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The more pain you expect, the more you feel, new study shows

Anonymous — Wed, 14 Nov 2018 18:22:43 +0000

The more pain you expect, the more you feel, new study shows Anonymous (not verified) Wed, 11/14/2018 - 11:22

Lisa Marshall

Expect a shot to hurt and it probably will, even if the needle poke isn’t really so painful. Brace for a second shot and you’ll likely flinch again, even though—second time around—you should know better.

That’s the takeaway of a new brain imaging study by CU �鶹ӰԺ neuroscientists which found that expectations about pain intensity can become self-fulfilling prophecies. Surprisingly, those false expectations can persist even when reality repeatedly demonstrates otherwise, the study found.

“We discovered that there is a positive feedback loop between expectation and pain,” said psychology and neuroscience professor Tor Wager, senior author of the paper published this month in Nature Human Behaviour. “The more pain you expect, the stronger your brain responds to the pain. The stronger your brain responds to the pain, the more you expect.”

Pain can be a self-fulfilling prophecy

Tor Wager (Credit: CU �鶹ӰԺ)

For decades, researchers have been intrigued with the idea of self-fulfilling prophecy, with studies showing expectations can influence everything from how one performs on a test to how one responds to a medication. The new study is the first to unpack the vicious cycle between increased pain expectations and increased pain and elucidate the neural mechanisms underlying it.

Marieke Jepma, then a postdoctoral researcher in Wager’s lab, launched the research after noticing that even when test subjects were shown time and again that something wouldn’t hurt badly, some still expected it to.

“We wanted to get a better understanding of why pain expectations are so resistant to change,” said Jepma, lead author of the study and now a researcher at the University of Amsterdam.

The researchers recruited 34 subjects and taught them to associate one symbol with low heat and another with high, painful heat.

Then, the subjects were placed in a functional magnetic resonance imaging (fMRI) machine, which measures blood flow in the brain as a proxy for neural activity. For 60 minutes, subjects were shown low or high pain cues (the symbols, the words Low or High, or the letters L and W), then asked to rate how much pain they expected.

Then varying degrees of painful but non-damaging heat were applied to their forearm or leg, with the hottest reaching “about what it feels like to hold a hot cup of coffee” Wager explains.

Then they were asked to rate their pain.

Unbeknownst to the subjects, heat intensity was not actually related to the preceding cue.

The study found that when subjects expected more heat, brain regions involved in threat and fear were more activated as they waited. Regions involved in the generation of pain were more active when they received the stimulus. Participants reported more pain with high-pain cues, regardless of how much heat they actually got.

“This suggests that expectations had a rather deep effect, influencing how the brain processes pain,” said Jepma.

‘Confirmation bias’ applies to pain too

Surprisingly, their expectations also highly influenced their ability to learn from experience. Many subjects demonstrated high “confirmation bias”—the tendency to learn from things that reinforce our beliefs and discount those that don’t. For instance, if they expected high pain and got it, they might expect even more pain the next time. But if they expected high pain and didn’t get it, nothing changed.

“You would assume that if you expected high pain and got very little you would know better the next time. But interestingly, they failed to learn,” said Wager.

This phenomenon could have tangible impacts on recovery from painful conditions, suggests Jepma.

Brain imaging from the study.

“Our results suggest that negative expectations about pain or treatment outcomes may in some situations interfere with optimal recovery, both by enhancing perceived pain and by preventing people from noticing that they are getting better,” she said. “Positive expectations, on the other hand, could have the opposite effects.”

The research also may shed light on why, for some, chronic pain can linger long after damaged tissues have healed.

Whether in the context of pain or mental health, the authors suggest that it may do us good to be aware of our inherent eagerness to confirm our expectations.

“Just realizing that things may not be as bad as you think may help you to revise your expectation and, in doing so, alter your experience,” said Jepma.

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A new brain imaging study has revealed the more pain people expect, the stronger their brain responds to pain, which may explain why chronic pain persists long after damaged tissue has healed.

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How ideas go viral in academia

Anonymous — Tue, 06 Nov 2018 07:00:00 +0000

How ideas go viral in academia Anonymous (not verified) Tue, 11/06/2018 - 00:00

Daniel Strain

How ideas move through academia may depend on where those ideas come from—whether from big-name universities or less prestigious institutions—as much as their quality, a recent study from CU �鶹ӰԺ suggests.

The new research borrows a page from epidemiology, exploring how ideas might flow from university to university, almost like a disease. The findings from CU �鶹ӰԺ’s Allison Morgan and her colleagues suggest that the way that universities hire new faculty members may give elite schools an edge in spreading their research to others.

Key takeaways

A small number of universities have trained the majority of tenure track faculty in computer science in the U.S. and Canada.
That bias may give elite universities an edge in spreading their ideas from university to university—even when those ideas aren't that good.
The good news: great ideas can still catch fire in academia, no matter where they come from.

In particular, the team simulated how ideas might spread out faster from highly-ranked schools than from those at the bottom of the pile—even when the ideas weren’t that good. The results suggest that academia may not function like the meritocracy that some claim, said Morgan, a graduate student in the Department of Computer Science.

She and her colleagues began by drawing on a dataset, originally published in 2015, that described the hiring histories of more than 5,000 faculty members in 205 computer science programs in the U.S. and Canada.

That dataset revealed what might be a major power imbalance in the field—with a small number of universities training the majority of tenure track faculty across both countries.

“This paper was really about investigating the implications of the imbalance,” Morgan said. “What does it mean if the elite institutions are producing the majority of the faculty who are, in turn, training the future teachers in the field?”

Academic roadmap

To answer that question, the researchers turned the 2015 dataset into a network of connected universities. If a university placed one of its PhD students in a job at another school, then those two schools were linked. The resulting “roadmap” showed how faculty might carry ideas from their graduate schools to the universities that hired them.

The researchers then ran thousands of simulations on that network, allowing ideas that began at one school to percolate down to others. The team adjusted for the quality of ideas by making some more likely to shift between nodes than others.

The findings, published in October in the journal EPJ Data Science, show that it matters where an idea gets started. When mid-level ideas began at less prestigious schools, they tended to stall, not reaching the full network. The same wasn’t true for so-so thinking from major universities.

“If you start a medium- or low-quality idea at a prestigious university, it goes much farther in the network and can infect more nodes than an idea starting at a less prestigious university,” Morgan said.

That pattern held up even when the researchers introduced a bit of randomness to the mix—allowing ideas to pop from one end of the network to another by chance. That simulated how university departments might learn about an idea through factors other than hiring, such as journals, conferences or word of mouth.

Diverse departments

The results seem to paint a dim picture of academia, said study coauthor Samuel Way, a postdoctoral research associate in computer science. He explained that recent sociological research demonstrates that workplaces benefit by having a lot of diversity—whether in gender, race or in how employees are trained.

“If you have five people who all have the exact same training and look at the world through the same lens, and you give them a problem that stumps one of them, it might stump all of them,” Way said.

He added that it may be possible for the academic world to blunt the impact of the sorts of biases the team revealed, including by adopting practices like double-blind peer review—in which the reviewers of a study can’t see the names or affiliations of the authors.

“In a setting like science where it’s incredibly difficult to come up with an objective measure of the quality of an idea, double-blind peer review may be the best you can do,” Way said.

The study did, however, contain a bit of good news: The bias toward big-name universities mattered a lot less for high-quality ideas. In other words, great thinking can still catch fire in academia, no matter where it comes from.

“I think it’s heartwarming in a way,” Morgan said. “We see that if you have a high-quality idea, and you’re from the bottom of the hierarchy, you have as good a chance of sending that idea across the network, as if it came from the top.”

Other coauthors on the study included graduate student Dimitrios Economou and Associate Professor Aaron Clauset, both in computer science.

New research shows that the spread of ideas through academia may depend on where they come from as much as their quality.

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Physician scientists shed light on origins of ALS, neuromuscular disease

Anonymous — Thu, 01 Nov 2018 19:22:46 +0000

Physician scientists shed light on origins of ALS, neuromuscular disease Anonymous (not verified) Thu, 11/01/2018 - 13:22

Lisa Marshall

Toxic protein assemblies, or "amyloids", gum up a cell. Credit: iStock

Toxic protein assemblies, or “amyloids,” long considered to be key drivers in many neuromuscular diseases, also play a beneficial role in the development of healthy muscle tissue, CU �鶹ӰԺ researchers have found.

“Ours is the first study to show that amyloid-like structures not only exist in healthy skeletal muscle during regeneration, but are likely important for its formation,” said co-first author Thomas Vogler, an M.D./PhD candidate in the Department of Molecular, Cellular, and Developmental Biology (MCDB).

The surprising finding, published today in the journal Nature, sheds new light on the potential origins of a host of incurable disorders, ranging from amyotrophic lateral sclerosis (ALS) to inclusion body myopathy (which causes debilitating muscle degeneration) to certain forms of muscular dystrophy.

Josh Wheeler, left, and Tom Vogler celebrate on the summit of Longs Peak. The friends, competitive runners, and M.D., PhD candidates published a paper this week that sheds new light on how neuromuscular diseases like ALS may originate.

The authors believe the findings could ultimately open new avenues for treating musculoskeletal diseases and age-related muscle decline. They could also lend new understanding to neurological disorders like Parkinson’s and Alzheimer’s disease, in which different amyloids play a role.

“Many of these degenerative diseases share a similar scenario in which they have these protein aggregates that accumulate in the cell and gum up the system,” said co-first author Joshua Wheeler, also an M.D./PhD candidate in the Department of Biochemistry. “Our data suggest that the cell is just damaged and trying to repair itself.”

Wheeler and Vogler, both competitive runners and participants in CU’s Medical Science Training Program, came up with the idea for the study while on a trail run in the hills West of �鶹ӰԺ.

Vogler studies muscle generation in MCDB Professor Brad Olwin’s lab. Wheeler studies protein assemblies in Biochemistry Professor Roy Parker’s lab. In pursuit of their medical degrees, both frequently see patients with neuromuscular disorders believed to be driven by amyloids.

“Each of our different fields were kind of on a collision course for each other,” says Wheeler.

That collision turned into a collaboration in which their two labs, and colleagues at Anschutz Medical Campus, set out to study a specific protein called TDP-43. TDP-43 has long been suspected to be a culprit in disease, having been found in the skeletal muscle of people with inclusion body myopathy and the neurons of people with ALS.

But surprisingly, when the researchers closely examined muscle tissue growing in culture in the lab, they discovered clumps of TDP-43 were present not only in diseased tissue but also in healthy tissue.

“That was astounding,” said Olwin. “These amyloid-like aggregates, which we thought were toxic, seemed to be a normal part of muscle formation, appearing at a certain time and then disappearing again once the muscle was formed.”

Key takeaways

Amyloids, or toxic protein assemblies, are often found in cells and neurons of people with neurodegenerative diseases and were believed to be toxic.
A new paper in Nature shows they are also present in healthy muscle tissue as it regenerates and likely key to its formation.
The research could lead to new treatment avenues for ALS, neurodegenerative diseases and age-related muscle wasting.

Subsequent studies in muscle tissue growing in culture showed that when the gene that codes for TDP-43 was knocked out, muscles didn’t grow. When the researchers looked at human tissue biopsied from healthy people whose muscles were regenerating, they found aggregates, or “myo-granules,” of TDP-43.

Further RNA-protein mapping analysis showed that the clusters - like shipping trucks traveling throughout the cell - appear to carry instructions for how to build contractile muscle fibers.

Wheeler, a competitive ultrarunner, says the data suggest that when healthy athletes push their muscles hard, via events like marathons or ultramarathons, they are probably also forming amyloid-like clusters within their cells.

The key question remains: Why do most people quickly clear these proteins while in others the granules – like sugar cubes that won’t dissolve – cluster together and cause disease?

“If they normally form and go away, something is making them dissolve,” said Olwin. “Figuring out the mechanisms involved could potentially open a new avenue for treatments.”

The team is also interested in exploring whether a similar process may occur in the brain after injury, kick-starting disease. And subsequent studies will go even further to identify what the protein clusters do. More research is already underway.

“This is a great example of how collaboration across disciplines can lead to really important work,” said Parker.

Someday, Wheeler and Vogler are hopeful the work they do in the lab will help the patients they see in the clinic.

“The holy grail of all this is to be able to treat devastating and incurable diseases like ALS and to develop therapeutic strategies to improve skeletal muscle and fitness,” said Wheeler. “We are just opening the door on this.”

Researchers from Johns Hopkins University School of Medicine, the University of California Los Angeles, St. Jude Children’s Research Hospital, Perleman School of Medicine at University of Pennsylvania, and Howard Hughes Medical Institute also contributed to this study.

Toxic protein assemblies, or "amyloids," long considered to be key drivers in many neuromuscular diseases, also play a beneficial role in the development of healthy muscle tissue.

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New gene therapy eases chronic pain in dogs; human trials underway

Anonymous — Mon, 29 Oct 2018 18:08:27 +0000

New gene therapy eases chronic pain in dogs; human trials underway Anonymous (not verified) Mon, 10/29/2018 - 12:08

Lisa Marshall

Taryn Sargent walks her dog Shane, who was recently treated with a new gene-therapy injection for chronic pain. (Credit: Casey Cass/CU �鶹ӰԺ)

When Shane the therapy dog was hit by a Jeep, life changed for him and his guardian Taryn Sargent.

The impact tore through the cartilage of Shane’s left shoulder. Arthritis and scar tissue set in. Despite surgery, acupuncture and several medications, he transformed from a vibrant border collie who kept watch over Sargent on long walks to a fragile pet who needed extensive care.

“Sometimes he would just stop walking and I’d have to carry him home,” recalls Sargent, who has epilepsy and relies on her walks with Shane to help keep her seizures under control. “It was a struggle to see him in that much pain.”

Today, 10-year-old Shane’s pain and reliance on medication have been dramatically reduced and he’s bounding around like a puppy again, 18 months after receiving a single shot of an experimental gene therapy invented by CU �鶹ӰԺ neuroscientist Linda Watkins

Thus far, the opioid-free, long-lasting immune modulator known as XT-150 has been tested in more than 40 Colorado dogs with impressive results and no adverse effects. With human clinical trials now underway in Australia and California, Watkins is hopeful the treatment could someday play a role in addressing the nation’s chronic pain epidemic.

“I’m hoping the impact on pets, their guardians and people with chronic pain could be significant,” said Watkins, who has worked more than 30 years to bring her idea to fruition. “It’s been a long time coming.”

An ancient survival system gone bad

Linda Watkins with Shane.

Watkins’ journey began in the 1980s when, as a new hire in the department of psychology and neuroscience, she began to rock the boat in the field of pain research.

Conventional wisdom held that neurons were the key messengers for pain, so most medications targeted them. But Watkins proposed that then-little-understood cells called “glial cells” might be a culprit in chronic pain. Glial cells are immune cells in the brain and spinal cord that make people ache when they’re sick. Most of the time, that function protects us.

“Glial cells are the reason that when you have the flu, even the bedsheets hurt,” explains Watkins. “They make you curl up and rest so you can get better.”

Watkins proposed that in the case of chronic pain, which can sometimes persist long after the initial injury has healed, that ancient survival circuitry somehow gets stuck in overdrive. She was greeted with skepticism.

“The whole field was like ‘what on earth is she talking about?’”

She and her students hunkered down in the lab nonetheless, ultimately discovering that activated glial cells produce specific inflammatory compounds which drive pain. They also learned that, after the initial sickness or injury fades, the cells typically produce a compound called Interleukin 10 (IL-10) to dampen the process they started.

“IL-10 is Mother Nature’s anti-inflammatory,” she explains. “But in the onslaught of multiple inflammatory compounds in chronic pain, IL-10’s dampening cannot keep pace."

Over the years, she and her team experimented with a host of different strategies to boost IL-10. They persisted and, in 2009, Watkins co-founded Xalud Therapeutics. Their flagship technology is an injection, either into the fluid-filled space around the spinal cord or the site of an inflamed joint, that delivers circles of DNA in a sugar/saline solution to cells, instructing them to ramp up IL-10 production.

With financial help from the National Institute of Neurological Disorders and Stroke, the MayDay Fund and CU’s Technology Transfer Office – which has provided intellectual property support, assistance with licensing agreements, and help obtaining a $100,000 research grant in 2018 – Watkins is edging closer to bringing her idea to clinical practice.

Healthy dog, healthy guardian

She has teamed up with veterinary chronic pain specialist Rob Landry, owner of the Colorado Center for Animal Pain Management in Westminster, to launch the IL-10 research study in dogs.

Their results have not been published yet. But thus far, the researchers say, the results look highly promising.

“They’re happier, more engaged, more active and they’re playing again,” said Landry, as he knelt down to scratch Shane’s belly after giving him a clean bill of health.

Rob Landry and Linda Watkins consult as Taryn walks Shane in the background.

With Shane able to accompany her on her walks again, Sargent has also seen her quality of life improve. Her seizures, which increased in frequency when Shane was injured, have subsided again.

Because the treatment is so localized and prompts the body’s own pain-killing response, it lacks the myriad side effects associated with opioids – including constipation and dependency – and it can last for many months after a single injection.

Ultimately, that could make it an attractive option for people with neuropathic pain or arthritis, Watkins says.

This summer, Xalud Therapeutics launched the first human study in Australia, to test the safety, tolerability and efficacy of the compound. Another one-year clinical trial of 32 patients with osteoarthritis of the knee is now underway in Napa, California.

More research is necessary in both pets and people, Watkins stresses. But she’s hopeful.

“If all goes well, this could be a game-changer.”

Landry and Watkins are seeking dogs with advanced osteoarthritis to participate in the ongoing IL-10 study. If a dog meets the requirements to be selected, the treatment and follow-up assessments are provided at no cost. For further information, contact Landry at 720-502-5823.

Neuroscientist Linda Watkins has developed an opioid-free, long-lasting shot for management of chronic pain. It's been tested in more than 40 dogs with impressive results and no adverse effects.

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Battling superbugs: New compounds could make old antibiotics new

Anonymous — Mon, 24 Sep 2018 18:19:29 +0000

Battling superbugs: New compounds could make old antibiotics new Anonymous (not verified) Mon, 09/24/2018 - 12:19

Lisa Marshall

[video:https://youtu.be/DePr4jBMWjE]

With antibiotic-resistant “superbugs” now infecting 2 million people per year and a dearth of new medications in the pipeline to treat them, CU �鶹ӰԺ researchers are taking a novel approach to addressing the looming public health crisis:

They’re helping develop new drugs to make old drugs work better.

“We believe the compounds we’ve discovered have the potential to rejuvenate existing antibiotics – to make bacteria that are now insensitive to multiple drugs sensitive again,” said Corrie Detweiler, a professor of Molecular, Cellular and Developmental Biology (MCDB) who recently outlined her discovery in the journal PLOS Pathogens.

More than 23,000 people die annually in the United States from bacterial infections that have evolved to resist antibiotics. Thousands more suffer life-threating bouts with once-easily treatable illnesses like strep throat, urinary tract infections and pneumonia. And some forms of tuberculosis and gonorrhea are now resistant to all available drugs.

“As our antibiotics work less and less, we risk essentially going back to a period 200 years ago when even a minor infection could mean death,” said Detweiler. “Even the risk from routine procedures like knee surgery is going to go up.”

Meanwhile, most antibiotics still in use today were developed in the 1950s, as pharmaceutical companies have scaled back investment in research and development. The last time a new class of antibiotics hit the market was in 1984, according to the Pew Charitable Trust.

“With industry largely turning away, it’s up to academic labs like ours to step up and help feed the pipeline,” said Detweiler.

Corrie Detweiler in her lab at CU �鶹ӰԺ. (Credit: Patrick Campbell/CU �鶹ӰԺ)

A new way to fight superbugs

To that end, she recently developed a new technique called SAFIRE for screening for new small molecules with anti-microbial properties.

“The old way of discovering antibiotics helped us get to the low-hanging fruit, but that stopped working a long time ago,” she said.

Rather than pour potential new antibiotics into a test tube teeming with bacteria (as in the past) SAFIRE uses cutting-edge cell imaging techniques to observe what the compounds do to mammalian cells infected with bacteria over 18 hours.

The method enables her laboratory to zero in on compounds that keep bacteria from replicating inside the host cell, but don’t harm the host.

“This filters out toxic compounds right off the bat,” she said.

Of 14,400 potential candidates screened, her team has zeroed in on at least three with strong potential.

They work not by killing the bacteria itself, but by getting inside it and shutting of cellular machines called “efflux pumps” which bacteria use to protect themselves from both antibiotic medications and the body’s own immune-boosting proteins.

“Bacteria are really smart, and they have learned to use these pumps to pump out whatever we throw at them to kill them, so they can live happily,” said Edward Yu, a professor of pharmacology at Case Western Reserve University who collaborated with Detweiler on the research. “The compounds Corrie is working on inhibit those pumps.”

Collaborating with industry

Senior research assistant Amy Crooks, right, works with Corrie Detweiler in the lab.

Yu notes that because the compounds don’t kill the bacteria themselves, the bacteria don’t learn to resist them – a fact that could give the treatments more staying power than conventional antibiotics have had.

The compounds are also potent.

In the recently published study, they synergized with the common antibiotics erythromycin and ciproflaxin to reduce replication of Salmonella in infected cells by 10 to 20 fold .

In September, the Colorado Office of Economic Development and International Trade awarded Detweiler $125,000, topping off $2 million in National Institutes of Health funding.

She’s now collaborating with �鶹ӰԺ-based pharmaceutical start-up Crestone Inc. to help refine the compounds, and hopes to begin testing them in animals soon.

“If you had a patient who had an infection that was resistant to available antibiotics, you might someday be able to treat them by giving them one of our compounds in addition to the antibiotic,” she said. “It could not only make the old antibiotic work better but also make the patient’s own immune system work better. It’s exciting to think about.”

Other co-authors of the PLOS Pathogens paper include: Abigail Reens, MCDB graduate student and first-author; Amy Crooks, senior research assistant; Toni Nagy, postdoctoral research associate; graduate student David Reens, Jessica Podoli, Madeline Edwards; Edward Yu and Chih-Chia Su of Case Western University.

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CU �鶹ӰԺ researchers have discovered three compounds that could someday be given alongside antibiotics to reinvigorate them, making them effective against drug-resistant bugs again.

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How skin begins: Study identifies origins, could lead to better grafts

Anonymous — Thu, 13 Sep 2018 22:48:27 +0000

How skin begins: Study identifies origins, could lead to better grafts Anonymous (not verified) Thu, 09/13/2018 - 16:48

Lisa Marshall

CU �鶹ӰԺ researchers have discovered a key mechanism by which skin begins to develop in embryos, shedding light on the genetic roots of birth defects like cleft palate and paving the way for development of more functional skin grafts for burn victims.

“This study maps how skin development starts, from the earliest stages,” said Rui Yi, senior author of the paper published online today in the journal Developmental Cell.

Thousands of people undergo skin grafts each year to repair burns, birth defects or wounds. Medical advancements, including the advent of stem cell therapy which uses the patient’s own skin cells to grow new skin, have improved skin transplants. But replacement skin often lacks important features like hair follicles, sweat glands or nerve endings.

“Skin is an incredibly complex system and the regeneration we are doing now is not even close to duplicating it,” said Yi, an associate professor of Molecular, Cellular and Developmental Biology. “The overarching goal is to someday be able to regenerate fully functional skin, and to do that, we have to know, fundamentally, what happens at the beginning.”

Rui Yi (Credit: Paul Muhlrad/CU �鶹ӰԺ)

For the study, Yi and postdoctoral associate Xiying Fan used state-of-the-art genomic tools and DNA sequencing techniques to observe what happens inside embryonic progenitor cells of mice as they coordinate to form skin.

The study focused on a transcription factor, a type of protein that can read genetic information from the genome, called p63, found mostly in skin cells and long-known to play a critical role in skin formation. Previous studies have shown that mice born without p63 have no skin and malformed limbs. Humans with p63 mutations often have cleft lips or other malformations of the teeth and skin. In adults, loss of p63 function is associated with metastatic cancer.

“We have known for a long time that this transcription factor is probably the most important for skin development. What we have not known is what it does,” said Yi.

Using fluorescent tags that illuminated cells where p63 was present, and RNA sequencing to examine patterns of gene expression , the researchers examined cells from day nine to 13 of a 19-day mouse gestation, the time when skin is believed to form.

They found that P63 was responsible for switching on at least 520 genes and igniting numerous critical signaling pathways, including the “Wnt” pathway (responsible for hair follicle formation) the “Eda” pathway (critical for the formation of hair follicle, sweat glands and teeth) and the “Notch” pathway (responsible for prompting stem cells to differentiate into the epidermis.)

They also found that this process was kick-started earlier than previously believed and impacted thousands of regions of the genome that govern skin and limb formation.

“Our study provides mechanistic insights into the critical role of p63 at the onset of skin development and reveals a molecular basis for explaining how p63 mutations in humans can cause so many skin diseases,” said Yi.

He stresses that the study was in mice and further studies using human cells are needed.

But, if replicated, the findings could help researchers develop new prenatal tests and treatments for skin-related birth defects.

The research could also inform development of methods to coax adult cells to behave more like embryonic ones and generate fully functional skin.

“Instead of just grafting a piece of skin to cover your body, you could regenerate it as if it were going through development for the first time,” he said.

Fan is now a research instructor at CU Denver’s Anschutz Medical Campus.
The National Institutes of Health and the American Cancer Society funded the study.

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'Leep' of faith: CU scientists testing world's fastest blade runner

Anonymous — Fri, 24 Aug 2018 16:51:52 +0000

'Leep' of faith: CU scientists testing world's fastest blade runner Anonymous (not verified) Fri, 08/24/2018 - 10:51

Lisa Marshall

Double-amputee sprinter Blake Leeper visited CU �鶹ӰԺ this week for testing that could determine whether he may vie for a spot at the 2020 Olympics. (Credit: Glenn Asakawa/CU �鶹ӰԺ)

One of the world’s fastest men visited CU �鶹ӰԺ this week, blazing around the corners of the track and clocking nearly 30 miles per hour on a treadmill in the Applied Biomechanics lab.

Grabowski with Leeper at the track.

The scientific question at hand: Does a double-amputee running on prosthetic blades have an advantage, or disadvantage, over sprinters with legs? The answer could ultimately determine whether he will be allowed to compete at the 2020 Olympics.

“We’re here to get the numbers and find out the truth with scientific nonbias,” said Blake Leeper, a 29-year-old elite sprinter from Kingsport, Tennessee.

In June, Leeper—who was born without legs and runs on Ottobock carbon fiber blades—ran the 400-meter sprint in 44.42 seconds, shattering his own record and that of Oscar Pistorius, who in 2012 became the first and only below-the-knee amputee to compete against able-bodied runners at the Olympics.

Leeper now has his eye on the 2020 games. However, the International Association of Athletics Federations maintains a rule prohibiting “mechanical aids” unless amputee athletes can prove their prostheses do not, as some have alleged, give them a competitive edge.

Alena Grabowski, assistant professor of integrative physiology, specializes in studying lower-limb prostheses and was instrumental in determining Pistorius was not at an advantage—a finding that enabled his 2012 Olympics debut.

“For kids who had an amputation and for adults who had some sort of physical disability—to see this guy push the boundaries like that, it opened a door,” Grabowski said.

Pistorius was convicted in 2015 of murdering his girlfriend and sentenced to more than a decade in prison. But his running achievements inspired a new generation of runners with disabilities—including Leeper—to think big.

Leeper sprints at the track.

Leeper notes that he faces numerous challenges that he sees as disadvantages, including sores and swelling in his stumps and balance problems that make it harder to lift weights at the gym.

He came to CU �鶹ӰԺ for scientific answers.

Grabowski took measurements of Leeper’s movement out of the starting blocks and around curves, measured his aerobic metabolism and fatigue levels on the treadmill and will compare the data to measurements of able-bodied runners and other runners with amputations, including Pistorius. She expects to have results within a few months.

Meanwhile, Leeper says he’ll keep his eye on 2020.

“My goal is to be the fastest man in the world.”

Read more about Grabowski’s work in the spring issue of the Coloradan Magazine.

Elite sprinter Blake Leeper recently visited CU �鶹ӰԺ for testing that could determine whether he can vie for a spot at the 2020 Olympics. Leeper was born without legs and runs with prosthetic blades.

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