Sentences with phrase «by normal mice»

Here, the AD model mice lacking PERK were able to successfully maneuver through the mazes at rates achieved by normal mice.

Not exact matches

But later, Javier Bravo at University College Cork managed to change the behaviour of normal adult mice by feeding them with a probiotic bacterium called Lactobacillus rhamnosus, often found in yoghurts and dairy products.

Heijtz could even shift her germ - free mice towards «normal» behaviour and genetic activity by giving them a microbiome transplant, but this only worked early in their lives.

For this study the researchers targeted very specific types of GABA receptors to improve social behaviors with clonazepam, but the team also found that by using a different drug, they could target other GABA receptors and actually reduce the ability to socially interact in normal mice — underscoring that future medications would need to target very specific receptors so as not to diminish the drug's impacts.

Skin grafts of such transgenic mice were rejected by normal C57BL / 10 mice, suggesting that the foreign SLA antigen expressed in the transgenic mice is recognized as a functional transplantation antigen.

Researchers led by Emory University pathologist Andrew Gewirtz found that mice genetically deficient in an immune system receptor have altered gut bacteria, eat more than normal mice do, and develop features of metabolic syndrome.

In the ovary of a normal mouse (left), a large follicle is shown at a late stage of development (a light pink oocyte surrounded by follicular cells, inset).

Older modified male mice metabolised sugar faster than normal mice and females, suggesting that SIRT6 might extend life by protecting against metabolic disorders such as diabetes.

A decade ago, he replicated the entire human leukemia disease process by introducing oncogenes into normal human blood cells, transplanting them into xenografts (special immune - deficient mice that accept human grafts) and watching leukemia develop — a motherlode discovery that has guided leukemia research ever since.

«Transplanted hematopoietic stem cells reverse damage caused by neuro - muscular disorder: In mouse model of Friedreich's ataxia, a single infusion measurably restored normal cellular functions.»

Four days later, the livers of the non-supressed mice had readjusted to a normal daily rhythm, as revealed by the daily rise and fall of liver - gene expression.

When they examined mice genetically incapable of producing Helios, they found the animals beset by a T - cell and antibody attack on normal tissue.

By examining the brains of these mice, the researchers observed a substantial decrease in inhibitory CA2 neurons, as compared to a control group of normal, healthy mice — a change remarkably similar to that previously observed in postmortem examinations of people with schizophrenia.

To investigate the longer - term effects of higher - than - normal acetylcholine levels on the brain, Hermona Soreq of the Hebrew University of Jerusalem and her colleagues first induced high levels of acetylcholine by forcing 26 mice to swim, an activity stressful to mice.

By 2003 other scientists had genetically manipulated mice to be relatively insensitive to either insulin or insulin - like growth factor; in both cases, the genetically engineered mice lived significantly longer than normal mice.

He and colleagues at the University of California, San Francisco, injected the brains of mice with prions they had created in the lab by misfolding normal prion protein, known as PrP.

The authors said that this result suggests that the reason bacterial numbers are so high in these mice, and, by extension, human LAD patients, is not because of a defect in the immune system's surveillance mechanism but because of the inflammation caused by the immune system's abnormal response to normal levels of bacteria in the gums.

Lastly, they plan to vary the timing of exposure to the various diets in the mouse model of autism, by, for example, giving pregnant mice a high - glycemic index diet and then keeping their pups on a normal diet.

However, cancer cells may instead be coaxed to turn back into normal tissue simply by reactivating a single gene, according to a study that found that restoring normal levels of a human colorectal cancer gene in mice stopped tumor growth and re-established normal intestinal function within only 4 days.

Because mice lacking both genes would not be born alive, the scientists followed up this lead by making «conditional knockout mice,» in which Esrp1 and Esrp2 activity was normal early in fetal development, but then was switched off in skin epithelial cells.

By contrast, these females retained a normal level of social interest in other females during estrus, and in male mice when not in estrus.

By switching Apc on, researchers turned swelling mobs of mouse cancer cells (above) back into normal intestinal tissue (below).

In previous studies, the research team, headed by Pier Paolo Di Fiore and Salvatore Pece, investigated the role of a protein called Numb in maintaining stem cells in normal mammary gland development in mice.

«It was particularly exciting to see plasticity in the neurons impaired by mHTT,» said Davidson, noting that in the HD mice, brain areas that had begun to atrophy recovered volume and permitted better motor function after the researchers restored mTORC1 activity to more normal levels.

Mice that made extra catalase in their mitochondria lived longer than normal mice, by about 1Mice that made extra catalase in their mitochondria lived longer than normal mice, by about 1mice, by about 19 %.

Researchers led by developmental biologist Hiroshi Hamada at the University of Osaka used a pump to reverse the normal leftward flow of fluid over mouse embryos.

To validate their findings, the scientists injected the novel nanoparticles into pancreatic tumor - bearing mice and observed that by balancing these two targets — bringing them to a normal level by increasing their expression or blocking the gene responsible for their expression — they significantly prolonged the survival of the mice.

Mice generated from embryonic stem cells in which ion channel genes have been mutated by homologous recombination often have a perfectly normal heart.

Remarkably, giving animals injections of lithium salts — which mimics WNT signaling by inhibiting the molecule GSK3 — or giving animals a more specific GSK inhibitor, the researchers were able to restore normal synapse and spine numbers and also improve some of the most significant psychiatric - like behavioral abnormalities in these mice.

These normal in vivo immune responses in IL -2-deficient mice question the importance of IL - 2 as defined by in vitro studies.

Longo also knew of research by molecular biologist John Kopchick at Ohio University, which showed that mice with a mutation in their growth hormone receptor gene lived 40 percent longer than normal mice — the equivalent of an average American living to age 110.

Notably, they also achieved the same effects on p300 and Tregs in mice by using a drug that inhibits p300 in normal mice.

By transferring part of the gut bacteria from healthy mice to diabetic mice, they are re-establishing a normal level of cathelicidin.

The blood sugar of the diabetic mice were made normal by the gene - therapy - treated human islets on the right.

By comparing the genome of mice with the HLHS heart defects to the genome of normal mice, Lo and her team identified several hundred mutations in the HLHS mutant strains.

When they restored normal nitric oxide levels by having mice breathe in the short - lived gas — as patients have done in clinical trials — cell adhesion did not increase when oxygen levels decreased.

His team could return their α - CaMKII levels to normal by giving the mice a drug that blocked only the engineered copy.

Faustman got her idea by chance while transplanting islets, the pancreatic bodies that contain beta cells, from normal mice into others that had lost theirs to type 1, or juvenile, diabetes.

Led by Massey's Deputy Director Steven Grossman, M.D., Ph.D., a team of scientists targeted the gene CtBP with a drug known as HIPP (2 - hydroxy - imino phenylpyruvic acid) and were able to reduce the development of pre-cancerous polyps by half and return a normal lifespan to mice born with a predisposition to intestinal polyps.

The investigators reached this conclusion by comparing the integrity and development of the blood - brain barrier between two groups of mice: the first group was raised in an environment where they were exposed to normal bacteria, and the second (called germ - free mice) was kept in a sterile environment without any bacteria.

The molecules are critical to normal development: When the genes for certain of these molecules are experimentally erased, the eggs made by female mice are invariably defective, and the errors fatally disrupt the normal choreography of egg maturation.

Malcolm Eames of the BUAV says Harvard supported its patent application by claiming that tests of potential carcinogens would need fewer onco - mice than normal mice.

The researchers, funded by the Medical Research Council (MRC), the Wellcome Trust and Cancer Research UK, compared the effects of two cancer - causing chemicals in normal mice and mice with the barrier defect (the knock - out mice).

The researchers found that levels of a substance called 4 - ethylphenylsulfate that is produced by gut bacteria increased 46-fold in the mice with autistic symptoms, but returned to normal after treatment with B. fragilis.

In contrast, in mice with normal immune systems, emulsifiers induced low - grade or mild intestinal inflammation and metabolic syndrome, characterized by increased levels of food consumption, obesity, hyperglycemia and insulin resistance.

Researchers at the University of Texas (U.T.) Southwestern Medical Center at Dallas noticed that mice used two primary methods to cope with defeat after being repeatedly pummeled by larger, more aggressive foes: Some of the weaker members withdrew, avoiding all types of social interaction for more than a month, whereas others rolled with the punches, so to speak, quickly bouncing back to their normal behavior.

The researchers looked for genes that were turned on by dHAND in normal mice, but nonfunctioning when dHAND was shut down.

By comparing mouse and cow embryos made either by normal fertilization, in vitro fertilization, or cloning, they discovered that developing embryos can fix short telomereBy comparing mouse and cow embryos made either by normal fertilization, in vitro fertilization, or cloning, they discovered that developing embryos can fix short telomereby normal fertilization, in vitro fertilization, or cloning, they discovered that developing embryos can fix short telomeres.

The fact that Connexin 30 knockout mice had a higher number of grafted cells than normal mice, and that some of the grafted cells expressed CONNEXIN 30 is a very important finding when considering cell transplantation as a treatment for hereditary hearing loss caused by CONNEXIN deficiency.

Moreover, normal mice, ordinarily killed or disabled by an ischemic stroke, were given a shot of a compound that blocks the action of IL - 21.