Not exact matches
«The successful restoration of
normal function demonstrated
in the
mouse models suggests that if we can develop therapies to address the loss of Mecp2,» Baylor's Zoghbi says, «we may be able to reverse neurological damage
in children and adults with Rett, autism and related neuropsychiatric disorders.»
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.
In their research, authors Sajedah M. Hindi, Ph.D., and Ashok Kumar, Ph.D., discovered that removing TRAF6 depletes Pax7, resulting in reduced muscle regeneration in both normal and Duchenne muscular dystrophy (DMD) mouse model
In their research, authors Sajedah M. Hindi, Ph.D., and Ashok Kumar, Ph.D., discovered that removing TRAF6 depletes Pax7, resulting
in reduced muscle regeneration in both normal and Duchenne muscular dystrophy (DMD) mouse model
in reduced muscle regeneration
in both normal and Duchenne muscular dystrophy (DMD) mouse model
in both
normal and Duchenne muscular dystrophy (DMD)
mouse models.
«Transplanted hematopoietic stem cells reverse damage caused by neuro - muscular disorder:
In mouse model of Friedreich's ataxia, a single infusion measurably restored
normal cellular functions.»
In this study, tungstate treatment in mouse models of colitis shifted gut microbiota to a more normal state in terms of the balance of bacterial species and also reduced gut inflammation, the researchers repor
In this study, tungstate treatment
in mouse models of colitis shifted gut microbiota to a more normal state in terms of the balance of bacterial species and also reduced gut inflammation, the researchers repor
in mouse models of colitis shifted gut microbiota to a more
normal state
in terms of the balance of bacterial species and also reduced gut inflammation, the researchers repor
in terms of the balance of bacterial species and also reduced gut inflammation, the researchers report.
Lastly, they plan to vary the timing of exposure to the various diets
in the
mouse model of autism, by, for example, giving pregnant
mice a high - glycemic index diet and then keeping their pups on a
normal diet.
Now, thanks to the new
mouse model, it will be possible to study how renal tumors are able to develop
in an environment with a
normal immune system, and how cancer cells manage to evade the immune system's attacks.
Dr. Baran Sumer (left) and Dr. Jinming Gao (right) and have invented a transistor - like threshold sensor that can illuminate cancer tissue, helping surgeons more accurately distinguish cancerous from
normal tissue
in mouse models.
In normal mice, stem cells (pink) express dystrophin (green) and are able to easily generate new muscle fibers, but in the disease model, there is no dystrophin and the stem cells lose their sense of direction and have trouble generating new muscle fiber
In normal mice, stem cells (pink) express dystrophin (green) and are able to easily generate new muscle fibers, but
in the disease model, there is no dystrophin and the stem cells lose their sense of direction and have trouble generating new muscle fiber
in the disease
model, there is no dystrophin and the stem cells lose their sense of direction and have trouble generating new muscle fibers.
The
normal mice and the AS
model mice with diminished expression of the Na / K - ATPase subunit searched the correct area of the maze
in the same amount of time.
They examined behaviors of the following types of
mice:
normal mice, AS
model mice,
mice that had reduced levels of the Na / K - ATPase, and AS
model mice in which expression of the subunit of Na / K - ATPase was reduced.
Finally, we generate new tools and
mouse models to study the role of de novo protein synthesis
in normal brain function and
in pathophysiology associated with neurodevelopmental and neurodegenerative disease.
The hTNFR1KI
mice have
normal phenotype and can be used
in combination to other genetic
models (e.g. Tg197hTNFR1KI) or with a variety of induced disease
models in order to test the efficacy of anti-human TNFR1 therapeutics.
Winkler, E. A., Bell, R. D. & Zlokovic, B. V. Pericyte - specific expression of PDGF beta receptor
in mouse models with
normal and deficient PDGF beta receptor signaling.
Another behavior that scientists have observed
in Huntington's disease
model mice is that they aren't as motivated as
normal mice to drink sweet water.
J147 increases the levels of BDNF
in the hippocampus of
normal rats, as well as
in huAPP / PS1 transgenic
mice [7], and its synthetic precursor, CNB - 001, increases BDNF levels
in rat traumatic brain injury
models [54].
A 50 % reduction
in HDAC4 restored these and other electrophysiological changes
in both the R6 / 2
model, a transgenic over-expresser of Exon 1 HTT with an expanded polyglutamine repeat, and heterozygous Q175 knock -
in mice (Q175 + / --RRB-, which carry one
normal and one mutant HTT allele with an expanded repeat of ~ 190 polyglutamines,
in addition to reversing behavioral alterations
in R6 / 2
mice (Mielcarek et al, 2013; PLOS Biology,
in press).
In order to better understand the liabilities associated with reducing normal htt in adult mice, we evaluated the effects of a robust knock down of WT htt both in CNS and periphery in a conditional htt knock - down (KD) model induced by doxycyclin
In order to better understand the liabilities associated with reducing
normal htt
in adult mice, we evaluated the effects of a robust knock down of WT htt both in CNS and periphery in a conditional htt knock - down (KD) model induced by doxycyclin
in adult
mice, we evaluated the effects of a robust knock down of WT htt both
in CNS and periphery in a conditional htt knock - down (KD) model induced by doxycyclin
in CNS and periphery
in a conditional htt knock - down (KD) model induced by doxycyclin
in a conditional htt knock - down (KD)
model induced by doxycycline.
In research funded by the Wellcome Trust, Professor Zernicka - Goetz and colleagues developed a mouse model of aneuploidy by mixing 8 - cell stage mouse embryos in which the cells were normal with embryos in which the cells were abnorma
In research funded by the Wellcome Trust, Professor Zernicka - Goetz and colleagues developed a
mouse model of aneuploidy by mixing 8 - cell stage
mouse embryos
in which the cells were normal with embryos in which the cells were abnorma
in which the cells were
normal with embryos
in which the cells were abnorma
in which the cells were abnormal.
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.
The researchers looked at the dentate gyrus, a specific area of the brain that is critical to memory and particularly vulnerable
in Alzheimer's disease, and compared the genes that were turned on and off
in normal mice and a
mouse model of Alzheimer's disease.
«This
mouse strain is great
model for this research because they are otherwise healthy and
normal, including
in their vision, so it allows us to conduct studies focused on cell integration,» said the publication's lead author, Jie Zhu, PhD, a postdoctoral researcher who started
in Lamba's lab three years ago.
◊
mouse models for diseases: phenotyping approaches: courses in English, March 14 - 17 in Illkirch - Strasbourg (CFE, PHENOMIN - ICS) ◊ European Advanced School for Mouse Phenogenomics: in English, June 12 - 16 at Liebfrauenberg in Alsace (PHENOMIN) ◊ necropsy, sampling and histology: June 19 - 23 in Toulouse (ENVT, Anexplo) ◊ normal and abnormal embryology of laboratory animals: March 13 - 17 + May 29 to June 3 + Décember 4 - 8 in Toulouse (ENVT, Ane
mouse models for diseases: phenotyping approaches: courses
in English, March 14 - 17
in Illkirch - Strasbourg (CFE, PHENOMIN - ICS) ◊ European Advanced School for
Mouse Phenogenomics: in English, June 12 - 16 at Liebfrauenberg in Alsace (PHENOMIN) ◊ necropsy, sampling and histology: June 19 - 23 in Toulouse (ENVT, Anexplo) ◊ normal and abnormal embryology of laboratory animals: March 13 - 17 + May 29 to June 3 + Décember 4 - 8 in Toulouse (ENVT, Ane
Mouse Phenogenomics:
in English, June 12 - 16 at Liebfrauenberg
in Alsace (PHENOMIN) ◊ necropsy, sampling and histology: June 19 - 23
in Toulouse (ENVT, Anexplo) ◊
normal and abnormal embryology of laboratory animals: March 13 - 17 + May 29 to June 3 + Décember 4 - 8
in Toulouse (ENVT, Anexplo)
Spermidine Ameliorates Neurodegeneration
in a
Mouse Model of
Normal Tension Glaucoma.