Malcolm Eames of the BUAV says Harvard supported its patent application by claiming that tests of potential carcinogens would need fewer onco -
mice than normal mice.
Not exact matches
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.
In experiments with
mice, the researchers found that Paneth cells engineered to lack a functional ATG16L1 gene were five times more likely to die in the face of rising TNF - alpha signals
than normal cells.
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.
The behavioral tests used here modeled one dimension of the disease — an inability to experience pleasure from
normal activities — but not others, such as stress and anxiety, and probably tap into different brain mechanisms in
mice than in humans, he says.
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.
Male
mice from both strains lived 15 per cent longer
than normal mice or females.
To their surprise, they found that these Th17 - deficient
mice experienced far more aggressive cancer growth
than normal mice — with the cancer completely smothering the lungs within 16 days.
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.
«
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 s
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 s
mice,» Shatz says.
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.
Older modified male
mice metabolised sugar faster
than normal mice and females, suggesting that SIRT6 might extend life by protecting against metabolic disorders such as diabetes.
The scientists exposed a group of
mouse lemurs to moderate chronic caloric restriction (30 % fewer calories
than their peers consuming a
normal diet) from the outset of early adulthood (Restrikal cohort, see visuals below).
Laboratory
mice that have received rapamycin have reduced the age - dependent decline in spontaneous activity, demonstrated more fitness, improved cognition and cardiovascular health, had less cancer and lived substantially longer
than mice fed a
normal diet.
In general, the mutant
mice also had much thicker skin
than the
normal animals did.
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.
In order to generate enough energy, the bone cells in our
mice therefore take up much more glucose
than normal.»
When they next measured responses in the auditory regions of the brain, a more sensitive test, the
mice responded to much quieter sounds: 19 of 25
mice heard sounds quieter
than 80 decibels, and a few could heard sounds as soft as 25 - 30 decibels, like
normal mice.
15 The results so far include short - legged
mice,
mice with fewer toes
than normal, and
mice that chirp like songbirds.
These modified
mice had significantly smaller testes and lower sperm counts
than their
normal counterparts — and when the group bred them with
normal females, they found that the litter size was around half
normal.
When the researchers examined
mice with disrupted IL - 27 function, they found that they were more likely
than normal mice likely to die when infected with the virus, and that they died as a consequence of rampant lung inflammation.
Then, he found that
mice lacking Klotho died young, after developing arteriosclerosis and other age - related conditions much earlier
than normal (Science, 7 November 1997, p. 1013).
That's because the boosted
mice produced
normal — rather
than high — levels of the amyloid precursor proteins from which plaques are made.
Their blood contained more insulin
than that of
normal mice.
The NK1R - deficient
mice consumed far less alcohol — especially later in the trial when alcohol concentration was higher —
than the
normal mice did.
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.
Expression of CXCL16 was higher in the colon and lung tissue of GF
mice than in
normal mice, and blocking that expression reduced the numbers of iNKT cells and the amount of inflammation in those tissues.
They were also more sensitive to alcohol's effects
than the
normal mice were; studies have shown that the more sensitive a person is to alcohol, the less likely he or she is to abuse it.
Six pairs of
mice — with one
mouse engineered to produce gobs of human A-beta and one
normal — were surgically joined for a year, causing blood mingling that's far more extensive
than that of a blood transfusion.
And because
mouse embryo cells with inactivated copies of BRCA2 are more sensitive to ionizing radiation
than normal cells are, «it's a reasonable extrapolation» that breast cancers with mutated copies of the gene may be especially good candidates for radiation therapy.
Pregnant
mice engineered to have higher levels of Zika virus had smaller fetuses (top)
than normal dams (bottom).
Both groups of animals are more resistant to insulin
than normal mice are, the researchers discovered.
Behaviourally, the stressed
mice were more daring yet more despairing
than normal mice.
By 2003 other scientists had genetically manipulated
mice to be relatively insensitive to either insulin or insulin - like growth factor; in both cases, the genetically engineered
mice lived significantly longer
than normal mice.
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.
But the males — despite having smaller testes and lower sperm counts
than normal mice — were clearly fertile and produced offspring.
In the new study, Ji's group put SHANK3 - deficient
mice through a battery of sensory tests, finding that the animals had lower sensitivity
than normal mice to heat and heat - related pain — akin to the soreness a person feels after a sunburn.
Removing a single gene from the brains of
mice and zebrafish causes these animals to become more anxious
than normal.
Put certain strains of
mice on near - starvation but nutrient - rich diets, and they live 50 % longer
than normal.
In subsequent tests, the
mice with the mutation did a worse job
than normal mice at learning new motor skills.
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 found that mutant
mice lacking Del - 1 had more severe attacks of the EAE
than normal mice, with more damage to myelin, the fatty sheath that coats neurons and helps in the transmission of signals along the cell.
When the researchers then induced stroke in
mice either with or without the PARP gene, they found that the resulting tissue damage in the
mice without the enzyme was 80 % less
than in
normal mice.
Moreover,
mice engineered to generate smaller
than normal quantities of SIRT1 carried relatively little fat in their blood, indicating that their cells hung onto it.
Mice that made extra catalase in their mitochondria lived longer than normal mice, by about 1
Mice that made extra catalase in their mitochondria lived longer
than normal mice, by about 1
mice, by about 19 %.
These
mice were then mated with females that hadn't been confined, and their resulting offspring had higher blood glucose
than normal.
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.
In contrast, M49, a less virulent strain of strep, caused larger skin lesions in
mice lacking cathelicidin
than in
normal, cathelicidin - producing
mice.
As a result, they have less
than half of the fat tissue found in
normal, aged
mice.
The
mice appear younger and more robust
than comparably - aged
normal mice, have better muscle tone, and do not develop age - related tumors.