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Big data, Bioengineering, NIH, Research, Science Policy, Stanford News

$23 million in NIH grants to Stanford for two new big-data-crunching biomedical centers

$23 million in NIH grants to Stanford for two new big-data-crunching biomedical centers

More than $23 million in grants from the National Institutes of Health – courtesy of the NIH’s Big Data to Knowledge (BD2K) initiative – have launched two Stanford-housed centers of excellence bent on enhancing scientists’ capacity to compare, contrast and combine study results in order to draw more accurate conclusions, develop superior medical therapies and understand human behaviors.

Huge volumes of biomedical data – some of it from carefully controlled laboratory studies, increasing amounts of it in the form of electronic health records, and a building torrent of data from wearable sensors – languish in isolated locations and, even when researchers can get their hands on them, are about as comparable as oranges and orangutans. These gigantic banks of data, all too often, go unused or at least underused.

But maybe not for long. “The proliferation of devices monitoring human activity, including mobile phones and an ever-growing array of wearable sensors, is generating unprecedented quantities of data describing human movement, behaviors and health,” says movement-disorders expert Scott Delp, PhD, director of the new National Center for Mobility Data Integration to Insight, also known as the Mobilize Center. “With the insights gained from subjecting these massive amounts of data to  state-of-the-art analytical techniques, we hope to enhance mobility across a broad segment of the population,” Delp told me.

Directing the second grant recipient, the Center for Expanded Data and Retrieval (or CEDAR), is Stanford’s Mark Musen, MD, PhD, a world-class biomedical-computation authority. As I wrote in an online story:

[CEDAR] will address the need to standardize descriptions of diverse biomedical laboratory studies and create metadata templates for detailing the content and context of those studies. Metadata consists of descriptions of how, when and by whom a particular set of data was collected; what the study was about; how the data are formatted; and what previous or subsequent studies along similar lines have been undertaken.

The ultimate goal is to concoct a way to translate the banter of oranges and orangutans, artichokes and aardvarks now residing in a global zoo (or is it a garden?) of diverse databases into one big happy family speaking the same universal language, for the benefit of all.

Previously: NIH associate director for data science on the importance of “data to the biomedicine enterprise”, Miniature wireless device aids pain studies and Stanford bioengineers aim to better understand, treat movement disorders

Humor, otolaryngology, Research, Stanford News

Pigs to the rescue: How salt pork stops nose bleeds

Pigs to the rescue: How salt pork stops nose bleeds

pig-214349_640With all the talk this week of Nobel Prizes, another recent prize won by a Stanford physician escaped notice. To secure this prize for inventive research in medicine, Stanford otolaryngologist Ian Humphreys, MD, didn’t need access to laboratories packed with MRIs and supercomputers or a team of never-sleeping postdocs. His experimental design couldn’t be called elegant or complex – or perhaps even an experiment at all.

He won for simply deploying a nasal pork tampon. Yes, you read that correctly: He stuck bacon in the bleeding nose of a small girl, and took home the 2014 IgNobel Prize in Medicine.

“We are squealing with pride,” Robert Jackler, MD, chair of Stanford otolaryngology department, wrote to me. “We only wish that the work for which he is so deservedly honored was actually done at Stanford, but we would not want to hog the glory [from] a distinguished university in Michigan.”

Oh, dear. Before your eyes glaze over with bad-piggy puns, here’s the thing: The nasal tampon worked — twice.

Humphreys was working with a team at Michigan State University when a 4-year-old girl came into the Children’s Hospital of Michigan with a bloody nose. The girl had a rare platelet bleeding disorder called Glanzmann thrombasthenia, which can cause fatal internal and nasal bleeding and bruising. To treat her nosebleed, the doctors applied pressure, gave her a clotting protein and sent her home.

She returned the next day, “a pale, ill-appearing child in moderate distress… with brisk bleeding” from the nose, according to the winning paper, “Nasal packing with strips of cured pork as treatment for uncontrollable epistaxis in a patient with Glanzmann thrombasthenia” from the Annals of Otology, Rhinology and Laryngology.

The team whisked her into surgery and inserted  a specialized dressing to control the bleeding. Two days later, however, the bleeding started again. The girl received a transfusion and they continued monitoring her. They took her back in surgery the next day, applying another type of packing material and a coagulating serum. They also gave another dose of coagulating proteins and a red blood transfusion. She remained intubated to allow her nasal cavity to heal.

Two days later, when doctors began to remove the packing material, bleeding began immediately. Quickly, they reapplied the high-tech gauze and upped her dose of coagulation protein. She remained hospitalized, sedated. Five days later, the team again tried to remove the packing. Again, the nosebleed returned.

“At this time, strips of cured salt pork were placed in both nasal vaults,” Humphreys and his colleagues wrote. Three days later, “the bleeding was significantly less evident than it had been on all previous postoperative evaluations.” Go pork!

About a month later, the little girl fell on her face, again causing a nose bleed. This time, the team whipped out the pork right away – bye, bye nosebleed.

It turns out this isn’t the first time salt pork has been used to control a nosebleed. “It’s a traditional therapy for hard to treat bleeding disorders,” Jackler told me. “When I was a resident in the 1980s, we would buy a lump of salt pork to use.”

The salt-packed pork is thought to work by inducing swelling, thereby blocking the bleeding blood vessel.

“It is not ignorant, even though they deem it ignoble,” Jackler said.

Previously: Ten-year-old YouTube star: Famous for her singing, not for her illness, Stanford physicians and engineers showcase innovative health-care solutions and Stanford chair of otolaryngology discusses future regenerative therapies for hearing loss
Photo by Mutinka

Bioengineering, Biomed Bites, Neuroscience, Research, Videos

Deciphering “three pounds of goo” with Stanford neurobiologist Bill Newsome

Deciphering "three pounds of goo" with Stanford neurobiologist Bill Newsome

Thursday means it’s time for Biomed Bites, a weekly feature that highlights some of Stanford’s most compelling research and introduces readers to innovative scientists from a variety of disciplines. If you aren’t hooked on this series yet, you will be after hearing from this neuroscientist.

Stanford neurobiologist Bill Newsome, PhD, doesn’t invent new drugs, develop creative treatments or diagnose mysterious afflictions. He mostly uses moving dots to study vision. So it makes sense that even Newsome’s own mother asks the point of his research.

Newsome, who directs the Stanford Neuroscience Institute, fields the question with grace in the video above:

I  am interested in the brain as a biological organ that gives rise to intelligence. We study vision because we believe it’s going to give us certain cues how the brain actually works and understanding the mechanisms by which the brain produces behavior will help us understand all kinds of diseases of the brain… how thought and decision-making and memory and attention go wrong in diseases like schizophrenia, in diseases like depression.

It’s not about the dots. It’s about deciphering the brain, which Newsome calls “three pounds of goo” by gesturing toward his own goo-container. (It’s a well-known goo-container: Newsome also co-chairs the federal BRAIN Initiative). How does what you see influence what you do? What you think? What you don’t see?

Newsome has spent more than 40 years poking around in the brain and he knows it works much better than any of our most advanced attempts to replicate it. Think of all the applications for a machine that can not only see, but can also make decisions based on what it spots. But now, Newsome says, the best artificial intelligence vision systems are only as perceptive as a fly or an ant.

The notion is that if we can understand how real biological vision works, we can build artificial intelligence systems that can do vision much, much better than our current ones can… and we can improve our lives in many ways.

Basic bio it is, and basically very important.

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving forward biomedical innovation here.

Previously: Even old brains can stay healthy, says Stanford neurologist, Marked improvement in transplant success on the way, says Stanford immunologist and Discover the rhythms of life with a Stanford biologist

Imaging, Research, Science, Stanford News, Videos

Breaking the light barrier in medical microscopy: More on today’s Nobel-winning work

Breaking the light barrier in medical microscopy: More on today's Nobel-winning work

Earlier today, Stanford University’s W.E. Moerner, PhD, was one of three scientists to be awarded the Nobel Prize in Chemistry for work in super-resolution microscopy. Before this technology, the only way to look at structures inside cells was with electron microscopy. But that requires researchers to kill the tissue in order to prepare it for the microscope. Essentially, the objects being examined were frozen in place; scientists could make out cellular structures but couldn’t watch them in action.

Microscopes that use refracted light, or optical microscopes, can be used to observe living cells, but for decades, they were limited from going below 220 nanometers, a hard limit imposed by the wavelength of light. Eric Betzig, PhD, of Howard Hughes Medical Institute, and Stefan W. Hell, PhD, of the Max Planck Institute for Biophysical Chemistry in Germany shared the prize with Moerner for work that helped break that barrier. Now, researchers can peek inside cells as they are going about their business and observe real-time changes as they happen.

This morning, Moerner spoke to Stanford’s news office via Skype from Brazil about his work and how other researchers, including Lucy Shapiro, PhD, and Matt Scott, PhD, of Stanford’s School of Medicine are applying the new methods to medical research (see above video). Shapiro, a 10-year collaborator of Moerner’s, is examining structures inside bacteria and Scott is looking at subcellular signalling structures. (Shapiro provides comment on her work in a Stanford press release.)

“Because of this revolutionary work, scientists can now visualize the pathways of individual molecules inside living cells,” Francis Collins, MD, PhD, director of the National Institutes of Health, which funds some of Moerner’s work, said in a statement. “Researchers can see how molecules create synapses between nerve cells in the brain, and they can track proteins involved in Parkinson’s, Alzheimer’s and Huntington’s diseases.”

Below is a clip of Moerner describing what those studying Huntington’s disease have learned using the prize-winning microscopy technology.

Previously: For third year in row, a Stanford faculty member wins the Nobel Prize in Chemistry
Videos courtesy of Stanford University Communications

Anesthesiology, Pain, Research, Stanford News

Miniature wireless device aids pain studies

Miniature wireless device aids pain studies

DSC_0053Here’s one thing I didn’t know: For every person who goes to the doctor to be treated for chronic pain, less than a half get their pain reduced even by half. I learned that from anesthesiologist David Clark, MD, who recently received a grant from Stanford Bio-X, which supports interdisciplinary teams working on biomedical problems, to improve those odds.

One of Clark’s collaborators is Scott Delp, PhD, who last spring developed a way of using light to activate and deactivate pain neurons in mice. To be clear, the nerves had to be genetically engineered to allow the light to work – not something that can currently be done in humans.

That work pointed to new ways of studying pain, but had a glitch. The light was delivered through fiber optic cables and the mice couldn’t behave normally in their cages. That’s where engineer Ada Poon, PhD, enters the picture. She’s been developing a variety of devices that work wirelessly in the body, and she’s now working on a wireless device to deliver the light to nerves in mice. Here’s what I wrote in an online story yesterday:

Coupling a wireless technology to optogenetics eliminates the wire and allows a mouse to move freely, use an exercise wheel and socialize. Clark said this combination will allow researchers to design experiments that more closely mirror a patient’s experience.

For example, Clark said that when he sees patients they don’t necessarily complain only about the pain. They complain about not wanting to see friends, not being able to go to work, or not being able to do activities they enjoy.

“What we will be able to look at is a more natural measure of pain relief,” Poon said. They could assess whether a treatment allows mice to return to normal activities by tallying time spent on an exercise wheel or socializing.

Clark went on to tell me the value of working in this team: “When you combine people with different skills you will come up with something with truly high impact.”

Previously: Using light to get muscles moving and Stanford researchers demonstrate feasibility of ultra-small, wirelessly powered cardiac device
Image courtesy of Ada Poon

Big data, Chronic Disease, Immunology, Research, Stanford News

Out of hiding: Found lurking in public databases, type-2 diabetes drug passes early test

Out of hiding: Found lurking in public databases, type-2 diabetes drug passes early test

lurking 3Way too often, promising-looking basic-research findings – intriguing drug candidates, for example – go swooshing down the memory hole, and you never hear anything about them again. So it’s nice when you see researchers following up on an upbeat early finding with work that moves a potential drug to the next peg in the development process. All the more so when the drug candidate targets a massively prevalent disorder.

Type 2 diabetes affects more than 370 million people worldwide, a mighty big number and a mighty big market for drug companies. (Unlike the much less common type 1-diabetes, where the body’s production of the hormone insulin falters and sugar builds up in the blood instead of being taken up by cells throughout the body, in type-2 diabetes insulin production may be fine but tissues become resistant to insulin.) But while numerous medications are available, none of them decisively halt progression, much less reverse the disease’s course.

About two-and-a-half years ago, Stanford data-mining maven Atul Butte, MD, PhD, combed huge publicly available databases, pooled results from numerous studies and, using big-data statistical methods, fished out a gene that had every possibility of being an important player in type 2 diabetes, but had been totally overlooked. (For more info, see this news release.) Called CD44,  this gene is especially active in fat tissue of insulin-resistant people and, Butte’s study showed, had a strong statistical connection to type-2 diabetes.

Butte’s study suggested that CD44′s link to type-2 diabetes was not just statistical but causal: In other words, manipulating the protein CD44 codes for might influence the course of the disease. By chance, that protein has already been much studied by immunologists for totally unrelated reasons. The serendipitous result is that a monoclonal antibody that binds to the protein and inhibits its action was already available.

So, Butte and his colleagues used that antibody in tests they performed on lab mice bioengineered to be extremely susceptible to type-2 diabetes, or what passes for it in a mouse. And, it turns out, the CD44-impairing antibody performed comparably to or better than two workhorse diabetes medications (metformin and pioglitazone) in countering several features of type 2 diabetes, including fatty liver, high blood sugar, weight gain and insulin resistance. The results appear in a study published today in the journal Diabetes.

Most exciting of all: In targeting CD44, the monoclonal antibody was working quite differently from any of the established drugs used for type-2 diabetes.

These are still early results, which will have to be replicated and – one hopes – improved on, first in other animal studies and finally in a long stretch of clinical trials before any drug aimed at CD44 can join the pantheon of type-2 diabetes medications. In any case, for a number of reasons the monoclonal antibody Butte’s team pitted against CD44 is far from perfect for clinical purposes. But refining initial “prototypes” is standard operating procedure for drug developers. So here’s hoping a star is born.

Previously: Newly identified type-2 diabetes gene’s odds of being a false finding equal one in 1 followed by 19 zeroes, Nature/nurture study of type-2 diabetes risk unearths carrots as potential risk reducers and Mining medical discoveries from a mountain of ones and zeroes
Photo by Dan-Scape.co.uk

In the News, Neuroscience, Research, Stanford News

Stanford neurobiologist shares insights from working in Nobel-winning lab

Stanford neurobiologist shares insights from working in Nobel-winning lab

Pic3Yesterday’s Nobel Prize announcement delighted Stanford neurobiologist Lisa Giocomo, PhD -  and not because she had taken home the coveted honor. Giocomo came to Stanford last year from Norway, where she worked first as a postdoc and later as a colleague of Edvard and May-Britt Moser (both PhDs), two of the three 2014 Nobel Prize winners in physiology or medicine.

Giocomo (to the right of the Mosers in the photo here) didn’t get a chance to congratulate her former mentors yesterday due to the time difference. But she said Edvard was shocked when he was greeted by reporters and colleagues bearing flowers as he stepped off a plane yesterday: “I don’t think they were expecting it at all,” Giocomo said.

The discovery that shot the Mosers to the top of the science world (along with London-based researcher John O’Keefe, PhD) involves the inner maps that humans and other animals use to navigate. The Mosers discovered grid cells, a type of nerve cell in the brain’s entorhinal cortex that fires when an animal moves to certain points (for example, when a rat stands on the holes of a giant Chinese checker board).

The Mosers lead a large lab group at the Kavli Institute for Systems Neuroscience, one that Giocomo was drawn to so she could pursue her investigation of computational models of single-cell biophysics. Yet despite the size of a lab, Giocomo said the group felt like a family.

“They’re very good scientists, but they’re also really nice people and very gracious mentors,” Giocomo said. “They were always very good at making time for everyone in the lab… It’s also very collaborative.”

And unlike many partnerships, the Mosers truly work together, Giocomo said. “The lab is really run as a single entity.”

Giocomo, a member of the Stanford Neurosciences Institute, said she considered staying to work with the Mosers, but ultimately chose to join the Stanford faculty. And when asked about her own Nobel aspirations, Giocomo laughed. “I’m just focusing on building a lab,” she said. “I have many other short-term goals.”

Previously: Say Cheese: A photo shoot with Stanford Medicine’s seven Nobel laureates, Stanford researcher Roger Kornberg discusses drive and creativity in Nobel Prize Talks podcast  and Stanford winners Michael Levitt and Thomas Südhof celebrate Nobel Week
Photo courtesy of Lisa Giocomo

Cancer, Infectious Disease, Pediatrics, Research, Stanford News

Summer’s child: Stanford researchers use season of birth to estimate cancer risk

Summer’s child: Stanford researchers use season of birth to estimate cancer risk

Four_seasons

One of the hardest parts of unraveling childhood cancers is understanding what causes them. In recent years, evidence has been mounting that cancer and many other chronic diseases begin early in life – and perhaps even in utero. To untangle some of these early causes of cancer in children and young adults, Stanford epidemiologist and family physician Casey Crump, MD, PhD, is partnering with researchers at Lund University in Sweden, a working relationship was set up by Marilyn Winkleby, PhD, MPH, professor emeritus of medicine here. The team is using Sweden’s national registries for birth certificates and medical records to track how factors during gestation and soon after birth – called perinatal factors – affect cancer risks.

Because Sweden has a national health care system, it’s relatively easy to track the course of illness in individuals. By comparison, the U.S.’s health care system is fragmented across dozens of health care providers and insurers, so getting medical records for a single person that might span decades is a much more difficult prospect.

Crump’s team is focusing on cancers that are common in childhood and early adulthood: brain tumors, leukemia and lymphoma among them. Two papers published earlier this year examine how the time of year a child is born affects cancer risk. The most recent, published ahead of print in April in the International Journal of Cancer, examined whether the season of birth was linked to the risk of developing either Hodgkin’s lymphoma or non-Hodgkin’s lymphoma later in life. Crump explained:

Lymphomas are among the most common cancers in childhood but the causes are still largely unknown. It’s been hypothesized that infectious exposures, such as Epstein Barr virus and others may play an important role, but it’s still unclear what the critical age window of susceptibility might be. We had an opportunity to use season of birth from birth records as a proxy for infectious exposures in the first few months of life, and see the relationship between that and subsequent risk of Hodgkin’s and non-Hodgkin’s lymphoma – following these people from birth through childhood and on into young adulthood.

The researchers found that children born in spring or summer had a higher risk of developing non-Hodgkin’s lymphoma later in life compared to kids born in winter. The team didn’t find any similar seasonal pattern for risk of Hodgkin’s lymphoma. The results lend additional support to the “delayed exposure hypothesis.” Children born in spring or summer may not be exposed to critical pathogens during a critical early period of immune system development, leaving them vulnerable later in life. Children born in the fall or winter, by comparison, do get that important exposure at just the right time. Crump was quick to note that season of birth provides only a rough estimate of these exposures, since the team didn’t have accurate measures of exposures to Epstein Barr or other viruses, but he also added that these results “shed additional light on possible pathways of risk that may contribute to the development of non-Hodgkin’s lymphoma.”

A similar study published in January in the International Journal of Epidemiology found that children born in spring and summer had a higher chance of developing melanoma later in childhood or early adulthood. The team hypothesized that spring and summer babies are exposed to more UV radiation in warm summer months in the first few months of life – an exposure that fall and winter babies are less likely to have.

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Genetics, In the News, Research, Science

Zebrafish: A must-have for biomedical labs

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Rats, mice and fruit flies be warned: The hippest lab critter around is a striped, little fish from South Asia called the zebrafish.

The fishies’ popularity is skyrocketing, as Susannah Locke recently wrote for Vox:

Zebrafish breed quickly, scientists can manipulate their genes easily, and the fish actually share a surprising number of similarities with humans.

As a result, researchers can study zebrafish to better understand how things like metabolism, birth defects, and even cancer work — and the results are often applicable to humans. So, for instance, it’s relatively quick and easy to test certain drugs on zebrafish. If those experiments yield promising results, the scientists can then do more targeted experiments with rodents. And then maybe, finally, with people.

Zebrafish have some unique characteristics that can be useful too: Zebrafish can regenerate heart, retina, spinal cord and fin tissue. Scientists are probing this ability to improve healing and potentially even cultivate new tissues. Their embryos are also transparent, allowing scientists to study organ development in real-time.

Scientists have grown quite masterful at manipulating their genes. As Locke writes: “Over the past five years, the cost of modifying a single gene in a zebrafish has dropped from $10,000 down to about $100.” That’s part of the reason why more than 2,000 biomedical papers are written each year using the fish.

Joseph Schech, DVM, knows these animals well:

“They’re very hardy. They’re very forgiving,” says Schech, a laboratory veterinarian in charge of roughly 200,000 zebrafish (and several other species) at the National Institutes of Health. ”They are very adaptable in the wild. They live in clear mountain streams. They live in muddy rice paddies. They can do a wide range of temperature if they have time to adapt to it.”

He’s in charge of keeping the creatures healthy in a NIH zebrafish facility that’s currently used by some 21 different laboratories. It’s one of the largest zebrafish facilities in the world — a single 78–80°F room that holds about 10,000 small tanks with a total of roughly 200,000 fish. The zebrafish eat a diet of brine shrimp grown in a nearby room and can be trained to spawn on cue.

Numerous Stanford labs use zebrafish for all sorts of research: William Talbot, PhD, is examining the development of the vertebrate nervous system; Gill Bejerano, PhD, is probing its genetics; and James Chen, PhD, is looking at its ability to regenerate tissue, to name just a few.

Previously: Researchers capture detailed three-dimensional images of cardiac dynamics in zebrafish, The importance of the zebrafish in biomedicineCellular-level video of brain activity in a zebrafish and A very small fish with very big potential
Image by Bob Jenkins

Big data, Research, Science, Stanford News, Technology

Gamers: The new face of scientific research?

Gamers: The new face of scientific research?

gamerMuch has been written about the lack of reproducibility of results claimed by even well-meaning, upright scientists. Notably, a 2005 PLoS paper (by Stanford health-research policy expert John Ioannidis, MD, DSci) with the unforgettable title, “Why Most Published Research Findings Are False”, has been viewed more than a million times.

Who knew that relief could come in the form of hordes of science-naive gamers?

The notion of crowdsourcing difficult scientific problems is no longer breaking news. A few years ago I wrote a story about Stanford biochemist Rhiju Das, PhD, who was using an interactive online videogame called EteRNA he’d co-invented to come up with potential structures for RNA molecules.

RNA is a wiggly wonder. Chemically similar to DNA but infinitely more flexible and mobile, RNA can and does perform all kinds of critical tasks within every living cell. Scientists are discovering more about RNA’s once-undreamed of versatility on a steady basis. RNA may even have been around before DNA was, making it the precursor that gave rise to all life on our planet.

But EteRNA gamers need know nothing about RNA, or even about biology. They just need to be puzzle-solvers willing to learn and follow the rules of the game. Competing players’ suggested structures for a given variety of RNA molecule are actually tested in Das’s laboratory to see whether they, indeed, stably fold into the predicted structures.

More than 150,000 gamers have registered on EteRNA; at any given moment, there are about 40 active players plugging away at a solution. Several broadly similar games devoted to pursuing biological insights through crowdsourcing  are also up and running.

Das and EteRNA’s co-inventor, Adrien Treuille, PhD, (now at Carnegie Mellon University) think the gaming approach to biology offers some distinct – and to many scientists, perhaps unexpected – advantages over the more-traditional scientific method by which scientists solve problems: form a hypothesis, rigorously test it in your lab under controlled conditions, and keep it all to yourself until you at last submit your methods, data and conclusions to a journal for peer review and, if all goes well, publication.

In this “think piece” article in Trends in Biochemical Sciences,  Treuille and Das write:

Despite an elaborate peer review system, issues such as data manipulation, lack of reproducibility, lack of predictive tests, and cherry-picking among numerous unreported data occur frequently and, in some fields, may be pervasive.

There is an inherent hint of bias, the authors note, in the notion of fitting one’s data to a hypothesis: It’s always tempting to report or emphasize only data that fits your hypothesis or, conversely, look at the data you’ve produced and then tailor the “hypothesis” accordingly (thereby presenting a “proof” that may never be independently and rigorously tested experimentally).

Das and Treuille argue that the “open laboratory” nature of online games prevents data manipulation, allows rapid tests of reproducibility, and “requires rigorous adherence to the scientific method: a nontrivial prediction or hypothesis must precede each experiment.”

Das says, “It only recently hit us that EteRNA, despite being a game, is an unusually rigorous way to do science.”

Previously: John Ioaniddis discusses the popularity of his paper examining the reliability of scientific researchHow a community of online gamers is changing basic biomedical researchParamecia PacMan: Researchers create video games using living organisms and Mob science: Video game, EteRNA, lets amateurs advance RNA research
Photo by Radly J Phoenix

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