Sentences with phrase «normal mice do»

At the same time, the rodents had an even greater response to social defeat stress than normal mice do, suggesting their brains also are more susceptible to a depressive - like state.

Normal mice do not develop disease if injected with human prions, presumably because the human prion binds only to human PrP.

«The mice also did not seem to gain weight when they got older, like normal mice do.

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.

The NK1R - deficient mice consumed far less alcohol — especially later in the trial when alcohol concentration was higher — than the normal mice did.

When these knockout mice were fed a high - fat diet, they gained as much weight as normal mice did, but they managed to remain sensitive to insulin.

Since more Cx43 means less room in the bladder, the team speculates that although normal mice didn't stop producing urine when asleep, their bladders were able to hold more due to decreased Cx43 concentrations.

Bone marrow from the p16 - deficient mice made 3 times as many blood - forming stem cells as bone marrow from the normal mice did.

Chen and colleagues report online today in Science that mice without GRPR neurons scratched significantly less than normal mice did — about 80 % less in each case.

The quest for better opioids got a much - needed jolt in 1999, when researchers at Duke University showed that mice lacking a protein called beta - arrestin 2 got more pain relief from morphine than normal mice did.

Gordon and his team found several years ago that genetically obese mice (the animals lacked the ability to make leptin, a hormone that limits appetite) had 50 percent fewer Bacteroidetes bacteria and 50 percent more Firmicutes bacteria than normal mice did.

Not exact matches

So did mice treated with breast milk that were genetically engineered to have guts lacking receptors to EGF, as well as normal mice treated with breast milk depleted of EGF.

The team found neonatal mice with the mutations had normal - appearing skin, and the dry itchy skin of dermatitis did not develop until the mice were a few months old, the equivalent of a young adult in human years.

These mice performed better than their normal counterparts on learning tests well into old age, and their brains did not exhibit the decline in neurogenesis typically seen in aged mice.

Both mouse and human males typically die early from the mutation in Mecp2, because their Y chromosome does not supply a normal copy of the gene.

Normal mice saw benefits, too: Muscles and pancreas cells healed better in middle - aged mice that got rejuvenation treatments than in mice that did not.

«Mice that don't have these molecules seem to be able to change their brain circuits with experience much more rapidly than normal mice,» Shatz sMice that don't have these molecules seem to be able to change their brain circuits with experience much more rapidly than normal mice,» Shatz smice,» Shatz says.

In general, the mutant mice also had much thicker skin than the normal animals did.

Clarke and colleagues compared normal mice, whose gastrointestinal tracts were teeming with bacteria, with mice bred in sterile environments, whose guts didn't contain any microbes.

For example, normal newborn mouse pups will emit frequent, high - pitched noises when they are separated from their littermates, but VPA - treated pups do not.

While 80 percent of normal mice are able to handle a temperature drop, all mice lacking ERRγ did not tolerate the cold.

Kingsley's team had no idea what the normal gene does, but a team at the University of Tokyo had recently identified the genetic defect behind a similar mouse disease — and determined that its protein product normally generates pyrophosphate on the outside of joint cells to keep the joints scale - free.

The researchers compared this result to normal mice, with both NOX proteins, and found that these mice did develop liver fibrosis after receiving the hepatotoxin.

In a study published October 30 in Neuron, the scientists show that mice genetically altered so they don't produce serotonin didn't scratch as much as normal mice when exposed to irritants.

However, when the researchers knocked out SIRT1 in endothelial cells of 10 - month - old mice, then put them on a four - week treadmill running program, they found that the exercise did not produce the same gains seen in normal 10 - month - old mice on the same training plan.

In subsequent tests, the mice with the mutation did a worse job than normal mice at learning new motor skills.

At first, when the genetically modified mice were put in a sterile, germ - free environment, they did not develop MS.. When exposed to a normal environment that would normally contain bacteria, the mice did develop MS - like disease and inflammation in their bowels, suggesting gut bacteria is a risk factor that triggers MS disease development.

Normal mice watching chronically itchy mice in other cages increased their own scratching in as little as 5 seconds, whereas mice placed near nonitchy mice didn't show any increase in scratching, researchers report in Science.

When the eyes of her mice looked normal, Xu Wang was certain she had done something wrong.

Furthermore, more than 75 % of mice infected with virus bearing the normal protein developed severe corneal autoimmune disease, whereas fewer than 20 % of mice infected with mutant virus did, and their symptoms were barely detectable.

Not only did the normal mice develop plaques, but also a pathology similar to «tangles» — twisted protein strands that form inside brain cells, disrupting their function and eventually killing them from the inside - out.

When fed a diet containing cholesterol, saturated fat, and bile acids for 3 weeks, the transgenic mice, in contrast to normal mice, did not develop a detectable increase in plasma LDL.

To prove that the UL6 protein sequence does in fact trigger the autoimmune attack of HSK, Cantor and his team have now infected mice with either normal HSV - 1 or a strain that they had genetically altered to lack the UL6 protein.

UBC Psychiatry Professor Dr. Weihong Song and Neurology Professor Yan - Jiang Wang at Third Military Medical University in Chongqing attached normal mice, which don't naturally develop Alzheimer's disease, to mice modified to carry a mutant human gene that produces high levels of a protein called amyloid - beta.

The team then administered progesterone inhibitors to normal mice and found that the animals behaved much as their knockout counterparts did.

The mice appear younger and more robust than comparably - aged normal mice, have better muscle tone, and do not develop age - related tumors.

When they exposed these mice to the cold, the animals developed far fewer beige fat cells than did normal animals, suggesting that macrophages were key to browning of white fat.

The normal mice adapted to the stress and didn't succumb to heart failure for weeks.

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.

Exposure to low - oxygen air sends EPO levels soaring in normal mice, but these conditions did not induce a rise in the hormone in the animals without HIF - 1α, the researchers report in the 18 April issue of Cell.

«When we stimulated D1 neurons in normal mice, we did not improve their timing»» he adds.

Bacterial counts from rodents» poop showed that although B. fragilis did not establish lasting colonies in the mice, they did «shake up the community,» of microorganisms, bringing it closer to that of the normal mice, Hsiao says.

The group also didn't investigate how the bacteria affect a normal animal, because the microbes were administered only to autistic mice, he says.

At 14 months, however, the J20 / caspase -2 null mice did significantly better in the water maze test than the J20 mice and similarly to the normal mice.

In mice with A-T, the cerebellum appears normal and they do not exhibit the obvious degeneration seen in the human brain.

Normal mice produced more than four times more melanocytes than did the p53 «knockout» mice.

He notes, however, that other attempts to stimulate bone growth in mice by manipulating cell signaling proteins have produced denser than normal bones — and he's surprised that Helms's team didn't see the same.

But he adds that the study does not show that human astrocytes are genetically normal when engrafted into the mouse brain, and it does not rule out the idea that the improved learning and memory «could be due to the persisting progenitor cells.»

Although muscle cells did not reduce in size or number in mice lacking a protective antioxidant protein, they were weaker than normal muscle cells, researchers from the Barshop Institute for Longevity and Aging Studies at The University of Texas Health Science Center San Antonio found.

The researchers found that in genetically - modified mice lacking Interferon - 1, who were also fed a high - fat diet, the CD8 + T cells did not produce an inflammatory response, and the mice had near normal blood sugar levels.