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Daily Archives: April 28, 2017
How Domestication Altered The Horse Genome – Forbes – Forbes
Posted: April 28, 2017 at 2:37 pm
Science Daily | How Domestication Altered The Horse Genome - Forbes Forbes A new study published today reveals the suite of traits that ancient nomadic peoples selected to develop the type of horse that best fit their purposes. Scythian horse breeding unveiled: Lessons for animal domestication ... Ancient Ritually Sacrificed Stallions Reveal How Humans Changed ... |
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Dog Genome Project Reveals Secrets of Canine Family Tree – Smithsonian
Posted: at 2:37 pm
smithsonian.com April 27, 2017
Researchers from the Dog Genome Project at the National Institutes of Health have released the most detailed canine family tree to date, creating a timeline of when and where dogs from 161 breeds emerged, reports Maggie Fox at NBC News. The researchers compiled the data by sequencing and comparing the genomes of 1,346 individual dogs over 20 years.
The new family tree isnt just a factoid for the kennel club. According to a press release, it has implications for archeology and human health as well. The study, published this week in the journal Cell Reports, suggests thatthe oldest dog breeds are varieties that served a specific function like herding dogs and pointers.
According to the results, herding dogs were bred independently in various parts of Europe with lineages tracing to the United Kingdom, northern Europe and southern Europe. In the past, reports Erin Ross at Nature, researchers had trouble mapping out the lineages of herding dogs, believing they came from a single source. In retrospect, that makes sense, says Elaine Ostrander, an author of the study. What qualities youd want in a dog that herds bison are different from mountain goats, which are different from sheep, and so on.
One of the most interesting finds was that some breeds from Central and South America like the Peruvian Hairless Dog and the Xoloitzcuintle possibly descended from canines that crossed the Bering land bridge with humans thousands of years ago. While there is some archeological evidence that dogs first entered the New World at that time, the study offers potential genetic confirmation. What we noticed is that there are groups of American dogs that separated somewhat from the European breeds, study co-author Heidi Parker of the NIH says in the press release. Weve been looking for some kind of signature of the New World Dog, and these dogs have New World Dogs hidden in their genome.
The study will also give researchers insight into which genes and mutations are associated with human diseases. As Fox reports for NBC, all domesticated dogs are part of the same species, Canis familiaris, and have the same genetic material. There are just a tiny fraction of changes in the genome that separate a Chihuahua from a Great Dane. We have a yellow brick road for figuring out how mutations move around the dog world. We recognize that everything humans get, dogs getepilepsy, cancer, diabetes, heart disease, Ostrander tells Fox. She points out that some diseases are more prevalent in certain breeds, like epilepsy in beagles. We can actually trace diseases as they move around the dog breed population.
The study suggests there were likely two intensive periods of dog breed diversification, writes Ross. The first happened in hunter-gatherer times when dogs were bred for their skills. During the second period, dogs were bred more frequently for their looks. Known as the "Victorian Explosion,"this period was whenmost modern breeds developed.
The canine family tree, however, is not finished. The team has sequenced less than half of the 400 or so recognized dog breeds in the world. The researchers tell Fox they haunt dog shows and Frisbee dog competitions looking for breeds they have not yet sampled. A list of hard-to-find breeds they are currently searching for is on the Dog Genome Project website. It's worth taking a look, perhaps your pup could be one of the missing branches on the canine family tree.
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Adam and the Genome Part Twelve – Patheos (blog)
Posted: at 2:37 pm
By historical Adam and Eve I simply mean real people in space and time, the progenitors of Gods people who were the sinners in question that set in motion the train of murder and death and iniquity that followed, no sooner than they stepped outside the garden (see the story of Cain and Abel). I do not think it is adequate to suggest that the writers of the NT or for that matter of the intertestamental period were simply referring to Adam and Eve as archetypal or literary figures in a story.
No, they believed these folks actually existed on planet earth long long ago. Indeed, so much did they take that for granted, that they argued from that basis to be able to say other things about Adam and Eve. I find weird the argument of John Walton cited on p. 109 that says because Christ is called the last Adam, since he was not the last biological specimen, one cannot conclude that when Paul refers to the first Adam he means the first biological specimen. Paul is talking about two founders of the race of Gods people the first one, who is the progenitor of Gods people and the last one who will also be the progenitor of Gods people. Biology is neither implied nor denied by this rhetorical comparison, for either Adam.
The chapter about the Twelve major theses, which begins on p. 111 makes up the bulk of Scots main argument. It begins with a very ironic quote from Walter Brueggemann on p. 112. Speaking about the theologians who wrote Gen. 1-11 he says of them they resist a scientific view of creation which assumes the world contains its own mysteries and can be understood in terms of itself without any transcendent referent. Indeed its a pity that the first half of this book didnt approach the matter more like the writers of Gen. 1-11. This quote accurately describes what we find in this book in the discussion on genetics.
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Adam and the Genome Part Eleven – Patheos (blog)
Posted: at 2:37 pm
In regard to point 5) (see the previous post) I agree with Scot that I dont think the later Christian notion of seminal transmission of a sin nature from Adam is a necessary conclusion from what the Bible says. It is the curse that affects the whole human tribe, not Adams sin nature. 6) since all have sinned and lack Gods glory now, it is not necessarily the case that without the historical Adam we dont need the Gospel of salvation, but I would say that Adams sin is the presenting cause which led to the curse which in turn led to fallen human beings.
It is hard for me to doubt that the sorry history of the human race, full of wickedness, bloodshed, hatred, wars etc. is not a profound testimony to sin and fallenness. And besides the Psalmist say in Ps. 51.5- surely I was sinful from the time my mother conceived me. That is hardly a statement about volitional sin after birth. I suspect as well that Pauls language about flesh and his discussion in Rom. 7.14-25 that people can know better, but apart from Christ cannot do the Law, should have some bearing on whether weve all fallen and cant get up without redemption.
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Here’s Why People Think Tesla Is the Most Innovative Company Today – Singularity Hub
Posted: at 2:36 pm
I did a quick Twitter poll asking which technology companies you think are the most innovative today. The options were:
(Note: Twitter polls only allow four options... yes, theres also Apple, Microsoft, Uber, Samsung and SpaceX, to name a few others).
With over 1,000 responses, a clear overwhelming winner emerged: Tesla.
Here was the final tally:
Google and Amazon each spend over $50 billion per year on R&D (2016 figures). In other words, they each spend more R&D dollars in a year than Teslas current market cap of $49 billion.
So why is it that Tesla garnered more votes than Google and Amazon combined?
What can an entrepreneur or CEO learn from this?
Here are my top four reasons (if you have others, please tweet them at me @PeterDiamandis):
Teslas MTP is to accelerate the worlds transition to sustainable energy. To this end, every product Tesla brings to market is focused on this vision and backed by a Master Plan Elon Musk wrote over 10 years ago. Google and Amazon, on the other hand, have scattered vision. Both are collectively working on dozens of innovations, from drone delivery to autonomous cars, that stray from their respective MTPs.
Musk has an eccentric, celebrity-like persona as a founder and has rallied a diehard fan base around himself. He believes 500 percent in what he is doing. He is crystal clear and driven 100 hours per week to execute. While he divides his time between Tesla and SpaceX (and now Neuralink), he doesnt do anything else or speak on any other subject. His companies reflect his clarity and confidence. To a large degree, like Steve Jobs and Apple, Tesla is a reflection of Musk himself.
Musk has garnered a cult-like following on social media, with 8.3 million Twitter followers. On the other hand, Larry Page does not even have a Twitter account, and scarcely speaks publicly; Jeff Bezos has tweeted less than 10 times per year since 2009 and has only 208,000 followers. Musk often responds directly to questions his followers throw his way, and has become famous for leaking product updates and launches on Twitter. He certainly has the news media eating out of his hands and effectively controls the perception of the Tesla brand himself.
Building hardware is HARD. And taking on complex industries like automotive and energy (not to mention space) with new tangible products is perceived by all to have a high degree of difficulty. Hard = Innovative.
In summary, there is a takeaway for entrepreneurs who want to build powerful, innovative companies to change the world. Theres a strong force-multiplier for your company if youre willing to be a powerful, outspoken CEO with a clear and dominant MTP/Moonshot, something you believe in with all your heart and soul.
Image Credit: Tesla
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Earth Day was about science and politics – mySanAntonio.com
Posted: at 2:36 pm
Tim Beach, For the Express-News
Photo: JIM BEST /UNIVERSITY OF ILLINOIS /NYT
Earth Day was about science and politics
Natural scientists would rather work in their labs or their natural labs, such as the Maya Tropical Forest or on Himalayan glaciers. Every part of this planet holds unanswered questions that scientists would joyously study for a hundred lifetimes. Activism takes scientists out of their comfort and confidence zones, but if there was ever a time to do it, now is that time.
Indeed, heroes of the environment include more policy people and artists, though I would like to think my own tribe of natural scientists was as important. Earth Day, which just concluded, started after the wild ride of the 1960s carried along with a growing scientific arsenal that showed nature in decline from burning rivers, toxic waste and sooty cities. Some scientists dared to speak up about those dangers in the 1960s, and some are still speaking up.
Earth Day and the broader zeitgeist that created it produced a phalanx of laws to protect the environment and human health, which made America greater for more people in terms of better health and new jobs. Air quality improved, water quality improved, and we have more sewage and water treatment that spread around the world.
But the divide of the environmental impacts on rich and poor has never been greater. We have improved air quality in rich nations in contrast with off-the-charts pollution levels in China and India, while the hammer of global warming, forged in richer nations, disproportionately pounds the worlds poor.
Two recent travels underscore this divide: through the streets of Rome and down the Tiber, and through the cities of Peru and down its El Nio-swollen quebradas. Despite its congestion, Rome is starkly cleaner. Both have hordes of people and motorcycles, but the lack of pollution laws and enforcement make every step along the garbage-strewn streets in Peru choked with life-shortening exhaust.
When I visited Rome in 1983, its air was also polluted from exhaust. Why Rome is cleaner today is partly due to the global impact of Earth Day and the fact that Europe, like America, is rich enough to care about clean air and water laws that increase human well-being and longevity.
For Earth Day 2017, bad news prevailed about species extinction and soil degradation. As a participant in a recent conference in the Vatican on biological extinctions, I can say that we have made less progress on these keystones of nature species diversity and soil health. Again, rich nations have made progress with such laws as the Endangered Species Act and attention on soils. But both are always in threat as administrations change and most of the hemorrhaging of species and soils is in the tropics, where poverty and politics trump the needs for preservation.
We have embarked on the sixth global extinction in the Earths 4.55 billion years.
Long before Earth Day, but a clear precursor to it, was the Dust Bowl. Many Americans know the role the New Deal and Civilian Conservation Corps played. But fewer know the outsized role that Big Hugh soil scientist Hugh Hammond Bennett played when he used a skillful mastery of science and politics to organize the Soil Erosion Service. Bennett and the service that became the Natural Resources Conservation Service put legions to work to restore soils, and their legion of ecosystem services made America greater, such as water purification, fertility and carbon sequestration.
Now enter President Donald Trump, who seems determined to cut environmental protection by slashing the very programs that grow the economy with clean technologies and save lives in the process. All types of scientists rose from their labs and rainforests this year to march for science on Earth Day in Washington, D.C., and across the country, standing against the ignorance of science by those in power who question even the basics of science.
Remember the Dust Bowl and Big Hugh, and hope these marching scientists will make an administration listen.
Tim Beach is the C.B. Smith Sr. Centennial Professor of Geography and the Environment at the University of Texas at Austin.
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9 Things You Should Never Do If You Have Eczema – Health.com
Posted: at 2:36 pm
Derived from the Greek language, the word eczema translates to something like to boil. And anyone who has atopic dermatitisthe most common form of eczemacan probably see why. The symptoms often shows up as red, itchy rashes on your arms and legs, and can sometimes cause open sores or resemble scaly skin.
Although its possible to develop atopic dermatitis for the first time as an adult, the majority of people experience it shortly after they were born, perhaps as young as two months old. Most people outgrow it in their early teens, but it can come back later in life, says Whitney High, MD, an associate professor of dermatology and pathology at the University of Colorado School of Medicine, in Denver. For some people, atopic dermatitis continues through into adulthood and never lets up.
The condition itself is likely hereditary, and usually runs in the same circles as allergic rhinitis and asthma. Families that have one child with eczema often have another child with asthma or even a third child with seasonal rhinitis or hay fever, he says.
To limit your odds of experiencing a flare up, here are nine things to avoid.
A long soak in the tub might sound fantasticbut if you have atopic dermatitis, spending too long in the bathtub can leave your skin feeling itchy and red. The next time you turn on the tap, remember the Goldilocks rule: the water should be not too hot, not too cold, but a lukewarm medium. Ideally, youll also limit your soak to no longer than 15 minutes a day, says Dr. High. We tell people to take good care of their skin by doing gentle bathing and not over-drying the skin, he says.
Any kind of abrasive texture, like wool or certain synthetic fibers, might irritate your skin, says Dr. High. A better wardrobe choice: soft, cotton clothing in a looser cut, which wont rub against your skin. You should also wash any new clothing you buy before wearing themsome contain dyes that make the fabric appear nicer in the store, but may trigger a flare-up on your skin.
Scented laundry detergents and some dryer sheets can also bother your skin. Choose products that are free of fragrances and dyes; liquid ones tend to leave less irritating residues behind compared to powder versions. We like the all-FREE CLEAR laundry detergent thats specifically designed for people with sensitive skin; the product received a seal of acceptance from the National Eczema Association (NEA), which keeps a list of other helpful products on their website.
RELATED: The Best Laundry Detergents for Sensitive Skin
Similar to scented laundry detergents, scented hand soaps, bubble baths, body washes, and lotions can all cause your skin to feel dry and itchy. Use bland soaps, not highly perfumed or scented soaps, says Dr. High.
Atopic dermatitis is sometimes called the itch that rashes. In other words, says Dr. High, some people think you have the itching sensation first, then do all the damage to the skin with the scratching and picking, which leads to the rash. And while its a good idea to reach for a moisturizer at the first sign of a tingle, you should also keep your fingernails trimmed and smooththat way, youll be less likely to puncture the skin if you do end up scratching at it.
During the warmer months, the high temperatures (or, the sensation of heat, says Dr. High) can sometimes bother peoples skin. Not only that, but sweating can cause irritation, too. Likewise, the cold, dry weather in winter can also trigger itchiness.
To avoid a flare-up, youll have to do more than just avoid certain products. You should also moisturize your skin at least twice a day to prevent it from becoming too dry or cracked, according to the American Academy of Dermatology. Look for mild, fragrance-free lotionsAveeno Eczema Therapy Moisturizing Cream and Cetaphils RestoraDerm Eczema Calming Body Moisturizer are two optionsor opt for petroleum jelly. Its also smart to try out a new product on a small area of your skin first, on the off chance that it causes your skin to feel itchy and irritated later on.
Although the majority of eczema flare-ups arent caused by a persons diet, there may be occasional cases where atopic dermatitis is exacerbated by food or drinks, says Dr. High. To pinpoint what might be triggering your flare, try keeping track of your daily routine (including meals) in a journal. By looking back at your past entries, you might be able to identify the culprits. For example, if you and your doctor think that milk is causing a flare, you might want to eliminate it from your diet while working with a nutritionist to help shore up your intake with other calcium-rich foods.
Although stress can certainly trigger a flare, Dr. High says that its usually the last factor that doctors consider. But he also notes that all of his patients feel itchier at night, whether they have atopic dermatitis or any other itching skin condition. Its the time of the day when its quiet, says Dr. High. Youre not going to feel itchy when youre going a million miles an hour at your job. You dont have time to plug into all those body sensations.
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No Excuses: Exercise Can Overcome the ‘Obesity Gene’ – Glens Falls Post-Star
Posted: at 2:35 pm
THURSDAY, April 27, 2017 (HealthDay News) -- Even if obesity is "in your genes," regular exercise can help keep extra pounds at bay, a new study suggests.
Researchers found that when people carried a particular gene variant that raises obesity risk, regular exercise seemed to reduce the effects of their DNA -- by about one-third.
The gene in question is known as FTO. Studies show that people with a particular variant of the gene have a heightened risk of obesity.
But the gene's effects are not huge, or written in stone. Research has found that people who carry two copies of the FTO variant (one inherited from each parent) weigh about 6.5 pounds more than non-carriers, on average.
The new findings underscore one way to counter the gene's impact: Exercise.
"There are genes that appear to directly impact weight, but the effects are small," said lead researcher Mariaelisa Graff, of the University of North Carolina at Chapel Hill. "You still have a lot of choice over your behavior."
The study results are not exactly surprising, according to Dr. Timothy Church, an obesity researcher who was not involved in the work.
"This shows, once again, that genes are not your destiny," said Church. He is a professor of preventative medicine at Louisiana State University's Pennington Biomedical Research Center.
Church said regular exercise is particularly key in preventing excess weight gain in the first place -- and in keeping the pounds off after someone loses weight.
Exercise is less effective in helping obese people shed weight, Church said. Diet changes are the critical step there.
But the bottom line is that exercise matters, regardless of your genes, according to Dr. Chip Lavie, of the John Ochsner Heart and Vascular Institute, in New Orleans.
Lavie, who was not involved in the study, pointed to findings from his own research.
"[We] have published data that suggests the main cause of increasing obesity over the past five decades is the dramatic decline in physical activity," he said.
Gym memberships aside, Americans these days are less active at work, at home (through housework) and during leisure time, according to Lavie.
And the benefits of exercise go beyond weight control, he stressed. Physical activity boosts people's fitness levels -- which, Lavie said, is critical in preventing heart disease and living a longer, healthier life.
The new findings are based on over 200,000 adults, mostly of European descent, who'd taken part in previous health studies.
Graff and her colleagues analyzed information on their weight and exercise habits, and looked at how those factors "interacted" with 2.5 million gene variants.
FTO is the gene that is most strongly linked to obesity, Graff said.
And overall, her team found, active people who carried the obesity-linked FTO variant appeared more resistant to its effects than sedentary people.
On average, exercise weakened the variant's effects by about 30 percent, the researchers reported in the April 27 issue of PLOS Genetics.
There were some hints that exercise also affected some other weight-related genes. But the only clear relationship was with the FTO variant, according to Graff.
That, she noted, could be related to the broad way the study looked at exercise. The 23 percent of people who were least active were considered "inactive," while everyone else was deemed "active."
Church said he thinks research into the genetics of body weight will increasingly become useful.
If certain gene variants affect people's response to a low-carb diet or aerobic exercise, for example, that could help in "tailoring" weight-loss plans, he suggested.
"The science is rapidly evolving," Church said, "and there's still a lot to learn. But I think that's the direction this is going."
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Exercise can help offset effects of ‘fat gene,’ study finds – ABC News
Posted: at 2:35 pm
Doctors have long known that genetics can predispose some people to gain weight despite a healthy lifestyle while others seemingly never gain an ounce no matter how much they eat. A new study sheds light on how people can counteract their genetic makeup, even if it's in their DNA to put on more weight than others.
Researchers from University of North Carolina Chapel Hill, the University of Copenhagen and other institutions conducted a meta-analysis examining 60 past genetic studies to see if physical activity could mitigate the effects a genetic predisposition to weight gain.
"Decline in daily physical activity is thought to be a key contributor to the global obesity epidemic," the authors wrote. However, they explained that genetic make-up may also play a role in weight gain for people who are not physically active.
They screened for 2.5 million genetic variants in 200,452 adults and also separated the subjects between those who were physically active -- about 77 percent -- and those who were physically inactive, about 23 percent. The researchers then looked at different markers that would indicate if a person was overweight including their body-mass index, waist circumference and hip-to-waist ratio.
They found those with a genetic variation that predisposed them to gain weight -- called an FTO gene -- had the ability counteract the effects that gene through exercise. By looking at the data they found that those with the FTO gene who were physically active were able to reduce the weight-gain effects associated with the gene by about 30 percent.
Dr. Goutham Rao, chairman of Family Medicine and Community Health at University Hospitals Cleveland Medical Center, said this type of research is key in helping patients better understand their weight and health.
"Despite that sort of bad luck of having a genetic predisposition to obesity if you are physically active ... you're not going to reduce risk of obesity entirely but you reduce it significantly," Rao said.
The mechanism that leads to people with FTO to be predisposed to gain weight is still not fully understood, but Rao said it's key to give people encouragement that taking healthy steps has an effect even if they haven't reached their goal weight.
"The message is to be sympathetic," Rao said. Explaining he tells frustrated patients, "if you weren't doing your best you would weigh a lot more and be much less healthy."
Dr. Kevin Niswender, associate professor of medicine, molecular physiology and biophysics at Vanderbilt University Medical Center, said the study took on the "really interesting question" of if people can counteract their genetics through their lifestyle.
"This study definitively confirms that lifestyle has an impact," he said.
During their research the team also discovered 11 new genetic variants that likely predispose a person to weight gain and they said more may be found through similar studies.
"In future studies, accounting for physical activity and other important lifestyle factors could boost the search for new obesity genes," said Mariaelisa Graff of the University of North Carolina at Chapel Hill, the lead author of the study. "To identify more genes whose effects are either dampened or amplified by physical activity, we need to carry out larger studies with more accurate measurement of physical levels."
Niswender said finding new variants that indicate predisposition for weight gain can help give a better understanding of the complex mechanisms behind obesity.
"For a long time we've been searching for this gene, the gene that causes obesity and it's just not like that," Niswender."there are a bunch of genes that cause obesity and the effect of each gene variant is really quite small."
Graff said more study should need to be done to get more accurate measurements of the participants' physical activity. The researchers classified those as having a sedentary job, commute and leisure time as "inactive" while everyone else was declared physically active. Additionally, the study was done primarily in people of European descent, so the findings may not be be easily extrapolated to other groups.
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Stem cells edited to fight arthritis – Washington University School of Medicine in St. Louis
Posted: at 2:35 pm
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Goal is vaccine that targets inflammation in joints
Using CRISPR technology, a team of researchers led by Farshid Guilak, PhD, at Washington University School of Medicine in St. Louis, rewired stem cells' genetic circuits to produce an anti-inflammatory arthritis drug when the cells encounter inflammation. The technique eventually could act as a vaccine for arthritis and other chronic conditions.
Using new gene-editing technology, researchers have rewired mouse stem cells to fight inflammation caused by arthritis and other chronic conditions. Such stem cells, known as SMART cells (Stem cells Modified for Autonomous Regenerative Therapy),develop into cartilage cells that produce a biologic anti-inflammatory drug that, ideally, will replace arthritic cartilage and simultaneously protect joints and other tissues from damage that occurs with chronic inflammation.
The cells were developed at Washington University School of Medicine in St. Louis and Shriners Hospitals for Children-St. Louis, in collaboration with investigators at Duke University and Cytex Therapeutics Inc., both in Durham, N.C. The researchers initially worked with skin cells taken from the tails of mice and converted those cells into stem cells. Then, using the gene-editing tool CRISPR in cells grown in culture, they removed a key gene in the inflammatory process and replaced it with a gene that releases a biologic drug that combats inflammation.
The research is availableonline April 27 in the journal Stem Cell Reports.
Our goal is to package the rewired stem cells as a vaccine for arthritis, which would deliver an anti-inflammatory drug to an arthritic joint but only when it is needed, said Farshid Guilak, PhD, the papers senior author and a professor of orthopedic surgery at Washington University School of Medicine. To do this, we needed to create a smart cell.
Many current drugs used to treat arthritis including Enbrel, Humira and Remicade attack an inflammation-promoting molecule called tumor necrosis factor-alpha (TNF-alpha). But the problem with these drugs is that they are given systemically rather than targeted to joints. As a result, they interfere with the immune system throughout the body and can make patients susceptible to side effects such as infections.
We want to use our gene-editing technology as a way to deliver targeted therapy in response to localized inflammation in a joint, as opposed to current drug therapies that can interfere with the inflammatory response through the entire body, said Guilak, also a professor of developmental biology and of biomedical engineering and co-director of Washington Universitys Center of Regenerative Medicine. If this strategy proves to be successful, the engineered cells only would block inflammation when inflammatory signals are released, such as during an arthritic flare in that joint.
As part of the study, Guilak and his colleagues grew mouse stem cells in a test tube and then used CRISPR technology to replace a critical mediator of inflammation with a TNF-alpha inhibitor.
Exploiting tools from synthetic biology, we found we could re-code the program that stem cells use to orchestrate their response to inflammation, said Jonathan Brunger, PhD, the papers first author and a postdoctoral fellow in cellular and molecular pharmacology at the University of California, San Francisco.
Over the course of a few days, the team directed the modified stem cells to grow into cartilage cells and produce cartilage tissue. Further experiments by the team showed that the engineered cartilage was protected from inflammation.
We hijacked an inflammatory pathway to create cells that produced a protective drug, Brunger said.
The researchers also encoded the stem/cartilage cells with genes that made the cells light up when responding to inflammation, so the scientists easily could determine when the cells were responding. Recently, Guilaks team has begun testing the engineered stem cells in mouse models of rheumatoid arthritis and other inflammatory diseases.
If the work can be replicated in animals and then developed into a clinical therapy, the engineered cells or cartilage grown from stem cells would respond to inflammation by releasing a biologic drug the TNF-alpha inhibitor that would protect the synthetic cartilage cells that Guilaks team created and the natural cartilage cells in specific joints.
When these cells see TNF-alpha, they rapidly activate a therapy that reduces inflammation, Guilak explained. We believe this strategy also may work for other systems that depend on a feedback loop. In diabetes, for example, its possible we could make stem cells that would sense glucose and turn on insulin in response. We are using pluripotent stem cells, so we can make them into any cell type, and with CRISPR, we can remove or insert genes that have the potential to treat many types of disorders.
With an eye toward further applications of this approach, Brunger added, The ability to build living tissues from smart stem cells that precisely respond to their environment opens up exciting possibilities for investigation in regenerative medicine.
Brunger JM, Zutshi A, Willard VP, Gersbach CA, Guilak F. Genome engineering of stem cells for autonomously regulated, closed-loop delivery of biologic drugs. Stem Cell Reports. April 27, 2017.
This work was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases and the National Institute on Aging of the National Institutes of Health (NIH), grant numbers AR061042, AR50245, AR46652, AR48182, AR067467, AR065956, AG15768, OD008586. Additional funding provided by the Nancy Taylor Foundation for Chronic Diseases; the Arthritis Foundation; the National Science Foundation (NSF), CAREER award number CBET-1151035; and the Collaborative Research Center of the AO Foundation, Davos, Switzerland.
Authors Farshid Guilak, and Vincent Willard have a financial interest in Cytex Therapeutics of Durham, N.C., which may choose to license this technology. Cytex is a startup founded by some of the investigators. They could realize financial gain if the technology eventually is approved for clinical use.
Washington University School of Medicines 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is one of the leading medical research, teaching and patient-care institutions in the nation, currently ranked seventh in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.
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Stem cells edited to fight arthritis - Washington University School of Medicine in St. Louis
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