Sentences with phrase «develop in human diseases»

Not exact matches

Since the human genome was decoded in 2003, researchers have been developing a powerful method for comparing the genomes of patients and healthy people, with the hope of pinpointing the DNA changes responsible for common diseases.

«This may contribute to antibiotic resistance, [and] scientists are more concerned about disease - causing bacteria that develops resistance in farm animals to then infect human beings.

Because the food we consume directly impacts our health, it is important to note that an infant who develops a «taste» for salty, sweet and fatty foods over fruits and vegetables will have a greater risk for diabetes, hypertension, cardiovascular disease and some cancers according to Mennella's and Beauchamp's Flavor Perception in Human Infants article.

Research in the United States, Canada, Europe, and other developed countries, among predominantly middle - class populations, provides strong evidence that human milk feeding decreases the incidence and / or severity of diarrhea,1 - 5 lower respiratory infection,6 - 9 otitis media,3,10 - 14bacteremia, 15,16 bacterial meningitis, 15,17 botulism, 18 urinary tract infection, 19 and necrotizing enterocolitis.20, 21 There are a number of studies that show a possible protective effect of human milk feeding against sudden infant death syndrome,22 - 24insulin - dependent diabetes mellitus,25 - 27 Crohn's disease, 28,29 ulcerative colitis, 29 lymphoma, 30,31 allergic diseases,32 - 34 and other chronic digestive diseases.35 - 37 Breastfeeding has also been related to possible enhancement of cognitive development.38, 39

Since the first human brain organoids were created from stem cells in 2013, scientists have gotten them to form structures like those in the brains of fetuses, to sprout dozens of different kinds of brain cells, and to develop abnormalities like those causing neurological diseases such as Timothy syndrome.

To better understand their findings, the team examined the animal model for APS1 (i.e. mice with the same genetic defect as human patients with the syndrome) and found that male mice spontaneously developed an inflammatory disease in their prostate glands — a so - called prostatitis — and reacted to transglutaminase 4.

A team of researchers at the Stanford University School of Medicine has used a gene - editing tool known as CRISPR to repair the gene that causes sickle cell disease in human stem cells, which they say is a key step toward developing a gene therapy for the disorder.

The team from the University made their discovery by studying the bacteria in a newly developed model, which closely reflected the human disease condition.

A recent study published in Annals of Neurology reports that healthy human tissue grafted to the brains of patients with Huntington's disease in the hopes of treating the neurological disorder also developed signs of the illness, several years after the graft.

«There are very few people in human history who get the privilege of developing a new therapy for any human disease, much less cancer.

The UCLA researchers plan to develop strategies to test the Duchenne - specific CRISPR / Cas9 platform to treat the disease in animals as the next step toward perfecting a method that can be used in humans.

In addition, the Izpisua Belmonte team is developing epigenetic editing technologies to reverse epigenetic alterations with a role in human aging and diseasIn addition, the Izpisua Belmonte team is developing epigenetic editing technologies to reverse epigenetic alterations with a role in human aging and diseasin human aging and disease.

A research team at The University of Texas at El Paso is one step closer to developing an effective human vaccine for cutaneous leishmaniasis, a tropical disease found in Texas and Oklahoma, and affecting some U.S. troops stationed in Afghanistan and Iraq.

The findings indicate that not only might Oprl1 become dysregulated in humans following the development of PTSD, but inherited variants of the disease could increase the likelihood of someone developing the disorder to begin with.

Further studies of processes in which GTPBP3 is involved will help towards the understanding of human diseases that are linked to mitochondrial DNA expression and to develop new therapies.

«Further work in our lab will be aimed at understanding the detailed mechanism of how these proteins regulate editing, in turn providing an inroad to developing therapeutics that modulate editing for the treatment of human diseases.»

His laboratory develops and deploys new biochemical and computational methods in functional genomics, to elucidate the genetic basis of human disease and human physiology, and to create and deploy novel techniques in next - generation sequencing and algorithms for tumor evolution, genome evolution, DNA and RNA modifications, and genome / epigenome engineering.

That way the researchers could ensure that each bird developed the disease as it would manifest in humans.

Scientists want to be able to clone early human embryos, using cells from patients with various diseases, so they can study the diseases in the lab and develop new treatments for them.

The findings, published in the journal Nature, explain why the human genome is so difficult to decipher — and contribute to the further understanding of how genetic differences affect the risk of developing diseases on an individual level.

«However, we were able to show for the first time that changes in this gene primarily cause Dowling - Degos disease and around half of the mutation carriers develop acne inversa,» emphasizes Damian Ralser, who is currently working on his doctorate at the Institute of Human Genetics.

«Using a technique developed by our collaborators at the University of Iowa, we were able to get long - term expression of these human gene variants in the fluid that bathes the entire brain,» says Bradley Hyman, MD, PhD, of the MassGeneral Institute for Neurodegenerative Disease (MGH - MIND), senior author of the report in the Nov. 20 Science Translational Medicine.

«It is possible that also in humans, inflammatory diseases that primarily develop outside the brain could trigger epigenetic reprogramming inside the brain,» says Neher.

UBC Psychiatry Professor Dr. Weihong Song and Neurology Professor Yan - Jiang Wang at Third Military Medical University in Chongqing attached normal mice, which don't naturally develop Alzheimer's disease, to mice modified to carry a mutant human gene that produces high levels of a protein called amyloid - beta.

His research interests include the molecular underpinnings of cervical cancer (including developing genetic screens), the identification of the genetic determinants of quantitative traits in humans, and the application of massively parallel sequencing technology for understanding the genetics of complex disease.

Dr. Funari's research interests include developing new approaches for obtaining mycobiome profiles in human disease and the translation of next generation sequencing applications into the clinic and personalized medicine.

Suspecting that the disease works differently in humans, whose brains are much bigger and more complex than those of lab animals, Brivanlou, along with research associates Albert Ruzo and Gist Croft, developed a cell - based human system for their research.

Using a recently developed genome - editing technique called CRISPR, a Chinese team has successfully altered two target genes in cynomolgus monkeys, paving the way for the development of monkey models that mimic human diseases.

«It's a bit like human disease but in plants, to understand the pathogen and its interaction with the plant allows to develop a functional cure to treat the affected plants» emphasizes the specialist in plant genomics.

However, since the novel genes that were identified, are known to lead to aging - associated diseases in humans, their further analysis seems to be promising for developing new approaches to understand and possibly cure these diseases and to contribute to a long life and healthy aging in humans — in a way, long - lived rodents do.

«If human offspring from obese mothers have a similar risk for developing fibrosis as we see in mice, we may be able to predict who is going to develop more serious disease,» said Thompson.

Researchers have discovered tell - tale signs of Alzheimer's disease in 20 elderly chimpanzee brains, rekindling a decades - old debate over whether humans are the only species that develop the debilitating condition.

Acute sleep loss in humans is associated with increased appetite and insulin insensitivity, while chronically sleep - deprived individuals are more likely to develop obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease.

Although common in humans, domestic pets, and zoo animals, periodontal disease does not typically develop in wild animals, leading to speculation that it is an oral microbiome disease resulting from modern human lifestyles.

Dartmouth researchers developed a new biological pathway - based computational model, called the Pathway - based Human Phenotype Network (PHPN), to identify underlying genetic connections between different diseases as reported in BioDataMining this week.

Since the sequencing of the human genome was completed in 2003, researchers have been trying to figure out which parts of the genome made some people more likely to develop certain diseases.

The monkey model has its own limitations: Monkeys don't develop severe disease when infected with different serotypes of dengue virus, which clearly happens in humans.

A computational tool developed at the University of Utah (U of U) has successfully identified diseases with unknown gene mutations in three separate cases, U of U researchers and their colleagues report in a new study in The American Journal of Human Genetics.

The Structural Genomics Consortium at the University of North Carolina at Chapel Hill (SGC - UNC), in partnership with the DiscoverX Corporation, has reached the milestone halfway point in its development of the Kinase Chemogenomic Set, a potent group of inhibitors which allow deeper exploration of the human kinome, a family of enzymes critical to understanding human disease and developing new therapies.

Professor Hong Wanjin, Executive Director at IMCB, said, «IMCB is now focusing research on molecular mechanisms underlying diseases, which is important in developing future treatments for prevailing human diseases.

Developing the capability to experiment with prions in bacteria could help to reveal more about the behavior of human prions, which may be linked to diseases such as Alzheimer's and Parkinson's, says Jeffrey Roberts, a molecular biologist at Cornell University in Ithaca, New York.

In humans, developing metabolic disease, particularly type 2 diabetes, is correlated with having bacteria that penetrate the mucus lining of the colon, according to a study led by Drs. Benoit Chassaing and Andrew Gewirtz at Georgia State University.

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.

«We believe it is the first example illustrating the process of a developing human heart chamber in vitro,» said Kevin Healy, a UC Berkeley professor of bioengineering, who is co-senior author of the study with Dr. Bruce Conklin, a senior investigator at the Gladstone Institute of Cardiovascular Disease and a professor of medical genetics and cellular and molecular pharmacology at UC San Francisco.

An accidental discovery of a flatworm's color - changing ability could help develop treatments for porphyria, a disease that causes pain and light sensitivity in humans.

«We know from previous human studies that changes in gut bacterial composition correlate with the early development of type 1 diabetes, and that the interactions between bacterial networks may be a contributing factor in why some people at risk for the disease develop type 1 diabetes and others don't,» said Jessica Dunne, Director of Discovery Research at JDRF, which funded the study.

Led by researchers at NYU Langone Medical Center, the study found that maintaining high levels of adenosine in rats with damage to the anterior cruciate ligament (ACL), which is known to lead to osteoarthritis in humans, prevented the rats from developing the disease.

To test this in an animal that is more closely related to humans, investigators in Japan directed iPSCs taken from a monkey to develop into certain neurons that are depleted in Parkinson's disease patients.

Last November, however, a team led by Mihael Polymeropoulos of the National Human Genome Research Institute in Bethesda, Maryland, reported that the disease afflicting the Italian family, which develops at an unusually early age, showed strong genetic linkage to a region on chromosome 4.

Research has shown that giving TMAO to rodents promotes atherosclerosis and that humans with higher concentrations of TMAO in the bloodstream are at increased risk of developing heart disease.