For example, he says,
because humans and mice have different metabolic rates, lower doses may have similar beneficial effects in humans.
«
Because humans and mice have similar responses, mice may be a good model for studying this further.»
Not exact matches
Both
mouse and human males typically die early from the mutation in Mecp2,
because their Y chromosome does not supply a normal copy of the gene.
Scientists aren't always thinking about the genetic differences between
mice and humans because they're focused elsewhere.
«Ninety to 95 percent of cervical cancer cases are HPV - related,
and there are very few studies of this type of cancer in
mice because HPV is a
human virus,» Schwarz said.
Part of the problem, he says, is that the incidence of many
human chronic diseases rises with age, yet many researchers prefer using young
mice because of the pressures of being published
and getting funding.
The summary of his experiment that Gage sent to the neuroscience meeting did not specify the size of the
human brain organoids he
and his colleagues implanted into
mice; he told STAT that he could not talk about the work
because he had submitted it to a journal.
While
mouse models have traditionally been used in studying the genetic disorder, Deng said the animal model is inadequate
because the
human brain is more complicated,
and much of that complexity arises from astroglia cells, the star - shaped cells that play an important role in the physical structure of the brain as well as in the transmission of nerve impulses.
«This is primarily
because of the difference between the
mouse and human immune systems.»
The authors said that this result suggests that the reason bacterial numbers are so high in these
mice,
and, by extension,
human LAD patients, is not
because of a defect in the immune system's surveillance mechanism but
because of the inflammation caused by the immune system's abnormal response to normal levels of bacteria in the gums.
These are not genes but must have an important role
because evolution has left them virtually unchanged in both
humans and mice since our evolutionary paths parted about 75 million years ago.
Studying aging
and its associated diseases has been challenging
because existing vertebrate models (e.g.,
mice) are relatively long lived, while short - lived invertebrate species (e.g., yeast
and worms) lack key features present in
humans.
Most animal studies of the disease are conducted with laboratory
mice that have been genetically engineered
and bred to model ALS, but for this research, investigators used rats with ALS
because they more accurately portray the disease's variable course in
humans.
This is
because the tumors in
mice mirror the genetics as well as the molecular
and cellular properties of tumors in
humans.
«These results are especially exciting
because they show that we can take findings in the
mouse and possibly apply them at the
human patient population,» said Koenig.
Another is that the transplanted bits of tumor act nothing like cancers in actual
human brains, Fine
and colleagues reported in 2006: Real - life glioblastomas grow
and spread
and resist treatment
because they contain what are called tumor stem cells, but tumor stem cells don't grow well in the lab, so they don't get transplanted into those
mouse brains.
But he cautions that
mouse and human livers aren't the same; what's more, whereas Atkins - like diets seem to work in
humans because they eat less,
mice lose the weight through exercise.
For the animal study, the researchers separated 52
mice with colon cancer tumors into three groups, including a control group
and groups that were fed either the grape compounds or sulindac, an anti-inflammatory drug, which was chosen
because a previous study showed it significantly reduced the number of tumors in
humans.
Belury
and colleagues were able to tie these findings to the
human tendency to skip meals
because of the behavior they expected to see — based on previous work — in the
mice on restricted diets.
Because neurogenesis surges in newborn
mice and humans and then tapers to a slow trickle by adulthood, Frankland
and colleagues wondered if that explosion of new neurons could help explain the widespread phenomenon of infantile amnesia — the inability of adults to remember events that occurred before they were 2 to 4 years old.
Because they are interested in
human heart failure, Lavine
and his colleagues developed a method to progressively damage
mouse cardiac tissue in a way that mimicked heart failure.
Previous attempts to do the same in monkeys, however, have failed — a disappointment
because monkeys are more similar than
mice to
humans,
and thus likely a better harbinger of how stem cell treatments will fare in people.
(Most of the research is still being done on
mice and other organisms
because human tests will take decades to complete.)
Because humans have the «identical circadian clock machinery» as
mice, adds Bass, the work has important implications for scientists studying obesity
and diabetes in people.
«Our results are important
because the process works in
mice and in
human muscle cells.»
Because mice with intact immune systems are resistant to S. stercoralis infection, the researchers began with an immunocompromised strain of
mice,
and then exposed some to a synthetic steroid called methylprednisolone (MPA) that is commonly used to treat asthma in
humans.
Because of the difficulties involved in harvesting
and culturing adult
human neurons, most research on DRG neurons has been done in
mice.
Embryonic stem (ES) cells, harvested from three -
and - a-half-day-old
mouse embryos or five -
and - a-half-day-old
human embryos, are referred to as pluripotent
because they can become any of the thousands of cell types in the body.
The findings have implications for all aspects of medical
and scientific research
because laboratory
mice underpin studies whose results have a transformative effect on
human and animal lives through vaccination
and other immune - based therapies.
The clinical applications are much more remote,
because mouse and human germs cells develop differently
and may require different conditions.
Because of altered Fgfr2 splicing, cells of the stria vascularis are missing in Esrp1 - deficient
mice,
and possibly in
humans.
The findings suggest that like (some)
humans,
mice and other animals may simply exercise
because they like to.
Because the
mouse and human brains have much in common, co-lead study investigator William Muñoz, an MD - PhD student at NYU Langone, says the team's findings advance the field's understanding of how the brain processes touch, smell, hearing, sight,
and taste.
Ross says that
because the hyperactivity
and decreased anxiety might be interpreted as «mania - like» symptoms, the researchers fed the
mice either lithium or valproic acid (an anti-seizure drug, also used to treat mania) over a two week period, as is often done in
human therapeutic trials.
Liang thinks rats make better models of
human feeding behaviors than
mice because rats are bigger mammals
and eat significantly more than
mice, making it easier to measure their food intake.
--
Mice and humans both have about 30,000 genes -
and share 99 % of them - but the
mouse genome is shorter than that of
humans (2.5 billion letters compared with 2.9 billion)---- About 1,200 new genes have been discovered in the
human because of
mouse -
human genome comparisons.
Because the
mouse and human brains have much in common, co-lead study investigator William Muñoz, an MD / PhD student at NYU Langone, says the team's findings advance the field's understanding of how the brain processes touch, smell, hearing, sight,
and taste.
That's
because most studies on single
human brain cells use dead rather than living tissue,
and many others rely on cells from common laboratory animals, especially
mice.
The germ cells made from stem cells stopped differentiating in the
mice before they produced mature sperm (likely
because of the significant differences between the reproductive processes of
humans and mice) regardless of the fertility status of the men from whom they were derived.
The findings,
and the techniques used to document them, are important to archaeological research in a broader sense
because they lend further support to the idea that fluctuations in ancient
mouse populations can be used as a proxy for tracking ancient shifts in
human mobility, lifestyle
and food domestication.
«We have to optimize how we can deliver these tools
because obviously, unlike the
mouse, we can't rely on genetic engineering to optimize
humans for CRISPRi
and CRISPRa.»
This was thought to be the case
because there were mutant Pax3 proteins in
mice and humans that had defects in the parts of the protein that bind to DNA,
and so, would not be able to properly turn genes «on» or «off.»
And, while the genetically - modified mice were made somewhat better by deactivating the HD gene in their hypothalamus, this approach isn't useable in human HD patients because their HD genes don't contain the sequences needed to turn them off with virus used by Petersen and colleagu
And, while the genetically - modified
mice were made somewhat better by deactivating the HD gene in their hypothalamus, this approach isn't useable in
human HD patients
because their HD genes don't contain the sequences needed to turn them off with virus used by Petersen
and colleagu
and colleagues.
We chose this model
because 1) it more closely recapitulates features of
human pancreatic cancer than do s.c. - implanted tumors, 2) it can be used in immunocompetent
mice to permit assessment of immune responses,
and 3) the cells grow in vivo with predictable kinetics (34).
Researchers at Georgetown University Medical Center have taken tissue from
human testicles that produce sperm, grafted them onto diabetic
mice and showed that blood sugar levels can be controlled for up to a week
because they produce insulin.
Because the symptoms resemble
human typhoid fever caused by STM,
mice infected by STM provide a model system to investigate the development
and immunology of typhoid fever in
humans.
There are lots of different HD
mice available,
and because every case of HD is caused by the same basic genetic mutation, it may be that «our»
mice will turn out to be better than those of other diseases, at predicting success in
human patients.
The lab chose to use the TCL1
mouse model to study B - cell leukemia
because ~ 90 percent of
human chronic lymphocytic leukemia (CLL) patients express the TCL1 protein,
and the overexpression of TCL1 in B cells leads to the development of CLL in
mice.
Among the early germ cell markers examined, VASA is a candidate gene for detecting pre-meiotic germ cell differentiation from monkey ES cells,
because its expression is detected earlier in the primordial stage of germ cell development in comparison to that of PIWI family genes in vivo in
mice and humans [11], [36]--[38], [49].
«That is significant
because mice and humans that lack or have substantial defects in regulatory T cells develop lethal autoimmune disease,» Vignali said.