Photo by John Amend/Cornell

I’ve always been fascinated with the rock solid bags of coffee bought at the store, which have all the density of a brick until opened, when they crumble into scoopable grounds. Turns out that’s a physical concept at work, known as “jamming transition,” when separate, particulate materials are pushed so close together they act like a solid structure. It turns out jamming transitions are useful for more than just compact packaging, but can also help solve a persistent, basic problem in robotics: how can you make a robot “hand” as good as the human hand at picking up objects?

An answer was published this week in the Proceedings of the National Academy of Sciences by researchers from the University of Chicago, Cornell University, and private company iRobot. The scientists created a finger-free “universal robot gripper” by filling a balloon-like elastic bag with particulate material - such as, yes, coffee grounds - pressing the bag down on to the object, then removing the air from the bag, triggering the jamming transition and creating a perfectly shaped, tight hold. There’s video below, demonstrating some of the objects and functions the device can be used for. But when will they be installed in prize claw machines?

[Coverage from Engadget, Gizmodo, and Wired]

Resurrection of the Beagle

The HMS Beagle was the Royal Navy ship that transported a very special passenger, a naturalist named Charles Darwin, around the world in 1831. What’s left of the ship may currently lie at the bottom of a marsh, but the name has lived on as a favorite for ambitious science projects. First, the Beagle name was attached to the Mars space probe Beagle 2, and now it has been affixed to the University of Chicago Computation Institute’s newest toy: a 150-teraflop supercomputer, one of the 50 fastest supercomputers in the world. Housed at Argonne National Laboratory, this Beagle will sail the seas of data produced by researchers in physics, biology, and medicine.

As discussed previously on ScienceLife, the next wave of science will be less about collecting data and more about actually doing constructive things with it. The Beagle’s maiden voyages will be to help projects such as the Membrane Protein Structural Dynamics Consortium, the UChicago-led effort to study the shape and function of cellular machines. Other immediate uses may be for genomics projects, where scientists have struggled to keep up with analysis of the data created by cheaper and cheaper gene sequencing technology. In the Beagle’s announcement, Conrad Gilliam, UChicago’s dean of research for the biological sciences division, looks forward to a time when electronic medical records provide valuable data for the development of more effective treatments.

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Racial disparities might seem to be an abstract, hard-to-visualize concept. But at least in Chicago, it can be simply portrayed with a neighborhood map. The picture at left is for violent crime in 2005, but if one inserted statistics for infant mortality, diabetes, obesity, or other health issues, roughly the same pattern would repeat.

This clustering of negative attributes in Chicago neighborhoods has been observed and studied since at least 1945’s Black Metropolis, a landmark sociological study of the South Side. Subsequent studies, such as the 1965 Moynihan Report and more recent observational research, have found the same concentrations, even if their exact locations have drifted south and west in the city. The sad persistence of that pattern raises two questions, one immense, one naive: what can be done to break the tragic cycle of these neighborhoods, and why don’t the people in those neighborhoods just move out?

In “The Social Reproduction of Health Disparities,” his talk in the MacLean Center for Clinical Medical Ethics seminar series, Harvard sociologists Robert Sampson addressed those two questions with a unique data set: the Chicago Neighborhoods Project. A longitudinal study that is following 6,500 children across the Chicago area, the project is producing reams of information about the structures of neighborhoods and how they affect the people within. It’s the kind of data that takes decades to sort through, but Sampson gave attendees a taste of how neighborhoods choose people, rather than the other way around.

The project, more formally called the Project on Human Development in Chicago Neighborhoods, tracked the children and their environments from 1995 to 2002. That involved not only surveying the children and their families at three different time points, but also measuring characteristics of their home neighborhoods. Researchers videotaped Chicago streets to measure aspects of social disorder such as graffiti and broken windows, and conducted unusual field experiments such as dropping fake letters in the street to see how many were returned to a mailbox by a neighborhood’s residents.

“The idea was we’re going to study individuals and follow them through time, but we’re also going to independently assess their context,” Sampson said.

When researchers looked at their neighborhood data, they didn’t find immobility; in fact, nearly half of their subjects moved over the 7 years of data collection. But deconstructed statistically, those movements were far from random, falling into regular networks along the lines of income, education, and racial factors. The nature of mobility is socially driven, Sampson said, putting restrictions on the ability of an individual to control their “escape” from neighborhoods with failing structures.

“Yes, you’re sorting, but neighborhoods are also sorting you. The idea that we are the controlling factor is a bit misleading,” Sampson said.

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When the novel H1N1 flu virus began to appear in North America and Europe in Spring 2009, it contained some worryingly familiar signs to flu experts. The new strain appeared suddenly in a season when flu typically declines, spread at a rapid pace, and seemed to disproportionately affect the young more than the old. The last influenza to display those features was the notorious 1918 flu, which killed as many as 100 million people around the world before burning out a year later.

“It was the most devastating infectious diseases episode in world history,” said Michael David, Instructor of Medicine at the University of Chicago Medical Center. “In numbers, it was probably 10 to 100 times more severe in terms of the absolute number of people killed than were killed in The Black Death.”

Of course, last year’s H1N1 pandemic was nowhere near as deadly, causing only an estimated 12,500 deaths in the United States despite approximately 60 million infections. The low mortality among elderly populations from H1N1 may have actually made the 2009-10 flu season less deadly than usual, as the Centers for Disease Control and Prevention estimate a yearly average of roughly 36,000 influenza deaths. But comparing 1918 to 2009 still reveals interesting similarities, David said in his October 14 talk at the Department of Pediatric Grand Rounds.

In the spring, when the virus first showed up on public health radar as a novel strain with all the right ingredients for a pandemic (jumped from animal to human, easily transmissable), the worst case scenario of 1918 couldn’t be ruled out. Like the 2009 strain, the 1918 influenza also made a relatively modest appearance in the spring, David said - graphs of the pandemic’s death rate revealed a small spike in the summer. Come October, that mild hill was overwhelmed by the shocking spike of influenza deaths that raged across the United States and Europe. In 8 weeks, 25 million people were infected with the virus, and some 600,000 died - in the U.S. alone.

“That’s more than the number of soldiers that were killed on both sides in the U.S. Civil War,” David said. “It’s something that’s really hard for us to grasp with our imaginations.”

[If you have a JAMA subscription, you can read this 1918 first-hand account of the pandemic at Cook County Hospital in Chicago - "During the past five weeks, more than 2,000 patients were admitted to the hospital. The disease is highly contagious and the mortality among our patients has totaled 31 percent. The epidemic has seriously crippled the medical and most especially the nursing staff of our hospital."]

In addition to its ferocious spread and mortality rate, the 1918 influenza was also unusual for the victims it chose: 20 percent of the deaths were in children under the age of 5, and 15 percent were between 20 and 25 years old. The line formed by these two mortality peaks combined with deaths in the elderly formed the pandemic’s characteristic “W curve” (pictured above), in contrast to the usual “U curve” seen when only the very young and old die from influenza.

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The common wisdom about kicking an addiction is to “isolate and conquer.” People trying to give up smoking, or coffee, or something more serious, are usually advised to stay away from reminders of their drug, such as other people smoking, the smell of coffee, or other cues that might remind them of their habit. Taken to its extreme, this isolation policy is the backbone of inpatient drug treatment programs, which remove an addict from their environment and away from addiction “triggers” for 30 days or more. At the hospital, addicts can safely pass through withdrawal symptoms, receive psychiatric care, and return to society equipped to resist the siren call of their vice.

However, research in animals throws a wrench into that theory of addiction treatment. In animals taught to hit a lever to receive addictive substances such as cocaine, heroin, or sucrose, an extended period of abstinence away from drug-related cues produces an unintended effect. Rather than decreasing the animals’ response to the cues (which in the world of a rat’s cage is usually a light or a sound rather than an ashtray or a syringe), longer periods of abstinence inspire a more robust and energetic “relapse” of lever-pressing.

This “incubation effect” suggests that the longer addicts stay away from their drug, the more likely they are to succumb to a relapse when they see or smell a drug-related trigger. But that idea had not been translated from rats to humans until an experiment performed by Gillinder Bedi and colleagues in the laboratory of Harriet de Wit, professor of psychiatry at the University of Chicago Medical Center. Published last month in the journal Biological Psychiatry, the experiment shows the first evidence that incubation of drug cues also occurs in humans. Further, their results suggest that current treatments for addiction may miss, or even run counter to, an important cause of relapse.

“Many factors contribute to relapse,” de Wit said. “One is the presence of withdrawal symptoms, the other is just the immediate difficulty of removing a habit that you had. But there might be this other factor, incubation, that grows over time without dissipating, at least for weeks or perhaps months.”

In Bedi’s experiment, cigarette smokers were paid $30 a day to abstain from smoking for as long as 35 days. As testament to the allure of nicotine, only half of the subjects recruited for the study reached their smoke-free target despite the financial rewards, de Wit said. The participants who did successfully abstain until their goal (7, 14, or 35 days) returned to the lab where they were exposed to either smoking-related cues (pictures of people smoking, lit cigarettes, ashtrays, etc.) or neutral cues or a matched show of neutral, non-smoking cues. To enhance the sensory experience, subjects held a lit cigarette while viewing the smoking cues or a pencil during the neutral session. Before and after the cues, subjects completed surveys to report how strongly they craved cigarettes.

Before the slide show sessions, participants reported expected, positive results of quitting: withdrawal symptoms and craving decreased with the more days since their last cigarette. But after viewing the parade of cigarette-related images, the opposite effect was observed. Subjects assigned to the group that abstained from smoking for a longer period of time (35 days) reported more cue-driven craving compared to those who only abstained for 7 or 14 days.

That looks a lot like the incubation effect seen in rats, and according to de Wit, may actually be an even more impressive effect than what was seen in animal studies. Whereas rats can be kept totally isolated from drug cues for as long as necessary, the subjects in Bedi’s study were presumably exposed to some smoking-related cues - friends smoking, cigarettes in movies, etc. - during a typical day of their paid abstinence. Yet in the laboratory, the cues still held the power to spark craving, and this craving increased with the number of days of abstinence. In a further surprise, most subjects returned to their smoking habits after their part in the research was finished, regardless of how long they had abstained from smoking for the study.

“I think one of the really interesting things is that almost everybody goes back to smoking, even after a month of not smoking,” de Wit said. “You would think if they could go drug-free for a month it would be pretty easy to stay quit after that, and yet they went back.”

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Designing a trial for the treatment of cancer is hard. Designing a trial to prevent cancer is even harder. In a typical population, such a small percentage of people will naturally contract a particular type of cancer that to test the ability of an intervention to reduce that number may require tens of thousands of subjects to be followed for decades. That’s not a cheap, or easy, study to run.

But in a population where the risk for a particular cancer is elevated, a prevention study might be both possible and immediately helpful. One such situation is found in the unfortunate case of Bangladesh, where charity efforts in the 1970’s to provide pathogen-free sources of drinking water accidentally exposed 40-70 million people to water tainted with arsenic. The disease epidemiology of that long-term exposure was recently characterized by Habibul Ahsan, director of the Center for Cancer Epidemiology and Prevention at the University of Chicago Medical Center, whose HEALS study found increased mortality and cancer in a study of more than 20,000 people.

In addition to characterizing what has been called “the largest mass poisoning of a population in history,” Ahsan has also been leading a study to try and offset some of its damage. The Bangladesh Vitamin E and Selenium Trial, or BEST, is testing two inexpensive nutritional supplements for their ability to prevent the non-melanoma skin cancer (NMSC) that commonly develops in people exposed to high levels of arsenic. The study, which recently received a $10 million renewal from the National Institutes of Health, has a twofold purpose, Ahsan explained.

“In the short term as well as unfortunately the long term, these people will be at an increased risk for arsenic-related cancers,” Ahsan said. “What we can do on the biomedical side, beyond solving the arsenic-contaminated water problem, is to identify low-cost, pharmacological or dietary/nutritional interventions. Something we can provide to these people that is feasible for millions of people at risk to take and reduce their future risk of these cancers.”

Like Ahsan’s HEALS project, the BEST study is massive in scope. In the first five years of the trial, roughly 7,000 Bangladeshi subjects were recruited and sorted into one of four groups, each required to take one pill a day for 6 years. Depending on the group, each subject will take a daily dose of vitamin E, selenium, vitamin E and selenium, or a control pill, with researchers tracking the amount of skin cancer, mortality, and other adverse events that develop by the end of the study.

Even at that size, the trial is smaller than it would be in a less vulnerable population. Because of the increased risk for NMSC among Bangladeshis exposed for decades to arsenic, a chemoprevention trial can operate with fewer subjects, Ahsan said. The infrastructure built by Ahsan’s team in Bangladesh (with collaborators at Columbia, Dartmouth, and the University of North Carolina) also saves money and ensures high compliance rates. More than 300 staff members have been hired to visit each subject on a daily basis to make sure they take their pill and to observe any side effects or illnesses.

“That’s something that’s impossible to do here,” Ahsan said. “It’s an expensive trial, but it’s a fraction of the cost had we conducted this trial here in the United States.”

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A cell’s DNA is its most valuable treasure. So it only makes sense that cells keep their genetic material protected under lock and key, wrapped tightly around spools called histones. When it’s time to make proteins from their DNA recipes, the right bit of DNA is unraveled so that the cell’s transcriptional machinery can gain access to the correct genes. But the process of spooling and unspooling the DNA is under tight security, controlled by a complex array of enzymes and signals attached to the histone’s tail.

Studying this security system is an important part of epigenetics, the growing field researching the many factors that control gene expression. Where the basic components of DNA were figured out by Watson, Crick, Franklin and their successors in the 20th century, the proteins and enzymes involved in epigenetics are still largely unknown. With dozens of enzymes that each recognize their own unique combination of signals moving in and out and changing conformation, it’s a fluid, complicated system that’s hard to pin down using traditional techniques.

But the laboratory of Anthony Kossiakoff, professor of Biochemistry and Molecular Biology, thinks it might have the method to help crack part of that epigenetic code. With a new grant totaling $7 million over 5 years from the National Institutes of Health (part of their Protein Structure Initiative), Kossiakoff and colleagues will apply their Chaperone-Enabled Biology and Structure (CEBS) technology to the complex riddle of how dynamic regulation of histone modifications regulate gene expression.

Scientists have long used the specificity of the immune system’s antibodies to create reagents that recognize and tightly attach to a target protein. Once captured, that reagent can help researchers look at the location abundance of their target in the cell. But the “natural” method of creating antibodies, by essentially tricking the immune system of rabbits or mice into producing the highly specific antibody you need, is expensive and may not always produce antibodies that work as advertised.

“Over half of those you buy don’t work, others work maybe for one application but not another that you want, and so it’s buyer beware,” Kossiakoff said.

Kossiakoff’s CEBS technology produces customized antibody-like reagents called synthetic affinity binders, or sABs, created via a process called phage display mutagenesis - akin to “evolution in a test tube.” Billions of synthetic antibody-like proteins compete for their ability to bind with high affinity and specificity to a chosen target. Instead of having the very few candidates produced by traditional monoclonal antibody production , the CEBS selections can generate as many as fifty different “synthetic antibodies” that can be used as highly specific reagents. Over the last five years, the laboratories of Kossiakoff, UChicago’s Shohei Koide, and Sachdev Sidhu of the University of Toronto have refined that process and established a pipeline where super-specific reagents can be created for virtually any stable protein a researcher would like to study.

As part of the Protein Structure Initiative, the laboratory will become what Kossiakoff called a “mothership” for research on histone modification enzymes, producing sABs useful in studying their structure and function. Some of those reagents will be used for experiments in Kossiakoff’s lab, others will go out to biologists and structural biology collaborators around the world. One goal is to generate sAB reagents to act as “crystallization chaperones” to enable the “freezing” of complex proteins for crystallization structural studies - a task that has proved difficult to impossible previously.

“Proteins are dynamic, and they can be floppy, especially if they have multiple domains, as is the case for these histone modifying enzymes” Kossiakoff said. “So many times, even with heroic efforts, you can’t crystallize them to study.”

Previous studies have succeeded in characterizing small stretches of the enzymes, but not all the domains together. Capturing the entire organization of the enzyme rather than one section at a time is an important leap forward, due to their complexity - each enzyme must read several different positions on a histone simultaneously to determine whether or not to bind and activate. It’s a flurry of activity, like a janitor with a full key ring trying to unlock three different doors at once.

“These interactions are pretty transient, on and off, on and off,” Kossiakoff said. “By having all the domains clicking into the right place, binding becomes additive. It literally is a trial and error process, and there is just so much stuff going on.”

Slowing down this whirlwind long enough to determine these complex structures could lead to new insights and understanding into how histone modifications regulate gene expression. The enzymes themselves are also major targets for drug discovery - for example, certain forms of cancer have been traced back to errors in histone modification. Some potential drugs could even be derived from the sABs, with more precise targeting than the “dirtier,” less specific compounds currently used in most pharmaceuticals. With the keys to the DNA’s security system unlocked, laboratories developing new drugs could save far more money than the amount invested by the NIH in this grant.

“One of the major shortcomings in drug development is defining what the actual target is,” Kossiakoff said. “There are many cases where drugs have been produced that worked perfectly based on what was attempted to be done, but they don’t work in terms of what they were supposed to do. We can test things out before a lot of time and money are spent developing these drugs against incorrect targets.”

Yesterday we talked about how Kathleen Cagney’s research appeared to reveal an effect of the 9/11 terrorist attacks on the body mass index of people more than a thousand miles away in Dallas. By coincidence, Discover magazine published a book excerpt (from “Origins: How the Nine Months Before Birth Shape the Rest of Our Lives” by Annie Murphy Paul) yesterday that touches on how the fall of the World Trade Center might have caused post-traumatic stress disorder not just in people near the towers that morning, but also the fetuses being carried by pregnant women near the towers. Can PTSD be transmitted from mother to unborn child? And did 9/11 leave a wide swath of medical impact across the country? Fascinating research.

Oh cruel search for alien habitable worlds: new data released at an astronomy symposium this week appears to refute the existence of Gliese 581g, the “Goldilocks” planet that had everyone daydreaming of intergalactic travel two weeks ago. Though the debate over the planet’s existence is far from settled, it’s a quick, nasty reminder that leaping from a handful of data points to bold claims of Earth-like planets and alien life is a dangerous gamble. (Also, Google News hits for original Gliese 581g story = 1407 articles. For the “Gliese 581g may not exist” story = 91.)

As part of the “It Gets Better” campaign reacting to the recent run of tragic suicides by homosexual teenagers, Scientific American’s psychology blogger Jesse Bering begins a long, detailed look at the evolutionary history of suicide. Why would an organism evolve the capacity to kill itself? Bering dials down to insects that are cannibalized after copulation and explains a mathematical equation for suicidal motivation in the first part of his series.

If University of Chicago evolutionary biologist Jerry Coyne is too prolific for you on his blog, Why Evolution is True, you can get a primer on his views regarding the incompatibility of science and religion from his USA Today editorial this week. There were, of course, letters,  and a blog response from Albert Mohler of the Southern Baptist Theological Seminary.

An in-depth Reuters article about the increasing use of cardiac assist devices and the end-of-life ethics questions they raise talks to our chief of cardiac and thoracic surgery Valluvan Jeevanandam, among other experts. For more on the topic, see our post on ethicist Daniel Sulmasy, who has written about when it is ethical for physicians to turn off a person’s cardiac device, knowing that it may hasten death.

It’s well established that environment can influence a person’s weight as much as their genes or their behavior. For people growing up in inner city environments where fast food restaurants and liquor stores far outnumber grocery stores with fresh food options, it’s a struggle to piece together healthy meals on a consistent basis. But beyond “food deserts,” can a person’s neighborhood also influence their weight and their health in more subtle ways? Could less tangible factors such as crime rates and community networks contribute to the health disparities of race and socioeconomic status?

University of Chicago researcher Kathleen Cagney and Christopher Browning of Ohio State University set out to answer those intriguing questions by merging enormous data sets of health information and crime rates. The results of that study, presented by Cagney on October 6 at the MacLean Center Seminar Series, suggested that a person’s social surroundings - and the local police blotter - can exert a great influence on their health and fitness.

Cagney and Browning started with the Dallas Heart Study, a survey of thousands of residents of the Texas city on parameters relevant to cardiovascular heath. Focusing on one measure - body mass index, or BMI - the researchers then plotted the data against changes in local crime rate from police data for each patient, focusing in particular on short-term “crime spikes.” The hypothesis was that an increase in crime nearby the person’s home could produce stress and discourage outdoor activity, leading to less exercise, increased consumption of unhealthy “comfort food,” and activation of the hormonal “fight-or-flight” response.

“If something changes dramatically in your environment or in your community, you can imagine that your life behaviors and patterns would change in concert with that,” Cagney said.

After controlling for several other factors (a necessity for so broad a research question), Cagney said a significant effect of crime spikes on BMI was found for one group: women. Females from neighborhoods that had experienced the largest increase in crime over the past six months experienced a rise in BMI, equivalent to roughly a 2.7-pound weight gain for a typical 130-pound person. The weight of men in the study was found to be slightly sensitive to the overall crime rate in their neighborhood, but not the short-term dynamics of crime spikes, Cagney said.

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RN Debbie Pienta of the Student Care Center at the University of Chicago gives a flu shot. (Photo by Yvette Marie Dostatni)

Until last year, the advent of the new influenza season was a pretty routine event on the health care calendar. Around October, people would be urged to receive vaccinations against the viral strains expected to plague North America in the coming months, with young children and older adults encouraged more strongly to get their annual shot. Other folks received their vaccine with all the enthusiasm of a trip to the dentist - something you know is good for you, but not exactly an urgent concern.

That all changed last year, thanks to the novel H1N1 virus, aka swine flu, aka the global flu pandemic. Suddenly, seasonal flu clinics used to a slow trickle of customers were faced with lines out the door and around the block, as the combination of limited H1N1 vaccine supply and media hysteria created unusual demand. Caught short by the late-breaking new strain, suppliers had to prepare a separate vaccine for the H1N1 virus, requiring people to get stuck with a needle twice for full protection.

The good news heading into the 2010-11 flu season is that many of those logistical headaches have been resolved. With no new strains rearing their head since last year, vaccine makers were able to consolidate protection against H1N1 and two seasonal strains into one injection or nasal spray. The Centers for Disease Control and Prevention recommendations have also been simplified: all people above the age of 6 months are advised to get the flu vaccine, full stop. All signs this season also point to better preparedness across the board from government and private organizations dispensing the vaccines - local Walgreens in Chicago were advertising vaccine availability well in mid-September.

To raise awareness of vaccine availability on the University of Chicago campus, ScienceLife talked to two of our flu experts: Stephen Weber, medical director of infection control at the Medical Center, and Ken Alexander, chief of pediatric infectious diseases. Here’s a few of their answers about this coming flu season and the research taking place one year post-epidemic.

Q: If 2010-11 is expected to be a routine flu season, what does that mean?

Weber: A regular flu season doesn’t mean that it’s easy or that people don’t get sick. We have to remember that while flu is a very common illness, folks who are not vaccinated are at an increased risk.

In many resepects we return to our usual state of flu awareness and preparedness. Bearing in mind, we are talking about infections that kill 24,000 Americans each year, and that’s not something that we want to neglect or that we want to be anything but vigilant about. We have an opportunity to save lives, and whether it happens to be a pandemic or a seasonal year, we still have an important responsibility.

Q: Why is it especially important for parents of infants to be immunized against flu?

Alexander: It’s the notion of a “cocoon.” The idea here is that babies under 6 months don’t respond well to flu vaccine, so we don’t get give shots. So you have this window of vulnerability, and babies are at high risk. With cocoon immunization, if can’t immunize the kid, we can immunize everybody around the child.

There are good data on pertussis transmission to babies, that they receive the virus one-third of the time from the mother, a quarter of the time from dad, and a quarter from their grandparents. Flu is probably pretty much the same, and the idea is we can protect them if we immunize people around the baby.

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There’s much conversation in the medical world today about how to use technology to improve health care and reduce unnecessary costs. Companies are currently racing to develop electronic medical records systems that promise to use the latest in database, encryption, and artificial intelligence programming to make medicine more efficient. But what about a form of computer technology that is much less cutting edge, so much so that even computer-shy grandmothers have embraced it?

The idea of incorporating e-mail communication into the doctor-patient relationship is far from novel, but has yet to gain a solid foothold in the health care community. Though many of us have been e-mailing at work and home for nearly two decades, a recent survey found that less than 7 percent of physicians routinely e-mail with their patients. Data shows that most patients would like to have e-mail access to their physician, and the benefits of quickly dealing with minor tasks such as prescription refills and test follow-up through the cheap form of e-mail are clear. But the survey’s results reflect the skepticism of many physicians about e-mail due to concerns about privacy, liability, compensation, and effectiveness.

Both the risks and benefits of medical e-mail communication were discussed last week at the University of Chicago Department of Medicine Grand Rounds, in a talk by visiting speaker Bernard Lo. A general internist at UCSF and director of their medical ethics program, Lo said he had fully embraced the potential of e-mail communication with patients in his practice. But that doesn’t mean he hasn’t encounter its limitations, from patients who over-use the channel to the lack of non-verbal cues from less-forthcoming patients.

For any doctor who has wasted time playing phone tag with a patient (read: all of them), e-mail should be a godsend for straightforward and simple questions, Lo said. Prescription refills, questions about medication dosage or minor side effects, and questions about referrals or appointment changes can be easily dealt with by the physician or an assistant when time allows, rather than trading voicemail messages. Lo said the more casual format of e-mail can sometimes draw out information from the patient that they may have hidden due to the stress of a visit to the doctor’s office. For some patients, talking about sensitive issues such as depression or sexual issues may be easier on  a computer screen than face to face, he said.

Of course, not every medical issue can be easily dealt with over e-mail. Lo said he makes sure his patients know to call the clinic if they need an immediate answer, or 911 if they have an emergency. But many issues fall into a gray area where it’s not clear that e-mail is the appropriate way to respond. One example Lo presented to the audience was a patient who wrote about a brief flash of chest pain and her brother’s history of heart problems. Clearly, she needed to be booked for a cardiac evaluation as soon as possible, but Lo said that a crucial part of the medical response was also addressing the patient’s anxiety about her health - something the impersonal medium of e-mail might not be equipped for.

“I know she’s worried, and how do I deal with that in an e-mail?,” Lo asked.

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This past week has been Nobel Prize week, and while none of the winners so far have had a University of Chicago connection (unlike last year’s trio), it’s still good fun for science spectators. Trying to divine a common theme from all of a year’s winners is probably futile - the selection process at the Royal Swedish Academy of Sciences is still pretty mysterious, and doesn’t seem to follow any consistent logic in the laureates it spits out. This year, the Thomson Reuters predictions - considered by many to be the best - have produced an ohfer so far, despite throwing out anywhere from 4-7 names for each of the prizes. The 2010 list is typically scattershot, with a mix of established science and science with yet unrealized potential; the only theme I can pick up is “non-American.”

Medicine: Occasionally, the Nobel committee is accused of waiting too long to award a prize. This year’s award in physiology or medicine, awarded to British scientist Robert G. Edwards for his work on in vitro fertilization, may fit that charge. The first baby produced by IVF procedures developed by Edwards and colleague Patrick Steptoe was born more than 30 years ago, on July 25, 1978. Since then, over 4 million “test tube babies” have been born to parents who would not otherwise have been able to have children. It’s kind of amazing, then, that the leaders of IVF had not previously been awarded the Nobel Prize - and sadly, Steptoe did not live to receive the honors, having died in 1988 (Nobel rules forbid posthumous awards). According to media reports, Edwards himself is in poor health and was unable to grant interviews about winning the award. Of course, the Vatican had its own criticisms of the winners.

Physics: Rather than rewarding a scientific discovery several decades after the fact, this award was given to science that, according to many experts, hasn’t yet ripened. Russian scientists Andre Geim and Konstantin Novoselov were recognized for the development of graphene, an extremely thin and extremely strong material thought to be useful in everything from solar panels to satellites. The emphasis is on “thought to be,” because the material was only discovered in 2004, and has yet to be incorporated into a commercially available product. Interestingly, the main gripe here was that it may have been more appropriate for the chemistry Nobel rather than the physics prize. Geim also notably becomes the first scientist to win both the Nobel Prize and its illegitimate brother, the Ig Nobel Prize, which he won for his research on levitating frogs.

Chemistry: If this were a fairytale, this prize would seem to be not too stale, not too fresh, but just right. Richard Heck, Ei-ichi Negishi, and Akira Suzuki each have an organic chemistry reaction that bears their name, and are considered to have laid important early groundwork for the burgeoning field of molecular engineering. The trio invented and refined the art of “palladium-catalyzed cross-coupling,” which finds a way to stick formerly contact-shy carbon atoms together. While the process is not exactly a household name, its impact is felt in medicine cabinets around the world. “Cross-coupling methods are now used in all facets of organic synthesis, but nowhere more so than in the pharmaceutical industry, where they are used on a daily basis by nearly every practicing medicinal chemist,” organic chemist Eric Jacobsen told ScienceNOW.

Elsewhere…

In the same issue of Archives of General Psychiatry where Daniel Le Grange’s study of family-based anorexia treatment was published, another Medical Center study probed the link between ADHD and teenage suicide. A study of 125 children diagnosed with attention deficit hyperactivity disorder between 4 and 6 years of age were three times as likely to attempt suicide between ages 9 and 18, compared to a control group of non-ADHD children. “The importance of this study is simply that it confirms that ADHD in children is not something to take lightly,” lead author Benjamin Lahey, professor of epidemiology, told WebMD.

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When long-hidden information about U.S. syphilis experiments on Guatemalan prisoners in the 1940’s surfaced last week, the shocking case contained echoes of the infamous Tuskegee study. Conducted from 1932 to 1972, the Tuskegee syphilis experiment followed African-American sharecroppers with the disease, and gained notoriety for withholding antibiotic treatment from the men in order to study the disease’s “natural progression.” The damage left by this unethical research persists to this day as an example frequently cited by minority communities distrustful of medical research.

“Most folks in the black community who know very little about research know about the Tuskegee study,” said Rick Kittles, in his Sept. 29 MacLean Center seminar “Race, Biomedical Research, and the Politics of Trust.” “It’s as if it was imprinted in our genes. There’s no Sunday morning breakfast discussion about it, but we know about it. We know something bad happened. We know that we were exploited. It has some serious implications still today.”

Indeed, the shadow of Tuskegee looms large over modern efforts to reduce the growing health disparities in the United States between Caucasian and minority populations, said Kittles, an associate professor at the University of Illinois School of Medicine. Many factors contribute to health gaps on parameters such as obesity, diabetes, and cancer: genes, socioeconomic status, environment, behavioral and cultural practices, and discrimination. But attempts to study any of these factors in the hope of reducing disparities must face the troubled history of research on the undeserved. As researchers find new ways to improve health, from advanced genetic medicine to improving access to fresh food with weekend farmers markets, community involvement is essential for such measures to close the disparity gap instead of further widening the distance between haves and have-nots.

“As this new technology and information is emerging - new treatments and intervention that could hopefully eliminate disparities - if [the community] is not involved, they’re not going to accept it. You have to bring them into the mix,” Kittles said.

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Losing weight can be described at its simplest as a matter of counting calories during the daytime. Consume fewer calories and burn more through activity and exercise, and you’re likely to lose weight. Eat more high-calorie foods and sit on the couch all day watching football, and you get the opposite effect. But according to a new study from University of Chicago Medical Center researchers, another number should be taken into account by dieters: hours of sleep.

Given people generally do not eat or exercise while asleep (aside from some Ambien users), the link between weight and sleep may seem unlikely. But previous research at the University of Chicago found that sleep loss can wreak havoc with a person’s endocrine system, the hormones that control appetite and metabolism. In a 2004 study, men limited to only four hours of sleep a night reported increased appetite and showed hormonal changes consistent with increased hunger - increased ghrelin, which signals hunger, and decreased leptin, which signals satiety. But the long-term influence of those sleep pattern changes on weight gain or loss remained to be studied.

Monday, an experiment testing that connection was published by Plamen Penev, assistant professor of medicine, and colleagues in the Annals of Internal Medicine. And this was no easy experiment: 10 subjects had to spend two 14-day periods essentially living in a laboratory, so that scientists could control their diet, their daily activity, and the amount of sleep. But the small study reached a compelling, unexpected conclusion.

On the surface, the results may look disappointing. Subjects were allowed 8-1/2 hours in bed during one two-week period, and limited to 5-1/2 hours in bed the other two weeks. Diet and exercise were kept the same between the two periods, so that the effect of sleep alone could be isolated. But when the researchers looked at weight loss during the two periods, it was almost identical. Subjects lost about 3 kilograms, or 6 pounds, over the two weeks, whether they were getting a long night’s sleep or the reduced amount.

But not all weight loss is created equal. When the researchers looked more closely at what kind of weight was lost over the two-week periods, an important difference was revealed. With adequate sleep time, more than half of what was lost was fat. But when sleep was limited to less than 5-1/2 hours, only a quarter of the lost weight was due to reduced fat, suggesting that important protein and muscle were being shed instead of unsightly flab.

“If your goal is to lose fat, skipping sleep is like poking sticks in your bicycle wheels,” Penev said. “Cutting back on sleep, a behavior that is ubiquitous in modern society, appears to compromise efforts to lose fat through dieting. In our study it reduced fat loss by 55 percent.”

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It’s great to have a treatment that’s proven to work in a difficult psychiatric condition such as anorexia nervosa. It’s even better to have two treatments for such a disorder. But having multiple options also creates a quandary for psychiatrists: with a new patient, which treatment do you try first? Creatures of habit like the rest of us, many doctors will simply stick with the method they know best until given convincing evidence that it’s worth switching gears. To be the new treatment of choice, a method must beat out the current champion in a head-to-head battle.

One such comparison, conducted by researchers at the University of Chicago Medical Center and Stanford University, was published yesterday afternoon in the Archives of General Psychiatry. The trial compared the most common form of treatment for adolescents with anorexia, known as adolescent-focused therapy (AFT), with the newer, family-based treatment (FBT), also sometimes known as the Maudsley Approach. The latter name comes from the Maudsley Hospital in London, where Daniel Le Grange, now director of the Eating Disorders Clinic at the University of Chicago, helped develop a new approach to bringing anorexic teens back to healthy weight and eating habits.

Under adolescent-focused therapy, the therapist works directly with the patient on a one-to-one basis, emphasizing the importance of weight gain and helping them accept personal responsibility for healthy eating. Family-based treatment, as you might expect from the name, does more to incorporate the parents into that process, equipping the patient’s mother and father with the tools to encourage healthy eating at home. By doing so, the therapist hopes to avoid hospitalizing the patient while permanently adjusting the home environment, removing factors that could lead to relapse after therapy is completed.

“No one is more available to care for the kids than the parents are; no one would put the time aside in the way that parents would, and no one loves their kids more than parents do,” Le Grange told NPR’s Morning Edition (where you can also hear the perspective of one patient’s mother on family-based treatment).

The two therapies had been compared previously, but in smaller studies with only two or three dozen patients. True convincing evidence requires a randomized trial, with enough patients for the statistics to make a strong case for one of the treatments. So, combining forces between Chicago and Stanford, Le Grange and his collaborator, James Lock at Stanford, were able to gather 120 patients with anorexia nervosa (with an average age of 14-1/2) for the study.

Split evenly between FBT and AFT, the patients were followed for a year of therapy and another year of follow-up. At the end of treatment, 42 percent of those enrolled in FBT showed full remission back to at least 95 percent of expected body weight, compared to only 23 percent of those enrolled in AFT. While that comparison fell just short of statistical significance, with a p-value of .055, Le Grange said that the higher standards used in the study spoke to the effectiveness of FBT.

“We used the higher yardstick for remission of 95 percent of body weight, which we felt was clinically more appropriate,” said Le Grange, a professor of psychiatry and behavioral neuroscience.

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Among evolution’s best tricks is the act of turning one species into two. Speciation, the foundation of a new species from an accumulation of small changes in an old one, has given birth to the incredible diversity of life on our planet. But in order for a new species to be founded, a sort of genetic restraining order must be put in place. Within a species, individual organisms can evolve extraordinary differences without spawning a new species - think dog breeds, for example. It’s only when two organisms grow so different that they lose the ability to come together and successfully reproduce, that a new speciation event can be declared - think the lion, the tiger, and the sad, sterile liger.

The nuts and bolts of speciation have given headaches to evolutionary biologists all the way back to the very first one. In his books, Charles Darwin laid out the outlines of how a new species could form from an old one, but left the dirty work of figuring out the actual mechanism to the field he created. Some of the most famed evolutionary biologists of the early 20th century took up the challenge and left the field with the DM model of hybrid dysfunction, named for Theodosius Dobzhansky and HJ Muller. For nearly 100 years, that theory stood as an explanation of how natural selection eventually produces sterile offspring, while being too technically difficult to explicitly test. But this year, in the laboratory of University of Chicago professor Jerry Coyne (and simultaneously and independently in an Indiana laboratory), the theory was finally confirmed.

With his first graduate student Allen Orr, Coyne had figured out the experiments and the mathematics that one could use to test the DM theory. The only problem was finding a set of species in which to do those experiments. Three species were necessary, and those three species had to still be closely related enough that breeding was possible, but not successful. A fast reproductive cycle would also be helpful, so the experiment wouldn’t require decades to execute, and the genetic information of those species would have to be fairly well characterized.

It wasn’t until two years ago that all those tools became available, and in a paper published in Science earlier this month, Coyne’s current graduate student Daniel Matute brings 100 years of theory and research into the end zone. Matute ran his experiments with the noble fruit fly from the Drosophila genus, and his project was made possible by the recent discovery of a new species in that genus, called Drosophila santomea. When Coyne and Matute realized that the new species finally completed the triad of closely-related species they would need to test the DM Theory, it launched Matute into a long series of breeding experiments.

Drosophia melanogaster (from Wikimedia Commons)

The central question was how quickly genes responsible for hybrid inviability accumulated. The DM Theory proposes that those genes don’t merely add up at a steady pace as two species split off from a common ancestor, they “snowball” at an exponential pace with time. To test that notion, Matute needed to count the genes responsible for inviability in two different pairs of species, with different divergence times. That meant a lot of time putting two Drosophila species together, allowing them to mate, and then counting their offspring under a microscope - essentially following the instructions Coyne and Orr had laid out 20 years prior.

Fortunately, all that work yielded exciting numbers. For Drosophila santomea and Drosphila melanogaster, estimated to have diverged 12.8 million years ago, 65 genes were found to cause inviability. For the more recently split Drosphila melanogaster and Drosophila simulans (who diverged only 5.4 million years ago), the number was far lower: only 10 genes caused inviability. Some simple math and curve-fitting later, and Matute had determined that the inviability genes were accumulating at an quadratic, faster than linear rate, confirming the central tenet of the DM Theory at long last.

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