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Determination of the correlation between the developmental patterns of expression of DMEs and regulatory pathways; Use of sensitive, specific, rapid methods (e.g., microarrays, proteomics, metabolomics) to identify predictive biomarkers of drug response and toxicity; Inducibility and imprinting of genes involved in pharmacokinetics or pharmacodynamics; Short-term or long-term alterations of genes involved in pharmacokinetics or pharmacodynamics in response to drug and environmental chemical exposure in early development; Ontogeny of both expression and functional characteristics of polymorphic expression of DMEs, receptors and transporters exhibiting genetic polymorphisms; Role of disease, ethnicity and sex in the ontogeny of DMEs, transporters, and receptors; The role played by intestinal and liver transporters in drug distribution and action; Environmental influences (e.g., nutrition, diet, chemicals, drugs of abuse) and modulating influences (hormones and other ligands) on DMEs, transporters and receptors (efficacy and toxicity) during development; Systems models, including, but not limited to, pharmacokinetic-pharmacodynamic approaches to assess the sensitivity of the CNS, and other organs, to therapeutic drugs (e.g., anesthetics) and drugs of abuse across the course of development; Analysis and comparison of cell, tissue and organ-specific effects of drug responses across various developmental stages: e.g., changes in receptor coupling, second messengers, and signal transduction pathways; Application of in vitro systems (e.g., transporter knockout and humanized transporter animal models) for evaluating transporters interactions during development; Identification of the effect of current drug therapies on critical developmental CNS processes such as synapse formation and remodeling, cell migration, cell replication and differentiation and cell survival; Role of the ontogeny of DMEs, transporters, and ion channels in the production of idiosyncratic and dose-related ADRs in children Use of sensitive, specific rapid methods (eg., microarrays, proteomics, metabolomics) to identify predictive biomarkers of drug response; Inducibility and imprinting of genes involved in pharmacokinetics or pharmacodynamics; Short-term or long-term alterations of genes involved in pharmacokinetics or pharmacodynamics in response to drug and environmental chemical exposure in early development; Ontogeny of both expression and functional characteristics of polymorphic expression of DMEs, receptors and transporters exhibiting genetic polymorphisms; Role of disease, ethnicity and sex in the ontogeny of DMEs, transporters, and receptors; The role played by ontogeny of intestinal, kidney and liver transporters in drug distribution action and toxicity; Environmental influences (e.g., nutrition, diet, chemicals, drugs of abuse) and modulating influences (hormones and other ligands) on DMEs, transporters and receptors (efficacy and toxicity) during development; Analysis and comparison of cell, tissue and organ-specific effects of drug responses across various developmental stages, e.g., changes in receptor coupling, second messengers, and signal transduction pathways; Application of in vitro systems (e.g., transporter knockout and humanized transporter animal models) for evaluating transporters interactions during development; Identification of the effect of current drug therapies on critical developmental CNS processes such as synapse formation and remodeling, cell migration, cell replication and differentiation and cell survival; Role of the ontogeny of DMEs, transporters, and ion channels in the production of idiosyncratic and dose-related ADRs in children; Use of genomics, proteomics and transcriptomics technology in the discovery and identification of toxicity biomarkers during development; In vitro and in vivo models to predict toxicity in pediatric populations due to fetal drug exposure; Study of the role of reactive metabolites produced in extrahepatic tissues as a result of oxidative stress, in the pathogenesis of toxic and/or hypersensitivity reactions in children , source: Lead is a Silent Hazard download pdf.

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