Not exact matches
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.
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.
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).
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.
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.
On the
other hand, as they aged, these «knockout
mice» grew fatter
than the
normal mice, especially when fed a high - fat diet.
The muscle fibers were larger and more numerous
than in
normal mice, and even after a year the mutant
mice show no
other abnormalities.
Researchers at the University of Texas (U.T.) Southwestern Medical Center at Dallas noticed that
mice used two primary methods to cope with defeat after being repeatedly pummeled by larger, more aggressive foes: Some of the weaker members withdrew, avoiding all types of social interaction for more
than a month, whereas
others rolled with the punches, so to speak, quickly bouncing back to their
normal behavior.
He notes, however, that
other attempts to stimulate bone growth in
mice by manipulating cell signaling proteins have produced denser
than normal bones — and he's surprised that Helms's team didn't see the same.
Mice with the PER1 phosphorylation defects ate earlier than other mice — causing them to wake up and snack before their sleep cycle was over — and ate more food throughout their normal waking per
Mice with the PER1 phosphorylation defects ate earlier
than other mice — causing them to wake up and snack before their sleep cycle was over — and ate more food throughout their normal waking per
mice — causing them to wake up and snack before their sleep cycle was over — and ate more food throughout their
normal waking period.
And, consistent with
other studies, when these
mice ate a high - fat diet, they gained weight faster
than their
normal counterparts.
When the researchers induced wounds in these
mice, they found that the
mice without TSP2 healed significantly better and faster
than other mice that had diabetes along with
normal levels of TSP2.
mouse studies, macrophages taken from obese
mice were less receptive to insulin
than normal (in
other words insulin resistant to a degree).