Sentences with phrase «genetic effects model»

Not exact matches

Zebrafish are commonly used to model human diseases, in part because their larvae are transparent, making it easy to see the effects of genetic mutations or drugs.

The research is also the first to demonstrate beneficial effects of UDCA on dopaminergic neurons, the nerve cells affected in Parkinson's disease, in a fly model of Parkinson's disease which carries the same genetic change as some patients with the condition.

«Besides being a great genetic model, it's also easier for us to study effects like sleep rebound in flies, as we have automatic equipment that can monitor thousands of them.

«So it might be genetic, or it might be a modeling effect.»

She did her master's degree research project at the Institute of Biochemistry and Biophysics (IBB), also in Warsaw, looking at the effect of genetic mutations on the function of an enzyme involved in the biosynthesis of heme, using Saccharomyces cerevisiae as a model organism.

«We have developed a mouse genetic model of Dravet syndrome, which is allowing us to probe more deeply into the possible beneficial effects of cannabidiol,» Catterall said.

The study, which compared each model's success in Caucasian women with those of Asian descent (Chinese, Japanese, Filipino, Korean and Vietnamese), also raised important questions about the effect of race on cancer development: When Caucasian and Asian patients with similar family histories of breast and ovarian cancer were compared, the Asian women had higher rates of genetic mutation, although the rates of these cancers for Asians have traditionally been lower.

The first genetic clues for slowing aging emerged from animal models in which the effect of individual genes on average life spans could be tested.

Zebrafish can be used as a model to understand what biological effects result from these genetic mutations.

The alternative model is that mutations of large phenotypic effect underlie most of these traits in dogs and that the same variants have been transferred to a wide diversity of dog breeds leading to phenotypic diversity from a narrow genetic base [5], [8], [12].

Epigenetically - effected hypothalamic GnRH secretion is central to my model of nutrient - dependent pheromone - controlled adaptive evolution, which was presented as «Olfactory - genetic - neuronal - hormonal reciprocity in learning, memory, behavior and in immune function» during a 1995 Anti-Aging medicine conference.

Dr. Parsons has provided similar insights into the mechanisms through which endocannabinoids modulate the rewarding effects of opiates, alcohol, and cocaine, and he is presently extending his evaluations of this stage of the addiction cycle to include animal models of commonly occurring genetic polymorphisms that are associated with problematic drug use and dependence in humans.

Differential effects of pharmacologic and genetic modulation of NMDA receptor activity on HIV / gp120 - induced neuronal damage in an in vivo mouse model.

These network models will help us to predict the functional effect of genetic variation, design interventions and therapies, and understand how living systems respond to changes in their environment.

-- 1) Improved understanding of adaptive genetic and phenotypic forest characteristics that would provide better guidance for breeding programs and management actions to maximize resilience to both direct and indirect climate impacts to forests; 2) Long - term studies to better understand effects of CO2 fertilization in Montana's forests; 3) Improved models of climate and vegetation effects on evapotranspiration and water balances throughout forested systems.

We are now using these models to study the gene function and complex mechanisms underlying disease pathways, with a focus on genetic background effects, genetic modifiers and interaction partners.

In addition, we are studying genetic background effects on onset and progression of ALS symptoms in the mouse model in hopes that these will provide novel targets for therapy.

Transgenic and gene knockout / knockin technologies have become important experimental tools for assigning functions to genes at the level of whole complexity of organism, creating models of genetic disorders, evaluating effects drugs and toxins, thus helping to answer fundamental issues in basic and applied research.

Chronic Class IIa HDAC inhibition only partially replicates the beneficial effects of HDAC4 genetic reduction in HD models O. AZIZ, C. A. LUCKHURST, T. HEIKKINEN, O. KONTKANEN, G. TOMBAUGH, S. GELMAN, D. YATES, K. MATTHEWS, R. WILLIAMS, P. BRECCIA, M. LAMERS, R. JARVIS, A. HAUGHAN, D. FISCHER, G. MCALLISTER, W. BLACKABY, A. GHAVAMI, G. OSBORNE, D. GOODWIN, G. BATES, I. MUNOZ - SANJUAN, C. DOMINGUEZ, L. PARK, M. MAILLARD, V. BEAUMONT... Abstract / Posters

The advent of human - induced pluripotent stem cell (hiPSC) technology has provided a unique opportunity to establish cellular models of disease from individual patients, and to study the effects of the underlying genetic aberrations upon multiple different cell types, many of which would not normally be accessible.

The Effect of Wolbachia on Genetic Divergence between Populations: Models With Two Way Migration.

In preclinical trials, the effect of chloroquine and hydroxychloroquine on tumorigenesis has been extensively investigated in mouse cancer models, including genetic and xenograft models (summarized in Table 2).

The effect of Wolbachia on genetic divergence between populations: Mainland - Island model.

A polygenic animal model, assuming additive genetic effects, was first applied for each breed.

The complete mixed inheritance model was where y = grades for hip dysplasia or elbow dysplasia; mean of the right and left joint, β = nongenetic fixed effects, b = random breeder effects, c = random litter effects, u = additive genetic effects, W = genotypes, m = genotype means, and e = random residuals.

Randomly drawn samples were made by shuffling, that is, each trait value and the corresponding model effects were reassigned to a new individual, while the individual's genetic links were retained (Churchill and Doerge, 1994).

The best - fitting Cholesky model revealed developmentally dynamic effects, mostly genetic attenuation and innovation.

In addition, behaviour - genetic analyses usually employ main effects models dividing up the total phenotypic variance into additive (or dominant) genetic, shared and non-shared environmental components.

The passive model can be used to explain the genetic effects as a result of the overlap in 50 % of the genes that a parent and a biological child share.

If the author wanted to bolster her argument for genetic influences, she could use the child - effects model or look to the vast array of behavior genetics research.

Main and interaction effects of genetic and environmental factors were analyzed by general linear models (GLMs).

Any genetic or environmental effects associated with baseline level or developmental change captured by the intercept and slope parameters of latent growth curve models can not be predicted from these intraclass correlations.

Models that estimate the effect of environmental exposures on developmental outcomes typically ignore genetic factors or focus on gene — environment interaction (whether individuals» response to environmental exposures depends on their genotype).

Genetic, shared, and non-shared environmental effects were estimated for each temperamental construct and psychiatric disorder using the statistical program MX. Multivariate genetic models were fitted to determine whether the same or different sets of genes and environments account for the co-occurrence between early temperament and preschool psychiatric disGenetic, shared, and non-shared environmental effects were estimated for each temperamental construct and psychiatric disorder using the statistical program MX. Multivariate genetic models were fitted to determine whether the same or different sets of genes and environments account for the co-occurrence between early temperament and preschool psychiatric disgenetic models were fitted to determine whether the same or different sets of genes and environments account for the co-occurrence between early temperament and preschool psychiatric disorders.