Sentences with phrase «which normal mice»

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Next, the researchers introduced into the bladders of the mice either Lactobacillus crispatus, a normal vaginal bacterium; G. vaginalis, which is associated with bacterial vaginosis; or sterile saltwater, as a control.
Damaged mouse sciatic nerves produced hundreds of times the normal amount of two «chemoattractant» molecules, Cxcl1 and Cxcl2, which attach to the surfaces of neutrophils and draw the immune cells into injured tissue.
Three groups of middle - aged mice (about a year old) were studied: one group ate a normal diet, in which fewer than 30 percent of calories came from fat, while two others were fed high - calorie diets in which 60 percent of the calories came from fat.
Aside from a food intake in laboratory mice that's about 40 percent fewer calories than normal, however, it's been found that another way to activate this pathway is with rapamycin, which appears to have a significant impact even when used late in life.
Lead author David W. Frederick, PhD, a postdoctoral fellow in the Baur lab, and the team generated mice in which they could restrict the amount of NAD in specific tissues in order to simulate this aspect of normal aging in otherwise healthy 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.
That's because the boosted mice produced normal — rather than high — levels of the amyloid precursor proteins from which plaques are made.
The researchers induced two groups of mice — germ - free (GF) mice, which are raised in a sterile environment, and specific - pathogen - free mice raised under normal laboratory conditions — to develop forms of asthma or ulcerative colitis.
The study compared intestinal wound healing in two groups of mice: 1) typical mice (wild type) found in nature and 2) mice genetically deficient in the healing factor IL - 10, specifically in macrophages, which impairs their ability to have normal wound repair.
They destroyed the T cells in 12 mice, five of which received marrow cells from normal mice while seven received marrow from mice with a defective Fas - ligand gene.
Other researchers had linked the ank mutation to mouse chromosome 15; in this week's Science, Kingsley's team reports that it's a single typo in a previously unknown gene, which they called ank, that led to a protein about 10 % shorter than the normal version.
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.
Using mice in which the production of the enzyme was blocked, the researchers found that mice lacking FIH in their muscles require more oxygen than normal when exercising.
The researchers studied both normal mice and mice genetically engineered without the Trpv4 gene (which produces TRPV4 channel protein).
They transplanted either normal or gene - corrected macrophages into the respiratory tracts of mice, which were bred to mimic the hereditary form of a human disease called hereditary pulmonary alveolar proteinosis (hPAP).
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.
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.
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.
«In a mouse, the optic nerve looks normal at birth, which is the equivalent of the third trimester of neonatal human development,» said Fox.
The octacosanol - administered mice also showed normal sleep, which was previously disturbed due to stress.
On the flip side, said Tran, PGC1 alpha transgenic mice, which had increased expression of these genes, were particularly resistant to various stressors and recovered from injury much more than quickly than animals with normal regenerative abilities.
One group consisted of normal mice, while the other group was genetically unresponsive to the hormone leptin, which promotes feelings of fullness after eating.
When the scientists applied nitroglycerin patches, which cause increased blood flow to the skin, to nine normal mice breathing air with adequate oxygen, EPO and red blood cell levels shot up, confirming that diverting blood into the skin drives the production of EPO.
The transgenic mice gave birth to fewer offspring than their normal relatives, which fits well with the evolutionary theory that there is a trade - off between longer life span and fertility.
When given the option to hang out with another mouse or an object like an empty cup, the mutant mice spent just as much time with the object as with the other mouse, unlike normal mice, which prefer a living companion.
The scientists found that transgenic mice in which phospholipase Cγ1 was unlinked from the TrkB receptor were less susceptible to seizures than normal mice.
Jetlagged mice lacking a receptor called FXR, which keeps bile acid level in the liver within a normal physiological range, had higher bile acid levels and much more liver cancer.
However, Brian Delaney, who is president of the Calorie Restriction Society, an organisation that supports the practice in people, says some who follow this diet are disappointed by the relatively modest benefits in monkeys compared with mice, which have lived up to 50 per cent longer than normal.
They examined behaviors of the following types of mice: normal mice, AS model mice, mice that had reduced levels of the Na / K - ATPase, and AS model mice in which expression of the subunit of Na / K - ATPase was reduced.
When these mice, which had normal diets, had pups, however, the methylation patterns disappeared from their offspring's DNA.
The team identified 186 different miRNAs, 11 of which were more highly expressed in the unhealthy mice than in normal mice, and five of which were expressed at lower levels than in normal mice.
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.
They compared the number of cytotoxic T cells — which help battle a virus by killing body cells that harbor it — in normal mice and animals missing IL - 33.
The researchers put the mice in a warm chamber for 6 hours, which raised their core temperature 2.7 C degrees above normal, to 39.5 C (about 103 F).
Interestingly NPGL levels, which plummeted in the 5 - week - long high - fat - diet mice — fell back to normal levels in mice who gorged themselves for the longer period of 13 weeks.
Next, Abadir and colleagues compared the effects of different concentrations of losartan and valsartan on young diabetic and aged mice during the proliferation / remodeling phase of wound healing, which involves the regrowth of normal tissue.
In their study «D - Serine and Serine Racemase are Localized to Neurons in the Adult Mouse and Human Forebrain,» the lab utilized SR deficient (SR - / --RRB- mice, which have < 15 % of normal D - serine levels, to validate and optimize a D - serine immunohistochemical method.
A 50 % reduction in HDAC4 restored these and other electrophysiological changes in both the R6 / 2 model, a transgenic over-expresser of Exon 1 HTT with an expanded polyglutamine repeat, and heterozygous Q175 knock - in mice (Q175 + / --RRB-, which carry one normal and one mutant HTT allele with an expanded repeat of ~ 190 polyglutamines, in addition to reversing behavioral alterations in R6 / 2 mice (Mielcarek et al, 2013; PLOS Biology, in press).
In research funded by the Wellcome Trust, Professor Zernicka - Goetz and colleagues developed a mouse model of aneuploidy by mixing 8 - cell stage mouse embryos in which the cells were normal with embryos in which the cells were abnormal.
Young said Celltex did a study in which it injected lab mice with 73 times the normal dose of 200 million cells that Celltex gives its clients, and none of the mice died, developed toxic organs or grew tumors.
This early hint that age - related changes in EP2 action in microglia might be promoting some of the neuropathological features implicated in Alzheimer's was borne out in subsequent experiments for which Andreasson's team used mice genetically predisposed to get the mouse equivalent of Alzheimer's, as well as otherwise normal mice into whose brains the scientists injected either A-beta or a control solution.
«We were careful to have all of the mice eating a normal diet during the actual memory testing which suggests the effects of the ketogenic diet were lasting.
Some studies have identified a number of regions of methylated DNA (one key way in which epigenetic changes occur) that are different in fat cells of mice fed high - fat diets than in cells of mice with normal diets.
Notably, mice in which MELK has been genetically ablated display normal development and hematopoiesis.
Normal mice had a gene which caused fat cells to secrete leptin, but the mutated obese mice lacked that gene.
«Low - Calorie Diet Slows Aging in Mice in Study,» claimed a recent headline.17 According to the article, «Putting elderly mice on a very low - calorie diet for as little as four weeks reversed many of the changes in the activity of various genes that had occurred during normal aging...» The resesearchers were not looking at actual signs of disease, nor were they measuring lifespan, but instead focused on the analysis of 11,000 different genes using a method called microarray technology in which Spindler has large financial holdiMice in Study,» claimed a recent headline.17 According to the article, «Putting elderly mice on a very low - calorie diet for as little as four weeks reversed many of the changes in the activity of various genes that had occurred during normal aging...» The resesearchers were not looking at actual signs of disease, nor were they measuring lifespan, but instead focused on the analysis of 11,000 different genes using a method called microarray technology in which Spindler has large financial holdimice on a very low - calorie diet for as little as four weeks reversed many of the changes in the activity of various genes that had occurred during normal aging...» The resesearchers were not looking at actual signs of disease, nor were they measuring lifespan, but instead focused on the analysis of 11,000 different genes using a method called microarray technology in which Spindler has large financial holdings.
The researchers also showed that regular feeding with the Lactobacillus strain caused changes in the expression of receptors for the neurotransmitter GABA in the mouse brain, which is the first time that it has been demonstrated that potential probiotics have a direct effect on brain chemistry in normal situations.
STUDY ONE — scientists gathered several sleep - deprived mice and discovered that when fed ashwagandha, their previously elevated lipid peroxide levels, which were caused by lack of sleep, fell to normal levels.
The enhanced endurance was seen in lab mice with a normal oxygen supply and those with oxygen restrictions which provided significant evidence that GW501516 targets and enhances skeletal muscle endurance and recovery time to a supraphysiological level.
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