Awards and Honors Across Weill Cornell Medicine - Week of April 18 - April 22


Dr. Dan Landau, an assistant professor of medicine and of physiology and biophysics, and a core member of the New York Genome Center, has received the 2016 Sidney Kimmel Foundation Scholar Award, which was established to advance the careers of gifted, young scientists involved in cancer research who demonstrate great promise and innovation in their work and have yet to receive a major grant from the National Institutes of Health or other funding sources. Dr. Landau will receive a $200,000 grant over the next two years for his translational research study, "Knowledge infrastructure for data-driven combination leukemia therapy engineering."

Dr. Gregory Sonnenberg, an assistant professor of microbiology and immunology in medicine and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease, has been chosen as a Searle Scholar for 2016. The Searle Scholar program awards grants to support the research of young, outstanding scientists who have been recently appointed as assistant professors — their first tenure-track position at an academic or of research institution. Dr. Sonnenberg will receive a $300,000 grant over the next three years for his project, "Harnessing the Co-evolution of Mammals and Microbes to Engineer Novel Vaccines."

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Bacteria in Immune Cells May Protect Against Chronic Inflammation

A population of bacteria inhabits human and mouse immune cells and appears to protect the body from inflammation and illness, Weill Cornell Medicine scientists discovered in a new study. The findings challenge conventional wisdom about the relationship between bacteria and the human body — and about how the microbes influence health and disease.

The study, published March 15 in Immunity, focused on "good" or "commensal" bacteria that live in the human intestine and are essential for digestion and proper immune function. The majority of these commensal bacteria are found in the tube-like inner core of the intestine, called the lumen. The intestine itself acts as a barrier, keeping the bacteria inside the lumen and ensuring that they do not enter the rest of the body. Many reports have demonstrated that if commensal bacteria managed to escape the lumen, they would activate the immune system and cause disease.

But in their study, Weill Cornell Medicine investigators identified a group of commensal bacteria residing in close contact with immune cells outside of the intestinal lumen that defy this thinking. The discovery may alter the way scientists understand diseases like HIV, inflammatory bowel disease, some cancers, and cardiovascular disease.

Sonnenberg Laboratory. Front center, Dr. Gregory Sonnenberg. Back (from left, clockwise): Dr. Jeremy Goc, Thomas Fung, Xinxin Wang, Dr. Nicholas Bessman and Stephane Pourpe Photo credit: Roger Tully

"For a long time, the assumption was that the human body is essentially sterile and that a physical separation between the immune system and our commensal bacteria was necessary to prevent chronic inflammation," said lead author Dr. Gregory Sonnenberg, an assistant professor of microbiology and immunology in medicine and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine. "While this is certainly true for most types of commensal bacteria, our new data demonstrate a special class of commensal bacteria that can closely associate with immune cells in a way that is mutually beneficial for both mammals and the microbes."

To learn more about this population of microbes, the researchers studied "germ-free" mice — rodents that are bred to have no bacteria in their bodies and have no contact with outside bacteria. They added this newly identified class of bacteria, called lymphoid tissue-resident commensal bacteria (LRC), to the mice.

The LRC colonized lymphoid tissues — specifically cells in the immune system — located outside of the intestinal lumen. When Dr. Sonnenberg and his colleagues investigated what the bacteria were doing, they found that they did not cause inflammation as expected. Rather, they did exactly the opposite — they limited the inflammatory response in the immune tissue.

The researchers then tried to experimentally induce intestinal tissue damage and inflammation in the rodents. They found that the mice that had LRC in their lymphoid tissue were protected.

"So it seems that these bacteria residing in lymphoid tissue are actually protecting the mice, rather than driving disease as would be expected," said lead author Thomas Fung, a graduate student in Dr. Sonnenberg's lab. "We further found that the immune responses induced by these bacteria are mutually beneficial; they not only protected mice from experimental tissue damage, but they also facilitated bacteria colonization of lymphoid tissues."

These are early findings, but the implications for human health are important to consider, Dr. Sonnenberg added. For example, the prevailing view is that in people with inflammatory bowel disease, colorectal cancer or HIV infection, commensal bacteria disseminate from the lumen of the intestine into the periphery of the body and promote inflammation.

"Our new data indicate that some unique bacteria residing in lymphoid tissues could instead promote tissue protection and limit inflammation," he said, "and our research highlights that it will be important to consider changes in lymphoid tissue-resident microbes during human health and disease."

The Sonnenberg Laboratory is also investigating whether LRCs can be developed as an innovative therapeutic approach to limit chronic inflammation and promote tissue repair in diseases such as inflammatory bowel disease.

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Innovative Therapeutic Approach Shows Promise in Treating Inflammatory Bowel Disease

inflamed mouse intestine with longer epithelial cells and an over-abundance of immune cells

Microscopic color-enhanced image of an inflamed mouse intestine, with longer epithelial cells and an over-abundance of immune cells (shown in yellow). Credit: Drs. Greg Sonnenberg and David Withers

An investigative therapy given to mice blocks the overactive immune responses that are a hallmark of inflammatory bowel disease without impairing the body's ability to fight infection, an international research team led by Weill Cornell Medicine investigators finds in a new study. The preclinical discovery may lead to more effective treatment strategies for IBD.

The prevailing scientific view of IBD — a chronic, debilitating inflammatory disorder of the digestive tract that affects an estimated 3.5 million individuals worldwide — is an over-reactive immune system attacking the normally beneficial bacteria that colonize the intestines. Treatments for the condition have been hampered by the challenge of stopping this aberrant immune response without hindering the immune system from protecting against harmful pathogens.

To get around this conundrum, investigators used an innovative therapeutic approach to block the production of an inflammation-promoting molecule in mice, while leaving key protective immune factors intact. In their study, published Feb. 15 in Nature Medicine, the investigators found that this approach effectively prevented inflammatory immune responses without making the mice more susceptible to infection. The results suggest that the drug may be effective in people.

Dr. Gregory F. Sonnenberg

Dr. Gregory F. Sonnenberg Photo credit: Carlos Rene Perez

"We really are excited by these new findings as they suggest that this therapeutic approach could be a safe and effective way to treat chronic intestinal inflammation," said senior author Dr. Gregory F. Sonnenberg, an assistant professor of microbiology and immunology in medicine and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine.

The pro-inflammatory molecule, called IL-17, has emerged as a target for treating IBD, but clinical trials that tested blocking it with antibodies have failed. Some patients became sicker or more susceptible to opportunistic infections by fungi in the intestine, Dr. Sonnenberg said. IL-17 is produced by both white blood cells called T cells and a recently discovered class of immune cells that play a role in the immune system's surveillance of infection and in tissue repair, known as innate lymphoid cells (ILCs). Some researchers believe that blocking IL-17 not only switches off the body's attack on its own cells, but also impedes the ability of ILCs to defend against new infections or promote tissue repair.

But scientists from Weill Cornell Medicine, the Children's Hospital of Philadelphia and the United Kingdom-based University of Birmingham and Babraham Institute, tried a different approach: Using both small-molecule compounds and genetic approaches, they targeted a molecule that regulates production of IL-17 in mice, called ROR gamma-t. The investigators found that inhibition of ROR gamma-t effectively prevented inflammatory immune responses without making the mice more susceptible to infection.

"The surprising finding we made was that temporary inhibition of ROR gamma-t did not impact the function of ILCs," said lead author Dr. David Withers, a Wellcome Trust Research Fellow at the University of Birmingham. "This effectively allowed us to limit the T cell responses that are promoting chronic intestinal inflammation, while preserving the protective ILC responses that mediate tissue repair and early protection from infections."

To test if this approach could selectively inhibit pro-inflammatory T cells in human cells, the researchers applied similar approaches to immune system cells taken from intestinal biopsies of pediatric patients diagnosed with Crohn's disease, one of the major forms of IBD. Similar to their observations in mice, the investigators found a reduction in the human T cells that make pro-inflammatory molecules, and the ILCs remained intact.

"There are a number of important questions remaining here that need to be addressed prior to taking these findings forward, such as developing innovative small-molecule compounds and further understanding what is maintaining ILC responses in the absence of ROR gamma-t," Dr. Sonnenberg said. "However, these findings suggest that small molecules that inhibit ROR gamma-t may be an attractive approach for therapeutically treating inflammatory bowel disease, as well as multiple other chronic inflammatory disorders."

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Symbiotic Relationship


Researchers Explore the Microbiome, Medicine's Newest Frontier

By Amy Crawford

Portraits by John Abbott

intestinal epithelium lining mouse's gastro-intestinal tract

A color-enhanced image of the intestinal epithelium that lines the gastro-intestinal tract of a mouse. Scientific images: Drs. Gregory Sonnenberg and David Artis

The most exciting discoveries can begin with the humblest material — and for researchers in the lab of immunologist Dr. David Artis, that often means mouse droppings. Once an obliging rodent provides a stool sample, a technician uses a chemical buffer to break down bacterial cell walls, unleashing the coils of DNA within. After further chemical preparation to enrich the genetic information, the sample is fed into an Illumina MiSeq, a desktop machine half the size of an office photocopier that, over the course of about 48 hours, sequences billions of base pairs to reveal a catalog of hundreds of types of bacteria: the mouse's microbiome. "After painstaking collection and preparation, you load your samples and allow the machine to run overnight," explains post-doctoral researcher Dr. Lisa Osborne, who has analyzed her share of murine fecal bacteria in the name of better understanding how the microbiome works in humans. "A lot of sophisticated magic happens inside that box."

The technology may not look flashy, but it's enabling a revolution in how scientists think about the bacteria that share our bodies — no longer as mere pathogens, but as members of a tiny ecosystem that coevolved with us, and on which our health depends. Dr. Artis and his colleagues hope these communities of microbes can offer insight into one of the most confounding problems in modern medicine: the set of painful chronic conditions known as inflammatory bowel disease (IBD). But IBD is not the only reason scientists at Weill Cornell and elsewhere are increasingly interested in microbiota. It turns out that the human microbiome may have far-reaching impact throughout the body, influencing how our immune systems develop, how our food is metabolized — and even, perhaps, the peculiarities of our personalities. New knowledge about the complex web of relationships between humans and the microbes that live within us is calling into question not only our understanding of disease, but of what it means to be human. "This is one of the major topics in contemporary biomedicine, and it's profoundly reshaping the way we think about health and disease and individuality," says Dr. Carl Nathan, the R. A. Rees Pritchett Professor of Microbiology and chairman of microbiology and immunology. "I grew up thinking that a given person has one genome, one set of genes that you inherit from your two parents. That's much too simple."

intestinal tissue of healthy mouse

A stained histologic section of intestinal tissue isolated from healthy mouse.

Medical training taught Dr. Nathan that the hereditary genome he learned about in school was not the only one that makes us who and what we are. There's also the somatic genome — the accumulated mutations and re-arrangements that some cells undergo, either as part of an abnormal process that can lead to cancer or as part of a healthy immune system, which adapts to recognize the myriad pathogens a person encounters throughout life. Another code is found within mitochondria, organelles that power our cells and, scientists believe, evolved in multicellular organisms like humans from symbiotic bacteria. "Then there's the fourth genome," Dr. Nathan says. "That's the collective complement of genes of all the bacteria that normally reside in us. And the ways that this impacts medicine are almost countless."

In a suite of gleaming new labs on the fifth floor of the Belfer Research Building, some 20 people are working to unravel the mysteries of the microbiome. Some are hunched over laptops, while others collect data from a machine called a flow cytometer set up in a corner. In a culture room, several sit at biosafety cabinets, manipulating cells collected from mice or human patients.

The team is led by Dr. Artis, who was recruited as the Michael Kors Professor in Immunology. Widely considered a world leader in his field, he has recently been involved in studies that uncovered links between the immune system's response to gut bacteria and systemic allergies, as well as how the immune system keeps gut bacteria where they belong. Last year, Dr. Artis, along with some of his longtime collaborators, was lured away from the University of Pennsylvania to head Weill Cornell's new Jill Roberts Institute for Research in Inflammatory Bowel Disease.

When Dr. Artis, who grew up in Scotland, was an undergraduate in the early '90s, he took a course on evolution and became fascinated by how the mammalian immune system had evolved in conjunction with the pathogens that infect us. After earning a Ph.D. in immunology at the University of Manchester, he crossed the Atlantic to do postdoctoral work at Penn, where he would later join the faculty. Some of his early research there centered on the immune system's interaction with helminths, tiny worms that can make their home in human intestines, into which they find their way via under-cooked meat or contaminated water. Broader interest in the human microbiome as anything but pathogenic had yet to take hold, but Dr. Artis and other researchers were beginning to recognize something that ran counter to our previous understanding of these parasites as little more than uninvited passengers that make us sick. "We were interested in the pathogens that infect us, and one class of pathogens is worms," Dr. Artis explains. "The interesting thing is that to eradicate worms, the body mounts the Type 2 inflammatory response. It's the same type of response in allergies, only there it's reacting to innocuous antigens in peanuts and milk products and so forth."

healthy mouse tissue with normal microflora

A color-enhanced tissue section from a healthy mouse showing the presence of normal microflora.

Over most of human history, the Type 2 response was an effective way to combat common parasites, and it's still called into action in much of the world, where helminths remain a problem. But in the United States and other industrialized countries, sanitation and medicine have virtually eliminated intestinal worms, leaving the Type 2 response a weapon without a proper target. That mismatch may contribute to the startling increase in allergic disease, asthma and other immune disorders, including certain forms of IBD.

As Dr. Artis' research looked at the ways in which immunity in the presence or absence of parasites could be involved with allergic reactions and chronic inflammation, a great shift was taking place in how researchers, doctors and even the general public think about other organisms that live in our bodies. It was a shift that paralleled the discovery of microorganisms themselves in the late 17th century, when the Dutch scientist Antonie van Leeuwenhoek trained his homemade microscopes on droplets of rainwater. "Like most discoveries in science," Dr. Artis says, "these quantum leaps are triggered by new technologies that allow us to see differently." A decade ago, studying the organisms living in someone's colon would have required culturing them in a petri dish, a time-consuming technique that could only begin to reveal the multitudes of bacteria that make up a complete human microbiome. That has changed, largely thanks to an international science project that some have compared to the 1969 moon landing in both its historical importance and its legacy of innovation.

In 2000, President Bill Clinton and British Prime Minister Tony Blair appeared on television to announce that an international team of scientists had completed a rough draft of the human genome, some 3 billion base pairs that make up roughly 20,500 genes. The project had been a massive undertaking, involving researchers in six countries working for more than a decade. In addition to the invaluable information about our own DNA that the project provided, it also spurred the development of new technology that would enable further discoveries. Today, commercially available genetic sequencing platforms like the Illumina MiSeq are considered de rigueur for any well-stocked research institution — Weill Cornell's Genomics Resources Core Facility has several — and what took the Human Genome Project years to accomplish can be done overnight. Now, researchers are using that technology to read and understand that fourth human genome, that of the bacteria that make their homes in our bodies. "Sequencing technology allows us to identify the microbiota at a level that we would never have been able to understand before," Dr. Artis says. "That technology has really accelerated our ability to profile the organisms in this complex ecosystem, and it also allows us to report how their composition changes in the context of disease."

Much as the sequencing of the human genome inspired the popular imagination a decade ago, today studies of the human microbiome have filtered from scientific journals and into the popular press. Breathless newspaper articles have told us how gut bacteria influence the workings of the mind, and that they might determine why some of us get fat while others stay slim on the same diet. In a 2013 New York Times Magazine cover story, the writer Michael Pollan recounted how sequencing the genes of the 100 trillion bacteria in his own body led him to think of himself "in the first-person plural — as a superorganism, that is, rather than a plain old individual human being."

Dr. Greg Sonnenberg, an assistant professor of microbiology and immunology in medicine, sees this as an asset to science. "The current level of excitement is fantastic," says Dr. Sonnenberg, who has collaborated on seminal studies with Dr. Artis and who was also recruited to lead a lab at the Roberts Institute. "The more you learn about the microbiome, the more it just touches upon everything; it is involved in probably every human disease out there. It's like the rainforest, where you can go through and find different bugs that may have the ability to provide therapeutic benefit in many diseases. And that's where the field is today. Now we need to get down to the nitty gritty in determining which species are important, which species are doing what and how are they interacting with each other. It's an extremely complex system."

Dr. Sonnenberg cautions that many recent papers based on sequencing data have likely uncovered mere correlations. While some members of the microbiome are clearly associated with certain medical conditions, he explains, that doesn't mean the bacteria caused the conditions. Much more work must be done to understand the functions of the bacteria that make up the human microbiome, and how the chemical signals and byproducts they produce affect us and each other. "Hopefully," he says, "that's going to translate to more research being done that advances us to the point where it will benefit patients more directly."

There is already one way in which doctors are using knowledge of the microbiome to benefit patients. Clostridium difficile (C. diff.) is a highly antibiotic-resistant bacterium that causes severe diarrhea and kills some 14,000 Americans each year. Patients most at risk are those in whom antibiotics have wiped out beneficial gut bacteria, leaving the coast clear for C. diff. to grow unimpeded. So far the most successful treatment involves replacing those good bugs with a fecal transplant — that is, inserting the stool of a healthy volunteer into the colon of a C. diff. sufferer — and restoring the normal, healthy balance of gut bacteria. "The concept is both intriguing and somewhat repulsive," admits Dr. Charlie Buffie, who will finish his medical degree at Weill Cornell in 2016, having completed his doctoral work at Sloan Kettering through the Tri-Institutional M.D.-Ph.D. program. "But the efficacy of a fecal transplant has been strikingly high under the right circumstances." Fecal transplant cures about 90 percent of C. diff. patients, but doctors aren't sure exactly why. And because the treatment by its very nature is impossible to standardize, government regulators are uneasy and doctors are reluctant to use it in immunocompromised patients. Dr. Buffie, however, may have found a partial answer to those quandaries.

Dr. Charlie Buffie

The components of a fecal transplant are as numerous as those of the human microbiome itself. But one that seems to be especially effective in controlling a C. diff. infection is a related species called Clostridium scindens. In a study published last year in Nature, Dr. Buffie and colleagues in the Sloan Kettering lab of immunologist Dr. Eric Pamer used C. scindens to defeat C. diff. in mice whose normal microbiomes had been disrupted with antibiotics. In the future, Dr. Buffie says, patients with C. diff. might be given precisely calibrated mixtures of beneficial bacteria or drugs that mimic the metabolic products of C. scindens that seem to prevent C. diff. from propagating. That would allow patients to avoid the potential safety risks — not to mention the ick factor — of a fecal transplant. Says Dr. Buffie: "Being able to isolate, define and construct compositions of bacteria that we know have positive effects and that do not have negative effects — that's definitely an attractive solution."

This line of research also holds promise for IBD patients, says Dr. Randy Longman '07, an assistant professor of medicine in gastroenterology and alumnus of the Tri-Institutional M.D.-Ph.D. Program who joined the Jill Roberts Center for Inflammatory Bowel Disease in 2013. Preliminary evidence suggests that fecal transplantation could help those with a form of IBD called ulcerative colitis, and Dr. Longman and his colleagues are working to figure out why. "The idea is to be able to get specific about the microbes," he says. "If we isolate some of these bugs from patient samples and then put them into gnotobiotic mice we may be able to understand how these microbes interact with the immune system within the intestine."

Although Dr. Longman's primary occupation is research, he spends one day a week in clinical practice, working to help patients manage their illness. "Inflammatory bowel disease, epidemiologically, affects people in the prime of life," Dr. Longman notes. "So many of the patients that I'm seeing for initial diagnoses are young people with so much of their lives in front of them. There is a tremendous need for new medicines and new therapeutic strategies." Like his colleagues, Dr. Longman is optimistic that cracking the secrets of the microbiome will lead to better treatments, and his patients will one day get relief from the stress of living with a chronic condition. "Right now, treating IBD is a management thing," he says. "We don't cure it right now. But we do hope for that."

Today, fecal transplantation remains the best microbiome-based treatment available. But as research points to gut bacteria's involvement with a variety of other ailments, scientists are hoping that future patients could be helped by targeted probiotics or drugs modeled after the chemical signaling of good bacteria. "There may be a point where it isn't necessary to cultivate certain bacteria in your body," Dr. Nathan says, "but rather to take a pill that provides the compounds those bacteria are making — to do the job they do, but in a more orderly, defined, predictable, consistent, safe way." In the future, such treatments might be used not only for C. diff. and IBD, but eventually for metabolic disorders, obesity and even neurological problems. "Whether the food you eat influences a predisposition to atherosclerosis — that's controlled by the bacteria in the body," Dr. Nathan says. "There are influences on behavior, on weight gain, probably on asthma. There's a connection to autism that's recently been reported." The microbiome may have an impact on every system in the human body, he stresses, and its importance is inestimable.

Dr. Artis echoes Dr. Nathan's enthusiasm, and notes that most breakthroughs are yet to come. He draws an analogy to the years after van Leeuwenhoek's microscope first revealed the hidden world in a water droplet. "The pace of discovery is so rapid; this field has really exploded," he says. "But in terms of understanding the complexities of microbiota in the body, we're in our infancy."

Living Underground

The New York Subway System Hosts a Complex Bacterial Ecosystem, Too

Infographic of DNA in New York subway forming bacteria in human body

Infographic showing the relative amount of DNA found in the New York subway system form bacteria associated with the human body. Click to enlarge.

Just as each human body holds a complex ecosystem of bacteria in the gut, every major metropolis is home to a medley of bacteria and pathogens, coexisting with that city's residents. Until recently, little was known about these native microbial communities, which surround us in streets, buildings and public transit areas.

Using the subway system as their testing ground, Weill Cornell investigators fanned out beginning in June 2013 and collected samples of hundreds of DNA from bacterial, viral, fungal, and animal species — like insects and domestic pets — in the underbelly of New York City. They then compiled the data and turned it into an interactive pathogen map, dubbed PathoMap, and recently published their findings in Cell Systems.

While most of the collected microbes are harmless, some are not — including live, antibiotic- resistant bacteria, which were found in 27 percent of the samples. Two samples included DNA fragments of anthrax, and three carried a plasmid associated with Bubonic plague. Reassuringly, those five were discovered at very low levels and showed no evidence of being alive. Other DNA — half of what was collected, in fact — could not be identified as any known organism, because the databases against which they are compared are still incomplete.

While this might sound troubling, there's no need to worry right now, says the study's senior investigator, Dr. Christopher Mason, the WorldQuant Foundation Research Scholar and an associate professor in Weill Cornell's Department of Physiology and Biophysics and in the HRH Prince Alwaleed Bin Talal Bin Abdulaziz Al-Saud Institute for Computational Biomedicine. These apparently virulent organisms are not linked to widespread sickness or disease in this environment, Dr. Mason says. "They are instead likely just the co-habitants of any shared urban infrastructure and city," he says, "but additional testing is needed to confirm this."

The knowledge that these bacteria are present and having no obvious negative effect on the 5.5 million daily subway riders demonstrates that most of them are neutral to human health, he adds. They may even be helpful, as they can out-compete dangerous bacteria. "The presence of these microbes and the lack of reported medical cases is truly a testament to our body's immune system," Dr. Mason says, "and our innate ability to continuously adapt to our environment." Would these pathogens be typical for other cities? With the aim of answering that question, collaborators are collecting samples from airports, taxis and public parks in 15 other cities around the world under a recent grant from the Sloan Foundation.

The PathoMap project involved investigators from Weill Cornell, five additional New York City medical centers and more than a dozen national and international institutions. Over the course of 17 months, medical students and other volunteers used nylon swabs to collect DNA from turnstiles, benches, railings, trashcans and kiosks in all operating subway stations across the five boroughs. The team also collected samples from inside trains, swabbing seats, doors, poles and handrails. They time-stamped each sample and tagged it using a GPS system, later sequencing about 1,500 samples (out of more than 4,200 collected) and analyzing those results. "PathoMap establishes the first baseline data for an entire city," Dr. Mason says, "revealing that 'molecular echoes' of commuters appear on all surfaces — from the bacteria on their skin to the food they eat, and even from the human DNA left behind, which matched U.S. Census data."

The data on New York City's ecosystem — an ingredient in building a smart city — already has potential real-world applications. Researchers could monitor the system for changes that would signal disease or a potential threat, or someday create a live model tracking real-time changes to this urban microbiome. The PathoMap, Dr. Mason says, is just the beginning.

— Anne Machalinski

This story first appeared in Weill Cornell Medicine, Vol. 14, No. 1.

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In the lab: Dr. David Artis with postdoc Dr. Anne-Laure Flamar
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