Next, Liao and his colleagues compared the effects of cardiac stress
on normal mice and on those lacking KLF4 in their hearts.
Not exact matches
Read this post for a refresher, but the short of it is they wreck your gut with inflammation that is
on the order of causing (in
mice anyway) IBD if predisposed, and if with a
normal immune system, say hello to chronic low - grade intestinal inflammation and metabolic syndrome.
Even in the first week after an election, the Whitehall agents of the 800 lb gorilla of executive power are hard at work
on the tiny but irritating squeak of the parliamentary
mouse rather than fixing the broken democracy in partnership with parliament, «back to
normal working» is not the slogan that will restore the reputation and capability of our democracy.
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.
Reporting in The Journal of Neuroscience, they showed that neurons of the
mouse forebrain depend heavily
on NAD in
normal cognitive function.
So Riqiang Yan, one of the discoverers of BACE1 and a neuroscientist at the Cleveland Clinic, and colleagues set out to learn what happens when
mice who start life with
normal amounts of BACE1 lose much of the enzyme later
on.
When they examined
mice genetically incapable of producing Helios, they found the animals beset by a T - cell and antibody attack
on normal tissue.
In experiments
on normal and MLL cells from
mice and humans, the researchers demonstrated that beta - catenin is activated in cancer stem cells that prompt leukaemic blood cells to multiply.
If one eye is deprived of sight, they rapidly rewire their brains to compensate, then beat
normal one - eyed
mice on tests of visual acuity.
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.
«The challenge is finding targets that exist
on other types of cancer cells but not
on normal cells,» says pediatric oncologist Stephan Grupp of the Children's Hospital of Philadelphia, who worked with Porter
on testing the treatment in
mice.
Mineral deposits and bone formation around toe joints of
mouse with mutation in the ank gene (mutant foot shown
on right,
normal skeleton
on left).
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.
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.
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.
Put certain strains of
mice on near - starvation but nutrient - rich diets, and they live 50 % longer than
normal.
The
mouse models of autism
on a
normal lab diet (with a medium glycemic index) are already known to generate fewer new neurons, and some of their existing cells and neuronal connections are abnormal compared with those of
normal mice.
By switching Apc
on, researchers turned swelling mobs of
mouse cancer cells (above) back into
normal intestinal tissue (below).
A new study has determined that
mice that spent time running
on wheels not only developed twice the
normal number of new neurons, but also showed an increased ability to distinguish new objects from familiar objects.
They then injected the protein into elderly
mice with
normal immune systems, and found this reproduced the beneficial effects of cord plasma
on both memory performance and LTP in the hippocampus whereas
mice engineered to lack TIMP2 showed reduced LTP.
To determine what effect this had
on fertility, Cook - Andersen's team set up an equal number of fertile male
mice with 10 females lacking L2 in their eggs and 10
normal females.
Klebsiella pneumoniae is usually a
normal resident in the mouth of healthy individuals, but as demonstrated in an experiment
on specific pathogen - free
mice treated and untreated with the antibiotic ampicillin, they can colonize in the gut and activate TH1 cells when antibiotics disturb the gut microbial balance and weaken tolerance for the colonization of oral bacteria reaching the intestine.
Knocking out a particular gene in muscle lets
mice run twice as far as
normal; knocking out the same gene in fat cells allows the animals to put
on weight without developing type - 2 diabetes.
Mice with obesity - related diabetes,
on the other hand, had
normal levels of Tregs within the tissue, despite having more fat tissue.
Notably, they also achieved the same effects
on p300 and Tregs in
mice by using a drug that inhibits p300 in
normal mice.
The control
mice with
normal C. mast
on the other hand were able to fend off the fungus.
To solve this mystery, the scientists generated
mice with
normal or reduced levels of A2A receptors in astrocytes and compared them
on tests of learning and memory.
Zeroing in
on this kinase was encouraging, Goga said, because other researchers have shown that genetic - knockout
mice that lack the entire family of PIM kinases are slightly smaller than
normal mice, but «basically fine,» indicating that a drug targeting just PIM1 may have manageable levels of toxicity in breast cancer patients.
The blood sugar of the diabetic
mice were made
normal by the gene - therapy - treated human islets
on the right.
Experiments with
mice show that after just four weeks
on a high - fat or a high - sugar diet, the performance of
mice on various tests of mental and physical function began to drop, compared to animals
on a
normal diet.
In this research, after just four weeks
on a high - fat or a high - sugar diet, the performance of
mice on various tests of mental and physical function began to drop, compared to animals
on a
normal diet.
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.
Photoswitches inserted into retinal ganglion cells (RGC) of blind
mice produce much less variety of response (all evenly red means the cells fire at the same time), while blind
mice with photoswitches inserted into bipolar cells (
ON - BC driven) exhibit much more variety in their retinal response to light, closer to that of
normal mice.
This time, they found that the
mice grew insulin - resistant, even when
on normal diets.
The scientists soon determined that
mice that lack IL - 17A activity healed wounds
on their skin much more slowly than
normal — very much like
mice that lack DETCs.
The researchers will use pieces of
normal mouse PrP as bait, hoping to fish out protein X when it latches
on.
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.
Despite higher glycogen levels, glycogenin - deficient
mice underperformed
normal mice, reaching exhaustion earlier and covering a shorter distance while running
on a treadmill.
On the other hand, as they aged, these «knockout
mice» grew fatter than the
normal mice, especially when fed a high - fat diet.
To overcome this hurdle, researchers genetically engineered human T cells to produce a CAR protein that recognizes a glycopeptide found
on various cancer cells but not
normal cells, and then demonstrated its effectiveness in
mice with leukemia and pancreatic cancer.
Researchers found that prior to treatment,
mice with tumors performed worse
on learning and memory tests compared to their
normal counterparts.
For comparison, bacteria grown in a laboratory
on Earth in
normal gravity infected another group of
mice.
Experiments
on mice and
on heart cells obtained from infants born with congenital heart disease suggest that neuregulin 1, a human growth factor, can put infant heart cells
on a path that mimics
normal growth rather than stalling out.
The Mecp2 mutant
mice were more sensitive to light touch; a small puff of air
on their backs startled the rodents more than
normal mice.
The one
on top is from a
normal mouse.
On one flank, the mice received healthy, normal cartilage; on the other, they received cartilage abundant with human RASF
On one flank, the
mice received healthy,
normal cartilage;
on the other, they received cartilage abundant with human RASF
on the other, they received cartilage abundant with human RASFs.
Sinclair's lab is now working
on developing what he calls a possible «supermouse» with elevated levels of NAMPT to see if it lives longer and is more disease - resistant than
normal mice.
That research showed that
mice on a
normal diet who were exposed to low doses of antibiotics throughout life, similar to what occurs in commercial livestock, packed
on 10 to 15 percent more fat than untreated
mice and had a markedly altered metabolism in their liver.
The news wasn't all bad: When Fischbach's team put obese
mice on a diet, their mammary fat tissue had fewer myofibroblasts, suggesting losing weight could make a woman's fat tissue structure more
normal and lower her breast cancer risk.
The researchers looked for genes that were turned
on by dHAND in
normal mice, but nonfunctioning when dHAND was shut down.