Sentences with phrase «cells in a mouse model of the disease»

An international research team led by biochemists at The University of Texas Health Science Center at Houston (UTHealth) reduced the sickling of red blood cells in a mouse model of the disease.

Not exact matches

He conducted his postdoctoral research at Brigham and Women's Hospital / Harvard Medical School, where he researched the role of the Wnt signaling pathway in mouse models of kidney disease, and was part of a team that discovered a stem cell subtype responsible for solid organ fibrosis.

Specifically, the Mount Sinai study was designed to test whether pharmacological compounds designed to block the function of XPO1 / CRM1 could stop disease progression in mouse models that exhibit some of the characteristics of MS. Researchers found that two chemical agents (called KPT - 276 and KPT - 350) prevented XPO1 / CRM1 from shuttling cargo out of the nucleus of nerve cells, which protected them from free radicals and structural damage.

The UT Southwestern group had previously used CRISPR - Cas9, the original gene - editing system, to correct the Duchenne defect in a mouse model of the disease and in human cells.

The scientists then tested three new mTOR inhibitors currently under development (pp242, AZD8055 and INK128) in combination with the chemotherapies AraC, Etoposide and Cisplatin to see how they affected laboratory lines of leukemia cells and mouse models of the disease.

«The compounds identified in this study, when administered orally, both reduced the inflammation that is a hallmark of multiple sclerosis and protected against the nerve cell damage seen in mouse models of the disease,» said Jeffery Haines, PhD, a post-doctoral fellow at Mount Sinai and the study's lead author.

In the study, exosomes, which are generated by all cells and are naturally present in blood, were modified as «iExosomes,» capable of delivering small RNA to specifically target mutant KRAS, resulting in disease suppression and increased overall survival in mouse modelIn the study, exosomes, which are generated by all cells and are naturally present in blood, were modified as «iExosomes,» capable of delivering small RNA to specifically target mutant KRAS, resulting in disease suppression and increased overall survival in mouse modelin blood, were modified as «iExosomes,» capable of delivering small RNA to specifically target mutant KRAS, resulting in disease suppression and increased overall survival in mouse modelin disease suppression and increased overall survival in mouse modelin mouse models.

Most importantly, these cells protected mice from developing diabetes in a model of disease, having the critical ability to produce insulin in response to changes in glucose levels.

This was observed in human ovarian cancer cells grown in culture, and then in mouse models of the disease.

Desgrosellier said the team will follow up with mouse models containing tumor fragments from patients to better reflect the diversity of cell types present in human disease.

In Remodeling of the Mononuclear Phagocyte Network Underlies Chronic Inflammation and Disease Progression in Heart Failure: Critical Importance of the Cardiosplenic Axis, Prabhu and colleagues showed that immune cells that are stored in the spleen were intricately involved in the heart failure that follows a heart attack, or infarction, in a mouse - model systeIn Remodeling of the Mononuclear Phagocyte Network Underlies Chronic Inflammation and Disease Progression in Heart Failure: Critical Importance of the Cardiosplenic Axis, Prabhu and colleagues showed that immune cells that are stored in the spleen were intricately involved in the heart failure that follows a heart attack, or infarction, in a mouse - model systein Heart Failure: Critical Importance of the Cardiosplenic Axis, Prabhu and colleagues showed that immune cells that are stored in the spleen were intricately involved in the heart failure that follows a heart attack, or infarction, in a mouse - model systein the spleen were intricately involved in the heart failure that follows a heart attack, or infarction, in a mouse - model systein the heart failure that follows a heart attack, or infarction, in a mouse - model systein a mouse - model system.

Using a combination of cell - based and mouse models, the researchers showed that the recently - evolved mycobacteria were more virulent, likely to cause more serious disease in patients.

Mouse embryonic stem cells, reported in 1981 by Martin Evans, Matthew Kaufman, and Gail Martin, have allowed scientists to generate genetically customized strains of mice that have revolutionized studies of organismic development and immunity and have provided countless models of human disease.

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 fiberIn 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 fiberin the disease model, there is no dystrophin and the stem cells lose their sense of direction and have trouble generating new muscle fibers.

When SphK1 was inhibited in a mouse model of sickle cell disease, red blood cells lived longer and had less sickling.

They show that this new formulation reduces the minimal curative dose in a disease model, based on infections in mice, by 100-fold and, most importantly, circumvents drug resistance in a cell line that is resistant as a result of mutations in the transporter that mediates drug uptake.

«We think that for the first time, we have a mouse model of anorexia that closely resembles the conditions leading up to the disease in humans,» said study leader Lori Zeltser, PhD, associate professor of pathology & cell biology and a researcher in the Naomi Berrie Diabetes Center.

«The dog has a retina very similar to ours, much more so than mice, so when you want to bring a visual therapy to the clinic, you want to first show that it works in a large animal model of the disease,» said lead researcher Ehud Isacoff, professor of molecular and cell biology at UC Berkeley.

With these cells in hand, the researchers injected them into the lacrimal glands of mouse models of Sjogren's syndrome, an autoimmune disease that results in ADDE, dry mouth and other symptoms.

The discovery was made by developing a mouse model of the disease that enabled researchers to track which of 15 genetic groups — or subclones — of myeloma cells spread beyond their initial site in the animals» hind legs.

By depriving the cancer cells of the amino acid cystine, the researchers were able to trigger a form of cell death called necrosis in mouse models of the disease.

The new Mount Sinai study reveals how loss of a protein called Sirtuin1 (SIRT1) affects the ability of blood stem cells to regenerate normally, at least in mouse models of human disease.

Engram cell in AD mouse — This image depicts a single memory engram cell (green) in the hippocampal dentate gyrus (DG) region of a mouse model of early Alzheimer's disease.

«We have shown for the first time that increasing synaptic connectivity within engram cell circuits can be used to treat memory loss in mouse models of early Alzheimer's disease,» says lead author Dheeraj Roy.

The work recently received a $ 1.7 million National Institutes of Health grant to delve into the mechanisms that occur as the cells reprogram, and to employ the cells for treating the Parkinson's - like symptoms in a mouse model of hypomyelinating disease.

Scientists at the Gladstone Institutes discovered that changing a specific part of the huntingtin protein prevented the loss of critical brain cells and protected against behavioral symptoms in a mouse model of the disease.

Scientists in the lab of Steve Finkbeiner, MD, PhD, discovered that modifying the huntingtin protein prevented cell death and motor impairment in a mouse model of Huntington's disease.

Roy, D. S., Arons, A., Mitchell, T. I., Pignatelli, M., Ryan T. J., & Tonegawa, S. (2016, March 24) Memory retrieval by activating engram cells in mouse models of early Alzheimer's disease [Abstract].

This approach is now being used to derive embryonic stem cells from a variety of strains including disease models from which in vitro tools are in demand, including mouse models of Alzheimer's disease, cytogenetic disorders (Turner's syndrome and Down syndrome), and tool strains for systems genetics.

Such techniques have the potential to enhance research into the origins of neurodevelopmental and neuropsychiatric disorders such as microcephaly, lissencephaly, autism and schizophrenia, which are thought to affect cell types not found in the mouse models that are often used to study such diseases.

They will then examine other mouse models with mutations involved in cell - adhesion and extracellular matrix molecules for signs of RPE diseases.

«We have shown for the first time that increasing synaptic connectivity within engram cell circuits can be used to treat memory loss in mouse models of early Alzheimer's disease,» said lead author Dheeraj Roy in a release.

The massive number of cells within the OSVZ of humans «tells us we have to be careful when modeling human brain diseases in mice,» says Kriegstein.

With the help of conditional and function - selective knockout mice for the glucocorticoid receptor (GR) the lab identified critical cell types and novel mechanisms for anti-inflammatory activities of glucocorticoids in different inflammatory disease models.

In recent years, researchers have developed so - called «senolytic» drugs that wipe out senescent cells in aging mice and mouse models of age - related disease, exploiting the high dependence of these cells on specific biochemical survival pathways.9, 10 In these studies, senolytic drugs have restored exercise capacity9 and formation of new blood and immune precursor cells11 in aging mice to near youthful norms, and prevented or treated mouse models of diseases of aging like osteoarthritis, 12 fibrotic lung disease, 13 hair loss, 14 atherosclerosis, 15,16 and age - related diseases of the heart itself.9 UNITY Biotechnology is leading a growing charge toward the clinic, with human clinical trials expected to begin in 201In recent years, researchers have developed so - called «senolytic» drugs that wipe out senescent cells in aging mice and mouse models of age - related disease, exploiting the high dependence of these cells on specific biochemical survival pathways.9, 10 In these studies, senolytic drugs have restored exercise capacity9 and formation of new blood and immune precursor cells11 in aging mice to near youthful norms, and prevented or treated mouse models of diseases of aging like osteoarthritis, 12 fibrotic lung disease, 13 hair loss, 14 atherosclerosis, 15,16 and age - related diseases of the heart itself.9 UNITY Biotechnology is leading a growing charge toward the clinic, with human clinical trials expected to begin in 201in aging mice and mouse models of age - related disease, exploiting the high dependence of these cells on specific biochemical survival pathways.9, 10 In these studies, senolytic drugs have restored exercise capacity9 and formation of new blood and immune precursor cells11 in aging mice to near youthful norms, and prevented or treated mouse models of diseases of aging like osteoarthritis, 12 fibrotic lung disease, 13 hair loss, 14 atherosclerosis, 15,16 and age - related diseases of the heart itself.9 UNITY Biotechnology is leading a growing charge toward the clinic, with human clinical trials expected to begin in 201In these studies, senolytic drugs have restored exercise capacity9 and formation of new blood and immune precursor cells11 in aging mice to near youthful norms, and prevented or treated mouse models of diseases of aging like osteoarthritis, 12 fibrotic lung disease, 13 hair loss, 14 atherosclerosis, 15,16 and age - related diseases of the heart itself.9 UNITY Biotechnology is leading a growing charge toward the clinic, with human clinical trials expected to begin in 201in aging mice to near youthful norms, and prevented or treated mouse models of diseases of aging like osteoarthritis, 12 fibrotic lung disease, 13 hair loss, 14 atherosclerosis, 15,16 and age - related diseases of the heart itself.9 UNITY Biotechnology is leading a growing charge toward the clinic, with human clinical trials expected to begin in 201in 2019.

In the study, which was conducted in collaboration with researchers at UC San Francisco and published today in the Journal of Neuroscience, scientists transplanted inhibitory neuron progenitors — early - stage brain cells that have the capacity to develop into mature inhibitory neurons — into two mouse models of Alzheimer's disease, apoE4 or apoE4 with accumulation of amyloid beta, another major contributor to Alzheimer'In the study, which was conducted in collaboration with researchers at UC San Francisco and published today in the Journal of Neuroscience, scientists transplanted inhibitory neuron progenitors — early - stage brain cells that have the capacity to develop into mature inhibitory neurons — into two mouse models of Alzheimer's disease, apoE4 or apoE4 with accumulation of amyloid beta, another major contributor to Alzheimer'in collaboration with researchers at UC San Francisco and published today in the Journal of Neuroscience, scientists transplanted inhibitory neuron progenitors — early - stage brain cells that have the capacity to develop into mature inhibitory neurons — into two mouse models of Alzheimer's disease, apoE4 or apoE4 with accumulation of amyloid beta, another major contributor to Alzheimer'in the Journal of Neuroscience, scientists transplanted inhibitory neuron progenitors — early - stage brain cells that have the capacity to develop into mature inhibitory neurons — into two mouse models of Alzheimer's disease, apoE4 or apoE4 with accumulation of amyloid beta, another major contributor to Alzheimer's.

In the current study, the scientists discovered that, in a mouse model of Alzheimer's disease, the accumulation of tau in neurons disrupts the cells» ability to strengthen their connections with other neurons, preventing them from stabilizing new memorieIn the current study, the scientists discovered that, in a mouse model of Alzheimer's disease, the accumulation of tau in neurons disrupts the cells» ability to strengthen their connections with other neurons, preventing them from stabilizing new memoriein a mouse model of Alzheimer's disease, the accumulation of tau in neurons disrupts the cells» ability to strengthen their connections with other neurons, preventing them from stabilizing new memoriein neurons disrupts the cells» ability to strengthen their connections with other neurons, preventing them from stabilizing new memories.

In the fall of 2012, their group demonstrated that misfolded versions of α - synuclein, the protein implicated in Parkinson's disease, can be transmitted from cell to cell in mouse models, adding weight to a hypothesis that a common mechanism of neurodegenerative disorders could involve the passage of misfolded proteins through the central nervous systeIn the fall of 2012, their group demonstrated that misfolded versions of α - synuclein, the protein implicated in Parkinson's disease, can be transmitted from cell to cell in mouse models, adding weight to a hypothesis that a common mechanism of neurodegenerative disorders could involve the passage of misfolded proteins through the central nervous systein Parkinson's disease, can be transmitted from cell to cell in mouse models, adding weight to a hypothesis that a common mechanism of neurodegenerative disorders could involve the passage of misfolded proteins through the central nervous systein mouse models, adding weight to a hypothesis that a common mechanism of neurodegenerative disorders could involve the passage of misfolded proteins through the central nervous system.

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.

Using genetic and epigenetic analyses coupled with powerful perturbation technologies to test gene functions in human cells and mouse models, we hope to identify the critical drivers of this disease and the basis for therapeutic responses.

Transgenic models session Chairs V.Korinek & Z. Kozmik 16.00 Bohumil Fafílek Cell tracking and manipulation in genetically modified mice 16.30 Michaela Krausová Mouse transgenic model to study tumor progression and metastasis in the gut 17.00 coffee break 17.20 Matej Durik Rodent transgenic models of cardiovascular diseases 17.50 Jan Masek The role of Wnt / beta - catenin signaling in neural crest development: an insight from transgenic and knockout mice 19.00 dinner

Adenovirally generated induced pluripotent stem cells mediate a preservation of motor function or behavioral recovery after transplantation in a mouse model of Huntington's Disease

The results were obtained from mice and human stem cells in cultivated brain tissue, and from a series of rodent models for human neurodegenerative diseases and acute brain injuries.

Previously, he worked in the laboratories of Dr. Paul Greengard and Dr. Myriam Heiman, utilizing similar cutting - edge cell - type specific techniques to investigate pathology of Huntington's disease model in mice.

In this work, we transplanted hematopoietic stem and progenitor cells into the substantia nigra of brains of two different mouse models of Parkinson's disease.

Working with Dr. Weiskopf, we established a model of human dengue disease using HLA transgenic mouse strains, and characterized human dengue - specific CD8 + and CD4 + T - cell responses in natural infection as well as following vaccination.

Recently, mouse neural stem cells (NSCs) have been shown capable of reprogramming into a pluripotent state by forced expression of Oct3 / 4 and Klf4; however it has been unknown whether this same strategy could apply to human NSCs, which would result in more relevant pluripotent stem cells for modeling human disease.

Research Interests: Molecular control of cell fate from stemness to differentiated skeletal and neuronal cell types; SOX transcription factors; skeletal malformation and degeneration diseases; intellectual disability and autism spectrum disorders; mouse genetic models; human pluripotent stem cell differentiation models in vitro

Changing a specific part of the huntingtin protein prevented the loss of critical brain cells and protected against behavioral symptoms in a mouse model of the disease.

Using red blood cells modified to carry disease - specific antigens, a team of scientists from Whitehead Institute and Boston Children's Hospital have prevented and alleviated two autoimmune diseases — multiple sclerosis (MS) and type 1 diabetes — in early stage mouse models.