Publications (103)1361.11 Total impact
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Article: Individual multi-locus heterozygosity is associated with lower morning plasma cortisol concentration.
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ABSTRACT: OBJECTIVE. STRESS IS IMPLICATED AS A RISK FACTOR FOR NUMEROUS ILLNESSES IN HUMANS, PUTATIVELY IN PART MEDIATED BY BIOLOGICAL RESPONSES TO STRESS, SUCH AS ELEVATED CORTISOL. THE THEORY OF GENETIC HOMEOSTASIS SUGGESTS THAT INDIVIDUAL HETEROZYGOSITY FACILITATES COMPENSATION FOR ENVIRONMENTAL STRESSES. WE HYPOTHESIZED THAT HETEROZYGOSITY AMELIORATES THE BIOLOGICAL RESPONSE TO A GIVEN LEVEL OF PERCEIVED STRESS, REFLECTED IN LOWER PLASMA CORTISOL CONCENTRATIONS.DESIGN. WE EXAMINE THE ROLE OF HETEROZYGOSITY ON THE ASSOCIATION BETWEEN PERCEIVED PSYCHOLOGICAL STRESS AND MORNING CORTISOL CONCENTRATIONS IN 854 INDIVIDUALS FROM THE ISOLATED ISLAND OF VIS, CROATIA.METHODS. CORTISOL WAS MEASURED IN MORNING PLASMA SAMPLES. 1184 AUTOSOMAL MICROSATELLITE MARKERS WERE GENOTYPED AND INDIVIDUAL MULTI-LOCUS HETEROZYGOSITY WAS CALCULATED AS THE PROPORTION OF HETEROZYGOUS MARKERS. GENERAL HEALTH QUESTIONNAIRE (GHQ-30) WAS USED TO ASSESS THE DEGREE OF PSYCHOLOGICAL DISTRESS.RESULTS. MEAN MULTI-LOCUS HETEROZYGOSITY WAS 34.850.45% (RANGE: 31.97-36.22%). Psychological distress (GHQ Likert score >31) was more prevalent in women (37% versus 18% in men, p<0.0001), in less educated people (β=-0.35 per year in school, p<0.001) and in lower socio-economic classes (β=-3.59, p<0.0001). Cortisol was positively associated with psychological distress (β=2.20, p=0.01). In a regression model adjusting for age, BMI, education and GHQ-30 score, multi-locus heterozygosity was independently and inversely associated with morning plasma cortisol (p=0.005).Conclusion. More heterozygous individuals, as measured by microsatellite markers, had lower morning plasma cortisol concentrations for a given level of perceived psychological stress. This may be important, as higher cortisol concentrations may increase allostatic load and be associated with higher risk of stress-related illness.European Journal of Endocrinology 05/2013; · 3.42 Impact Factor -
Article: Genome-wide association study identifies genetic risk underlying primary rhegmatogenous retinal detachment.
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ABSTRACT: Rhegmatogenous retinal detachment (RRD) is an important cause of vision loss and can potentially lead to blindness. The underlying pathogenesis is complex and incompletely understood. We applied a two-stage genetic association discovery phase followed by a replication phase in a combined total of 2,833 RRD cases and 7,871 controls. The discovery phase involved a genome-wide association scan of 867 affected individuals and 1953 controls from Scotland, followed by genotyping and testing 4,347 highest ranking or candidates SNPs in independent sets of cases (1,000) and controls (2,912) of Dutch and British origin. None of the SNPs selected reached a Bonferroni-corrected threshold for significance (p<1.27x10(-7)). The strongest association, for rs12960119 (p=1.57x10(-7)) located within an intron of the SS18 gene. Further testing was carried out in independent case-control series from London (846 cases) and Croatia (120 cases). The combined meta-analysis identified one association reaching genome-wide significance for rs267738 (OR=1.29, p=2.11x10(-8)), a missense coding SNP and eQTL for CERS2 encoding the protein ceramide synthase 2. Several of the top signals showing suggestive significance in the combined meta-analysis encompassed genes with a documented role in cell adhesion or migration, including SS18, TIAM1, TSTA3 and LDB2, which warrant further investigation. This first genetic association study of RRD supports a polygenic component underlying RRD risk since 27.4 % of the underlying RRD liability could be explained by the collective additive effects of the genotyped SNP from the discovery genome-wide scan.Human Molecular Genetics 04/2013; · 7.64 Impact Factor -
Article: Genome-wide meta-analysis identifies 11 new loci for anthropometric traits and provides insights into genetic architecture
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ABSTRACT: Approaches exploiting trait distribution extremes may be used to identify loci associated with common traits, but it is unknown whether these loci are generalizable to the broader population. In a genome-wide search for loci associated with the upper versus the lower 5th percentiles of body mass index, height and waist-to-hip ratio, as well as clinical classes of obesity, including up to 263,407 individuals of European ancestry, we identified 4 new loci (IGFBP4, H6PD, RSRC1 and PPP2R2A) influencing height detected in the distribution tails and 7 new loci (HNF4G, RPTOR, GNAT2, MRPS33P4, ADCY9, HS6ST3 and ZZZ3) for clinical classes of obesity. Further, we find a large overlap in genetic structure and the distribution of variants between traits based on extremes and the general population and little etiological heterogeneity between obesity subgroups.Nature Genetics 04/2013; · 35.53 Impact Factor -
Article: Genome-wide meta-analysis identifies 11 new loci for anthropometric traits and provides insights into genetic architecture.
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ABSTRACT: Approaches exploiting trait distribution extremes may be used to identify loci associated with common traits, but it is unknown whether these loci are generalizable to the broader population. In a genome-wide search for loci associated with the upper versus the lower 5th percentiles of body mass index, height and waist-to-hip ratio, as well as clinical classes of obesity, including up to 263,407 individuals of European ancestry, we identified 4 new loci (IGFBP4, H6PD, RSRC1 and PPP2R2A) influencing height detected in the distribution tails and 7 new loci (HNF4G, RPTOR, GNAT2, MRPS33P4, ADCY9, HS6ST3 and ZZZ3) for clinical classes of obesity. Further, we find a large overlap in genetic structure and the distribution of variants between traits based on extremes and the general population and little etiological heterogeneity between obesity subgroups.Nature Genetics 04/2013; · 35.53 Impact Factor -
Article: Meta-Analysis of Genome-wide Association Studies in 5 cohorts reveals common variants in RBFOX1, a regulator of tissue-specific splicing, associated with refractive error.
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ABSTRACT: Visual refractive errors are complex genetic traits with a largely unknown etiology. To date, genome-wide association studies (GWAS) of moderate size have identified several novel risk markers for refractive error, measured here as mean spherical equivalent. We performed a GWAS using a total of 7,280 samples from 5 cohorts: the Age-Related Eye Disease Study (AREDS); the KORA study ("Cooperative Health Research in the Region of Augsburg"); the Framingham Eye Study (FES); the Ogliastra Genetic Park-Talana (OGP-Talana) Study; and the Multiethnic Study of Atherosclerosis (MESA). Genotyping was performed on Illumina and Affymetrix platforms with additional markers imputed to the HapMap II reference panel. We identified a new genome-wide significant locus on chromosome 16 (rs10500355, p=3.9 x 10-9) in a combined discovery and replication set (26,953 samples). This SNP is located within the RBFOX1 gene which is a neuron-specific splicing factor regulating a wide range of alternative splicing events implicated in neuronal development and maturation, including transcription factors, other splicing factors and synaptic proteins.Human Molecular Genetics 03/2013; · 7.64 Impact Factor -
Dataset: Verhoeven 2013 meta-GWAS refractive error and myopia supp
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Article: Genome-wide meta-analyses of multiancestry cohorts identify multiple new susceptibility loci for refractive error and myopia.
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ABSTRACT: Refractive error is the most common eye disorder worldwide and is a prominent cause of blindness. Myopia affects over 30% of Western populations and up to 80% of Asians. The CREAM consortium conducted genome-wide meta-analyses, including 37,382 individuals from 27 studies of European ancestry and 8,376 from 5 Asian cohorts. We identified 16 new loci for refractive error in individuals of European ancestry, of which 8 were shared with Asians. Combined analysis identified 8 additional associated loci. The new loci include candidate genes with functions in neurotransmission (GRIA4), ion transport (KCNQ5), retinoic acid metabolism (RDH5), extracellular matrix remodeling (LAMA2 and BMP2) and eye development (SIX6 and PRSS56). We also confirmed previously reported associations with GJD2 and RASGRF1. Risk score analysis using associated SNPs showed a tenfold increased risk of myopia for individuals carrying the highest genetic load. Our results, based on a large meta-analysis across independent multiancestry studies, considerably advance understanding of the mechanisms involved in refractive error and myopia.Nature Genetics 02/2013; · 35.53 Impact Factor -
Article: Inference of identity by descent in population isolates and optimal sequencing studies.
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ABSTRACT: In an isolated population, individuals are likely to share large genetic regions inherited from common ancestors. Identity by descent (IBD) can be inferred from SNP genotypes, which is useful in a number of applications, including identifying genetic variants influencing complex disease risk, and planning efficient cohort-sequencing strategies. We present ANCHAP - a method for detecting IBD in isolated populations. We compare accuracy of the method against other long-range and local phasing methods, using parent-offspring trios. In our experiments, we show that ANCHAP performs similarly as the other long-range method, but requires an order-of-magnitude less computational resources. A local phasing model is able to achieve similar sensitivity, but only at the cost of higher false discovery rates. In some regions of the genome, the studied individuals share haplotypes particularly often, which hints at the history of the populations studied. We demonstrate the method using SNP genotypes from three isolated island populations, as well as in a cohort of unrelated individuals. In samples from three isolated populations of around 1000 individual each, an average individual shares a haplotype at a genetic locus with 9-12 other individuals, compared with only 1 individual within the non-isolated population. We describe an application of ANCHAP to optimally choose samples in resequencing studies. We find that with sample sizes of 1000 individuals from an isolated population genotyped using a dense SNP array, and with 20% of these individuals sequenced, 65% of sequences of the unsequenced subjects can be partially inferred.European Journal of Human Genetics advance online publication, 30 January 2013; doi:10.1038/ejhg.2012.307.European journal of human genetics: EJHG 01/2013; · 3.56 Impact Factor -
Dataset: Kornfeld JCEM Brief Figure1
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Dataset: Kornfeld JCEM Brief pre-final-draft
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Dataset: Kornfeld JCEM Brief Supplement Final
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Article: Genome-wide association analyses identify multiple loci associated with central corneal thickness and keratoconus.
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ABSTRACT: Central corneal thickness (CCT) is associated with eye conditions including keratoconus and glaucoma. We performed a meta-analysis on >20,000 individuals in European and Asian populations that identified 16 new loci associated with CCT at genome-wide significance (P < 5 × 10(-8)). We further showed that 2 CCT-associated loci, FOXO1 and FNDC3B, conferred relatively large risks for keratoconus in 2 cohorts with 874 cases and 6,085 controls (rs2721051 near FOXO1 had odds ratio (OR) = 1.62, 95% confidence interval (CI) = 1.4-1.88, P = 2.7 × 10(-10), and rs4894535 in FNDC3B had OR = 1.47, 95% CI = 1.29-1.68, P = 4.9 × 10(-9)). FNDC3B was also associated with primary open-angle glaucoma (P = 5.6 × 10(-4); tested in 3 cohorts with 2,979 cases and 7,399 controls). Further analyses implicate the collagen and extracellular matrix pathways in the regulation of CCT.Nature Genetics 01/2013; · 35.53 Impact Factor -
Article: Genome-wide association analyses identify 18 new loci associated with serum urate concentrations.
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ABSTRACT: Elevated serum urate concentrations can cause gout, a prevalent and painful inflammatory arthritis. By combining data from >140,000 individuals of European ancestry within the Global Urate Genetics Consortium (GUGC), we identified and replicated 28 genome-wide significant loci in association with serum urate concentrations (18 new regions in or near TRIM46, INHBB, SFMBT1, TMEM171, VEGFA, BAZ1B, PRKAG2, STC1, HNF4G, A1CF, ATXN2, UBE2Q2, IGF1R, NFAT5, MAF, HLF, ACVR1B-ACVRL1 and B3GNT4). Associations for many of the loci were of similar magnitude in individuals of non-European ancestry. We further characterized these loci for associations with gout, transcript expression and the fractional excretion of urate. Network analyses implicate the inhibins-activins signaling pathways and glucose metabolism in systemic urate control. New candidate genes for serum urate concentration highlight the importance of metabolic control of urate production and excretion, which may have implications for the treatment and prevention of gout.Nature genetics. 01/2013; 45(2):145-54. -
Article: Loci associated with N-glycosylation of human immunoglobulin g show pleiotropy with autoimmune diseases and haematological cancers.
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ABSTRACT: Glycosylation of immunoglobulin G (IgG) influences IgG effector function by modulating binding to Fc receptors. To identify genetic loci associated with IgG glycosylation, we quantitated N-linked IgG glycans using two approaches. After isolating IgG from human plasma, we performed 77 quantitative measurements of N-glycosylation using ultra-performance liquid chromatography (UPLC) in 2,247 individuals from four European discovery populations. In parallel, we measured IgG N-glycans using MALDI-TOF mass spectrometry (MS) in a replication cohort of 1,848 Europeans. Meta-analysis of genome-wide association study (GWAS) results identified 9 genome-wide significant loci (P<2.27×10(-9)) in the discovery analysis and two of the same loci (B4GALT1 and MGAT3) in the replication cohort. Four loci contained genes encoding glycosyltransferases (ST6GAL1, B4GALT1, FUT8, and MGAT3), while the remaining 5 contained genes that have not been previously implicated in protein glycosylation (IKZF1, IL6ST-ANKRD55, ABCF2-SMARCD3, SUV420H1, and SMARCB1-DERL3). However, most of them have been strongly associated with autoimmune and inflammatory conditions (e.g., systemic lupus erythematosus, rheumatoid arthritis, ulcerative colitis, Crohn's disease, diabetes type 1, multiple sclerosis, Graves' disease, celiac disease, nodular sclerosis) and/or haematological cancers (acute lymphoblastic leukaemia, Hodgkin lymphoma, and multiple myeloma). Follow-up functional experiments in haplodeficient Ikzf1 knock-out mice showed the same general pattern of changes in IgG glycosylation as identified in the meta-analysis. As IKZF1 was associated with multiple IgG N-glycan traits, we explored biomarker potential of affected N-glycans in 101 cases with SLE and 183 matched controls and demonstrated substantial discriminative power in a ROC-curve analysis (area under the curve = 0.842). Our study shows that it is possible to identify new loci that control glycosylation of a single plasma protein using GWAS. The results may also provide an explanation for the reported pleiotropy and antagonistic effects of loci involved in autoimmune diseases and haematological cancer.PLoS Genetics 01/2013; 9(1):e1003225. · 8.69 Impact Factor -
Article: Genome-wide association analyses identify 18 new loci associated with serum urate concentrations.
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ABSTRACT: Elevated serum urate concentrations can cause gout, a prevalent and painful inflammatory arthritis. By combining data from >140,000 individuals of European ancestry within the Global Urate Genetics Consortium (GUGC), we identified and replicated 28 genome-wide significant loci in association with serum urate concentrations (18 new regions in or near TRIM46, INHBB, SFMBT1, TMEM171, VEGFA, BAZ1B, PRKAG2, STC1, HNF4G, A1CF, ATXN2, UBE2Q2, IGF1R, NFAT5, MAF, HLF, ACVR1B-ACVRL1 and B3GNT4). Associations for many of the loci were of similar magnitude in individuals of non-European ancestry. We further characterized these loci for associations with gout, transcript expression and the fractional excretion of urate. Network analyses implicate the inhibins-activins signaling pathways and glucose metabolism in systemic urate control. New candidate genes for serum urate concentration highlight the importance of metabolic control of urate production and excretion, which may have implications for the treatment and prevention of gout.Nature Genetics 12/2012; · 35.53 Impact Factor -
Dataset: Hum.Mol.Genet.2012
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Article: Discovery and Fine Mapping of Serum Protein Loci through Transethnic Meta-analysis.
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ABSTRACT: Many disorders are associated with altered serum protein concentrations, including malnutrition, cancer, and cardiovascular, kidney, and inflammatory diseases. Although these protein concentrations are highly heritable, relatively little is known about their underlying genetic determinants. Through transethnic meta-analysis of European-ancestry and Japanese genome-wide association studies, we identified six loci at genome-wide significance (p < 5 × 10(-8)) for serum albumin (HPN-SCN1B, GCKR-FNDC4, SERPINF2-WDR81, TNFRSF11A-ZCCHC2, FRMD5-WDR76, and RPS11-FCGRT, in up to 53,190 European-ancestry and 9,380 Japanese individuals) and three loci for total protein (TNFRS13B, 6q21.3, and ELL2, in up to 25,539 European-ancestry and 10,168 Japanese individuals). We observed little evidence of heterogeneity in allelic effects at these loci between groups of European and Japanese ancestry but obtained substantial improvements in the resolution of fine mapping of potential causal variants by leveraging transethnic differences in the distribution of linkage disequilibrium. We demonstrated a functional role for the most strongly associated serum albumin locus, HPN, for which Hpn knockout mice manifest low plasma albumin concentrations. Other loci associated with serum albumin harbor genes related to ribosome function, protein translation, and proteasomal degradation, whereas those associated with serum total protein include genes related to immune function. Our results highlight the advantages of transethnic meta-analysis for the discovery and fine mapping of complex trait loci and have provided initial insights into the underlying genetic architecture of serum protein concentrations and their association with human disease.The American Journal of Human Genetics 09/2012; 91(4):744-753. · 10.60 Impact Factor -
Article: FTO genotype is associated with phenotypic variability of body mass index.
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ABSTRACT: There is evidence across several species for genetic control of phenotypic variation of complex traits, such that the variance among phenotypes is genotype dependent. Understanding genetic control of variability is important in evolutionary biology, agricultural selection programmes and human medicine, yet for complex traits, no individual genetic variants associated with variance, as opposed to the mean, have been identified. Here we perform a meta-analysis of genome-wide association studies of phenotypic variation using ∼170,000 samples on height and body mass index (BMI) in human populations. We report evidence that the single nucleotide polymorphism (SNP) rs7202116 at the FTO gene locus, which is known to be associated with obesity (as measured by mean BMI for each rs7202116 genotype), is also associated with phenotypic variability. We show that the results are not due to scale effects or other artefacts, and find no other experiment-wise significant evidence for effects on variability, either at loci other than FTO for BMI or at any locus for height. The difference in variance for BMI among individuals with opposite homozygous genotypes at the FTO locus is approximately 7%, corresponding to a difference of ∼0.5 kilograms in the standard deviation of weight. Our results indicate that genetic variants can be discovered that are associated with variability, and that between-person variability in obesity can partly be explained by the genotype at the FTO locus. The results are consistent with reported FTO by environment interactions for BMI, possibly mediated by DNA methylation. Our BMI results for other SNPs and our height results for all SNPs suggest that most genetic variants, including those that influence mean height or mean BMI, are not associated with phenotypic variance, or that their effects on variability are too small to detect even with samples sizes greater than 100,000.Nature 09/2012; 490(7419):267-72. · 36.28 Impact Factor -
Article: Integration of genome-wide association studies with biological knowledge identifies six novel genes related to kidney function.
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ABSTRACT: In conducting genome-wide association studies (GWAS), analytical approaches leveraging biological information may further understanding of the pathophysiology of clinical traits. To discover novel associations with estimated glomerular filtration rate (eGFR), a measure of kidney function, we developed a strategy for integrating prior biological knowledge into the existing GWAS data for eGFR from the CKDGen Consortium. Our strategy focuses on single nucleotide polymorphism (SNPs) in genes that are connected by functional evidence, determined by literature mining and gene ontology (GO) hierarchies, to genes near previously validated eGFR associations. It then requires association thresholds consistent with multiple testing, and finally evaluates novel candidates by independent replication. Among the samples of European ancestry, we identified a genome-wide significant SNP in FBXL20 (P = 5.6 × 10(-9)) in meta-analysis of all available data, and additional SNPs at the INHBC, LRP2, PLEKHA1, SLC3A2 and SLC7A6 genes meeting multiple-testing corrected significance for replication and overall P-values of 4.5 × 10(-4)-2.2 × 10(-7). Neither the novel PLEKHA1 nor FBXL20 associations, both further supported by association with eGFR among African Americans and with transcript abundance, would have been implicated by eGFR candidate gene approaches. LRP2, encoding the megalin receptor, was identified through connection with the previously known eGFR gene DAB2 and extends understanding of the megalin system in kidney function. These findings highlight integration of existing genome-wide association data with independent biological knowledge to uncover novel candidate eGFR associations, including candidates lacking known connections to kidney-specific pathways. The strategy may also be applicable to other clinical phenotypes, although more testing will be needed to assess its potential for discovery in general.Human Molecular Genetics 09/2012; · 7.64 Impact Factor -
Article: Uncovering Networks from Genome-Wide Association Studies via Circular Genomic Permutation.
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ABSTRACT: Genome-wide association studies (GWAS) aim to detect single nucleotide polymorphisms (SNP) associated with trait variation. However, due to the large number of tests, standard analysis techniques impose highly stringent significance thresholds, leaving potentially associated SNPs undetected, and much of the trait genetic variation unexplained. Pathway- and network-based methodologies applied to GWAS aim to detect associations missed by standard single-marker approaches. The complex and non-random architecture of the genome makes it a challenge to derive an appropriate testing framework for such methodologies. We developed a rapid and simple permutation approach that uses GWAS SNP association results to establish the significance of pathway associations while accounting for the linkage disequilibrium structure of SNPs and the clustering of functionally related elements in the genome. All SNPs used in the GWAS are placed in a "circular genome" according to their location. Then the complete set of SNP association P values are permuted by rotation with respect to the genomic locations of the SNPs. Once these "simulated" P values are assigned, the joint gene P values are calculated using Fisher's combination test, and the association of pathways is tested using the hypergeometric test. The circular genomic permutation approach was applied to a human genome-wide association dataset. The data consists of 719 individuals from the ORCADES study genotyped for ∼300,000 SNPs and measured for 51 traits ranging from physical to biochemical measurements. KEGG pathways (n = 225) were used as the sets of pathways to be tested. Our results demonstrate that the circular genomic permutations provide robust association P values. The non-permuted hypergeometric analysis generates ∼1400 pathway-trait combination results with an association P value more significant than P ≤ 0.05, whereas applying circular genomic permutation reduces the number of significant results to a more credible 40% of that value. The circular permutation software ("genomicper") is available as an R package at http://cran.r-project.org/.G3 (Bethesda, Md.). 09/2012; 2(9):1067-75.
Top co-authors
Top Journals
- Nature Genetics (18)
- PLoS Genetics (12)
- PLoS ONE (7)
- Nature Genetics (6)
- Human Molecular Genetics (6)
Institutions
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2009–2013
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University of Zagreb
- • Faculty of Pharmacy and Biochemistry (PHARMA)
- • School of Medicine (MEF)
Zagreb, Grad Zagreb, Croatia -
University of Split-School of Medicine
Split, Splitsko-Dalmatinska Zupanija, Croatia
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2012
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McGill University
- Department of Epidemiology, Biostatistics and Occupational Health
Montréal, Quebec, Canada -
Johns Hopkins Bloomberg School of Public Health
Baltimore, MD, USA -
National Institute of Livestock and Grassland Science
Ibaraki, Osaka-fu, Japan
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2008–2012
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The University of Edinburgh
- • Centre for Population Health Sciences
- • Division of Health Sciences
Edinburgh, SCT, United Kingdom
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2011
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Medizinische Universität Innsbruck
- Sektion für Genetische Epidemiologie
Innsbruck, Tyrol, Austria -
Ludwig Boltzmann Institute for Cancer Research
Vienna, Vienna, Austria
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2009–2011
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Institute of Genetics and Molecular Medicine
Edinburgh, SCT, United Kingdom
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2008–2011
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Uppsala University
- • The Rudbeck Laboratory
- • Department of Immunology, Genetics and Pathology
Uppsala, Uppsala, Sweden
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2010
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Trinity College Dublin
- Department of Psychiatry
Dublin, L, Ireland (Republic of Ireland) -
Universitätsklinikum Regensburg
Regensburg, Bavaria, Germany -
Europaeische Akademie Bozen - Accademia Europea Bolzano
Bolzano - Bozen, Trentino-Alto Adige, Italy -
University of Michigan
- Department of Biostatistics
Ann Arbor, MI, USA -
Johns Hopkins University
- Department of Epidemiology
Baltimore, MD, USA
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2005–2010
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Medical Research Council (UK)
- MRC Human Genetics Unit
London, ENG, United Kingdom
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