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Category Archives: Transhuman News
High-fat diet leads to same intestinal inflammation as a virus – UCLA Newsroom
Posted: June 22, 2017 at 4:47 am
FINDINGS
A new study by scientists at UCLA found that when mice eat a high-fat diet, the cells in their small intestines respond the same way they do to a viral infection, turning up production of certain immune molecules and causing inflammation throughout the body. The scientists also found that feeding the mice tomatoes containing a protein similar to that in HDL, or good cholesterol, along with the generic cholesterol drug Ezetimibe, reversed the inflammation.
The results could lead to new types of drugs, targeting the intestinal cells, to reduce peoples risk of heart attacks and strokes, or to treat other conditions linked to inflammation, including cancer and inflammatory bowel disease.
Researchers already knew that prolonged obesity can cause inflammation of the liver and fat tissues, and that this inflammation contributes to the development of diabetes and heart disease. Studies have also shown that higher levels of high-density lipoprotein, or HDL, cholesterol, reduces a persons risk of heart disease.
The UCLA research team, led by Alan Fogelman, chair of the department of medicine at the David Geffen School of Medicine at UCLA,previously developed genetically engineered tomatoes that contained 6F, a protein resembling the main protein in high-density lipoprotein. In early experiments on 6F, they found that the compound was active in the small intestines of mice, and that it reduced inflammation. But exactly how it did this was unclear.
The scientists fed either a standard chow or a high-fat, high-cholesterol Western diet to mice that were especially prone to developing clogged arteries. They also treated some of the mice with either 6F, in the form of a tomato concentrate containing the protein, Ezetimibe, or both. After two weeks, cells from the small intestines of the mice were collected and blood samples were taken. The researchers measured cholesterol levels as well as the levels of inflammatory and immune molecules in both the intestines and throughout the body.
The findings shed light on the molecular details of how high-fat diets cause inflammation in the body, by making the intestines activate the pathway normally triggered by a virus. This suggests that blocking this immune reaction as 6F and Ezetimibe do may treat inflammatory diseases and decrease peoples risk of heart attack and stroke.
The authors of the study are all faculty and researchers at UCLA, affiliated with the Department of Medicine; Department of Molecular and Medical Pharmacology; Department of Human Genetics; Department of Microbiology, Immunology & Molecular Genetics; Department of Pathology and Laboratory Medicine; Department of Obstetrics and Gynecology; Semel Institute for Neuroscience and Human Behavior; and Department of Molecular, Cell and Developmental Biology. The first author is Pallavi Mukherjee; Fogelman is the senior author.
The studywas published June 7, 2017, in the Journal of Lipid Research.
The study was funded by the United States Public Health Service (2P01 HL-30568) and the Castera, Laubisch, and Milt Grey funds at UCLA.
Alan Fogelman, Mohamad Navab and Srinivasa Reddy are principals in Bruin Pharma, which is working to commercialize apoA-I mimetics, including the 6F peptide studied in this paper; Fogelman is additionally an officer of the company.
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Rare genetic variants found to increase risk for Tourette syndrome – UCLA Newsroom
Posted: at 4:47 am
An international team led by researchers from UCLA and Massachusetts General Hospital has identified the first definitive genes associated with Tourette syndrome, giving scientists a long-sought foothold on the biology of the disease.
The report in the June 21 issue of Neuron describes the discovery of rare mutations either deletions or duplications of genetic material in two neurodevelopmental genes, NRXN1 and CNTN6, in people with Tourette syndrome, a disorder characterized by multiple chronic, involuntary motor and vocal tics.
This is a first, key step in understanding the role of these genes in the disease process and ultimately in pointing the field toward possible therapeutic strategies, said Dr. Giovanni Coppola, a professor of psychiatry and neurology at UCLAs Semel Institute for Neuroscience and Human Behavior, and the studys co-senior author. All of us in the field have been trying to understand which genes increase the risk of disease.
Theres no cure for Tourette syndrome, and no one medication that is helpful to all people with Tourette syndrome or suppresses all symptoms.
Previous research has shown Tourette syndrome has a clear genetic component. But genetic risk appears to be very complex, possibly involving different genes in different individuals. Several small studies have identified genes that appear to contribute to Tourette syndrome risk, Coppola said, but none of them met the statistical threshold of significance.
For this study, researchers analyzed data collected by the Tourette Syndrome Association International Consortium for Genetics and the Gilles de la Tourette Syndrome GWAS (genome-wide association studies) Replication Initiative from more than 2,400 people with Tourette syndrome.
Of those people, only two dozen shared rare genetic mutations onNRXN1, which has a role in the development of synapses that transmit signals between neurons, orCNTN6, which is important in the development of neuronal connections involved in movement control.
To test whether these findings were specific to Tourette syndrome and not coincidence, researchers looked for the mutations in 4,100 people without Tourette syndrome. They found that the mutations were vastly predominant in people with Tourette syndrome.
The finding is also relevant to other neuropsychiatric disorders. More than 85 percent of people with Tourette syndrome have attention deficit hyperactivity disorder or obsessive-compulsive disorder, or elevated risk for mood, anxiety, major depressive and autism spectrum disorders. Next, scientists plan to study cells from people with these rare genetic variantsto understand more precisely how they are involved in these diseases.
Tourette syndrome has long been considered a model disorder to study the parts of the brain that function at the intersection of our traditional concepts of neurology and psychiatry, said Dr. Jeremiah Scharf of the psychiatric and neurodevelopmental genetics unit in the Massachusetts General Hospital departments of psychiatry and neurology and co-senior author. Identifying additional genes will give us additional points on the map to let us focus in on exactly which cells in the brain are not functioning correctly at which specific times.
John Miller, president and CEO of the Tourette Association of America, which provided support for the study, called the identification of the two genes an enormous step forward. We congratulate our colleagues on this important discovery and on the real progress it means for individuals with Tourette.
The studys first author is Alden Huang, a doctoral student in the UCLA bioinformatics program. Additional co-senior authors of the study are Dr. Carol Mathews of the University of Florida and Peristera Paschou of Purdue University. Other support for the study came from the National Institute of Neurologic Disorders and Stroke grants U01 NS040024, K02 NS085048, P30 NS062691 (Informatics Center for Neurogenetics and Neurogenomics, ICNN) and NS016648; National Institute of Mental Health grants K23 MH085057 and MH096767; and American Recovery and Reinvestment Act grant NS040024-07S.
Coppola said that he is especially grateful to patients who agreed to be part of the study. As a neurologist in Italy, where he trained, people volunteering for genetic studies would ask him, What is the possible outcome of this? and he would say, Most likely, nothing.
Now, with this studys results, Coppola can point to a success story: Next time your doctor asks you to give your DNA for testing, and tells you chances are dim for the result being relevant, keep in mind sometimes it works. And the more people enrolled, the better it works.
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Genetic modelling adds a new twist to hobbit ancestry question – Cosmos
Posted: at 4:47 am
An artists impression of Homo floresiensis.
Katrina Kenny
Just when we thought we were getting a firm grip on the place of the diminutive early human Homo floresiensis, better known as the hobbit, in our evolutionary family tree, new research keeps alive at least part of a long-held theory about the one-metre-tall hominid being a dwarf descendant of Homo erectus, the first hominid believed to have left Africa.
This hitherto widely accepted theory has been challenged of late. A study published in April and credited as the most comprehensive analysis to date of the bones of H floresiensis confidently reported that the tiny human also known as Flores Man, because his remains were discovered on the Indonesian island of Flores in 2003 was not descended from H erectus but most likely from another ancestor in Africa.
That study, led by Debbie Argue of the Australian National University (ANU), used 133 data points ranging across the skull, jaws, teeth, arms, legs and shoulders of the H. floresiensis fossil to conclude that many features were more primitive than H. erectus, and that therefore the hobbits were most likely a sister species of Homo habilis, one of the earliest known species of human found in Africa 1.75 million years ago. It was possible, Argues team said, that H. floresiensis evolved in Africa and migrated, or that a common ancestor moved from Africa then evolved into H. floresiensis.
Now Jos Alexandre Felizola Diniz-Filho of the Federal University of Gois, Brazil, and Pasquale Raia of University of Naples Federico II have revisited the controversy through their application of quantitative evolutionary genetics modelling, using simulations to evaluate the possible trajectories of body dwarfing between H. erectus (with an estimated body size value of 50 kg) and H. floresiensis (with a body size value of 27 kg).
The pair state their results, published in the journal Proceedings of the Royal Society B, do not say any final word on the matter, but their analysis does consistently support a relatively large-bodied hominid as the ancestor to H. floresiensis.
If H. floresiensis originated from an early small-bodied Homo such as such as H. habilis, they note, its small body and brain would just reflect deeper ancestry followed by little evolutionary change. However, that still leaves deep implications for the so-called Out of Africa I hypothesis, which portrays H. erectus or related forms as the first hominin to leave Africa.
On the other hand, the theory that H. floresiensis evolved from H. erectus also required understanding how Flores Man, given the small size not just of its body but also its brain, could be the evolutionary result of insular dwarfism due to the island rule, where the limited environment and resources of islands see smaller mainland animals become larger, while larger animals become smaller.
The pair report that the hobbits small body and brain size are perfectly consistent with dwarfing driven by strong directional selection under the island rule. Our results also show that the exceedingly small cranial volume of H. floresiensis might have required additional and independent selective forces acting on brain size alone, reinforcing the role of energetic constraints underlying the island rule.
Thus their findings also support previous conclusions that H. floresiensis may be most likely derived from an early Indonesian H. erectus, which is coherent with currently accepted biogeographical scenario for Homo expansion out of Africa.
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Genetic modelling adds a new twist to hobbit ancestry question - Cosmos
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DNA Replication Filmed for First Time Shows How Awkward and Random Genetics Is – Newsweek
Posted: at 4:47 am
Researchers at the University of California, Davis, have just reported a small but significant accomplishment: catching the replication of a single DNA molecule on video for the first time. And the footage has revealed some surprising details about this structure on which all life depends.
DNA is composed of two strands bound together in a helical shape, like a twisting ladder. These strands are made of four basesadenine, guanine, cytosine and thymine, abbreviated as A, G, C and T, respectivelystrung together in various patterns and paired in specific ways across the rungs of the ladders. A always pairs with T, and C always pairs with G. Sugar and phosphate molecules help provide architectural support to the ladder-like structure. Human DNA contains about 3 billion bases. Discrete, repeated sequences of bases form the individual genes that encode the instructions for all our working parts. And every time a cell divides, which happens incredibly often, DNA replicates so that each new cell contains a complete copy of our entire genome, or genetic blueprint.
A digital representation of the human genome. Scientists at UC Davis have discovered that DNA replication is not as smooth as they thought. Mario Tama/Getty Images
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The process of DNA replication isa tremendous source of wonder and focus forresearch. The helix must unwind and have each strand copied smoothly and quickly. An enzyme called helicase triggers the unwinding and another called primase initiates the replication process. Athird, called polymerase, travels the length of a strand, adding the requisite base pairs along the way, leaving behind a new strand. Imagine splitting a ladder down the middle and assembling matching halves so that where there was once one ladder now there are two. That is DNA replication, only in place of saws, nails, wood and glue, there are enzymes and many microscopic and complex processes. Mysteries aboundwhen it comes to thishereditary material.
To better probe those mysteries, geneticist and microbiologist Stephen Kowalcyzkowski and colleagues watched DNA from bacteria replicate. They wanted to see exactly how fast the enzymes worked on each strand.
This first-ever view, shown in the video above, revealed a surprise: replication stopped unpredictably and moved at a varying pace. "The speed can vary about 10-fold," Kowalczykowski said in a statement. The two strands also replicated at different speeds.Sometimes the copying stalled on one strand while proceeding on the other. "We've shown that there is no coordination between the strands," said Kowalczykowski. "They are completely autonomous." The process, the researchers report in their study, published in Cell, is much more random than previously suspected.
The three enzymeshelicase, primase and polymeraseare also not alwys in sync. Even if polymerase stops its replication work, helicase can keep unzipping the helix. That lack of coordination leaves the half-helix of DNA exposed and vulnerable to damage. Such exposure is known to trigger repair mechanisms within the cell. Errors in replicating DNA, while often corrected, can also result ingenetic abnormalities that in turn lead to diseases.
This new look at DNA transforms the scientific understanding about replication. "It's a real paradigm shift," saidKowalcyzkowski, "and undermines a great deal of what's in the textbooks."
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DNA study reveals cats traveled with humans centuries ago – New York Post
Posted: at 4:47 am
Long before cats became the darlings of Facebook and YouTube, they spread through the ancient human world.
A DNA study reached back thousands of years to track that conquest and found evidence of two major dispersals from the Middle East, in which people evidently took cats with them. Genetic signatures the felines had on those journeys are still seen in most modern-day breeds.
Researchers analyzed DNA from 209 ancient cats as old as 9,000 years from Europe, Africa and Asia, including some ancient Egyptian cat mummies.
They are direct witnesses of the situation in the past, said Eva-Maria Geigl of the Jacques Monod Institute in Paris. She and colleagues also looked at 28 modern feral cats from Bulgaria and east Africa.
Its the latest glimpse into the complicated story of domesticated cats. They are descendants of wild ancestors that learned to live with people and became relatively tame though some cat owners would say that nowadays, they dont always seem enthusiastic about our company.
The domestication process may have begun around 10,000 years ago when people settled in the Fertile Crescent, the arch-shaped region that includes the eastern shore of the Mediterranean Sea and land around the Tigris and Euphrates rivers. They stored grain, which drew rodents, which in turn attracted wild cats. Animal remains in trash heaps might have attracted them too. Over time, these wild felines adapted to this man-made environment and got used to hanging around people.
Previous study had found a cat buried alongside a human some 9,500 years ago in Cyprus, an island without any native population of felines. That indicates the cat was brought by boat and it had some special relationship to that person, researchers say.
Cats were clearly tame by about 3,500 years ago in Egypt, where paintings often placed them beneath chairs. That shows by that time, the cat makes its way to the household, said Geigl.
But the overall domestication process has been hard for scientists to track, in part because fossils skeletons dont reveal whether a cat was wild or domesticated.
Its easier to distinguish dogs, our first domesticated animal, from their wolf ancestors. Dogs evolved from wolves that had begun to associate with people even before farming began, perhaps drawn by the food the humans left behind.
The new study tracked the spread of specific cat DNA markers over long distances through time, a sign that people had taken cats with them. Results were released Monday by the journal Nature Ecology & Evolution.
The study strengthens and refines previous work, said Carlos Driscoll of the Wildlife Institute of India. The extensive sampling of cat DNA going back so far in time is unprecedented, he said.
Researchers also looked for a genetic variant that produces the blotchy coat pattern typical of modern-day domestic cats, rather than the tiger-like stripes seen in their wild cousins. It showed up more often in samples from after the year 1300 than earlier ones, which fits with other evidence that the tabby cat markings became common by the 1700s and that people started breeding cats for their appearance in the 1800s.
Thats late in the domestication of cats, in contrast to horses, which were bred for their appearance early on, Geigl said.
Most of the study focused on the ancient dispersals of cats. In the DNA samples analyzed, one genetic signature found first in the Asian portion of Turkey and perhaps once carried by some Fertile Crescent cats showed up more than 6,000 years ago in Bulgaria.
That indicates cats had been taken there by boat with the first farmers colonizing Europe, Geigl said. It also appeared more than 5,000 years ago in Romania, as well as around 3,000 years ago in Greece.
A second genetic signature, first seen in Egypt, had reached Europe between the first and fifth centuries, as shown by a sample from Bulgaria. It was found in a seventh-century sample from a Viking trading port in northern Europe, and an eighth-century sample from Iran.
The dispersal of the cats across the Mediterranean was probably encouraged by their usefulness in controlling rodents and other pests on ships, the researchers said.
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A baby’s DNA may kick off mom’s preeclampsia – Science News Magazine
Posted: at 4:47 am
A protein made by the fetus may lead to preeclampsia in moms.
People born to mothers who had the prenatal disorder were more likely to have certain DNA variationsnear a gene known to influence blood vessels. The results, published online June 19 in Nature Genetics, point to that gene as a possible preeclampsia culprit, and may help scientists develop ways to stop or prevent the pregnancy complication. Preeclampsia, which is marked by a dangerous spike in blood pressure, affects about 5 percent of pregnancies and is estimated to kill over 70,000 women a year globally.
Scientists have known that preeclampsia can run in families, but the genetics of the fetus hadnt been scrutinized. Over the years, people have looked at mothers genes, says geneticist Linda Morgan of the University of Nottingham in England. This is the first large study to look at babies genes.
Morgan and colleagues compared DNA variations in 2,658 babies, children and adults born to mothers who had preeclampsia with those in more than 300,000 people. (This large group probably included some people born to mothers with the condition, but the vast majority were not.)
A genome-wide association study (GWAS), a technique used to comb through DNA looking for genetic variations that may be linked to a disorder, pinpointed a spot on chromosome 13, near a gene called FLT1. That gene is involved with blood vessel formation, an intricate process for the placenta as it grows into the inside wall of the uterus and merges the babys blood supply to the mothers. The same genetic hot spot turned up in tests of a second group of offspring from mothers who had preeclampsia, Morgan and colleagues report. Another DNA variation near the gene also showed a link to the disorder.
Identifying FLT1 makes a lot of sense, says Ananth Karumanchi, a vascular biologist at Beth Israel Deaconess Medical Center in Boston, who was not involved in the study. Earlier experiments by Karumanchi and others suggest that the gene plays a role in preeclampsia.
Preeclampsia is kicked off by the placenta, an organ grown mostly from fetal cells that helps provide nutrients to the fetus. And though the details are unclear, some scientists suspect that unhealthy placentas start to pump out too much Flt-1 protein. A version of the protein called sFlt-1 can then slip into a mothers bloodstream, where it may damage blood vessels in a way that leads to high blood pressure.
The GWAS results cant explain the bulk of preeclampsia cases. A fetus carrying a single copy of one of the troublesome variants near FLT1 raised a mothers risk of preeclampsia by about 20 percent, the analysis suggests. Other risk factors are known to be much stronger, Morgan says, including previous high blood pressure, former preeclampsia diagnoses or carrying twins.
Karumanchi says that the genetic results might not be strong enough on their own to make the case that the gene is involved. But other work points to FLT1. We feel its the right target, he says.
In Europe, a preliminary clinical trial is testing a filtration method that removes excess sFlt-1 protein from the blood of women with signs of preeclampsia. So far, about 20 women have undergone the procedure, says nephrologist Ravi Thadhani of Massachusetts General Hospital in Boston. Early results are quite encouraging, he says, and he hopes to expand the study soon.
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Alleged burglar identified through DNA – Muskogee Daily Phoenix
Posted: at 4:47 am
A lost hat while fleeing police led to a DNA match and an arrest in a burglary attempt at a local storage facility.
Matthew Kelly Carpenter, 34, was allegedly caught in the act by law enforcement at the storage facility on South Cherokee Street in Muskogee in late January, according to the probable cause affidavit filed in the case Wednesday.
Carpenter fled officers, losing his hat in the progress. DNA from the hat was sent to the Oklahoma State Bureau of Investigation for testing, and it came back as a match to Carpenter, the court documents state.
He has two prior convictions of second-degree burglary, according to supplemental information filed with the charges.
Carpenter was arrested Tuesday and is held without bond on four charges of second-degree burglary and two charges of attempted second-degree burglary, according to court documents.He returns to court June 26.
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Researchers find new mechanism for genome regulation – Phys.org – Phys.Org
Posted: at 4:46 am
June 21, 2017 Liquid-like fusion of heterochromatin protein 1a droplets in the embryo of a fruit fly. Credit: Amy Strom/Berkeley Lab
The same mechanisms that quickly separate mixtures of oil and water are at play when controlling the organization in an unusual part of our DNA called heterochromatin, according to a new study by researchers at the Department of Energy's Lawrence Berkeley National Laboratory (Berkeley Lab).
Researchers studying genome and cell biology provide evidence that heterochromatin organizes large parts of the genome into specific regions of the nucleus using liquid-liquid phase separation, a mechanism well known in physics but whose importance for biology has only recently been revealed.
They present their findings June 21 in the journal Nature, addressing a long-standing question about how DNA functions are organized in space and time, including how genes are regulated to be silenced or expressed.
"The importance of DNA sequences in health and disease has been clear for decades, but we only recently have come to realize that the organization of sections of DNA into different physical domains or compartments inside the nucleus is critical to promote distinct genome functions," said study corresponding author, Gary Karpen, senior scientist at Berkeley Lab's Biological Systems and Engineering Division.
The long stretches of DNA in heterochromatin contain sequences that, for the most part, need to be silenced for cells to work properly. Scientists once thought that compaction of the DNA was the primary mechanism for controlling which enzymes and molecules gain access to the sequences. It was reasoned that the more tightly wound the strands, the harder it would be to get to the genetic material inside.
That mechanism has been questioned in recent years by the discovery that some large protein complexes could get inside the heterochromatin domain, while smaller proteins can remain shut out.
In this new study of early Drosophila embryos, the researchers observed two non-mixing liquids in the cell nucleus: one that contained expressed genes, and one that contained silenced heterochromatin. They found that heterochromatic droplets fused together just like two drops of oil surrounded by water.
In lab experiments, researchers purified heterochromatin protein 1a (HP1a), a main component of heterochromatin, and saw that this single component was able to recreate what they saw in the nucleus by forming liquid droplets.
"We are excited about these findings because they explain a mystery that's existed in the field for a decade," said study lead author Amy Strom, a graduate student in Karpen's lab. "That is, if compaction controls access to silenced sequences, how are other large proteins still able to get in? Chromatin organization by phase separation means that proteins are targeted to one liquid or the other based not on size, but on other physical traits, like charge, flexibility, and interaction partners."
The Berkeley Lab study, which used fruit fly and mouse cells, will be published alongside a companion paper in Nature led by UC San Francisco researchers, who showed that the human version of the HP1a protein has the same liquid droplet properties, suggesting that similar principles hold for human heterochromatin.
Interestingly, this type of liquid-liquid phase separation is very sensitive to changes in temperature, protein concentration, and pH levels.
"It's an elegant way for the cell to be able to manipulate gene expression of many sequences at once," said Strom.
Other cellular structures, including some involved in disease, are also organized by phase separation.
"Problems with phase separation have been linked to diseases such as dementia and certain neurodegenerative disorders," said Karpen.
He noted that as we age, biological molecules lose their liquid state and become more solid, accumulating damage along the way. Karpen pointed to diseases like Alzheimer's and Huntington's, in which proteins misfold and aggregate, becoming less liquid and more solid over time.
"If we can better understand what causes aggregation, and how to keep things more liquid, we might have a chance to combat these types of disease," Strom added.
The work is a big step forward for understanding how DNA functions, but could also help researchers improve their ability to manipulate genes.
"Gene therapy, or any treatment that relies on tight regulation of gene expression, could be improved by precisely targeting molecules to the right place in the nucleus," says Karpen. "It is very difficult to target genes located in heterochromatin, but this understanding of the properties linked to phase separation and liquid behaviors could help change that and open up a third of the genome that we couldn't get to before."
This includes targeting gene-editing technologies like CRISPR, which has recently opened up new doors for precise genome manipulation and gene therapy.
Explore further: Discovery of a novel chromosome segregation mechanism during cell division
More information: Amy R. Strom et al, Phase separation drives heterochromatin domain formation, Nature (2017). DOI: 10.1038/nature22989
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The same mechanisms that quickly separate mixtures of oil and water are at play when controlling the organization in an unusual part of our DNA called heterochromatin, according to a new study by researchers at the Department ...
Gelada malesa close relative to baboonspay attention to the loud calls of a rival to gain information about his relative fighting ability compared to themselves, a new study indicated.
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Researchers find new mechanism for genome regulation - Phys.org - Phys.Org
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Genes that affect diseases and other traits may be scattered across genome – Scope (blog)
Posted: at 4:46 am
Biomedical researchers tend to envision genes for traits from height to Alzheimers disease as being clustered in a limited number of pathways.
Two assumptions have guided this perspective: that specific traits or diseases are influenced by a few dozen genes andthat this limited menu of genes tends to be governed bymolecular pathways known to be associated with the disease.
For example, researchers might look for genes promoting diabetes in molecular pathways associated with sugar metabolism. Similarly, a hunt for genes that increase the risk for Alzheimers would focus on pathways active in the brain.
But while those assumptions make intuitive sense, Jonathan Pritchard, PhD, professor of genetics and of biology, said he has found that data dont always agree.
Recently, Pritchard and colleagues (shown above) published apaper in Cellsuggesting that the bulk of the inheritance of complex traits comes not from those few dozen core genes but from thousands of gene variants scattered across the genome. Graduate student Evan Boyle and postdoctoral scholar Yang Li, PhD, share lead authorship.
As Ireported in anews release:
The gene activity of cells is so broadly networked that virtually any gene can influence disease, the researchers found. As a result, most of the heritability of diseases is due not to a handful of core genes, but to tiny contributions from vast numbers of peripheral genes that function outside disease pathways.
Any given trait, it seems, is not controlled by a small set of genes. Instead, nearly every gene in the genome influences everything about us. The effects may be tiny, but they add up.
Its an interesting perspective, one that is sure to spur a host of inquiries.
Previously:New technique offers glimpse at human evolution in action,Genetics: A look back at the first 100 years,Computing our evolution Photo by Steve Fisch
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Genes that affect diseases and other traits may be scattered across genome - Scope (blog)
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Human Longevity, Inc. Announces … – finance.yahoo.com
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SAN DIEGO, June 15, 2017 /PRNewswire/ --Human Longevity, Inc. (HLI), the genomics-powered, health intelligence company, announced today that the company has signed an agreement with Merck KGaA, Darmstadt, Germany, which operates its biopharmaceutical business as EMD Serono in the U.S. and Canada, with the goal of pioneering the application of advanced genomics and expert analysis with machine learning to transform drug development and medical use of next generation therapeutics. As part of the agreement, the companies have started a joint pilot project to identify treatment response biomarker signatures in patients with advanced melanoma. Financial terms of the deal were not disclosed.
Human Longevity, Inc. (PRNewsFoto/Human Longevity, Inc.)
Cindy Collins, HLI CEO said, "Our agreement with Merck KGaA, Darmstadt, Germany will enable us to work together to discover novel insights that improve patient survival in melanoma, the deadliest form of skin cancer. With more than 230,000 new cases of melanoma diagnosed worldwide each year, and rates on the rise for the last 30 years, we believe our first pilot project is of great importance for society and look forward to working with Merck KGaA, Darmstadt, Germany to impact the treatment of melanoma."
In the pilot project, Merck KGaA, Darmstadt, Germany and HLI are working together to identify treatment response biomarkers in patients with locally advanced or metastatic NRAS mutated cutaneous melanoma that preferentially respond to Merck KGaA Darmstadt, Germany's MEK1/2 inhibitor, pimasertib. To enable this goal, HLI is generating genomic sequencing data from clinical trial participants' tumor and germline and utilizing its machine learning and analytical tools and expertise to interpret and analyze this data in the context of survival and other clinical data.
HLI is building the world's largest database of genomic, phenotypic, and clinical information. HLI has sequenced approximately 40,000 high-quality genomes and is building an unparalleled database of genomic and phenotypic integrated health records. HLI's customers include pharmaceutical and biotechnology companies, life insurance companies, large academic medical centers, physicians and individuals.
About Human Longevity, Inc
Human Longevity, Inc. (HLI) is the genomic-based, health intelligence company empowering proactive healthcare and enabling a life better lived. HLI combines the largest database of genomic and phenotypic data with machine learning to drive discoveries and revolutionize the practice of medicine. HLI's business areas include the HLI Health Nucleus, a genomic powered clinical research center which uses whole genome sequence analysis, advanced clinical imaging and innovative machine learning, along with curated personal health information, to deliver the most complete picture of individual health; HLIQ Whole Genome and HLIQ Oncology. For more information, please visit http://www.humanlongevity.com or http://www.healthnucleus.com.
To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/human-longevity-inc-announces-agreement-with-merck-kgaa-darmstadt-germany-to-engage-in-cancer-biomarker-discovery-in-advanced-melanoma-300474439.html
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Human Longevity, Inc. Announces ... - finance.yahoo.com
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