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Printable Handouts
Navigable Slide Index
- Introduction
- Mendelian vs. complex diseases (1)
- Mendelian vs. complex diseases (2)
- The genetic epidemiology of complex diseases (1)
- Case example: asthma phenotype
- The genetic epidemiology of asthma
- Linkage regions and candidate genes
- Southern California Children's Health Study
- Exposure assessment
- Effects of particulates on bronchitis
- Familial aggregation of asthma
- Familial aggregation/maternal smoking interaction
- GSTM1, maternal smoking, and active asthma
- Pathways in asthma
- Oxidative stress
- Determinants of oxidative stress
- Conceptual model for oxidative stress pathway
- Genes involved in oxidative stress
- Oxidative stress pathways (1)
- Oxidative stress pathways (2)
- The genetic epidemiology of complex diseases (2)
- USC colorectal polyps study
- Other pathways for sporadic colorectal cancer (1)
- Multivariate analyses of polyps data (1)
- Polyps data: main effects
- Polyps data: mEH x well done red meat interaction
- Interactions in polyps data
- Problems with these approaches
- Multivariate analyses of polyps data (2)
- Bayes model averaging (1)
- Bayes model averaging (2)
- Bayes factors
- Graphical illustration
- Hierarchical model
- Bayes factors for models (1)
- Bayes factors for models (2)
- Bayes factors for terms averaging across models
- Graphical illustration
- Incorporation of "prior covariates"
- Multivariate analyses of polyps data (3)
- Conceptual model for HCA and PAH pathways
- HCA pathway
- PAH pathway
- Mathematical representation (1)
- Mathematical representation (2)
- Graphical illustration (1)
- Graphical illustration (2)
- Genotype-phenotype relationship for one step
- Details of one step
- Models for individual metabolic rates
- Toxicogenetic models
- Intermediate metabolites
- Nonlinear toxixokinetics
- Markov chain Monte Carlo
- Details of MCMC sampling
- Convergence of interaction term
- Contribution of smoking to PAH pathway (1)
- Contribution of smoking to PAH pathway (2)
- Contribution of smoking to PAH pathway (3)
- Contribution of exposures to both pathways
- Contribution of pathways to polyps risk
- Genetic effect estimates
- Simulation studies
- Graphical illustration
- Simulated vs. estimated beta
- Simulated vs. estimated gamma
- Simulated vs. estimated delta
- Simulated vs. estimated omega
- Simulated vs. estimated phi
- Simulated vs. estimated psi
- Limitations: biological
- Limitations: statistical
- Other pathways for sporadic colorectal cancer (2)
- Folate pathways
- Folate (DNA methylation) pathway (1)
- Genes involved in folate (DNA methylation) pathway
- Folate (DNA methylation) pathway (2)
- Folate (DNA repair) pathway (1)
- Genes involved in folate (DNA repair) pathway
- Folate (DNA repair) pathway (2)
- Combined folate pathways
- Other pathways for sporadic colorectal cancer (3)
- Bile acids pathways (1)
- Bile acids pathways (2)
- Genes involoved in bile acid reabsorption
- Bile acids pathways (3)
- Genes involved in bile acid degredation
- Bile acids pathways (4)
- Bile acids biosynthesis
- The bigger picture
- Conclusions
- A cautionary comment
Topics Covered
- Case study: asthma
- Multiple environmental agents
- Polygenic factors
- Standard approaches: contingency tables and logistic regression methods
- Latest approaches: Bayesian model averaging and pharmacokinetic modelling
- Case study: colorectal cancer
- Taking account of prior knowledge
- The potential for application to other pathways
- Biological and statistical limitations
Talk Citation
Thomas, D. (2004, September 1). Bayesian approaches for modelling complex metabolic pathways [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 21, 2024, from https://doi.org/10.69645/HAHR3177.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Duncan Thomas has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.