studies, our findings further emphasize the importance of measures to reduce the global epidemic of childhood obesity and encourage mechanistic studies.
Data from: Analysis of genome-wide structure, diversity and fine mapping of Mendelian traits in traditional and village chickens
Extensive phenotypic variation is a common feature among village chickens found throughout much of the developing world, and in traditional chicken breeds that have been artificially selected for traits such as plumage variety. We present here an assessment of traditional and village chicken populations, for fine mapping of Mendelian traits using genome-wide single-nucleotide polymorphism (SNP) genotyping while providing information on their genetic structure and diversity. Bayesian clustering analysis reveals two main genetic backgrounds in traditional breeds, Kenyan, Ethiopian and Chilean village chickens. Analysis of linkage disequilibrium (LD) reveals useful LD (r2greater than or equal to0.3) in both traditional and village chickens at pairwise marker distances of ~10 Kb; while haplotype block analysis indicates a median block size of 11–12 Kb. Association mapping yielded refined mapping intervals for duplex comb (Gga 2:38.55–38.89 Mb) and rose comb (Gga 7:18.41–22.09 Mb) phenotypes in traditional breeds. Combined mapping information from traditional breeds and Chilean village chicken allows the oocyan phenotype to be fine mapped to two small regions (Gga 1:67.25–67.28 Mb, Gga 1:67.28–67.32 Mb) totalling ~75 Kb. Mapping the unmapped earlobe pigmentation phenotype supports previous findings that the trait is sex-linked and polygenic. A critical assessment of the number of SNPs required to map simple traits indicate that between 90 and 110K SNPs are required for full genome-wide analysis of haplotype block structure/ancestry, and for association mapping in both traditional and village chickens. Our results demonstrate the importance and uniqueness of phenotypic diversity and genetic structure of traditional chicken breeds for fine-scale mapping of Mendelian traits in the species, with village chicken populations providing further opportunities to enhance mapping resolutions.
Causality of 486 human blood metabolites on gastric cancer: a two-sample Mendelian randomization study
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Mental disease and risk of autoimmune disease: a Mendelian randomization study
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The causal links between gut microbiota and diabetic nephropathy: A Mendelian randomization study. Supplementary material
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Integration of Single-Cell Analysis and Mendelian Randomization Reveals NET1 as a Potential Key Player in Lung Cancer Pathogenesis
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Supplementary Data forExploring Potential Druggable Gene Targets for Hypertrophic Cardiomyopathy through Mendelian Randomization
<p><em>该数据集包含探索肥厚型心肌病可成药基因靶点的手稿的补充材料</em>。</p>
raw data - Causal relationship of immune cells and primary open-angle glaucoma: A Mendelian randomization study
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Data from: Diabetes mellitus, glycemic traits, and cerebrovascular disease: A Mendelian randomization study
<p><span><span><span><span><span><span><span><span><span><span><span><b>Objective: </b>We employed Mendelian randomization (MR) to explore the effects of genetic predisposition to type 2 diabetes (T2D), hyperglycemia, insulin resistance, and β-cell dysfunction on risk of stroke subtypes and related cerebrovascular phenotypes.</span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><a name="_Hlk49339275"><b>Methods: </b></a>We selected instruments for genetic predisposition to T2D (74,124 cases, 824,006 controls), HbA1c levels (n=421,923), fasting glucose levels (n=133,010), insulin resistance (n=108,557), and β-cell dysfunction (n=16,378) based on published genome-wide association studies. Applying two-sample MR, we examined associations with ischemic stroke (60,341 cases, 454,450 controls), intracerebral hemorrhage (1,545 cases, 1,481 controls), and ischemic stroke subtypes (large artery, cardioembolic, small vessel stroke), as well as with related phenotypes (carotid atherosclerosis, imaging markers of cerebral white matter integrity, and brain atrophy). </span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><b>Results: </b>Genetic predisposition to T2D and higher HbA1c levels were associated with higher risk of any ischemic stroke, large artery stroke, and small vessel stroke. Similar associations were also noted for carotid atherosclerotic plaque, fractional anisotropy, a white matter disease marker, and markers of brain atrophy. We further found associations of genetic predisposition to insulin resistance with large artery and small vessel stroke, whereas predisposition to β-cell dysfunction was associated with small vessel stroke, intracerebral hemorrhage, lower grey matter volume, and total brain volume.</span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><b>Conclusions: </b>This study supports causal effects of T2D and hyperglycemia on large artery and small vessel stroke. </span></span></span></span></span></span></span></span></span></span></span><a name="_Hlk52240657">We show associations of genetically predicted insulin resistance and β-cell dysfunction with large artery and small vessel stroke that might have implications for anti-diabetic treatments targeting these mechanisms.</a></p> <p><span><span><span><span><span><span><span><span><span><span><span><b>Classification of Evidence:</b> This study provides Class II evidence that genetic predisposition to T2D and higher HbA1c levels are associated with a higher risk of large artery and small vessel ischemic stroke.</span></span></span></span></span></span></span></span></span></span></span></p>
Food Liking and Risk of Sepsis: A Two-Sample Mendelian Randomization Study_Supplementary Materials
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Fetal/maternal-determined birth weight and adulthood type 2 diabetes and its subtypes: a Mendelian randomization study
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Effects of blood cell traits on cardiovascular morpho-functional phenotypes: Evidence from Mendelian randomization analysis
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Unraveling the Impact of Nutrients and Dietary Patterns on Periodontitis: A Mendelian Randomization Study
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Proteome-wide Mendelian randomization study identifies potential therapeutic targets for Coronary atherosclerosis
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Data from: Unlinked Mendelian inheritance of red and black pigmentation in snakes: implications for Batesian mimicry
Identifying the genetic basis of mimetic signals is critical to understanding both the origin and dynamics of mimicry over time. For species not amenable to large laboratory breeding studies, widespread color polymorphism across natural populations offers a powerful way to assess the relative likelihood of different genetic systems given observed phenotypic frequencies. We classified color phenotype for 2,175 ground snakes (Sonora semiannulata) across the continental United States to analyze morph ratios and test among competing hypotheses about the genetic architecture underlying red and black coloration in coral snake mimics. We found strong support for a two-locus model under simple Mendelian inheritance, with red and black pigmentation being controlled by separate loci. We found no evidence of either linkage disequilibrium between loci or sex linkage. In contrast to Batesian mimicry systems like butterflies in which all color signal components are linked into a single "supergene," our results suggest that the mimetic signal in colubrid snakes can be disrupted through simple recombination and that color evolution is likely to involve discrete gains and losses of each signal component. Both outcomes are likely to contribute to the exponential increase in rates of color evolution seen in snake mimicry systems over insect systems.
Insight into modifiable risk factors for tuberculosis : a Mendelian randomization study(supplementary materials)
<p>Detailed results of the above 5 statistical methods.</p>
Systematic comparison of Mendelian randomization studies and randomized controlled trials using electronic databases
<p><strong>Supplementary Dataset 1. </strong>Select ClinicalTrials.Gov data fields for the RCT studies identified as the<br> <em>main </em>dataset.<br> <strong>Supplementary Dataset 2.</strong> Select ClinicalTrials.Gov data fields for the RCT studies identified as the<br> <em>literature </em>dataset.<br> <strong>Supplementary Dataset 3.</strong> Comparison of frequency of RCT general features between the <em>Main</em><br> dataset and background of all RCTs available in ClinicalTrials.Gov.</p> <p><strong>Supplementary Dataset 4. </strong>PubMed and SemMedDB data for published MR and RCT studies.<br> <strong>Supplementary Dataset 5. </strong>Case series of MR and RCT studies with matching exposures<br> (interventions) and outcomes (conditions).</p>
Study of the Causal Link Between Rheumatoid Arthritis and Periodontitis Using Mendelian Randomization
ClinicalTrials.gov study NCT06603207. IPD Sharing: Not stated. Countries: 0. Publications: 0.
Parathyroid hormone and bone mineral density: a Mendelian randomization study
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Data from: Risky behaviors and Parkinson’s disease: a Mendelian randomization study
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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)
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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.