Sentences with phrase «in normal mice»

The scientists then set out to see whether they could use a drug to achieve the same effect in normal mice.

By changing the times the lights went on and off during the night each week, the researchers modeled the effects of chronic jet lag in normal mice who were fed a healthy diet.

The researchers then decided to see what would happen if they boosted sirtuin levels in normal mice as they aged.

We found that, indeed, it's much easier to trigger these blackouts experimentally in the brainstem of those mice, while in normal mice we could not trigger them at all,» said Noebels.

In those mice, but not in normal mice, they found that caerulein caused existing alpha cells in the pancreas to differentiate into insulin - producing beta cells.

Some fell into a pattern of two to three separate cycles of sleep and activity per day, in contrast to the single daily cycle found in normal mice, while others» rhythms were completely disorganized, Blackshaw says.

The researchers also showed that DENV NS1 caused similar levels of blood vessel leak in normal mice as in mice bred to have inhibited cytokine activity, suggesting that cytokines were not necessary for this effect.

This was easily discernible objectively in the normal mouse with the aid of the cage movement registration method.

DNA sequencing of sperm from the grandfather mice and their pups also revealed epigenetic marks on the gene encoding M71 that weren't seen in normal mice.

So this is big not for the degree of life extension, but rather for the rest of what this effort represents: a venture backed startup with big names doing SENS research and development in a very public way, and pushing the SENS line into the media via their university and venture capital PR machines, as well as one of the first life span studies in normal mice for a SENS rejuvenation biotechnology.

Given this, I assume it would have to mean those max lifespan extending interventions you mentioned that work in normal mice (CR, Met Restriction, GH Knockout, IGF - 1 and Insulin Signalling Manipulation) reduce ALL major forms of fatal aging damage?

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.

In comparison, succinate was barely detectable in the normal mice.

In normal mouse groups, the dominant mouse trims the whiskers and facial hair of subordinate mice, but the mutant mice, which were housed together, all had full sets of whiskers.

The researchers found that Sp7 in normal mice was expressed only in the dental mesenchymal tissue that gives rise to odontoblasts; it was not expressed in the oral epithelium that gives rise to ameloblasts.

However, a high - fat / low - carbohydrate ketogenic diet stimulated water drinking in normal mice while mice genetically unable to produce FGF21 failed to increase water intake in response to that nutritional stress.

In normal mice there was more TRPV4 expressed in trigeminal sensory neurons when inflammation was induced.

After LPS was added, the neutrophils in a mouse lung deficient in CD11b crawled about a third of the distance as the neutrophils in a normal mouse lung.

The authors observed that activation of the FAT10 gene in normal mice increases in fat tissue with age.

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

They decided to look at the effects of endotoxin in normal mice, and in those who had been genetically engineered to lack the enzyme.

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.

Intrigued, Turek joined with endocrinologist Joseph Bass, also at Northwestern, to study the effects of regular and high - fat diets in normal mice and mice with a dysfunctional Clock gene.

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

To do this they will compare prostate cancer formation in normal mice and mice lacking Runx2 in their prostates.

In a normal mouse model (left), cell growth is controlled but in a mouse model with the ERK1 / 2 pathway blocked (right) increased cell proliferation and loss of organization occurred.

Notably, these miR - 34a - deficient tumors invaded into neighbouring tissue, which was not observed in 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).

So far, all the experiments have been conducted in normal mice and human follicles.

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

Raised alongside unaltered mice and fed the same diet rich in omega - 6's, the transgenic mice maintained a one - to - one omega - 6 to omega - 3 fatty acid ratio, compared to a 20 - to - 1 ratio in the normal mice.

A fractured leg bone heals in normal mice (left), but mice lacking the protein PlGF have globs of cartilage (red).

To see whether point mutations, which affect just one DNA base in mtDNA, are directly involved in aging, a team of researchers at the University of Washington in Seattle charted mtDNA mutation frequency in normal mice and «mitochondrial mutator» mice.

When the researchers examined various tissues in normal mice 3 hours to 2.5 days after birth, they found active autophagy in heart, diaphragm, and lung cells, but not in the brain.

The researchers measured 40 % more of the enzyme PDE4A5 in the brains of sleep - deprived mice than in normal mouse brains.

Light stimulation did not boost the number of spines in normal mice or strengthen the fear memory, nor did indiscriminately shining light in the dentate gyrus result in any long - term memory improvement.

When the scientists fed these mice a high - fat diet that clogged their arteries and performed a procedure similar to stent insertion, they found that the arteries in these animals were less clogged than in normal mice given the same procedure.

This is in keeping with previous reports indicating that orthotopic corneal allografts in mice do not normally induce detectable CTL responses to donor alloantigens in normal mice and corneal allograft rejection occurs in CD8 KO mice and perforin KO mice, which can not generate allospecific CTL (8, 9).

Dr. Verdin further found that prolonged intake of a high - fat diet, even in normal mice, can itself reduce the activity of the enzyme produced by SIRT3 — an enzyme his laboratory originally discovered.

We have found that expression of C3 in normal mouse eyes leads to pathology similar to AMD in humans, including the creation of anaphylatoxins and the MAC.

If the causes of death in normal mice (which i've heard mostly die from cancer, though haven't verified) differ from those in humans (for example cardiovascular disease is the number one killer), the conclusion I draw is that resveratrol could very well be effective on man and species closer to man.

The scientists found a striking reduction in colon tumors in the AIM2 - deficient mice and an increase in tumors in the normal mice.

Further, tumor to lung volume ratio was substantially lower in mice without Notch1 function; this ratio was 6 % at 6 weeks, 17 % at 18 weeks, and 20 % at 24 weeks in normal mice, and 4 %, 11 %, and 9.5 %, respectively, in the Notch1 - knockdown mice.

The researchers also found you could boost the receptor in a normal mouse and see OCD - like symptoms appear.

Enard found that in the basal ganglia and connected regions involved in learning, the human version of FOXP2 caused some neurons to develop longer branches than those found in normal mice.

In normal mice with working photoreceptors (PR driven), stimulating the retina produces a variety of responses in retinal ganglion cells, the output of the eye.

But in the new study, these pathways continued to function in mice in which the actions of miR - 30a - 5p had been tamped down — the mice retained the preference for a sweetened solution over plain water that is seen in normal mice.

The mouse lifespan study is the important news here, as it demonstrates meaningful extension of median life span through removal of senescent cells, the first such study carried out in normal mice for this SENS - style rejuvenation technology.

And when researchers experimentally increased deltaFosB levels in normal mice, calbindin expression was suppressed and the animals» memory deteriorated, demonstrating that deltaFosB and calbindin are key regulators of memory.

To our amazement, the clearance was unchanged from that in normal mice.