by Rob Mitchum

An advantage and disadvantage of hypothesis-free studies looking for genes associated with various traits or diseases is that they often point to genetic candidates that don’t make immediate sense. One example of this occurrence was the 2005 discovery of an association between the gene Glo1 and anxiety-like behaviors in mice. Previously, scientists knew Glo1’s protein product, glyoxylase 1, primarily as a enzyme involved in in glycolysis — the cellular digestion of glucose. Nobody had considered that glyoxylase 1 played a role in brain function, much less behavior, leading some to question the validity of the genetic association.

“When people discover a gene, they’re always most comfortable when they discover something they already knew,” said Abraham Palmer, assistant professor of human genetics at the University of Chicago Medicine. “The alarming thing here was there was a discovery of something that nobody knew, and therefore it seemed less likely to actually be correct.”

But Palmer’s laboratory continued chasing down the Glo1/anxiety connection, and their experiments paid off in the discovery of an entirely new mechanism for anxiety disorders. Their study, published today in the Journal of Clinical Investigation, also describes a previously unrecognized inhibitory neural factor, offers a promising new target for the treatment of anxiety disorders and other psychiatric symptoms, and suggests an intriguing connection between metabolism and neurobiology.

“What’s neat is that we started with exploratory, open-ended genetic studies in mice, and we’ve now gotten into some fundamental new physiology that nobody had appreciated or put together before,” Palmer said. “Now we’re starting to reap some of the fruit from those types of genetic studies to enrich our understanding of more classical aspects of biology.”

Lead author Margaret Distler, an MD/PhD student in the Pritzker School of Medicine, started her examination of the Glo1/anxiety link by testing it in a new way. In a 2009 paper, Palmer’s group hypothesized that mice with more copies of the Glo1 gene — a genetic phenomenon known as copy number variants — were more likely to show anxious behaviors. Distler tested this theory by inserting two, eight, or ten copies of the gene into mouse lines, and measuring their anxiety with various laboratory tests, including the open field test and the light-dark box test. As predicted, more Glo1 copies equated to more anxiety-like behavior, lending more evidence to the link.

“Animals transgenic for Glo1 had different levels of anxiety-like behavior, and more copies made them more anxious,” Palmer said. “We showed that Glo1 was causally related to anxiety-like behavior, rather than merely correlated.”

The next step was to figure out how Glo1 accomplished its unexpected influence. In glycolysis, glyoxylase 1’s job is to metabolize and reduce levels of a byproduct called methylglyoxal, or MG for short. So Distler tried an experiment so simple it almost obvious: if increasing Glo1 increases anxiety, would increasing MG levels alleviate it? After injecting mice with MG, the mice were less anxious in the behavioral experiments, suggesting that the metabolic byproduct does in fact play a role in anxiety — and a relatively fast role, at that.

“Methylglyoxal changed behavior within 10 minutes of administration, which means it’s a rapid onset. It’s not changing gene expression, and it’s not having long-term downstream effects,” Distler said. “That was our first breakthrough.”

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The rise of optogenetics — where flashes of light can manipulate brain activity and rat behavior — have excited scientists looking for more precise ways of manipulating cells and their components in the laboratory and the clinic. Two papers published this month by University of Chicago laboratories explore new methods with great scientific potential of controlling cells through light  We’ll cover them in two installments.

Many important cellular functions are principally the result of factors being in the right place at the right time. The complex pathways that handle important jobs such as cell growth or migration can have hundreds of components that must arrive at the same location within the busy cellular environment. As such, biologists would like the ability to move proteins to different parts of the cell at will, giving them control over the staging of these pathways and their functions. With a new system that draws upon the work of several University of Chicago laboratories, researchers have figured out how to achieve this power with light.

Like many good ideas in science, the collaboration that created TULIPs began with a question posed at a bar. At the annual Molecular Biosciences retreat in Galena, Illinois, Devin Strickland and Tobin Sosnick challenged their colleague Michael Glotzer with a provocative question.

“They asked, ‘If you could control any protein you wanted, what would you control?’,” recalled Glotzer, Professor of Molecular Genetics & Cell Biology at the University of Chicago.

Strickland, then a graduate student in the laboratory of Sosnick, Professor and Chair of Biochemistry & Molecular Biophysics, were looking for applications of  their strategy of using light to control the activity of a specific protein. Glotzer realized that the system could bring two proteins together in a cell, whenever and wherever researchers wanted. The result was an exciting new technique, called TULIPs, published this month in Nature Methods.

The acronym TULIPs stands for TUnable, Light-controlled Interacting Protein tags. Instead of  the light-activated ion channels or gene transcription used by other optogenetic methods, the TULIPs use a LOV domain, a light-sensitive component from a protein plants use to detect and grow toward sunlight. By attaching different proteins to this domain and another known as an ePDZ “clamp,” the researchers built a customizable way of precisely manipulating cellular signals in both space and time.

“Basically nothing previously had been designed to control cell signaling that wasn’t engineered on a case-by-case basis,” said Strickland, now a postdoctoral researcher in Glotzer’s laboratory. “We started off wanting to be the first people to create an adaptable system.”

In the Nature Methods paper, the authors describe testing the system by attaching it to fluorescent proteins and applying it to Glotzer’s chosen target, a GTPase pathway that controls growth and genes related to mating in yeast. The experiments demonstrated both that the TULIPs worked, and that it could be easily adapted to manipulate a wide range of cellular signals.

“The idea was let’s solve this generic problem once, and then we’ll be able to reuse that solution in many different contexts,” Glotzer said. “Looking at lots of different biological phenomena, it’s pretty clear that a lot of functions correlate with changes in sub-cellular localization of specific proteins. So there’s almost no limit; you’re only limited by your imagination.”

[Light flashes on the right demonstrate the successful localization of fluorescent proteins attached to the TULIPs system. Video by Elizabeth Wagner]

The TULIP system is made up of two components that draw upon work done previously by the University of Chicago laboratories of Shohei Koide, who developed the ePDZ clamp, and Keith Moffat, who characterized the LOV domain and first suggested its use in the TULIP system.

“It’s really a nice story of how basic research can lead to things that aren’t really anticipated,” Strickland said.

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By John Easton

There are ways in which patients who leave the hospital against medical advice wind up paying for that decision. Being saddled with the full cost of their hospital stay, however, is not one of them.

Insurance companies know this. Patients who walk out may know this. But many physicians, according to a study published in the Journal of General Internal Medicine, do not.

A survey of general internal medicine doctors at the University of Chicago Medicine found that two-thirds of residents and almost half of attending physicians believe that when a patient leaves the hospital against medical advice, insurance companies will not pay for the patient’s hospitalization, leaving the patient liable for the full hospital bill.

“We have all heard this, and many physicians may have passed it on to their students, even to patients threatening to leave on their own,” said study author Vineet Arora, MD, associate professor of medicine at the University of Chicago Medicine. “But a closer look revealed this to be a myth, a medical urban legend, albeit a pervasive one.”

In this video, Arora discusses this myth, how she and her colleagues tracked it down and how rumors like this persist in a hospital environment.

Video produced by Matt Wood

By Dianna Douglas

A pregnancy is considered at “term” after 37 weeks. But there are critical growth stages that come next–a baby’s lungs, brain, and liver develop in the last few weeks in the womb. Women in the United States are often induced before the baby has fully gestated, which leads to a host of negative consequences. Kenneth Nunes, MD, assistant professor of obstetrics and gynecology, led an effort to slow down the rate of elective “early-term” deliveries between 37 and 39 weeks at the University of Chicago. In these video interviews, he discusses his motivations, methodology, and results.

In the first, Nunes discusses the risk of delivering early versus the risk of prolonging a pregnancy.

Nunes discusses how a pregnancy is induced, when it is necessary, and the possible effects of inducing.

Nunes discusses how he and the Women’s Care Group reversed the number of elective “early-term” deliveries at the University of Chicago.

By Rob Mitchum

Treating a brain tumor in a lab dish is easy. Scientists have developed a full arsenal of treatments to kill tumor cells, using natural toxins, chemotherapeutic drugs, and even gene therapy to send them to an early grave. But making those therapies work in the actual setting of the brain is a much different ballgame. The first major challenge is even delivering the therapy to the right place, as any drug must get past the brain’s defense systems and navigate the organ’s complex architecture. In addition, the therapy must be a picky killer, eradicating tumor cells while leaving the healthy brain cells intact.

Researchers are therefore searching for a smarter delivery system that can maximize the effectiveness of these brain tumor therapies, collaborating with experts in the world of chemistry, materials science, and engineering. Bakhtiar Yamini, an assistant professor of surgery at the University of Chicago Medicine, is collaborating on one such effort with a biotechnology company in Nebraska, targeting the most difficult malignant brain tumors Yamini sees in his neurosurgery practice. By designing a new nanoparticle “shell” capable of selectively targeting therapeutics to brain tumor cells — and capable of being watched as it travels through the brain — the research team hopes to make eradicating these cells in their native environment as simple as killing them in a dish.

“Even though new therapies are being developed that can kill cells in culture, getting them into the brain tumor is a big problem, so development of a vehicle is an important step,” Yamini said. “People have previously used both targeting and image guidance in the treatment of other cancers, but bringing these two strategies together in one vehicle is something that would be really useful.”

In Phase I of their NIH-funded project, Yamini and collaborators at LNKChemsolutions developed a nanoparticle made from materials such as polylactic acid and polycaprolactone. Despite the complicated chemical names, these materials are commonly used in biodegradable products — a feature that offers an advantage over other nanoparticles made from gold, titanium, and other metals. The nanoparticles are also customizable, able to carry a variety of therapeutics and different targeting signals, and incorporate a metal, iron oxide, that allows doctors to visualize the nanoparticles’ travels using MRI technology.

For Phase II of the project, funded late last year, the team is taking their technology to animal models. A nanoparticle designed to target a protein called the EGF receptor (often overexpressed by tumor cells) and deliver the chemotherapy drug temozolomide will be tested in mice and rats that have brain tumors. If those experiments are a success, the team will try the therapy on a larger animal model: dogs. Partnering with veterinary clinics in Chicago and Minnesota, the researchers will offer the treatment to pet owners willing to volunteer their sick dog for a cutting-edge therapy.

“That’s how we will develop the treatment, but at the same time it should be effective at helping the dogs,” Yamini said. “It’s essentially a clinical trial for dogs that have brain tumors, and because their tumors are very similar to human ones, the results in the dogs will have relevance to humans.”

Because of the blood-brain barrier, which prevents most molecules from passing from the body’s blood supply into the brain, just injecting the nanoparticles into a vein won’t work. Directly infusing particles into the brain during surgery to remove the tumor is possible, but the spread of particles by that method can be unpredictable and may miss the target. Instead, Yamini will use a method known as convection enhanced delivery to push the nanoparticles very slowly into the desired area of the brain, squeezing them through the space between brain cells. The iron oxide tags will allow surgeons to monitor the path of the nanoparticles by MRI as they are being infused through the brain.

“The image guidance is a big factor, because ‘blind’ infusion of the nanoparticles can be problematic,” Yamini said. “If you plan to treat the upper right corner and you see, on MRI, that the infusion actually went to the lower left, you can put your catheter back in and try again. This paradigm of ‘adaptive image guidance’ allows you to adjust subsequent treatments to target the areas that were missed on the original injection.”

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Roughly 30 million Americans suffer from migraines, and as you might expect, there’s a large pharmaceutical market to prevent or stop these debilitating headaches. Drugs such as Imitrex and Verapamil employ different pharmacological modes of action, reducing migraines by adjusting neurotransmitter levels, blocking ion channels, or simulating the body’s natural painkillers. There’s also a less pharmaceutical migraine treatment strategy, recommended by many headache specialists, that follows the old adage: “Active Body, Active Mind.” One recent study even found that 40 minutes of exercise three times a week can be as effective at preventing migraines as popular anti-migraine medications.

Still, prescribing exercise or environmental enrichment (keeping the mind busy through activities such as reading, crossword puzzles, exercise, or socialization) can strike some doctors and patients as frustratingly vague. Understanding the biological mechanism that makes these activities protective against migraines could help convince doctors and patients of their utility, while also giving researchers the opportunity to translate the factors associated with environmental enrichment into highly effective treatments.  In the laboratory of Richard Kraig, William D. Mabie Professor in the Neurosciences at University of Chicago Medicine, that very effort is underway.

“We are interested in environmental enrichment as a way to stop cognitive decline from aging, injury after stroke, Parkinson’s disease, and cell death after seizures.  With our new work, we apply this search for how the brain protects itself against disease to include migraines,” Kraig said.  ”The ‘why’ of it has sometimes been left in the realm of holistic medicine, with little scientific support.  So establishing the hard science makes it more credible to the psychologists, physiologists, physiatrists, because here’s the chemistry.”

Working with graduate students Yelena Grinberg and Aya Pusic as well as senior technician Heidi Mitchell, Kraig discovered three different natural signals elevated by exercise and environmental enrichment: insulin-like growth factor-1 (IGF-1), interleukin-11 (IL-11), and interferon gamma (IFN-γ). When these “cytokines” are applied to brain slices, they reduce the probability of triggering a spreading depression — a transient wave of reduced brain activity associated with migraines. Understanding how those cytokines stop spreading depression — and the nasal route by which they might be delivered — may revolutionize how migraines and other neurological conditions are treated.

A spreading depression of brain is a chain reaction of dramatic events. After an initial burst of increased neuronal activity, a subsequent ripple of absent activity slowly spreads across involved brain at a rate of about 3 mm per minute — lasting a few minutes overall.  While the event sounds brief, the consequences can last from hours to days, causing harmful oxidative stress, elevated inflammatory factors, moving microglia, and significant pain and discomfort for the migraine sufferer.

Paradoxically, the way to stop this chain reaction may not be to simply reduce or block the byproducts of a spreading depression, but to expose the brain to moderate levels of inflammatory factors, which include the cytokines described above. To interrupt the cycle of repeated migraines, treatments could take place before the process begins or in small steps after the recurrent spreading depression that underlies chronic migraine. While these factors may have negative effects in the short-term, in the long-term they prime the neurons to make antioxidants that are protective against oxidative stress.

“Spreading depression increases oxidative stress in a big fashion — it depolarizes all the brain cells. It’s like an engine kicking out a lot of exhaust, and the exhaust makes the brain hyper-excitable,” Kraig said. “But you have to let the engine run. The engine is running with stimuli that include cytokines that are initially irritative, but then adapt to stop spreading depression.”

The trick, Kraig said, is to mimic the natural cycles of cytokine levels the brain would experience during healthy, active behavior, rather than drowning the system in abnormally high concentrations of the factors that can occur with disease. The cytokines would be delivered to the brain in an on/off pattern rather than chronically, theoretically recreating the rise and fall of natural cytokines during a person’s sleep/wake cycle. By giving just a little bit of a factor normally considered harmful, the treatment could strengthen the brain’s resistance to spreading depression and migraines via the principle of hormesis, or “what doesn’t kill me makes me stronger.”

“The treatment is unique in that it’s the opposite of putting a Band-Aid on something,” Grinberg said. “It’s triggering cells to produce their own antioxidants instead of just providing the antioxidants exogenously. In that way it’s really unique and the opposite of how a lot of people think about medical treatment.”

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As the weather finally starts to get seriously cold, we thought this would be a good time to revisit our conversation with Dr. Ginard Henry on Cold Hands Syndrome. While it seems like your frozen fingertips could be fixed by simply wearing a good pair of gloves, Cold Hands Syndrome is a real medical condition caused by a range of different diseases that restrict blood flow to extremities. It can strike at any time, not just the dark days of winter.

For more, check out our four-part video Q&A with Dr. Henry:

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If you called someone a rat, they probably wouldn’t take it as a compliment. But in a clever new study published today in Science, a team of University of Chicago neurobiologists show that rodents could serve as role models for how humans should behave. Rats were given a difficult choice between heart and stomach: either open a container of chocolate chips and enjoy the feast, or free a companion and share the chocolate chip bounty. The results argue that humans aren’t the only species to feel empathy for the distress of another and act upon it, suggesting a deep evolutionary basis for helping your fellow creature.

When Inbal Ben-Ami Bartal was a master’s student in Israel researching immunosuppression after surgery, she noticed a strange phenomenon in her laboratory rats. When rats were brought to the room where she regularly conducted surgical procedures, they grew extremely agitated.

“It was very obvious that rats could sense what was going on with other rats,” Bartal said. “They freaked out and were affected by the emotional state of the other rats once they were removed from the cages.”

Other researchers had previously noticed this phenomenon in both humans and animals and gave it the name “emotional contagion,” describing when the distress or pain of one individual spreads to others. In 2006, Jeffrey Mogil of McGill University found evidence of this effect in mice, observing that when one mouse is given a mildly painful stimulus, a second mouse viewing the first mouse’s pain will exhibit increased sensitivity to pain. When that paper was published, it was considered by some to be the first evidence for empathy in a rodent. But Bartal, having started as a graduate student advised by Jean Decety, Irving B. Harris Professor of Psychology and Psychiatry at the University of Chicago, wanted to find more definite proof of rat compassion.

Collaborating with the laboratory of Peggy Mason, professor of neurobiology, Bartal designed a test to see whether emotional contagion could actually drive a rat to take action. Two rats who live together in the same cage were placed in a special arena, with one held in a transparent, tube-shaped restrainer and one allowed to roam free. The restrainer’s door could be opened by a nudge from the outside, though the free rat - at least initially - didn’t know that. But after several sessions where the free rat was visibly agitated by his trapped companion’s distress, he figured out how to pop open the restrainer. As you can see in this video from Science, once the free rat learned this trick, he would take action almost immediately upon being placed in the arena during subsequent sessions.

“We are not training these rats in any way,” Bartal said. “These rats are learning because they are motivated by something internal. We’re not showing them how to open the door, they don’t get any previous exposure on opening the door, and it’s hard to open the door. But they keep trying and trying, and it eventually works.”

Proving that the free rat’s actions were motivated by empathy required more experimental conditions. When the restrainer was left empty, or when researchers put a stuffed toy rat in the tube, the free rat showed no interest in opening the restrainer door. He did, however, when the arena was rigged so that opening the restrainer released the trapped rat into a separate compartment from the free rat, showing that the free rat was not motivated by the “reward” of social interaction. The experiments left behavior motivated by empathy as the simplest explanation for the rats’ behavior.

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By Matt Wood

Celiac disease is an inherited autoimmune disorder that affects the digestive process of the small intestine. When a person who has celiac disease consumes gluten, a protein found in wheat, rye and barley, the individual’s immune system responds by attacking the small intestine and inhibiting the absorption of important nutrients into the body. At least 1% of Americans, or nearly 3 million people, have celiac, but 97% of them are undiagnosed.

The University of Chicago Celiac Disease Center is an international center of excellence providing comprehensive patient and professional education, expert diagnosis and treatment for both children and adults, groundbreaking bench and clinical research, and active leadership in advocacy efforts. Their goal is finding a cure for celiac disease by 2026. We spoke to Dr. Stefano Guandalini, medical director of the Celiac Disease Center, about this unique, comprehensive research and treatment approach. We also discussed the link between celiac and diabetes, and asked pediatric dietitian Lara Field from Comer Children’s Hospital how people with both diseases manage their diets. Lara also discussed how children with celiac disease can learn to go gluten-free.

Medical students spend the first half of their education learning anatomy and physiology, and the second half applying that knowledge in the hospital. But where in that process do they learn the very important skill of listening and talking to their patients? In the panel discussion that followed yesterday’s announcement of The Bucksbaum Institute for Clinical Excellence, it was clear that even physicians who graduated from medical school decades ago remember exactly when and from whom they learned those important lessons. In some cases, that mentor was sitting just a few feet away, such as when Mark Siegler spoke of his time as a medical student learning from the now 102-year-old Joseph Kirsner.

“The way you learn medicine is by seeing, not by talking. You have to show what good care is about. I learned from studying people like Joe,” Siegler said. “Joe told us that everything was important, [including] science and clinical inquiry, but patients came first, patients were the absolute first priority.”

The Bucksbaum Institute, made possible by a $42 million pledge from The Matthew and Carolyn Bucksbaum Family Foundation, has borrowed that sentiment as its defining principle. Teaching bedside manner may not be as straightforward as teaching biology, but creating a system of mentorship can help experienced physicians pass lessons down to young and aspiring doctors. Perhaps with serendipity, the panel represented that kind of mentorship family tree, with Dr. Siegler seated next to his former trainee Holly Humprey, dean for medical education, and Dr. Humphrey adjacent to current Pritzker 4th-year medical student Rebecca Levine.

[Watch video of yesterday's announcement and panel discussion.]

Each panelist and speaker at the event talked about the doctor-patient relationship as a phenomenon under threat in the modern health care system. Though better tests, treatments, and procedures have saved and extended countless lives, an increased reliance upon technology can interfere with the “old-fashioned” methods of taking a good patient history and answering patients’ questions.

“We were always taught that 90 percent of the diagnosis in medicine was based on what the patient tells you,” said Kenneth Polonsky, dean of the Division of the Biological Sciences and the Pritzker School of Medicine. “There are tendencies on the part of physicians to rely more on technologies than on what the patients tell them, their interactions with patients, and what they learn at the bedside.”

It makes sense then to start with doctors-in-training, and the foundation of the Bucksbaum Institute is the financial support of three to five new medical students a year as Bucksbaum Student Scholars [read more on the Insitute's organization in the FAQ]. Because of the Pritzker School of Medicine’s reputation as a “teacher of teachers,” (30 percent of Pritzker graduates go on to faculty positions at academic medical centers, Humphrey said), the hope is that the emphasis on doctor-patient communication seeded at the University of Chicago will spread around the country.

“This gift allows our medical school to make a very public statement to our students at the time they are applying to medical school and then during their experience in medical school, that the doctor-patient relationship is fundamentally important in the education of a physician,” Humphrey said. “Then, upon graduation, our students populate schools across the country and carry on that Bucksbaum tradition wherever they go.”

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In the physician’s office, the communication between doctor and patient can be just as important as any medical exam or test. To set a patient on a healthy path, a doctor must explain diseases and treatments in a manner that is accessible and relevant to each individual. The conversation must also be a two-way street, with the doctor listening to the patient instead of merely lecturing. In the increasingly technical and hurried world of medicine, more and more of that critical interaction is lost to 10-minute appointments and physician switching.

To counter that trend, an exciting new institute was announced at the Medical Center this morning. The Bucksbaum Institute for Clinical Excellence at the University of Chicago will be made possible by a $42 million pledge from The Matthew and Carolyn Bucksbaum Family Foundation. The institute, inspired by the relationship between the Bucksbaums and their long-time physician Mark Siegler, will focus on how to improve doctor-patient interaction and train the next generation of doctors how to be advisers, counselors, and navigators for their patients.

“These generous donors have pinpointed a fundamental aspect of medical practice that deserves greater attention,” said Kenneth S. Polonsky, MD, dean of the Division of the Biological Sciences and the Pritzker School of Medicine at the University of Chicago. “They are giving us the resources to concentrate on training physicians who not only possess extraordinary technical knowledge but can work effectively with patients to reach the best clinical decisions.”

An announcement ceremony this morning will be followed by a panel discussion of the patient-doctor relationship and patient outcomes, with Siegler, dean of medical education Holly Humphrey, and Pritzker medical student Rebecca Levine participating. That event will be webcast live, and coverage will follow here on the blog this afternoon. In the meantime, you can read more about the institute at the New York Times, hear a story about it at WBEZ, and watch the official announcement video below.

Actin is the Lego of the cell. The small proteins can be assembled into many different forms for a wide variety of uses: serving as a scaffold to keep the cell’s shape, a railroad for shipping packages, or a powerful motor to propel the cell or tear it in half. But actin itself is a blank slate, an interchangeable material that needs guidance to do anything more than stick together in chains called filaments. To truly understand the Lego of the cell, you have to understand the factors that prompt it to form into its many useful conformations.

“The actin itself is boring. It’s just a building block,” said David Kovar, assistant professor of cell & molecular biology and molecular biophysics at the University of Chicago. “These filaments have to be assembled at the right time and place, they have to be organized with the right architecture, and the dynamics have to be correct - some structures are assembled and stable for minutes to hours, whereas others are assembled and disassembled on the order of seconds.”

Kovar’s lab studies actin-binding proteins, the cellular tools that shape formless actin into functional filaments. This area of research has exploded as scientists discovered multiple actin-binding proteins, each with their own unique properties. One element, the actin-related protein 2/3 complex (Arp2/3 for short), creates branches in the normally linear filaments. Another, called formin, attaches to the end of the filament and steps on the gas, causing it to grow at an accelerated rate.

Scientists have learned a lot about actin engineering by using a method called TIRF microscopy, which allows them to watch as actin filaments form, grow, and take shape. [A short video of Arp2/3-induced branching is available below.]

“This enables us to actually watch these things in real time, and it has revolutionized the field,” Kovar said.

In a new paper, published last week in the journal Nature Structural & Molecular Biology, Kovar’s laboratory and collaborators at the University of Pennsylvania eavesdropped on the activity of a newly-discovered class of actin-binding proteins, named for a shared feature called the WH2 domain. By studying one such WH2 domain protein, isolated from a water-dwelling bacteria that causes gastrointestinal problems in humans, the lab found themselves watching a new, chaotic kind of actin-forming behavior - akin to how a toddler might choose to play with Legos.

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Since the Roe v. Wade decision of 1973, abortion has been a woman’s legal right (with ever-changing state-specific restrictions) in the United States. But one factor often trumps the legal status of abortion: access. Though abortion training is required for medical residents studying to become obstetrician-gynecologists, physicians are not required to perform the procedure or even to refer a patient to a ob-gyn who will. That voluntary basis can create pockets of the country where access to an abortion provider is a larger obstacle than any legislation.

As a window into these access issues, a team led by Debra Stulberg, assistant professor of family medicine, conducted a survey of more than 1,000 Ob-Gyn physicians on their experience regarding abortion requests and providing the procedure. Their answers, published in Obstetrics & Gynecology, reflected how commonly ob-gyns are approached for the procedure - 97% of respondents said they had encountered patients seeking abortions. However, only 1 in 7 (14.4%) of those surveyed said that they had provided abortions themselves.

The data collected from other question on the survey allowed Stulberg and her colleagues to paint a picture of who was more or less likely to provide an abortion. Some of the results were unsurprising: female ob-gyns were more like to perform the procedure than men, those with strong religious beliefs were less likely to provide abortions, and those who worked at Catholic hospitals were very unlikely to provide the option to their patients. Geographically, ob-gyns from the Northeastern, Western, and urban regions of the United States were more likely to have performed an abortion, while those from the South, Midwest, and rural areas were less likely. That could contribute to large areas of the country where there are limited options for women seeking abortion - regions that happen to be where abortion providers commonly experience harassment, the authors note.

Breaking down the responses by age also reveals an interesting U-shaped curve. The most likely age group to provide abortions was ob-gyns 35 years or younger. But the second most likely were those aged 56-65 years old - the generation that was in medical school around the time of the Roe v. Wade decision. As that age group heads toward retirement, the number of abortion providers could drop even lower, the authors speculate, should the younger generation not pick up the slack. For responses to this data from both sides of this always polarized issue, see U.S. News & World Report. More coverage can be found at the Los Angeles Times, NPR, and the State Column.

Our New Facebook Home

Thanks to the hard work of our colleague Matt Wood, the Medical Center has a new Facebook page! The page will be updated daily with articles and videos about Medical Center care and research, including the occasional article from this here blog. If you are so inclined, please visit the page and click the all-important Like button.

Elsewhere…

It sounds counter-intuitive: burning the smooth muscle of the lung to improve symptoms for people suffering from severe asthma. But bronchial thermoplasty is a promising new procedure, and has worked for patients like swimmer Stephanie Manikas, featured in this CBS Early Show piece from Thursday. Manikas’ physician, the Medical Center’s Kyle Hogarth, has previously explained the procedure as part of ScienceLife’s Dr. FAQ series.

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The future of genetic medicine comes in many flavors, from the discovery of the rare mutations responsible for uncommon diseases to the cataloging of variants that may be responsible for common diseases such as high blood pressure and diabetes. A segment from last night’s ABC 7 Chicago news focused on both aspects of this potential, jumping from a young man in Utah with Miller Syndrome to the 1200 Patient Project of the Medical Center’s Mark Ratain and Peter O’Donnell. Results from the project, currently underway, could help physicians customize medical treatments for individual patients, maximizing effectiveness while reducing side effects. As the segment says, if we really are heading toward a future where every patient has their genetic code read as routinely as they receive a doctor’s check-up, such research will be essential for unleashing the power of genetic medicine.

When the media hypes the healthy effects of drinking red wine in moderation, they’re talking about resveratrol, the chemical responsible for wine’s benefits. Scientists have long tested whether isolating that chemical can turn it into a super-pill for good health and long life without the alcoholic “side effects” of its normal route, with mixed results. But a new study featured in the New York Times this morning finds an intriguing benefit of a resveratrol derivative called SRT-1720. Obese mice given the experimental drug lived 30 percent longer - as long as control mice - rather than expiring earlier from obesity-related diseases such as fatty liver and diabetes. As the article states, such a drug may represent “more a moral hazard than an incentive to good health,” seen by some as a way of avoiding the consequences of excess. But with trials of the drug in humans still in their earlier stages, the ethical discussions will have to wait on the science.

Since our piece remembering famed bio-statistician Paul Meier ran last week, two more fine obituaries of the UChicago professor emeritus have appeared. Read the Chicago Tribune take to learn what instrument Meier learned to play at the Old Town School of Folk Music, and the New York Times version for the context of how Meier changed randomization in clinical trials forever.

Living shoulder to shoulder (or even closer, on the subway) in an urban environment feels like a particularly modern phenomenon. But as friend of the blog Tim de Chant explains in his guest blog at Scientific American, human societies have concentrated themselves since even the prehistoric hunter-gatherer days. For more of Tim’s great writing on the science of population density, visit his Per Square Mile blog.

Stress can have all sorts of negative effects on your health, but what about the stress of your spouse or partner? Not Exactly Rocket Science looks at a study in finches that suggests a high-strung life mate could actually shorten your life.

Last November, a barrier was broken in the prolific Bollywood film industry of India. A film called Dunno Y featured the first on-screen male-male kiss - a provocative scene in a country that only the year before repealed a law making homosexuality illegal. Many tagged the film as India’s version of Brokeback Mountain, a controversial and progressive step in depicting male-male romance in popular culture that reflected a growing social acceptance of homosexuality. But the full significance of those cultural changes in the South Asian country have yet to be studied, and will require perspectives from law, anthropology, medicine, and more.

Just such a discussion will take place this Saturday morning at the University of Chicago and on the internet in the roundtable event, “Sexual Identity, Health and Stigma in India: Traditional Statuses and Western Influences.” Organized by John Schneider, assistant professor of medicine and epidemiology at the University of Chicago Medical Center and director of Global Health Programs, the discussion will be available worldwide on a webcast broadcast by the UChicago Facebook page, the Global Health Initiative website, and here on ScienceLife (watch this space).

“What I tried to do is bring together scholars from a number of different disciplines to make this a truly interdisciplinary discussion,” Schneider said. “I want it to be like a Sunday morning news program - but smarter - where a topic area is chosen and everybody fires away with their background about it, leaving room for remote viewer input.”

The central topic of whether sexual identity in India is truly shifting can be addressed from any number of angles. There’s the legal status of homosexuality after the 2009 repeal of Section 377 of the Indian Penal Code by the High Court of Mumbai. Or the sexual and mental health consequences after centuries of stigmatization of men having sex with men, including the spread of HIV and other sexually transmitted diseases. Or the pop culture ripples, such as Dunno Y, that may reflect changing attitudes and sexual roles in Indian culture. All of which are set against the backdrop of a country rapidly modernizing and playing an increasingly powerful role in global economy and society.

“I think that India is going through tremendous social and cultural changes as it emerges from what would be, in old terms, a less-developed economy to now becoming something of an economic powerhouse,” said Niranjan Karnik, assistant professor of psychiatry and behavioral neuroscience and another participant in the event. “This has the potential to really change the dynamics of the society and change the way people see themselves and behaviors.”

The participants in the roundtable are all accomplished researchers and experts on India. The keynote speaker, Lawrence Cohen of the University of California, Berkeley, studies medical anthropology in the country, and has written on homosexuality, aging, and organ transplant markets. Philip Kumar and Sanjay Srivastava are researchers based in India studying sexuality and advising the government on health issues related to men who have sex with men. Schneider himself has an extensive project underway in Indian truck drivers, where he is using cell phones in building a network of men who have sex with men to study their behavior and identify potential peer outreach points.

“One of the issues we are looking at is what changes in sex position roles might be occurring over time in India,” Schneider said. “Is a Western identity rubbing off on India, or is it developing a new identity? My work will help address those questions because of the cell phone network data that triangulates often sensitive self-reported data,” Schneider said.

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