5 edition of Genetic Variability in Responses to Chemical Exposure found in the catalog.
by Cold Spring Harbor Laboratory Pr
Written in English
|Contributions||Harry Victor Gelboin (Editor)|
|The Physical Object|
|Number of Pages||421|
Understanding the genetic basis of responses to chemical and physical exposures can help to predict which individuals will respond best, and with the least side effects, to particular pharmaceutical agents and also to predict which individuals will be most at risk from specific occupational and environmental exposures. Ecogenetics is a branch of genetics that studies genetic traits related to the response to environmental substances. Or, a contraction of ecological genetics, the study of the relationship between a natural population and its genetic structure. Ecogenetics principally deals with effects of preexisting genetically-determined variability on the response to environmental agents.
Specifically, we compare how genetic variability in feeding responses among the studied Daphnia clones changed across increasing nonlethal exposure levels (expressed as increased exposure levels of feeding inhibition, EC) and how these changes converge relative to acute lethal responses (expressed in terms of the 48‐h LC50). Our data show Cited by: A number of factors, including the population’s genetic structure and the environment (Figure ) influence population variation, the distribution of phenotypes among individuals. Understanding phenotypic variation sources in a population is important for determining how a population will evolve in response to different evolutionary pressures.
This FOA solicits Phase I (R43), Direct to Phase II (R44) and Fast-track (R44) SBIR grant applications from SBCs to develop resources and approaches that reflect the variability in responses to chemical exposures based on genetic diversity in the human population. The team from NC State and Oregon State analyzed high throughput screening data to find patterns of interindividual variability in response to chemical exposure: in .
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Abstract. Individuals differ in their response to environmental exposures. In the following, we describe examples and paradigms of studying heritable differences in response to exposure—commonly known as “gene–environment interaction” or “ecogenetics”—and their relation to Cited by: 2.
In addition to offering increased biological sensitivity, the use of inbred, isogenic strains increases statistical power since variability in phenotypic response to chemical exposure is minimized. However, by the same token, they may fail to take into account the full spectrum of genetic variation and responses in natural by: 6Application to Analyzing Variation in Human Susceptibility.
As a rule, humans vary in their responses to environmental factors because of variability in their genes and their genes’ epigenetic modification. Consequently, the same level of exposure to a chemical compound may give rise to different biologic effects in different individuals.
Researchers from North Carolina State University and Oregon State University have pinpointed a genetic difference in zebrafish tied to differing responses to the same environmental chemical.
The work could have implications for identifying genetic factors that explain differential chemical sensitivity. Everyone has a unique combination of polymorphic traits that modify susceptibility and response to drugs, chemicals and carcinogenic exposures. The metabolism of exogenous and endogenous chemical toxins may be modified by inherited and induced variation in CYP (P), acetyltransferase (NAT) and glutathione S-transferase (GST) genes.
Ecotoxicological tests may be biased by the use of laboratory strains that usually contain very limited genetic diversity. It is therefore essential to study how genetic variation influences stress tolerance relevant for toxicity outcomes.
To that end we studied sensitivity to cadmium in two distinct genotypes of the parthogenetic soil ecotoxicological model organism Folsomia by: 9. Environmental Toxicology is the third volume of a three-volume set on molecular, clinical and environmental toxicology that offers a comprehensive and in-depth response to the increasing importance and abundance of chemicals of daily life.
By providing intriguing insights far down to the molecular level, this three-volume work covers the entire range of modern toxicology with special. The toxicity associated with PAHs exposure is the result of genetic variability and epigenetic mechanisms. With regard to genetic susceptibility, polymorphisms in PAHs metabolizing—CYP1A1, mEH, GSTP1, GSTM1, NAT2, and DNA repair—APEX1, XPA, XPC—enzymes may have a role in PAHs associated by: Genetic disorder associated with an imbalance in the ratio of alpha and beta globin caused by reduced or absent synthesis of beta globin.
Fetal hemoglobin has two alpha globins and two gamma globins. Gamma globins, part of the beta cluster, are switched off at birth, and beta gene is activated. Start studying Review Book Quiz #2. Learn vocabulary, terms, and more with flashcards, games, and other study tools.
genetic basis of variation 4)competition. the bacteria that survived exposure to penicillin learned to avoid it 3)the bacteria that caused the new outbreaks were from populations that had never been exposed to.
What are the highlights of the chemistry and physical-chemical properties of the drug Exposure-Response Does genetic variation impact exposure and/or response?. 31 Extrinsic Factors. Genetic variability in responses to chemical exposure. [Cold Spring Harbor, N.Y.]: Cold Spring Harbor Laboratory, (OCoLC) Online version: Genetic variability in responses to chemical exposure.
[Cold Spring Harbor, N.Y.]: Cold Spring Harbor Laboratory, (OCoLC) Material Type: Conference publication: Document Type: Book. To date, studies on genetic variability in the tolerance of aquatic biota to chemicals have focused on exposure to. single chemicals. In the ﬁeld, metals occur as elemental mixtures, and thus it is essential to study whether the genetic.
consequences of exposure to such mixtures differs from response to single chemicals. Genetic variability is the cornerstone of wheat breeding. Variability can be sourced from hexaploid wheat or its near and distant relatives.
Traits can be introgressed into hexaploid wheat from these sources using conventional hybridization techniques. variability in exposure (AUC, Cmax, Cmin) in patients with the target disease and how much of the variability is explained by the identified covariates?.
28 Based upon what is known about E-R relationships in the target population and their variability, what dosage regimen adjustments are. The vision, raised by the sequencing of the human genome, of applying this information to more broadly understand the genetic basis of variability in drug responses is tantalizing, but faces.
And are there genetic factors that explain differential sensitivity?” The team from NC State and Oregon State analyzed high throughput screening data to find patterns of interindividual variability in response to chemical exposure: in other words, they looked for chemicals that elicited differing responses.
we believe that identifying genetic differences between races and ethnic groups, be they for random genetic markers, genes that lead to disease susceptibility or variation in drug response, is.
Individual variability in drug efficacy and drug safety is a major challenge in current clinical practice, drug development, and drug regulation. For more than 5 decades, studies of pharmacogenetics have provided ample examples of causal relations between genotypes and drug response to account for phenotypic variations of clinical importance in drug by: Performing genetic association studies on drug response can be especially challenging .
A key challenge is that the detection of a drug-response phenotype requires accurate identification of at least two “phenotypes”—the drug exposure and the outcome. In some cases, it requires resolving temporal sequences of more than two phenotypes.
Mutations. DNA polymerase occasionally makes uncorrected mistakes when copying a cell’s genetic information during DNA replication.
These mistakes are called spontaneous mutations, and they introduce changes into the genetic code. In addition, exposure of cells to mutagens (environmental agents, such as X-rays and certain chemicals that cause changes in DNA) can increase the number.
The authors review recent advances and current debates in epigenetics, including how epigenetic mechanisms interact with genetic variation, ageing, disease and the by: In contrast, adapting to novel contaminants such as synthetically produced chemicals with no precedent of occurrence in the environment may prove especially challenging, for example, if adaptive responses require novel genetic variation (Barrett and Schluter ).
Moreover, the occurrence of contaminants alongside numerous other human Cited by: