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Article ; Online: The exhaustive genomic scan approach, with an application to rare-variant association analysis.

Kanoungi, George / Nothnagel, Michael / Becker, Tim / Drichel, Dmitriy

European journal of human genetics : EJHG

2020 Volume 28, Issue 9, Page(s) 1283–1291

Abstract: Region-based genome-wide scans are usually performed by use of a priori chosen analysis regions. Such an approach will likely miss the region comprising the strongest signal and, thus, may result in increased type II error rates and decreased power. Here, ...

Abstract	Region-based genome-wide scans are usually performed by use of a priori chosen analysis regions. Such an approach will likely miss the region comprising the strongest signal and, thus, may result in increased type II error rates and decreased power. Here, we propose a genomic exhaustive scan approach that analyzes all possible subsequences and does not rely on a prior definition of the analysis regions. As a prime instance, we present a computationally ultraefficient implementation using the rare-variant collapsing test for phenotypic association, the genomic exhaustive collapsing scan (GECS). Our implementation allows for the identification of regions comprising the strongest signals in large, genome-wide rare-variant association studies while controlling the family-wise error rate via permutation. Application of GECS to two genomic data sets revealed several novel significantly associated regions for age-related macular degeneration and for schizophrenia. Our approach also offers a high potential to improve genome-wide scans for selection, methylation, and other analyses.
Keywords	covid19
Language	English
Publishing date	2020-05-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1141470-4
ISSN	1476-5438 ; 1018-4813
ISSN (online)	1476-5438
ISSN	1018-4813
DOI	10.1038/s41431-020-0639-3
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Article ; Online: A genome-wide association meta-analysis implicates Hedgehog and Notch signaling in Dupuytren's disease.

Riesmeijer, Sophie A / Kamali, Zoha / Ng, Michael / Drichel, Dmitriy / Piersma, Bram / Becker, Kerstin / Layton, Thomas B / Nanchahal, Jagdeep / Nothnagel, Michael / Vaez, Ahmad / Hennies, Hans Christian / Werker, Paul M N / Furniss, Dominic / Nolte, Ilja M

Nature communications

2024 Volume 15, Issue 1, Page(s) 199

Abstract: Dupuytren's disease (DD) is a highly heritable fibrotic disorder of the hand with incompletely understood etiology. A number of genetic loci, including Wnt signaling members, have been previously identified. Our overall aim was to identify novel genetic ... ...

Abstract	Dupuytren's disease (DD) is a highly heritable fibrotic disorder of the hand with incompletely understood etiology. A number of genetic loci, including Wnt signaling members, have been previously identified. Our overall aim was to identify novel genetic loci, to prioritize genes within the loci for functional studies, and to assess genetic correlation with associated disorders. We performed a meta-analysis of six DD genome-wide association studies from three European countries and extensive bioinformatic follow-up analyses. Leveraging 11,320 cases and 47,023 controls, we identified 85 genome-wide significant single nucleotide polymorphisms in 56 loci, of which 11 were novel, explaining 13.3-38.1% of disease variance. Gene prioritization implicated the Hedgehog and Notch signaling pathways. We also identified a significant genetic correlation with frozen shoulder. The pathways identified highlight the potential for new therapeutic targets and provide a basis for additional mechanistic studies for a common disorder that can severely impact hand function.
MeSH term(s)	Humans ; Animals ; Dupuytren Contracture/genetics ; Dupuytren Contracture/metabolism ; Genome-Wide Association Study ; Hedgehogs/genetics ; Wnt Signaling Pathway ; Genetic Loci ; Polymorphism, Single Nucleotide ; Genetic Predisposition to Disease
Language	English
Publishing date	2024-01-03
Publishing country	England
Document type	Meta-Analysis ; Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-44451-0
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Article ; Online: METAINTER: meta-analysis of multiple regression models in genome-wide association studies.

Vaitsiakhovich, Tatsiana / Drichel, Dmitriy / Herold, Christine / Lacour, André / Becker, Tim

Bioinformatics (Oxford, England)

2015 Volume 31, Issue 2, Page(s) 151–157

Abstract: Motivation: Meta-analysis of summary statistics is an essential approach to guarantee the success of genome-wide association studies (GWAS). Application of the fixed or random effects model to single-marker association tests is a standard practice. More ...

Abstract	Motivation: Meta-analysis of summary statistics is an essential approach to guarantee the success of genome-wide association studies (GWAS). Application of the fixed or random effects model to single-marker association tests is a standard practice. More complex methods of meta-analysis involving multiple parameters have not been used frequently, a gap that could be explained by the lack of a respective meta-analysis pipeline. Meta-analysis based on combining p-values can be applied to any association test. However, to be powerful, meta-analysis methods for high-dimensional models should incorporate additional information such as study-specific properties of parameter estimates, their effect directions, standard errors and covariance structure. Results: We modified 'method for the synthesis of linear regression slopes' recently proposed in the educational sciences to the case of multiple logistic regression, and implemented it in a meta-analysis tool called METAINTER. The software handles models with an arbitrary number of parameters, and can directly be applied to analyze the results of single-SNP tests, global haplotype tests, tests for and under gene-gene or gene-environment interaction. Via simulations for two-single nucleotide polymorphisms (SNP) models we have shown that the proposed meta-analysis method has correct type I error rate. Moreover, power estimates come close to that of the joint analysis of the entire sample. We conducted a real data analysis of six GWAS of type 2 diabetes, available from dbGaP (http://www.ncbi.nlm.nih.gov/gap). For each study, a genome-wide interaction analysis of all SNP pairs was performed by logistic regression tests. The results were then meta-analyzed with METAINTER. Availability: The software is freely available and distributed under the conditions specified on http://metainter.meb.uni-bonn.de. Supplementary information: Supplementary data are available at Bioinformatics online.
MeSH term(s)	Data Interpretation, Statistical ; Diabetes Mellitus, Type 2/genetics ; Gene-Environment Interaction ; Genome, Human ; Genome-Wide Association Study ; Haplotypes/genetics ; Humans ; Linear Models ; Logistic Models ; Models, Statistical ; Polymorphism, Single Nucleotide/genetics ; Software
Language	English
Publishing date	2015-01-15
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btu629
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Article ; Online: mARC1 in MASLD: Modulation of lipid accumulation in human hepatocytes and adipocytes.

Jones, Amanda K / Bajrami, Besnik / Campbell, Morgan K / Erzurumluoglu, Abdullah Mesut / Guo, Qiusha / Chen, Hongxing / Zhang, Xiaomei / Zeveleva, Svetlana / Kvaskoff, David / Brunner, Andreas-David / Muller, Stefanie / Gathey, Vasudha / Dave, Rajvee M / Tanner, James W / Rixen, Sophia / Struwe, Michel A / Phoenix, Kathryn / Klumph, Kaitlyn J / Robinson, Heather /

Veyel, Daniel / Muller, Annkatrin / Noyvert, Boris / Bartholdy, Boris Alexander / Steixner-Kumar, Agnes A / Stutzki, Jan / Drichel, Dmitriy / Omland, Steffen / Sheehan, Ryan / Hill, Jon / Bretschneider, Tom / Gottschling, Dirk / Scheidig, Axel J / Clement, Bernd / Giera, Martin / Ding, Zhihao / Broadwater, John / Warren, Curtis R

Hepatology communications

2024 Volume 8, Issue 5

Abstract: Background: Mutations in the gene MTARC1 (mitochondrial amidoxime-reducing component 1) protect carriers from metabolic dysfunction-associated steatohepatitis (MASH) and cirrhosis. MTARC1 encodes the mARC1 enzyme, which is localized to the mitochondria ... ...

Abstract	Background: Mutations in the gene MTARC1 (mitochondrial amidoxime-reducing component 1) protect carriers from metabolic dysfunction-associated steatohepatitis (MASH) and cirrhosis. MTARC1 encodes the mARC1 enzyme, which is localized to the mitochondria and has no known MASH-relevant molecular function. Our studies aimed to expand on the published human genetic mARC1 data and to observe the molecular effects of mARC1 modulation in preclinical MASH models. Methods and results: We identified a novel human structural variant deletion in MTARC1, which is associated with various biomarkers of liver health, including alanine aminotransferase levels. Phenome-wide Mendelian Randomization analyses additionally identified novel putatively causal associations between MTARC1 expression, and esophageal varices and cardiorespiratory traits. We observed that protective MTARC1 variants decreased protein accumulation in in vitro overexpression systems and used genetic tools to study mARC1 depletion in relevant human and mouse systems. Hepatocyte mARC1 knockdown in murine MASH models reduced body weight, liver steatosis, oxidative stress, cell death, and fibrogenesis markers. mARC1 siRNA treatment and overexpression modulated lipid accumulation and cell death consistently in primary human hepatocytes, hepatocyte cell lines, and primary human adipocytes. mARC1 depletion affected the accumulation of distinct lipid species and the expression of inflammatory and mitochondrial pathway genes/proteins in both in vitro and in vivo models. Conclusions: Depleting hepatocyte mARC1 improved metabolic dysfunction-associated steatotic liver disease-related outcomes. Given the functional role of mARC1 in human adipocyte lipid accumulation, systemic targeting of mARC1 should be considered when designing mARC1 therapies. Our data point to plasma lipid biomarkers predictive of mARC1 abundance, such as Ceramide 22:1. We propose future areas of study to describe the precise molecular function of mARC1, including lipid trafficking and subcellular location within or around the mitochondria and endoplasmic reticulum.
MeSH term(s)	Animals ; Humans ; Mice ; Adipocytes ; Biomarkers ; Ceramides ; Fatty Liver ; Hepatocytes ; Mendelian Randomization Analysis
Chemical Substances	Biomarkers ; Ceramides ; MTARC2 protein, human (EC 1.-) ; Mtarc2 protein, mouse
Language	English
Publishing date	2024-04-12
Publishing country	United States
Document type	Journal Article
ISSN	2471-254X
ISSN (online)	2471-254X
DOI	10.1097/HC9.0000000000000365
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Article: Analysis of the progression of systolic blood pressure using imputation of missing phenotype values.

Vaitsiakhovich, Tatsiana / Drichel, Dmitriy / Angisch, Marina / Becker, Tim / Herold, Christine / Lacour, André

BMC proceedings

2014 Volume 8, Issue Suppl 1, Page(s) S83

Abstract: We present a genome-wide association study of a quantitative trait, "progression of systolic blood pressure in time," in which 142 unrelated individuals of the Genetic Analysis Workshop 18 real genotype data were analyzed. Information on systolic blood ... ...

Abstract	We present a genome-wide association study of a quantitative trait, "progression of systolic blood pressure in time," in which 142 unrelated individuals of the Genetic Analysis Workshop 18 real genotype data were analyzed. Information on systolic blood pressure and other phenotypic covariates was missing at certain time points for a considerable part of the sample. We observed that the dropout process causing missingness is not independent of the initial systolic blood pressure; that is, the data is not missing completely at random. However, after the adjustment for age, the impact of systolic blood pressure on dropouts was no longer significant. Therefore, we decided to impute missing phenotype values by using information from individuals with complete phenotypic data. Progression of systolic blood pressure (∆SBP/∆t) was defined based on the imputed phenotypes and analyzed in a genome-wide fashion. We also conducted an exhaustive genome-wide search for interaction between single-nucleotide polymorphisms (7.14 × 10(10) tests) under an allelic model. The suggested data imputation and the association analysis strategy proved to be valid in the sense that there was no evidence of genome-wide inflation or increased type I error in general. Furthermore, we detected 2 single-nucleotide polymorphisms (SNPs) that met the criterion for genome-wide significance (p≤5 × 10(-8)), which was also confirmed via Monte-Carlo simulation. In view of the rather small sample size, however, the results have to be followed-up in larger studies.
Language	English
Publishing date	2014-06-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2411867-9
ISSN	1753-6561
ISSN	1753-6561
DOI	10.1186/1753-6561-8-S1-S83
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Article ; Online: Identification of de novo variants in nonsyndromic cleft lip with/without cleft palate patients with low polygenic risk scores.

Ishorst, Nina / Henschel, Leonie / Thieme, Frederic / Drichel, Dmitriy / Sivalingam, Sugirthan / Mehrem, Sarah L / Fechtner, Ariane C / Fazaal, Julia / Welzenbach, Julia / Heimbach, André / Maj, Carlo / Borisov, Oleg / Hausen, Jonas / Raff, Ruth / Hoischen, Alexander / Dixon, Michael / Rada-Iglesias, Alvaro / Bartusel, Michaela / Rojas-Martinez, Augusto /

Aldhorae, Khalid / Braumann, Bert / Kruse, Teresa / Kirschneck, Christian / Spanier, Gerrit / Reutter, Heiko / Nowak, Stefanie / Gölz, Lina / Knapp, Michael / Buness, Andreas / Krawitz, Peter / Nöthen, Markus M / Nothnagel, Michael / Becker, Tim / Ludwig, Kerstin U / Mangold, Elisabeth

Molecular genetics & genomic medicine

2022 Volume 11, Issue 3, Page(s) e2109

Abstract: Background: Nonsyndromic cleft lip with/without cleft palate (nsCL/P) is a congenital malformation of multifactorial etiology. Research has identified >40 genome-wide significant risk loci, which explain less than 40% of nsCL/P heritability. Studies ... ...

Abstract	Background: Nonsyndromic cleft lip with/without cleft palate (nsCL/P) is a congenital malformation of multifactorial etiology. Research has identified >40 genome-wide significant risk loci, which explain less than 40% of nsCL/P heritability. Studies show that some of the hidden heritability is explained by rare penetrant variants. Methods: To identify new candidate genes, we searched for highly penetrant de novo variants (DNVs) in 50 nsCL/P patient/parent-trios with a low polygenic risk for the phenotype (discovery). We prioritized DNV-carrying candidate genes from the discovery for resequencing in independent cohorts of 1010 nsCL/P patients of diverse ethnicities and 1574 population-matched controls (replication). Segregation analyses and rare variant association in the replication cohort, in combination with additional data (genome-wide association data, expression, protein-protein-interactions), were used for final prioritization. Conclusion: In the discovery step, 60 DNVs were identified in 60 genes, including a variant in the established nsCL/P risk gene CDH1. Re-sequencing of 32 prioritized genes led to the identification of 373 rare, likely pathogenic variants. Finally, MDN1 and PAXIP1 were prioritized as top candidates. Our findings demonstrate that DNV detection, including polygenic risk score analysis, is a powerful tool for identifying nsCL/P candidate genes, which can also be applied to other multifactorial congenital malformations.
MeSH term(s)	Humans ; Cleft Palate/genetics ; Cleft Lip/genetics ; Genome-Wide Association Study ; DNA-Binding Proteins/genetics ; Risk Factors
Chemical Substances	DNA-Binding Proteins
Language	English
Publishing date	2022-12-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2734884-2
ISSN	2324-9269 ; 2324-9269
ISSN (online)	2324-9269
ISSN	2324-9269
DOI	10.1002/mgg3.2109
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Article ; Online: Integrated genome-wide pathway association analysis with INTERSNP.

Herold, Christine / Mattheisen, Manuel / Lacour, André / Vaitsiakhovich, Tatsiana / Angisch, Marina / Drichel, Dmitriy / Becker, Tim

Human heredity

2012 Volume 73, Issue 2, Page(s) 63–72

Abstract: Objectives: Pathway association analysis (PAA) tests for an excess of moderately significant SNPs in genes from a common pathway.: Methods: We present a Monte-Carlo simulation framework that allows to formulate the main ideas of existing PAA ... ...

Abstract	Objectives: Pathway association analysis (PAA) tests for an excess of moderately significant SNPs in genes from a common pathway. Methods: We present a Monte-Carlo simulation framework that allows to formulate the main ideas of existing PAA approaches using a self-contained rather than a competitive null hypothesis. A stand-alone implementation in INTERSNP makes time-consuming communication with standard GWAS software redundant. By additional parallelization with the OpenMP API, we achieve a reduction in running time for PAA by orders of magnitude, making a power simulation study for PAA feasible. Our approach properly accounts for linkage disequilibrium and is robust with respect to residual λ inﬂation. Results: We demonstrate that under simple, realistic disease models, PAA can actually strongly outperform the GWAS single-marker approach. PAA methods that make use of the strength of the SNP association (GenGen, Fisher's combination test), in general, perform better than ratio-based methods (ALIGATOR, SNP ratio), whereas the relative performance of gene-based scoring (ALIGATOR, GenGen) and pathway-based scoring (SNP ratio, Fisher's combination test) depends on the architecture of the assumed disease model. Finally, we present a new PAA score that models independent signals from the same gene in a regression framework and show that it is a reasonable compromise that combines the advantages of existing ideas.
MeSH term(s)	Genome-Wide Association Study/methods ; Humans ; Monte Carlo Method ; Polymorphism, Single Nucleotide ; Software
Language	English
Publishing date	2012
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2424-7
ISSN	1423-0062 ; 0001-5652
ISSN (online)	1423-0062
ISSN	0001-5652
DOI	10.1159/000336196
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Article ; Online: Quick, “Imputation-free” meta-analysis with proxy-SNPs

Meesters Christian / Leber Markus / Herold Christine / Angisch Marina / Mattheisen Manuel / Drichel Dmitriy / Lacour André / Becker Tim

BMC Bioinformatics, Vol 13, Iss 1, p

2012 Volume 231

Abstract: Abstract Background Meta-analysis (MA) is widely used to pool genome-wide association studies (GWASes) in order to a) increase the power to detect strong or weak genotype effects or b) as a result verification method. As a consequence of differing SNP ... ...

Abstract	Abstract Background Meta-analysis (MA) is widely used to pool genome-wide association studies (GWASes) in order to a) increase the power to detect strong or weak genotype effects or b) as a result verification method. As a consequence of differing SNP panels among genotyping chips, imputation is the method of choice within GWAS consortia to avoid losing too many SNPs in a MA. YAMAS ( Y et A nother M eta A nalysis S oftware), however, enables cross-GWAS conclusions prior to finished and polished imputation runs, which eventually are time-consuming. Results Here we present a fast method to avoid forfeiting SNPs present in only a subset of studies, without relying on imputation. This is accomplished by using reference linkage disequilibrium data from 1,000 Genomes/HapMap projects to find proxy-SNPs together with in-phase alleles for SNPs missing in at least one study. MA is conducted by combining association effect estimates of a SNP and those of its proxy-SNPs. Our algorithm is implemented in the MA software YAMAS. Association results from GWAS analysis applications can be used as input files for MA, tremendously speeding up MA compared to the conventional imputation approach. We show that our proxy algorithm is well-powered and yields valuable ad hoc results, possibly providing an incentive for follow-up studies. We propose our method as a quick screening step prior to imputation-based MA, as well as an additional main approach for studies without available reference data matching the ethnicities of study participants. As a proof of principle, we analyzed six dbGaP Type II Diabetes GWAS and found that the proxy algorithm clearly outperforms naïve MA on the p -value level: for 17 out of 23 we observe an improvement on the p-value level by a factor of more than two, and a maximum improvement by a factor of 2127. Conclusions YAMAS is an efficient and fast meta-analysis program which offers various methods, including conventional MA as well as inserting proxy-SNPs for missing markers to avoid unnecessary power loss. MA with YAMAS can be readily conducted as YAMAS provides a generic parser for heterogeneous tabulated file formats within the GWAS field and avoids cumbersome setups. In this way, it supplements the meta-analysis process.
Keywords	Computer applications to medicine. Medical informatics ; R858-859.7 ; Biology (General) ; QH301-705.5
Subject code	310
Language	English
Publishing date	2012-09-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: A one-degree-of-freedom test for supra-multiplicativity of SNP effects.

Herold, Christine / Ramirez, Alfredo / Drichel, Dmitriy / Lacour, André / Vaitsiakhovich, Tatsiana / Nöthen, Markus M / Jessen, Frank / Maier, Wolfgang / Becker, Tim

PloS one

2013 Volume 8, Issue 10, Page(s) e78038

Abstract: Deviation from multiplicativity of genetic risk factors is biologically plausible and might explain why Genome-wide association studies (GWAS) so far could unravel only a portion of disease heritability. Still, evidence for SNP-SNP epistasis has rarely ... ...

Abstract	Deviation from multiplicativity of genetic risk factors is biologically plausible and might explain why Genome-wide association studies (GWAS) so far could unravel only a portion of disease heritability. Still, evidence for SNP-SNP epistasis has rarely been reported, suggesting that 2-SNP models are overly simplistic. In this context, it was recently proposed that the genetic architecture of complex diseases could follow limiting pathway models. These models are defined by a critical risk allele load and imply multiple high-dimensional interactions. Here, we present a computationally efficient one-degree-of-freedom "supra-multiplicativity-test" (SMT) for SNP sets of size 2 to 500 that is designed to detect risk alleles whose joint effect is fortified when they occur together in the same individual. Via a simulation study we show that the SMT is powerful in the presence of threshold models, even when only about 30-45% of the model SNPs are available. In addition, we demonstrate that the SMT outperforms standard interaction analysis under recessive models involving just a few SNPs. We apply our test to 10 consensus Alzheimer's disease (AD) susceptibility SNPs that were previously identified by GWAS and obtain evidence for supra-multiplicativity ([Formula: see text]) that is not attributable to either two-way or three-way interaction.
MeSH term(s)	Genome-Wide Association Study/methods ; Humans ; Models, Genetic ; Polymorphism, Single Nucleotide/genetics
Language	English
Publishing date	2013-10-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0078038
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Conference proceedings: Imputation-free GWAS Meta-Analysis with YAMAS

Becker, Tim / Drichel, Dmitriy / Herold, Christine / Meesters, Christian / Leber, Markus

2011 , Page(s) 11gmds053

Event/congress	56. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 6. Jahrestagung der Deutschen Gesellschaft für Epidemiologie (DGEpi); Mainz//2011; Mainz; ; Deutsche Gesellschaft für Epidemiologie; 2011
Keywords	Medizin, Gesundheit ; GWAS Meta Analysis Imputing ; 1000 Genomes
Publishing date	2011-09-20
Publisher	German Medical Science GMS Publishing House; Düsseldorf
Document type	Conference proceedings
DOI	10.3205/11gmds053
Database	German Medical Science

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