The RNAs of enhancers are expressed before the genes they regulate
during human and mouse cell differentiation.
Not exact matches
Infant calming responses
during maternal carrying in
humans and mice.
Infant Calming Responses
during Maternal Carrying in
Humans and Mice.
A study by researchers at the University of Chicago Medicine shows that when
mice that are genetically susceptible to developing inflammatory bowel disease (IBD) were given antibiotics
during late pregnancy
and the early nursing period, their offspring were more likely to develop an inflammatory condition of the colon that resembles
human IBD.
The study examined specific immune pathways known to be activated
during flu infections in both
humans and mice, which makes the findings relevant to children.
The researchers, reporting online March 5 in the American Journal of Reproductive Immunology, also say they found that an anti-inflammatory drug that is FDA - approved for rheumatoid arthritis
and is believed to be safe for
humans to take
during pregnancy halted the brain injury in
mouse offspring.
«Even the timing of the emergence of symptoms in the
mice —
during young adulthood — parallels the onset of schizophrenia in
humans,» said Joseph Gogos, PhD, a professor of physiology
and neuroscience at CUMC, a principal investigator at the Zuckerman Institute
and a lead author of the paper.
Using a
mouse model of HSV - 1 as well as autopsied samples of
human adult
and fetal tissues, investigators from Dartmouth College's Geisel School of Medicine found that antibodies against HSV - 1 produced by adult women or female
mice could travel to the nervous systems of their yet unborn babies, preventing the development
and spread of infection
during birth.
Before birth,
mouse and human ovaries contain an abundant supply of germ cells, some of which will develop into the eggs that will ultimately be released from follicles
during ovulation.
Fittingly, most of these genes reside in ampliconic regions of the X
and appear to have been acquired independently
during the 80 million years since
mouse and human diverged from a common ancestor.
This factor is the first lung molecular marker
during mouse and human development
and is essential for lungs to mature properly in an embryo.
Walford's new research is based on the fact that in
mice and humans, the immune system malfunctions
during aging, losing the ability to distinguish between healthy cells
and invasive pathogens such as bacteria
and viruses.
To find out why, they examined genes in both
mice and humans that turned on
during peak brain development
and spotted a DNA snippet, ARHGAP11B, that was active only in
humans.
Galatzer - Levy analyzed data from large studies in
humans and mice that involved «fear conditioning»
and «fear extinction,»
during which subjects receive a mild aversive stimulus when exposed to a sound or light,
and «fear extinction learning,»
during which conditioning is reversed by applying sound or light without the stimulus.
What we do know is that in
mice (
and so, presumably, in
humans) FOXP2 is active in the brain
during embryonic development.
She looked after her children
during the first year
and took a postdoc on
mouse models of
human fertility in a genetics group at the Stanford School of Medicine in their second year in California.
Next steps include He's collaboration with Piedmont Atlanta Hospital to retrieve T cells, liver cancer cells
and healthy tissue normally removed from patients
during surgery, put the
mouse receptor genes on these T cells
and monitor in a dish both how those cells now fight the tumor
and react to healthy
human tissue.
During this BSA Lecture, Kevin Esvelt of Massachusetts Institute of Technology discusses his lab's work with communities on Nantucket
and Martha's Vineyard to prevent tick - borne
human illness by developing hereditary traits in
mice that could immunize them, removing a vital link in the spread of Lyme disease.
In fact, though many
human and mouse genes appear to be similar, they may have taken on slightly different roles, or be active at different times
during the life of a person or a
mouse.
During its Preparatory Phase, INFRAFRONTIER aimed at resolving the major issues required for implementing a sustainable INFRAFRONTIER Research Infrastructure for systemic phenotyping, archiving
and distribution of
mouse models of
human diseases:
Appearance of an oocyte activation - related substance
during spermatogenesis in
mice and humans.
«Over the past ten years, several research groups, including our own, have shown the importance of certain immune cell subsets in preventing or exacerbating heart disease in
mice, but we are just beginning to understand how the metabolism
and function of these immune cells change
during cardiovascular disease progression in
humans,» says Hedrick.
During his work, Clarence also carried out investigations into cancer
and observed that many
mouse tumours acted in the same way as
human ones.
They went on to show that Sox10, a factor needed for the formation of skin pigment cells from neural crest stem cells
during development, was present at high levels in naevi
and melanoma samples obtained from both the
mouse model
and human patients.
On the basis of studies on the XMRV - producing
human prostate cancer cell lines CWR22Rν1
and CWR - R1
and their progenitor tumour xenograft CRW22, they concluded that XMRV infections were caused by contamination
during in vivo passaging in nude
mice.
267/4: 30 Extremely high resolution 3D maps of
human and mouse genomes across lineages
and during differentiation reveal principles of chromatin looping.
Our lab uses both cardiomyoctes derived from
human stem cells (iPS cell - derived cardiomyocytes)
and mouse models harboring the
human mutation to study which exact changes occur
during the onset
and development of the disease.
CAST / EiJ mTR — / —
mice exhibit significant deficits in tissue renewal
during adulthood, even in the first generation,
and progressive worsening of the phenotype with successive generations, similar to what is seen in other background strains with these mutations
and in the genetic anticipation observed in successive generations of families with autosomal dominant forms of the
human genetic disorder of telomerase components, dyskeratosis congenita.
Intrigued by recent findings that neuron firing rates in the regions of
mouse and fly brains associated with visual processing increase
during physical activity, UC Santa Barbara psychologists Barry Giesbrecht
and Tom Bullock wanted to know if the same might be true for the
human brain.
Different mutations in HSF4 have been reported to cause both
human autosomal dominant
and recessive cataracts [97 — 99]
and studies in
mice have shown HSF4 is required for normal fibre cell differentiation
during lens development [100, 101].