Sentences with phrase «gene in mice resulted»

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After determining the proper dosage of tamoxifen — an early trial resulted in a number of mouse deaths due to overactivation of Mecp2 — researchers settled on a four - week regimen of ramping up the gene's function.
This suggested that obesity in both obese and db mouse strains resulted from a mutation in a single gene in each case.
Bone marrow transplant cured compulsive behaviour in mice whose OCD symptom seems to be the result of a mutation in a gene never before linked to behaviour.
So far, gene therapy attempts have only resulted in partial improvements of hearing in mouse models of specific human deafness forms that did not include severe anomalies in hair cell structure.
With a single local injection of the USH1G gene just after birth, the scientists observed a restoration of the structure and mechanosensory function of the inner ear hair bundles — profoundly damaged before birth -, resulting in a long - term partial recovery of hearing, and complete recovery of vestibular function in these mice.
In a test of this theory, researchers have demonstrated that mice harboring a human SCN1A gene mutation that results in Dravet Syndrome (DS), a severe and intractable genetic epilepsy, have electrical disturbances in the heart that culminate in ventricular fibrillation and sudden cardiac deatIn a test of this theory, researchers have demonstrated that mice harboring a human SCN1A gene mutation that results in Dravet Syndrome (DS), a severe and intractable genetic epilepsy, have electrical disturbances in the heart that culminate in ventricular fibrillation and sudden cardiac deatin Dravet Syndrome (DS), a severe and intractable genetic epilepsy, have electrical disturbances in the heart that culminate in ventricular fibrillation and sudden cardiac deatin the heart that culminate in ventricular fibrillation and sudden cardiac deatin ventricular fibrillation and sudden cardiac death.
That means that the approach that worked so well for finding the sweet receptor — identifying a likely gene for the receptor, destroying it in mouse embryos, and proving that the resulting mice are unable to taste sweetness — will not work in the search for the salt receptor.
Scientists had been searching in vain for such a gene since 1994 when Rockefeller University scientist Jeffery Friedman found that lab mice with a specific genetic mutation fail to produce leptin and as a result have uncontrollable appetites, and become huge.
The research team found that when the SMAD4 gene is eradicated in mice, it also results in depletion of ME2 levels.
In Martin's view, the result strongly suggested that the patients had inherited the silenced gene from one of their parents, like the case with agouti mice.
To find out what BRCA2 does normally, the team reporting the new results, which includes Allan Bradley of Baylor College of Medicine in Houston and Paul Hasty of Lexicon Genetics Inc. in The Woodlands, Texas, created «knockout» mice in which the gene was inactivated.
She and her colleagues will be exploring the role of YY1 further, using clinical samples as well as mouse models, to look at the protein in diseases like lupus to deepen their understanding of how autoimmunity could result from the «escape» of immune genes from X chromosome inactivation.
When the researchers then induced stroke in mice either with or without the PARP gene, they found that the resulting tissue damage in the mice without the enzyme was 80 % less than in normal mice.
When his team looked at gene expression changes in the mice, then applied them to humans with early stage cancer, the results revealed a breakdown of which patients have a high or low chance of survival.
«To our knowledge, our model is the first in which expression of a single gene in postnatal hair cells results in hair cell survival and hearing preservation in mice that otherwise suffer from age - related and noise - induced hearing loss,» Dr. Chen said.
In this mouse model, mutations in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different colorIn this mouse model, mutations in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different colorin Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different colorin the formation of individual tumor cell populations that were labeled with different colors.
«No gene is truly off, and the off state in this case resulted in enough leaky DUX4 expression to kill the mice
Scientists deleted the LZK gene in astrocytes of one group of injured mice, which decreased the cells» injury response and resulted in a larger wound on the spinal cord.
The genetically modified mice distort the results because of the human growth hormone, so in many cases the effect of that gene was either overvalued or undervalued.
Results showed that naturally healthy macrophages and gene - corrected macrophages worked equally well in correcting the disease in the mice.
In mice lacking the NDST1 gene, and therefore the NDST1 enzyme, nature substitutes with an NDST1 isoform (NDST2, NDST3, and NDST4), but the results — like substitutions in cooking — are noticeablIn mice lacking the NDST1 gene, and therefore the NDST1 enzyme, nature substitutes with an NDST1 isoform (NDST2, NDST3, and NDST4), but the results — like substitutions in cooking — are noticeablin cooking — are noticeable.
In tests on human breast cancer cells and in special immunodeficient mice with tissue grafts, the scientists found that both agents interfered with genes involved with breast cancer cell growth, resulting in more cancer cellIn tests on human breast cancer cells and in special immunodeficient mice with tissue grafts, the scientists found that both agents interfered with genes involved with breast cancer cell growth, resulting in more cancer cellin special immunodeficient mice with tissue grafts, the scientists found that both agents interfered with genes involved with breast cancer cell growth, resulting in more cancer cellin more cancer cells.
Dr. Je and his team analysed signalling activity in neuronal cultures that either did not have the DTNBP1 gene or had lowered levels of the gene, because reduced DTNBP1 levels and genetic disruptions of DTNBP1 in mice resulted in schizophrenia - like behaviours.
Petris found that young mice missing the ATP7A gene in their intestinal cells were unable to absorb copper from food, resulting in an overall copper deficiency that mimics symptoms of Menkes disease in children.
Scientists compared urination patterns, both volume and frequency, in normal mice and in mice genetically engineered without two circadian genes, Cryptochrome - 1 and Cryptochrome - 2, resulting in dysfunctional circadian rhythms.
Results of previous studies in mice of bexarotene's effect on AD have been mixed, and none of those studies were done in mice that carry a human APOE gene and also develop progressive, AD - like pathology.
This gene therapy resulted in high - fat diet mice having a reduced body weight, building up less fat, expending more energy, and showing evidence of improved leptin - signalling.
Furthermore, organ cultured cartilage from ACH mice treated with statin resulted in increased expression of the aforementioned three genes and also in Runx2 and Col10a1, which indicated that statin stimulated both the differentiation and maturation of ACH mouse chondrocytes.
Consistent with these results, genetic inactivation of an HR gene (Fancd2) and Polq in mice results in embryonic lethality.
PER2: Deletion of the PER2 gene in mice, associated with the mechanisms of circadian rhythm, appears to improve DNA repair in stem cell populations relevant to the immune system, resulting in a healhier immune cell population, better immune function in old age, and a modestly extended life span.
The resulting change in the appearance, behaviour or biochemical characteristics of the mouse then gives an indication of the gene's normal role in the mouse, and perhaps in humans.
Catalase: Gene therapy to increase levels of the antioxidant catalase in the mitochondria in mice have produced mixed results, but some studies show improved health and extended life.
In Yeast, Worms, Flies, and Mice, Only About 1 in 3 Genes is Essential for Viability The consequences of some genomic perturbations can not be compensated for by normal epigenetic processes and result in the death of the organism prior to adulthooIn Yeast, Worms, Flies, and Mice, Only About 1 in 3 Genes is Essential for Viability The consequences of some genomic perturbations can not be compensated for by normal epigenetic processes and result in the death of the organism prior to adulthooin 3 Genes is Essential for Viability The consequences of some genomic perturbations can not be compensated for by normal epigenetic processes and result in the death of the organism prior to adulthooin the death of the organism prior to adulthood.
Südhof used genetic engineering to «knock - out» the synaptotagmin gene in mice, with the result that synapses from the forebrains of mice that lacked synaptotagmin lost their capacity for fast calcium - triggered release of neurotransmitter, thus confirming the importance of synaptotagmin in vivo.
The scientists removed the gene region containing the risk variant from the mouse genome, and found that as a result the mice were healthy but displayed a small decrease in the expression of a nearby cancer gene, called MYC.
Here we present an experimental reannotation of the GENCODE intergenic lncRNA populations in matched human and mouse tissues that resulted in novel transcript models for 3,574 and 561 gene loci, respectively.
To better illustrate gene expression profiles in mouse ES cells, we have organized the results in an interactive database with a number of features and tools.
Results: Here, we profile genome - wide changes in DNA methylation, gene expression and lipidomics in response to DR and aging in female mouse liver.
A gene that naturally occurs on the mouse's sex chromosome can be moved to another chromosome where it results in all - male offspring.
The results implicate GPC6 as a novel determinant of BMD, and also identify abnormal skeletal phenotypes in knockout mice associated with a further 100 prioritized genes.
In one mouse study, the IGF - 1 gene was placed in the animals» glutes and calves, which resulted in up to a 115 % increase in muscle - cross-sectional areIn one mouse study, the IGF - 1 gene was placed in the animals» glutes and calves, which resulted in up to a 115 % increase in muscle - cross-sectional arein the animals» glutes and calves, which resulted in up to a 115 % increase in muscle - cross-sectional arein up to a 115 % increase in muscle - cross-sectional arein muscle - cross-sectional area.
The researchers noted that the mouse results may have implications for human health as well, as they also found an E. coli variant with the suspect genes in high percentages of human patients with colorectal cancer and irritable bowel disease.
Calorie Restriction - like Effects of 30 Days of Resveratrol Supplementation on Energy Metabolism and Metabolic Profile in Obese Humans Cell Metabolism 2011 (Nov 2); 14 (5): 612 — 622 ~ FULL TEXT The result of just 30 days on resveratrol were impressive: (1) The same gene regulators (AMPK, SIRT1 and PGC - 1a) were activated in this study as are activated by caloric restriction and resveratrol in mice and endurance training in humans.
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