However, the Connexin 30 knockout mice had more grafted
cells than the normal mice, and some of the grafted cells were found to express CONNEXIN 30.
The fact that Connexin 30 knockout mice had a higher number of grafted
cells than normal mice, and that some of the grafted cells expressed CONNEXIN 30 is a very important finding when considering cell transplantation as a treatment for hereditary hearing loss caused by CONNEXIN deficiency.
Not exact matches
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.
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.
In order to generate enough energy, the bone
cells in our
mice therefore take up much more glucose
than normal.»
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.
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.
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.
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.
When they exposed these
mice to the cold, the animals developed far fewer beige fat
cells than did
normal animals, suggesting that macrophages were key to browning of white fat.
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.
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.
In another experiment,
mice lacking the
cells that produce serotonin scratched less
than normal mice when exposed to a skin irritant.
Although muscle
cells did not reduce in size or number in
mice lacking a protective antioxidant protein, they were weaker
than normal muscle
cells, researchers from the Barshop Institute for Longevity and Aging Studies at The University of Texas Health Science Center San Antonio found.
To see what was happening in the brains of these ankyrin - G mutant
mice, the researchers analyzed the
cell components in inhibitory synapses connecting with pyramidal neurons, finding that two proteins known as GAT1 and GAD67 — responsible for making the neurochemical GABA that dials back nerve impulses — were at much lower levels in the synapses on pyramidal neurons in ankyrin - G mutant
mice than in
normal mice.
When the researchers injected extra copies of the betatrophin gene into the liver of
normal mice, the animals» pancreases responded by making as much as 30 times more β
cells than usual.
However, by the time these
mice reached adulthood, around 8 months old, the level of photoreceptor
cells in these knockout
mice was less
than half the
normal level.
«The successful retrieval of memories in AD
mice by increasing the number of spines for
normal memory processing only in the memory
cells, rather
than in a broad population of
cells, highlights the importance of highly - targeted manipulation of neurons and their circuits for future therapies.
First, they found that the
mice on a high - fat diet had many more intestinal stem
cells than mice on a
normal diet.
«The successful retrieval of memories in AD
mice by increasing the number of spines for
normal memory processing only in the memory
cells, rather
than in a broad population of
cells, highlights the importance of highly - targeted manipulation of neurons and their circuits for future therapies,» said Tonegawa in a statement.
They found that the
mice developed earlier and more severe disease
than mice that had
normal Tob1 expression in all
cells including CD4 +.
It should be noted, however, that while a study on senescent
cell ablation in genetically
normal mice would provide at least some evidence on the effect of senescent
cells (and their ablation) on promoting cancer, even such a study would likely show less effect
than could be anticipated in a large mammal model, since even normally - aging
mice rarely suffer metastatic disease to the extent of aging humans, as sheer primary tumor volume is generally sufficient to be fatal to
mice.
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.
Remarkably, outcomes following loss of the switch mirrored what the group had previously observed when they physically removed the gene itself: the lungs of mutant
mice contained many more melanoma
cells than did lungs of
normal mice.
It was even lower in the early lesions of I10
mice than in those of age - matched virgin
mice, suggesting that the molecular network activated in
normal epithelia at involution to arrest the
cell cycle (Figure 1 — figure supplement 3B) also operates in these premalignant
cells.
Takeda et al. engineered
mice that were either unable to produce a particular LPA receptor on their T -
cells, or that produced less LPA
than normal.