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Research Interest
Our lab develops and utilizes statistical genetics, computational biology, and population genetics-based approaches to understand the biological underpinnings and evolutionary history of human traits and complex disease.
Keywords
Population Genetics, Statistical Genetics, Bioinformatics, Computational Biology, Statistics, Systems Biology, Metabolic Disorder, Type-2 Diabetes, Coronary Heart Disease, non-Alcoholic Fatty Liver Disease, Obesity, Myocardial Infarction, Cholesterol Levels, Natural Selection, Demography, Genome-wide Association Study (GWAS), Next-Generation Sequencing, Mendelian randomization.
Research Summary
The central aim in my lab is to understand the genetic, biological, and evolutionary basis of metabolic and cardiovascular phenotypes in human populations. To build this understanding, the lab constructs computational and statistical tools grounded in principles of population biology and quantitative genetics. These tools are then applied to genetic data collected across thousands of whole human genomes.
My research has answered population genetic questions about recent demographic and selective events in human populations, and work to develop new statistics to identify selective pressures is ongoing. Recent work in the lab has focused on statistical models which capture variability in the rate of mutation in the human genome.
I have an active interest in mapping risk alleles for common diseases, particularly type-2 diabetes and coronary heart disease, but perhaps more importantly, to identify the causal variant, gene, and mechanism that influences risk to these diseases from existing non-coding associations identified by genome-wide association studies.
I continue to utilize the framework of Mendelian Randomization, to perform causal inference studies between genetically-heritable biomarkers and complex diseases. Work in the lab is toward applications, but also development of novel methodologies.
In the coming years, the lab activities will focus on several key areas of interest, which includes:
- Developing statistical models to capture variability in the rate of mutation in human genomes, with application to identifying de novo mutations and rare variation related to human disease
- Computational methods and functional characterization of the causal variants and genes related to non-coding associations for type 2 diabetes and heart disease
- Developing informational and statistical tools which interrogate human genetic association data together with other sources of 'omics data to construct credibly actionable information on pathways responsible for disease susceptibility
- Population genetic methods to identify loci in the human genome which are targets of natural selective pressures, and to further identify the causal variants and genes responsible
- Performing large-scale genomic studies using data from the Million Veteran Program, a large (>1M) multi-ethnic cohort enriched for cardiometabolic disease.
Positions Available!
For the 2020-2021 academic year, my lab has openings for computational post-doctoral positions. Please see the following site for further details on how to apply.
The lab also has a number of potential graduate student rotation projects available for the 2020-2021 academic year. Ideal students will have a strong background in computational sciences, and projects will be built around human genetic data, bioinformatic applications, statistical genetic analysis, epidemiology, and/or population and systems biology. Please contact me if you are interested.
Our lab develops and utilizes statistical genetics, computational biology, and population genetics-based approaches to understand the biological underpinnings and evolutionary history of human traits and complex disease.
Keywords
Population Genetics, Statistical Genetics, Bioinformatics, Computational Biology, Statistics, Systems Biology, Metabolic Disorder, Type-2 Diabetes, Coronary Heart Disease, non-Alcoholic Fatty Liver Disease, Obesity, Myocardial Infarction, Cholesterol Levels, Natural Selection, Demography, Genome-wide Association Study (GWAS), Next-Generation Sequencing, Mendelian randomization.
Research Summary
The central aim in my lab is to understand the genetic, biological, and evolutionary basis of metabolic and cardiovascular phenotypes in human populations. To build this understanding, the lab constructs computational and statistical tools grounded in principles of population biology and quantitative genetics. These tools are then applied to genetic data collected across thousands of whole human genomes.
My research has answered population genetic questions about recent demographic and selective events in human populations, and work to develop new statistics to identify selective pressures is ongoing. Recent work in the lab has focused on statistical models which capture variability in the rate of mutation in the human genome.
I have an active interest in mapping risk alleles for common diseases, particularly type-2 diabetes and coronary heart disease, but perhaps more importantly, to identify the causal variant, gene, and mechanism that influences risk to these diseases from existing non-coding associations identified by genome-wide association studies.
I continue to utilize the framework of Mendelian Randomization, to perform causal inference studies between genetically-heritable biomarkers and complex diseases. Work in the lab is toward applications, but also development of novel methodologies.
In the coming years, the lab activities will focus on several key areas of interest, which includes:
- Developing statistical models to capture variability in the rate of mutation in human genomes, with application to identifying de novo mutations and rare variation related to human disease
- Computational methods and functional characterization of the causal variants and genes related to non-coding associations for type 2 diabetes and heart disease
- Developing informational and statistical tools which interrogate human genetic association data together with other sources of 'omics data to construct credibly actionable information on pathways responsible for disease susceptibility
- Population genetic methods to identify loci in the human genome which are targets of natural selective pressures, and to further identify the causal variants and genes responsible
- Performing large-scale genomic studies using data from the Million Veteran Program, a large (>1M) multi-ethnic cohort enriched for cardiometabolic disease.
Positions Available!
For the 2020-2021 academic year, my lab has openings for computational post-doctoral positions. Please see the following site for further details on how to apply.
The lab also has a number of potential graduate student rotation projects available for the 2020-2021 academic year. Ideal students will have a strong background in computational sciences, and projects will be built around human genetic data, bioinformatic applications, statistical genetic analysis, epidemiology, and/or population and systems biology. Please contact me if you are interested.
研究兴趣
论文共 234 篇作者统计合作学者相似作者
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Arteriosclerosis, thrombosis, and vascular biology (2024)
Genome Biologyno. 1 (2024): 1-19
medRxiv (Cold Spring Harbor Laboratory) (2023)
引用2浏览0引用
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medRxiv (Cold Spring Harbor Laboratory) (2023)
biorxiv(2023)
Daniel Hui, Eric Sanford, Kimberly Lorenz, Scott M Damrauer,Themistocles L Assimes, Christopher S Thom,Benjamin F Voight
medRxiv : the preprint server for health sciences (2023)
medRxiv : the preprint server for health sciences (2023)
Varun Bahl, Eric Waite, Reut Rifkind, Zenab Hamdan,Catherine Lee May,Elisabetta Manduchi,Benjamin F. Voight,Michelle Y.Y. Lee, Mark Tigue, Nicholas Manuto, the HPAP Consortium,Benjamin Glaser,
biorxiv(2023)
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