Sentences with phrase «as models of human disease»

These changes may influence the cells» abilities to serve as models of human disease and development.

Not exact matches

«Future studies need to determine the health effects of these cocoas in models of human disease and to evaluate the consumer acceptability of the cocoas as part of a chocolate product.»

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.

With our human gut - on - a-chip, we can not only culture the normal gut microbiome for extended times, but we can also analyze contributions of pathogens, immune cells, and vascular and lymphatic endothelium, as well as model specific diseases to understand complex pathophysiological responses of the intestinal tract.»

«Computational models like this one might one day be able to predict the clinical course of a disease or injury, as well as make it possible to do less expensive testing of experimental drugs and interventions to see whether they are worth pursuing with human trials,» he said.

«We know that urate has neuroprotective properties in animal models, and an unusual convergence of human studies suggested its possible use as a disease - modifying strategy in Parkinson's; so the positive results of this trial are very encouraging.»

These techniques include: human tissue created by reprogramming cells from people with the relevant disease (dubbed «patient in a dish»); «body on a chip» devices, where human tissue samples on a silicon chip are linked by a circulating blood substitute; many computer modelling approaches, such as virtual organs, virtual patients and virtual clinical trials; and microdosing studies, where tiny doses of drugs given to volunteers allow scientists to study their metabolism in humans, safely and with unsurpassed accuracy.

«If human organs on chips can be shown to be robust and consistently recapitulate complex human organ physiology and disease phenotypes in unrelated laboratories around the world, as suggested by early proof - of - concept studies, then we will see them progressively replace one animal model at a time.

But if homologous recombination could be worked out in human (embryonic) stem cells, then cardiomyocytes with mutations in ion channels could be derived, as well as a large number of other very useful disease models of other tissues.

His research focuses on the cancer biology, drug resistance, and signaling pathway networks of human diseases as well as on ways to model these disorders.

Given the rapid succession of generations in yeast, we can use it as a model organism — and study the mechanisms of aneuploidy in much greater detail to find out whether we can derive from it new approaches for diagnosing and treating human diseases.»

The finding, by researchers at the University of Illinois at Chicago College of Medicine, was reported July 16 at the Alzheimer's Association International Conference in Copenhagen by Mary Jo LaDu, who in 2012 developed a transgenic mouse that is now regarded as the best animal model of the human disease.

Clevers and other scientists have developed organoids of the gut, liver, lung, brain, and many other human organs that can be used to model disease or to serve as test beds for drugs.

In a Philadelphia Inquirer op - ed, he wrote that such eternal life was in our reach because «Being able to decode the human genome allows us to develop detailed models of how major diseases, such as heart disease and cancer, progress, and gives us the tools to reprogram those processes away from disease.»

-- 90 percent of genes associated with disease are identical in the human and the mouse, supporting the use of mice as model organisms.

No, studies using animal models of human disease as well as «humanized mice» are expressly forbidden.

Investigating mouse models for biological for research The congress aims to promote the International Mouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imaging.

Human embryonic stem cells derived from affected embryos during a pre-implantation diagnostic (PGD), as well as the conversion of somatic cells, such as skin fibroblasts, into induced pluripotent stem cells by genetic manipulation, offer the unique opportunity to have access to a large spectrum of disease - specific cell models.

Historically, researchers have generated their own lines of knockout mice to serve as models for human disease, such as heart disease or cancer.

This animal model closely resembles lesion kinetics as seen in human disease [34] and use of non-human primates allows for repetitive surgical sampling for multiple time point analysis.

After their initial in vitro testing, therapeutic proofs of concept must be tested in a living model that recapitulates as closely as possible both the phenotype and biological defects associated to the human disease.

However, mouse models are not always exact replicas of the human condition, and they are inadequate to study the onset and evolution of diseases that are caused by human - tropic infectious agents, such as HIV - 1.

Animal gait is affected in models of human disorders such as Parkinson's Disease, Multiple Sclerosis, Amyotrophic Lateral Sclerosis, spinal cord injury and many others.

Now, the use of diverse model organisms to explore human disease is truly starting to gain the recognition it deserves as a scientific approach.

«Amy's video is both beautiful to watch on an aesthetic level and beautiful to watch as an illustration of how simple model organisms like Ashbya can give us insights into human diseases like Alzheimer's,» Atkinson continues.

NYSCF partners with a broad range of institutions, foundations, centers and companies in a variety of ways ranging from the creation of fundamental research resources such as iPSC lines for a disease area to developing human disease models in vitro to enable drug discovery and toxicity testing.

If successful, this model of making human genomic data accessible to the world might become a paradigm for other diseases, as a way to catalyze scientific advances throughout all fields of human biology.

As a result of these findings, the team were able to conclude that the Drosophila model was an effective and accurate model of human kidney disease.

Furthermore, new genome - editing technologies such as CRISPR / Cas9 now enable the efficient derivation of precision disease models incorporating patient - specific genetic variants as a means of recapitulating essential aspects of human disease in mouse and other model organisms.

We focus on developing computational methods and tools for (a) analyzing large - scale gene expression data related to human cancer in search for gene markers and disease sub-categories, (b) identifying regulatory elements such as miRNA precursors and their targets in whole genomes of plants and mammals, (c) building theoretical models of gene regulatory networks.

Now this latter element, it turns out that we have a real opportunity because as Dave Calkins and others have now demonstrated very beautifully in animal models, and we even have very good data now in humans; in glaucoma there's an injury that happens first, and it's the death or loss of the cell that happens later in the disease.

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.

Clinicians and investigators in the fields of veterinary and human endocrine oncology, clinical trials, pathology, and drug development will be joined in this consortium, in order to improve knowledge, development of, and access to naturally occurring canine endocrine tumours, as a model for human disease.

Moreover, PHENONIM - ICS is involved in European projects presenting a strong impact on human health: Interreg CARDIOGENE (Genetic mechanisms of cardiovascular diseases), GENCODYS (Genetic and epigenetic networks involved in cognitive dysfunctions), AgedBrainSYSBIO (Basic studies of brain aging), as well as projects in partnership with industry: MAGenTA (an Industrial Strategic Innovation project supported by Bpifrance about the treatment of major urogenital diseases) and CanPathPro (H2020 program), to develop a predictive modeling platform of signaling pathways involved in cancers.

The congress aims to promote the International Mouse Phenotyping Consortium (IMPC) mouse lines, importance of mouse phenotyping & clinical and drug discovery collaboration, to present progresses performed by IMPC with regards CRISPR editing genome, rare diseases, microbiota and ageing pipeline, as well as illustration of examples of scientific projects about «Animal models for human diseases» and recent developments in mouse models phenotyping imaging.

Here we tested whether human NSCs could be reprogrammed into iPS cells utilizing a similar strategy as described above since they represent a more clinically relevant source of cells for basic studies and modeling human 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.

Biomedcode offers preclinical testing using complex mouse models closely recapitulating the complexity of human disease as they also exhibit co-developing pathologies also observed in human patients.

We therefore suggest that the presence of the mutated transgenes (AβPP and PS1), which are per se the basis for the genetic form of Alzheimer's disease in humans, directly interferes with gut function as shown here for the disease model mice.

Potential projects include identifying common pathways that modify retinal degenerative disease from a large collection of actively maintained mouse models; determining molecular networks implicated in pathological disruption of the retinal pigment epithelium; identifying molecular pathways that regulate postnatal ocular growth; and using mouse models to assess the pathogenic role of gene variants that increase the risk of age - related macular degeneration as identified by human genome - wide association studies.

The use of nonhuman primates to model this disease provides the most accurate representation of human Lyme disease as demonstrated in this work.

Dr. Nobrega has modeled the impact of mutations implicated in various human diseases, such as congenital heart defects, heart failure, cancer, type 2 diabetes, obesity, and asthma.

«We already knew that the buildup of fibrin appears early in the development of MS — both in animal models and in human patients, so we wondered whether thrombin activity could in turn serve as an early marker of disease.»

Fruit flies serve as a good model organism for understanding the molecular mechanisms behind many human diseases — around 75 percent of disease - causing genes are found in the species in a similar form.

Dr. Falk is also PI of an NIH, pharma, and philanthropic funded translational research laboratory group at CHOP that investigates the causes and global metabolic consequences of mitochondrial disease, as well as targeted therapies, in C. elegans, zebrafish, mouse, and human tissue models of genetic - based respiratory chain dysfunction, and directs multiple clinical treatment trials in mitochondrial disease patients.

Because of the pivotal role that diet plays in causing the MS in humans, most metabolic disease animal models do (and we believe should) use diet as a way to precipitate this syndrome.

«Drosophila as a Model for Human Neurodegenerative Disease,» by Julide Bilen and Nancy M. Bonini, Annual Review of Genetics, December 2005.

Furthermore, the heterozygous knock in mouse serves as a better animal model of the human disorder, as compared to the homozygous mouse, given that Huntington disease homozygosity is very rare in humans.

The Ellerby lab is known for its pioneering studies on Huntington's disease (HD), and Karen is now using human stem cell models of HD to understand why important molecular signaling pathways, such as the TGF - β pathway, are dysregulated in HD.

These mouse models could shed light on a wide range of human diseases such as diabetes, many types of cancers, and even neurological diseases such as depression.