Studies in mice indicated that drugs that activate the surface protein TRPA1 on pain - sensing nerve cells intensify postoperative pain.
Not exact matches
While
study results
indicated that combining capsaicin with the chemicals «might promote cancer cell survival,» the report clearly stated that the control group of
mice treated only with capsaicin ``... did not induce any skin tumors...»
In addition, the study repeatedly cited other research studies in which the anti-cancer properties of capsaicin were solidly demonstrate
In addition, the
study repeatedly cited other research
studies in which the anti-cancer properties of capsaicin were solidly demonstrate
in which the anti-cancer properties of capsaicin were solidly demonstrated.
The new
study indicates that such infections
in the
mice cause the number of tuft cells to increase by five - to tenfold, leading the norovirus to replicate more efficiently.
Mouse study indicates signaling molecules at play
in cancer may also promote atherosclerosis
Although we did observe positive effects on some aging traits, such as memory impairments and reduced red blood cell counts, our
studies showed that similar drug effects are also seen
in young
mice,
indicating that rapamycin did not influence these measures by slowing aging, but rather via other, aging - independent, mechanisms.»
Evolution has preserved the «neuropeptide Y (NPY) system», as it is known,
in most species —
indicating its importance — and much of our understanding comes from
studying it
in mice.
Remarkably, although
mouse studies had
indicated that different transcription factors were differently important for generating pain and itch sensing neurons versus pressure and limb position neurons,
in the dish these factors produced equal numbers of each of the three main subtypes.
«Previous
studies in mice have
indicated that bacteria that are able to encroach upon the epithelium might be able to promote inflammation that drives metabolic diseases, and now we've shown that this is also a feature of metabolic disease
in humans, specifically type 2 diabetics who are exhibiting microbiota encroachment.»
Previous research
indicated this was the case
in mice, but this is the first
study to document presymptomatic dysfunction
in humans.
Their
study in aged
mice indicates that high folic acid intake causes lowered immune function because natural killer (NK) cells, a particular type of immune cell, are less effective.
Combined with previously published
studies, our data
indicate that infection with all three major North American T. gondii clonal lineages results
in loss of innate, hard - wired aversion to feline predator urine
in mice.
In this regard, animal model studies with FIPV in cats and RSV in mice have indicated that viral surface proteins may be the sensitizing protein of inactivated vaccines for immunopathology with infection [32], [45
In this regard, animal model
studies with FIPV
in cats and RSV in mice have indicated that viral surface proteins may be the sensitizing protein of inactivated vaccines for immunopathology with infection [32], [45
in cats and RSV
in mice have indicated that viral surface proteins may be the sensitizing protein of inactivated vaccines for immunopathology with infection [32], [45
in mice have
indicated that viral surface proteins may be the sensitizing protein of inactivated vaccines for immunopathology with infection [32], [45].
In addition to the reduction in total numbers of activated microglia in AFF 1 - treated TG mice, it is of note that costaining studies indicated that those activated microglia that did emerge in treated mice were highly colocalized with recalcitrant (proteinase K - resistant) AS aggregate as compared to untreated PDGF - AS mic
In addition to the reduction
in total numbers of activated microglia in AFF 1 - treated TG mice, it is of note that costaining studies indicated that those activated microglia that did emerge in treated mice were highly colocalized with recalcitrant (proteinase K - resistant) AS aggregate as compared to untreated PDGF - AS mic
in total numbers of activated microglia
in AFF 1 - treated TG mice, it is of note that costaining studies indicated that those activated microglia that did emerge in treated mice were highly colocalized with recalcitrant (proteinase K - resistant) AS aggregate as compared to untreated PDGF - AS mic
in AFF 1 - treated TG
mice, it is of note that costaining
studies indicated that those activated microglia that did emerge
in treated mice were highly colocalized with recalcitrant (proteinase K - resistant) AS aggregate as compared to untreated PDGF - AS mic
in treated
mice were highly colocalized with recalcitrant (proteinase K - resistant) AS aggregate as compared to untreated PDGF - AS
mice.
Our mechanistic
studies,
in both
mouse and human mammary cancer cells,
indicate that leptin and LepR are necessary for NANOG expression.
However, recent evidence
indicates that apoE4 expression compromises the blood - brain barrier (as does apoE deficiency).40
Studies of brain histology, neurodegenerative markers, cholinergic activity, and neuronal function in knockout mice have been equivocal.39 Failure of detailed neurocognitive and retinal studies to demonstrate defects in our patient suggests either that the functions of apoE in the brain and eye are not critical or that they can be fulfilled by a surrogate p
Studies of brain histology, neurodegenerative markers, cholinergic activity, and neuronal function
in knockout
mice have been equivocal.39 Failure of detailed neurocognitive and retinal
studies to demonstrate defects in our patient suggests either that the functions of apoE in the brain and eye are not critical or that they can be fulfilled by a surrogate p
studies to demonstrate defects
in our patient suggests either that the functions of apoE
in the brain and eye are not critical or that they can be fulfilled by a surrogate protein.
For example, results of a
mouse study conducted by the National Institutes of Health (NIH)
in collaboration with ChromaDex published
in November 2014
indicated that NR was effective at restoring NAD + levels
in mitochondria and rescuing phenotypes associated with a devastating accelerated aging disease known as Cockayne Syndrome (CS).