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52 results for “Mendelian Randomization”
Collider Bias Correction for Multiple Covariates in GWAS Using Robust Multivariable Mendelian Randomization
<p>This repository contains the data underlying the figures in paper "Collider Bias Correction for Multiple Covariates in GWAS<br>Using Robust Multivariable Mendelian Randomization".</p> <p> </p> <p> </p> <p>The file names and sheet names in the xlsx file indicate the corresponding figures of data. </p> <p><br>The underlying data of manhattan plots and QQ plots are in text file. For other figures, the underlying data are in the spreadsheet.</p> <p>In each file, column names indicate the MVMR method used to obtain the result. </p> <p>For example: </p> <p>In text files:</p> <p>The abbreviation "mPC" refers to metabolomic principle components.</p> <p>beta_no_correction: the SNP effect estimate without bias correction.</p> <p>beta_cml or beta_MVMR_cml: the standard error of SNP effect estimate after the bias correction of MVMR-cML.</p> <p>SE_UVMR_cml: the standard error of SNP effect estimate after the bias correction of UVMR-cML.</p> <p>p_value_Egger or p_value_MVMR_Egger: the p-value of SNP effect estimate after the bias correction of MVMR-Egger regression.</p> <p><br>In the spreadsheet, column names follow the same style. </p> <p>The GWAS data is also available. The column names follows the plink output file. The detailed explanations are available at https://www.cog-genomics.org/plink/2.0/formats#glm_linear</p>
Summary statistics from "Sex-Specific Causal Relations between Steroid Hormones and Obesity—A Mendelian Randomization Study"
<p>GWAMA summary statistics of four steroid hormone levels and one steroid hormone ratio using fixed-effect model.</p> <p>When using this data, please cite: Pott J, Horn K, Zeidler R, et al.. Sex-Specific Causal Relations between Steroid Hormones and Obesity - A Mendelian Randomization Study. <em>Metabolites</em> <strong>2021</strong>, <em>11</em>, 738. https://doi.org/10.3390/metabo11110738</p> <p>All txt files contain the following columns:</p> <ul> <li>markername</li> <li>chr</li> <li>bp_hg19 (base position according to hg19)</li> <li>ea (effect allele)</li> <li>oa (other allele)</li> <li>eaf (effect allele frequency)</li> <li>info (minimal info score across all used studies)</li> <li>nSamples (sample size per SNP)</li> <li>nStudies (number of studies)</li> <li>beta (effect estimate)</li> <li>se (standard error)</li> <li>p (p-value)</li> <li>I2 (SNP heterogeneity across studies)</li> <li>phenotype (phenotyp setting)</li> </ul>
Vitamin B12 deficiency anaemia and gestational diabetes mellitus: a two-sample Mendelian randomization study
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Supplementary table for "Deciphering the Relationship Between Circulating Metabolites and Osteoarthritis: A Comprehensive Genetic Correlation and Mendelian Randomization Studies"
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Supplement to "Endogenous DHEAS is causally linked with lumbar spine bone mineral density and forearm fractures in women - A mendelian randomization study"
<p>Supplemental tables to "Endogenous DHEAS is causally linked with lumbar spine bone mineral density and forearm fractures in women - A mendelian randomization study" by Johan Quester, Maria Nethander, Anna Eriksson and Claes Ohlsson.</p>
Data from: Genetic susceptibility, Mendelian randomization and nomogram model construction of gestational diabetes mellitus
<p>The dataset contains subjects' basic information, including the Identification number of the test sample, fasting plasma glucose (FPG), oral glucose tolerance test 1h plasma glucose (1hPG), oral glucose tolerance test 2h plasma glucose (2hPG), glycated hemoglobin (HbA1c), Systolic blood pressure (SBP), Diastolic blood pressure (DBP), triglyceride (TG), total cholesterol (TC), High-density lipoprotein cholesterol (HDL-c), Low-density lipoprotein cholesterol (LDL-c), and also involves subjects' genetic variant information used for analysis of the association of functional polymorphisms and GDM. The variables including SBP_M, DBP_M, FPG_M, 1hPG_M, 2hPG_M, HbA1c_M, TG_M represent the mean value of SBP, DBP, FPG, 1hPG, 2hPG, HbA1c, TG, which are used for the stratification analysis. This study has obtained the support from the Ethics Committee of Guilin Medical University. All included subjects signed the informed consent.</p>
Investigating the causal association between immune cell phenotypes and allergic diseases and non-allergic asthma using conventional Two-sample and Bayesian weighted Mendelian randomization
<p>Investigating the causal association between immune cell phenotypes and allergic diseases and non-allergic asthma using conventional Two-sample and Bayesian weighted Mendelian randomization</p>
Data from: Genetic susceptibility, Mendelian randomization and nomogram model construction of gestational diabetes mellitus
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Supplementary Materials of the article:The relationship between circulating inflammatory proteins mediating gut microbiota and postherpetic neuralgia: A Mendelian Randomization study
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Appendix: Association between hemostatic profile and migraine: a Mendelian randomization analysis
<p><b>Objective: </b><span>To assess support for a causal relationship between </span>hemostatic measures and migraine susceptibility using genetic instrumental analysis.</p> <p><b>Methods: </b>Two-sample Mendelian randomization (MR) instrumental leveraging available genome-wide association study (GWAS) summary statistics was applied to hemostatic measures as potential causal for migraine and its subtypes, migraine with aura (MA) and migraine without aura (MO). Twelve blood-based measures of hemostasis were examined, including plasma level or activity of eight hemostatic factors and two <span>fibrinopeptides together with </span>two hemostasis clinical tests<span>.</span></p> <p><b>Results: </b>There were significant instrumental effects between increased coagulation factor VIII activity (FVIII, odds ratio[95% confidence interval]=1.05[1.03, 1.08]/standard deviation (SD), <i>P</i>=6.08×10<sup>-05</sup>), von Willebrand factor level (VWF, 1.05[1.03, 1.08]/SD, <i>P</i>=2.25×10<sup>-06</sup>), and phosphorylated <span>fibrinopeptide A level</span> (1.13[1.07, 1.19]/SD, <i>P</i>=5.44×10<sup>-06</sup>) with migraine susceptibility. When extended to migraine subtypes, FVIII, VWF, and phosphorylated <span>fibrinopeptide A</span> showed slightly stronger effects with MA than overall migraine. Fibrinogen level was inversely linked with MA (0.76[0.64, 0.91]/SD, <i>P</i>=2.32×10<sup>-03</sup>) but not overall migraine. None of the hemostatic factors was linked with MO. In sensitivity analysis, effects for fibrinogen and phosphorylated <span>fibrinopeptide A</span> were robust, while independent effects of FVIII and VWF could not be distinguished, and FVIIII associations were potentially affected by pleiotropy at the <i>ABO</i> locus. Causal effects from migraine to the hemostatic measures were not supported in reverse MR. However, MA was not included due to lack of instruments.</p> <p><b>Conclusions:</b> The current study supports potential causality of increased FVIII, VWF, and phosphorylated <span>fibrinopeptide A,</span> and decreased fibrinogen in migraine susceptibility, especially for MA, and may provide insights into the etiology underlying the relationship between <span>hemostasis</span> and migraine.</p>
Supplementary data for: Maternal testosterone and offspring birth weight: A Mendelian randomization study
<p><span>Evidence showed maternal androgen levels in both healthy/general population and populations with hyperandrogenic disorders were inversely associated with offspring's birth weight. We aimed to investigate the causal effect of maternal testosterone levels in general population on offspring's birth weight and preterm delivery risk using two-sample Mendelian randomization (MR) method.</span></p> <p><span>We obtained independent genetic instruments from a sex-specific genome wide association study with up to 230,454 females of European descent from UK biobank. Genetic instruments with consistent testosterone effects but no aggregate effect on sex-hormone binding globulin were used to perform the main analysis. Summary-level data of offspring's birth weight with offspring's genotype adjusted was obtained from a study with 210,406 females of European descent. Summary-level data of preterm delivery was obtained from the FinnGen study (6,736 cases and 116,219 controls).</span></p> <p><span>For outcome of offspring's birth weight, the numbers of instruments included in final MR analyses were 123, 128 and 91 respectively. For outcome of preterm delivery, the numbers were 115, 120 and 83 respectively. The present data files show the genetic instruments and their effects on exposures and outcomes. Pleiotropic genetic instruments that excluded in the MR analysis were also provided in the files.</span></p>
Supplemental material for "Statins, type 2 diabetes and body mass index: a univariable and multivariable Mendelian randomization study"
<p>Supplemental material for "Statins, type 2 diabetes and body mass index: a univariable and multivariable Mendelian randomization study" by Guoyi Yang and C Mary Schooling.</p>
Genetically predicted lipid traits, diabetes mellitus liability and carotid intima-media thickness in African ancestry individuals: a Mendelian randomization study
<p>Genetic variants used for the analysis of 'Genetically predicted lipid traits, diabetes mellitus liability and carotid intima-media thickness in African ancestry individuals: a Mendelian randomization study'.</p>
Potential drug targets for benign prostatic hyperplasia: A proteome-wide Mendelian randomization study
<p>Additional file 3</p>
Investigating the Casual Associations among the Gut Microbiota, Metabolites, and Bladder Cancer: A Mediation Mendelian Randomization Study
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Association between plasma lipids and ischemic stroke: a multivariable and drug-target Mendelian randomization study
<p>The sensitivity analysis results using the leave-one-out approach revealed that no individual SNP substantially drove the association between plasma lipids and each disease outcome (Figure S1-S4).</p> <p> </p> <p>The STROBE-MR checklist is also attached.</p>
Supplementary data to the paper: Causal association between serum thyroid-stimulating hormone and obesity: A bidirectional Mendelian randomization study
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Supplementary data for: Maternal testosterone and offspring birth weight: A Mendelian randomization study
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Appendix: Association between hemostatic profile and migraine: a Mendelian randomization analysis
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Data from: Risky behaviors and Parkinson's disease: a Mendelian randomization study
Objective: To examine causal associations between risky behavior phenotypes on Parkinson's disease using a Mendelian randomization approach. Methods: We used two-sample Mendelian randomization to generate unconfounded estimates using summary statistics from two independent, large meta-analyses of genome-wide association studies on risk taking behaviors (n=370,771-939,908) and Parkinson's disease (cases: n=9581, controls: n = 33,245). We used inverse variance weighted as the main method for judging causality. Results: Our results support a strong protective association between the tendency to smoke and Parkinson's disease (OR=0.714 per log odds of ever smoking; 95% CI=0.568-0.897; p-value=0.0041; Cochran Q test; p-value=0.238; I2 index=6.3%). Furthermore, we observed risk association trends between automobile speed propensity as well as the number of sexual partners and Parkinson's disease after removal of overlapping loci with other risky traits (OR=1.986 for each standard deviation increase in normalized automobile speed propensity; 95% CI=1.215-3.243; p-value=0.0066, OR=1.635 for each standard deviation increase in number of sexual partners; 95% CI=1.165-2.293; p-value=0.0049). Conclusion: These findings provide support for a causal relationship between general risk tolerance and Parkinson's disease and may provide new insights in the pathogenic mechanisms leading to the development of Parkinson's disease.
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Allen Brain Atlas
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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.