Not exact matches
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 holdi
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 holdi
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 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.