We’ve been keeping a close eye on the University of Chicago Medical Center’s activity in Haiti to help recovery efforts after the earthquake of January 12th. It’s been two weeks since the first batch of physicians and nurses from the Medical Center left, with one emergency medicine physician joining others in Port-au-Prince while six volunteers went to a hospital camp in Fond Parisien, near the border with the Dominican Republic. Yesterday, the first members from a second batch of volunteers traveled to Haiti to take over for the initial crew, most of which will be returning tonight. All told, 22 employees of the Medical Center will be headed to Haiti this week - a dozen to Fond Parisien, 6 to Port-au-Prince, and 4 plastic surgeons traveling to Santo Domingo in the Dominican Republic, where they will see injured Haitians transported by airlift. 

John Easton, our director of communications, was present at the preparation meeting for the 22 volunteers on Saturday evening at the Medical Center. In the video below, you can hear from Chrissy Babcock, co-leader of the Haiti effort, and from several of the physicians, nurses, physical therapists and logistics personnel who are joining the recovery effort. Note the giant red duffel bags of supplies - each person traveling to Haiti will check the maximum allowed luggage on their flight to bring the supplies requested by the teams already in the field.

You can also listen to an interview with the other team co-leader, emergency medicine physician Christian Theodosis, that ran today on Chicago Public Radio’s Worldview program. Theodosis was interviewed via satellite phone from the field hospital in Fond Parisien.

  Banda Aceh before the 2004 tsunami

A populace is devastated by natural disaster, without access to medical care for trauma and infectious disease. Physicians and nurses from around the world rush to help, but good intentions are handicapped by logistical challenges - a lack of diagnostic technology, operating room facilities, and clean environments where the severely injured can recover. To alleviate the medical crisis, the U.S. Navy sends one of its two massive floating hospitals, which sits offshore and starts providing advanced medical care for survivors of the disaster with the help of volunteers from non-governmental organizations in a unique military/civilian partnership.

That, in a nutshell, is the current situation in Port-au-Prince, Haiti. But, according to Matthew Wynia, assistant professor of infectious disease at the University of Chicago Medical Center, it could also describe the situation five years ago in Banda Aceh, Indonesia, in the weeks after a deadly tsunami killed as many as 170,000 people in the country. In the rush to provide critically-needed medical resources to the region, strange bedfellows were made between the U.S. Navy and Project HOPE, an international health care organization that provides medical care to developing countries. As part of that effort, roughly 100 physicians and nurses from around the world worked from the USNS Mercy, a Navy hospital ship, to treat the wounded of Banda Aceh - a mission that set the mold for efforts such as the current use of the USNS Comfort to treat survivors of the Haiti earthquake.

Wynia, also director of the Institute for Ethics at the American Medical Association, spoke about that experience Wednesday as part of the MacLean Center for Clinical Medical Ethics weekly lecture series. In light of current events, the talk was particularly interesting - though the Medical Center teams in Haiti are not working from the USNS Comfort, they will be receiving patients discharged from the ship to clear space so that more people can receive operations and care. Usefully, Wynia recapped his experience with candor, addressing the ethical issues that faced medical volunteers working alongside the U.S. military administering care to a nation wary of American intentions.

At the end of 2004, when the tsunami struck Indonesia, public opinion of the heavily Muslim country about the United States was precariously low: only 15 percent positive, Wynia said. What’s more, the country had been in the midst of a civil war before the disaster, and neither side particularly welcomed a naval ship nearly the size of an aircraft carrier floating only 2 miles off shore. As a result, the ship was only allowed to be in Indonesian waters for 90 days following the tsunami, and given the time it takes to sail a gigantic ship from San Diego to Indonesia, it didn’t arrive until a month after the disaster.

By that point, as with the current situation in Haiti, many of the severe trauma victims had already undergone surgery or succumbed to their injuries, Wynia said. As such, despite the fact that the USNS Mercy was equipped to serve as a floating trauma center for severe war injuries, the medical team only saw 300 operating room cases during their 60 days off Banda Aceh. On a ship equipped with 1000 hospital beds (though as Wynia pointed out, half of them were upper bunks unsuited for severely-ill patients), only 170 inpatient admissions were made. Much of the care supplied by the physicians and nurses was either diagnostic (using the state-of-the-art CT scanner on board) or primary care - providing dental care, eyeglasses, and prescriptions for management of chronic disease.

The USNS Mercy alongside the USS Abraham Lincoln

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Very busy today, so please forgive the light posting.

In December, we wrote about a unique collaboration between Argonne National Laboratory and the University of Chicago Medical Center to fight brain tumors with microscopically tiny gold nano-discs. ABC-7-Chicago recently ran a story on that research which you can watch below:

 

And if you have time for two science videos today, enjoy this neurobiological explanation of why the good guys always win gunfights in old Westerns. (from the University of Birmingham)

photos by Christian Theodosis

One week after two medical teams from the University of Chicago traveled to the earthquake-ravaged nation of Haiti, the situation remains critical. In a conference call Monday from the field hospital camp in Fond Parisien, where a six-person Medical Center team, including physicians, nurses and a pharmacist, are stationed, Haiti team co-leader Christian Theodosis gave a sobering reminder that the nation’s recovery is only beginning: “Being injured and homeless and without legs in Haiti is a very bad outcome.”

Though the focus has shifted in some parts of the country from acute surgery to post-operative care and the medical issues that accompany hundreds of thousands of newly homeless people, the need for expert help and supplies remains great. The Fond Parisien camp (pictured above and on Theodosis’ online gallery) is somewhere between a tent hospital and a refugee camp. Built on the grounds of a Haitian orphanage, the rows of tents sheltered 500 people when the University of Chicago team arrived, and now house 230 patients and their families. More patients are arriving every day by helicopter or bus; hospitals in Port au Prince and the USS Comfort - a US Navy ship that has served as a floating hospital since the quake - are sending recovering patients to the camp to clear space in their facilities for more operations. With only one facility equipped for surgical operations on site, medical personnel at the camp have largely tended to the post-operative and displaced, building shelters, vaccinating patients and their families, and providing rehabilitation services.

John Easton and I spoke to Richard Cook, associate professor of anesthesia and critical care at the University of Chicago Medical Center, by phone this morning from the Fond Parisien camp. Though Cook hasn’t been using his primary specialty - “You know, I haven’t given an anesthetic since I arrived,” he said - he has been incredibly busy acting as physician, electrician, construction worker, and anything else the camp needs. He says he’s been shaken by the severity of the injuries, but is comforted by the resilience of the Haitian people.

“I’ve seen more pediatric amputations in my nine days here than I have in the rest of my career combined. The devastation is almost incalculable,” Cook said. “But the Haitian people are stoic, gracious, polite, optimistic, and deeply faithful. They are responding as well as any community possibly could to such a disaster.”

The full interview is after the jump.

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Addiction is a hard disease to define. We all understand in a general sense what addiction to drugs or sex or food means or looks like, but when it comes to an explicit definition, even the experts struggle. In the DSM-IV, the manual for psychiatric disease, addiction is bifurcated into “substance abuse” and “substance dependence,” and anyone who shows a handful from a grab bag of symptoms (such as “failure to fulfill major obligations,” “withdrawal,” and “large amounts over a long period”) meets the diagnosis.

So imagine trying to model this complex behavior in animals, where experiments can attempt to unravel some of the brain changes that underlie addiction. Not easy. But one DSM-IV symptom may offer a clue - “continued use despite adverse consequences.” Addicts appear to find their chosen drug to be much more important than other people, and are willing to put up with more adversity in order to acquire and take the drug, fighting through physical illness and loss of work, home, and family. You can’t threaten a lab rat with losing his job, but you can measure how important the drug is to an animal through self-administration, measuring how many times the rat will press a lever to receive a hit of drug.

That model has been the central approach in the behavioral addiction laboratory of Paul Vezina, professor of psychiatry and behavioral neuroscience at the University of Chicago Medical Center. Rats in Vezina’s lab are given a series of injections of cocaine or amphetamine over the course of a couple weeks to induce sensitization, a well-studied phenomenon where the behavioral effects of the drug - running around, in rats - increases after multiple exposures. Sensitized rats will work much harder for drug, sometimes hitting a lever as many as 1000 times for just one single burst of amphetamine, suggesting a similar imbalance of motivation as one sees in addicted humans.

“The drug short circuits your system and makes your system sensitized, which is associated with the pathological pursuit of this behavior - that’s the problem,” Vezina said. “With alcohol, there’s no problem having a glass of wine with dinner, but there’s a problem having three bottles. Our argument is that exposure to the drug in select individuals will lead to a sensitization of these pathways and some behaviors.”

The hunt, then, is focused on determining what changes in the brain to produce this dramatically exaggerated motivation for drug. In a new paper, published earlier this month in The Journal of Neuroscience, Vezina’s laboratory presents a series of intriguing experiments that demonstrate just one molecule can push a rat into becoming a furry model of human addiction, hammering away at the drug-lever to the exclusion of all other activity.

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A brain from a person with mad cow disease, caused by prions (compared to a normal brain).

A Place for Prions

We previously discussed the bizarre infectious proteins called prions in the context of kuru, the disease of muscle tremors and uncontrollable laughter spread by cannibalistic rituals in Papua New Guinea. In diseases such as kuru or mad cow disease, abnormal prion proteins wreak havoc by binding to native prions and other cellular elements, creating clumps that kill off cells in the nervous system. But one important thing I didn’t mention in the kuru article - nobody’s really sure what the native, normal prions actually do!

That mystery may have been somewhat dispelled by an article published by Nature Neuroscience last weekend from a team of scientists in Sweden and Germany. Those researchers knocked out or interrupted the gene for prions in a number of different mouse strains, a strategy that had previously yielded a pretty normal mouse without much to say about the prion’s purpose. But for the current experiment, the researchers were patient, allowing the mice to live to the grand old age of 60 weeks (mice typically live for about two years) before looking for deficiencies related to their lack of prions.

What they found in their elderly mice links back to another ScienceLife post - peripheral neuropathy, a motor disorder marked by the demyelination of peripheral neurons. The nerve cells running from the spinal cord to muscles of the prion-free mouse’s body were normal, save for a thinned-out sheath of myelin along the axon. As discussed previously for multiple sclerosis (where central nervous systems neurons are demyelinated), this loss of myelin leaves cells less insulated and like a frayed power cable, unable to transmit signals at optimum speeds. Hence, the motor difficulties associated with peripheral neuropathy, which in humans manifests itself as twitching, paralysis, and loss of dexterity.

That could be a promising finding for not just one field but two. Recall that motor difficulties are usually one of the first symptoms of prion diseases - “kuru” is the word for “shiver” in the Fore language of Papua New Guinea’s Eastern Highlands. Prion gene knockout mice may have their issues, but have the small consolation of being resistant to prion diseases. And the study of peripheral neuropathies (plural, because the term covers several different diseases) could benefit from the new identity of the prion as a mediator of myelin maintenance.

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The University of Chicago Medical Center team currently working in Jimani, Haiti. (L to R: Rex Haydon, Elvire LaPlanche, Richard Cook, Nicole Muse, Christian Theodosis)

More than two weeks after the earthquake that devastated the Caribbean nation of Haiti, the situation remains a humanitarian crisis as hundreds of thousands of injured and homeless seek treatment and shelter. There are more and more signs of hope: Hundreds of millions of dollars have been donated from around the world, some semblance of daily life is resuming on Haitian streets, and roughly 150 temporary hospitals and clinics - including a US Navy ship docked off the coast of Port-au-Prince - have set up to treat the wounded. Yet beyond the immediate triage, long-term health care worries about illness, infection and serious injuries persist, including the need for an estimated 200,000 amputations due to wounds suffered in the quake.

To bolster this continued effort to provide high-quality medical care in the coming weeks and months, two teams left the University of Chicago Medical Center for Haiti earlier this week. Made up of emergency medicine specialists, orthopedic surgeons, anesthesiologists and nurses, the teams are suited to assist both the immediate and long-term challenges of the medical crisis. One team, made up of physicians from the UCMC-affiliated North Shore University Health System as well as Northwestern University and Johns Hopkins University, flew into Port-au-Prince. Another team, with three physicians and two nurses (both Haitian natives), will set up in Fond Parisien, a town near the border between Haiti and the Dominican Republic that has become a hub of medical care to earthquake survivors. The team also brought more than 1,000 pounds of medical supplies with them, and additional teams of UCMC personnel will rotate into the camp every two weeks - more than 100 physicians and nurses have already volunteered for the effort.

The first dispatch from the arriving team underscored the urgency of the need for medical care and supplies. “Just finished getting crushed,” wrote team co-leader and emergency medicine physician Christian Theodosis the day after their arrival. “67 patients on 3 buses, after dark. Conditions quite intense, quite rough. Running short on tents, short on hands, several generators now, security intact. Many, quite vulnerable people. Hungry and tired.”

Updates from the latter team will be posted at Haiti Relief, a blog set up by the Medical Center’s Global Health Initiative. That space also hopes to start conversations among experts across the University of Chicago campus about how best to treat and rebuild Haiti, its health care, infrastructure and beyond. From there, you can read articles from UChicago anthropologist Greg Beckett on the underlying issues Haiti faced before the earthquake. If you would like to donate to efforts in Haiti, the University’s Chicago Studies project have set up a blog with links and information about local and global campaigns.

After the jump, some pictures from Dr. Theodosis of the Fond Parisien hospital camp.

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The protein structure of human interferon-alpha

As discussed yesterday, lupus is not an equal-opportunity disease. Ninety percent of lupus cases occur in women, the disease is three times more likely to affect African-American women than Caucasian women, and lupus is more common and severe in other minority populations as well. Given that the general cause of lupus remains unknown, the reason for these discrepancies is also mysterious. But a grant from the Lupus Research Institute recently awarded to Timothy Niewold, assistant professor of rheumatology at the University of Chicago Medical Center, hopes to turn the focus of science to this issue, looking for genetic factors that may explain why minority women are more seriously afflicted by lupus.

One of the few things that is clear about lupus is that it must have a strong genetic component. The disease is strongly inherited - if someone has a close relative with lupus, their own chances of having the disease are increased twenty-fold. Genetic linkage studies have found a number of promising genes and clusters of genes that are associated with an increased risk of contracting lupus. But while such results are promising, they also contain a couple of problems. 1) The genes don’t account for everything, suggesting an environmental role in triggering the disease. 2) The multiple linkages indicate that lupus cannot be traced back to just one gene, backing theories that the complexity of the disease is due to multiple genetic factors. 3) The linkage studies were conducted in patient populations that were predominantly Caucasian, obfuscating any genetic differences that could account for the increased incidence of lupus in minorities.

“We are excited that we are mapping a bunch of different genes, but it is kind of like we’re sketching some of the first maps of the continent,” Niewold said. “We’re getting something here, something there, and not everything is connected. It’s kind of a vague diagram.”

If all those caveats and complexities are giving you a headache, you’re not alone. But Niewold’s approach is to focus on particular portions of the map that look like they may be relevant to at least a large portion of lupus patients, while expanding genetic studies to start filling in some of the blank parts on the map.

One part of that effort is to focus on a likely suspect in lupus - cytokines. Small signaling molecules that play a role in the immune system, cytokines are normally responsible for helping marshal immune defenses to fight off infections. But one particular cytokine, called interferon-alpha, or IFN-α, may go awry in lupus patients, with elevated levels of the cytokine producing the disease’s characteristic overactive immune response. The theory is backed by both genetic linkage data (where several genes associated with the IFN-α pathway pop up) and acute measurements revealing high levels of IFN-α in lupus patients.

“One of the most common and consistent pathways dysregulated in lupus is type I interferon,” Niewold said. “It doesn’t give us a complete answer, but the data suggests that it’s an important pathway in lupus.”

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Autoimmune disorders are a strange type of disease, a case where the body’s biology isn’t breaking down but rather is functioning too well. In disorders such as Type I diabetes, arthritis and multiple sclerosis, the body’s natural defenses stage something of an internal coup, mistakenly attacking the body’s own tissues instead of viral or bacterial invaders. In a lot of these diseases, the immune system chooses just one system to mistakenly attack - the pancreas in diabetes, or the joints in arthritis. But one autoimmune disorder is less specific, striking out against multiple targets that can differ from patient to patient - lupus.

Known clinically by its longer name, systemic lupus erythematosus (SLE), lupus afflicts roughly 1% of the American population, according to CDC statistics. But that number could also be three times higher, the CDC cautions, an imprecise figure partially down to the difficulty of diagnosing the disease. As Tammy Utset, associate professor in the Section of Rheumatology at the University of Chicago Medical Center describes in the videos below, lupus can present with any number of different symptoms, from fever, rash and fatigue to hair loss, joint pain and kidney disorders.

“It’s a little tricky because the symptoms are so varied from person to person,” Utset said. “That’s why it can take a long time for lupus to come to diagnosis after the symptoms start, because the symptoms early on can be relatively non-specific.”

The diverse range of symptoms is only one of lupus’ mysteries. The disease also has a very skewed incidence between genders, with 9 out of 10 cases in women. Across ethnic lines, lupus strikes minority populations more often - the CDC states that the disease is three times more likely to strike African-American women than Caucasian women, and symptoms tend to be more severe in these populations. At the University of Chicago, the Gwen Knapp Center for Lupus and Immunology Research has been grappling with research questions regarding this discrepancy and potential genetic factors in the development of lupus. Tomorrow, I’ll discuss some of the genetic research coming from that group, but today, here are four videos of Dr. Utset talking about the unique clinical character of this unusual, but hardly rare, autoimmune disease.

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Illustration by Clint May

Most people who have spent any length of time in a laboratory know the pain and frustration of Western blots. There’s probably a little bit of PTSD in every cell biologist related to gels falling apart, leaky electrophoresis chambers, or bands that should be there but aren’t, causing you to wonder which of the preceding 40 steps went wrong.

But don’t hate the method, hate the human error - Western blots, for all the agony they’ve caused, have been one of the most widely-used and productive lab methods of the past 30-some years. Used to detect the amount of protein in a given cell or tissue sample, Western blots have furthered our understanding of the intricate machinery of the cell, from the assembly line that builds it to the defects that can lead to cancer and other diseases. More specific than another protein assay, mass spectrometry, Western blots are the weapon of choice for laboratories that want to characterize the amount and status of a specific protein.

Nevertheless, Western blots have their limits, and the key word is “protein,” singular. Due to the limited size of a Western blot gel and the expense of the antibodies needed to “visualize” the proteins within, blots can only assay, at most, a handful of proteins in each run. Given that the protein networks of cells can contain hundreds or even thousands of proteins, that’s like trying to figure out the image on a puzzle by looking at only one piece at a time. The search was on for a better method, one that could take a snapshot of hundreds of proteins from a cell sample simultaneously.

Such a breakthrough was announced over the weekend in the journal Nature Methods, where a team of scientists led by Richard Jones, assistant professor at the University of Chicago’s Ben May Department for Cancer Research and the Institute for Genomics and Systems Biology described a promising new technique: micro-western arrays.

“When you walk into a dark room and don’t have much information, it’s difficult to predict where everything is going to be,” Jones said. “If someone can simply turn on the light, you don’t have to progress one step at a time by bumping into things. With this new technology, you can potentially see everything at the same time.”

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Videogame Learning & Brain Size

Many a member of the older generations will tell you how video games are rotting our children’s brains, turning kids into button-pushing, drooling zombies. Such warnings linger on despite the fact that my generation - the one that desperately wanted a Nintendo for Christmas - turned out pretty okay…though obviously I’m a little biased. Heard less often are whispers that video games might actually be beneficial to players, helping them fine-tune hand-eye coordination, spatial learning and perceptual tasks. But such research is out there; last year, I wrote about research showing that video games and other parental bogeymen such as Facebook and texting might actually be improving people’s brains rather than destroying them.

Some new research in that community was released this week in the journal Cerebral Cortex, in a study that was rapidly misunderstood as merely Bigger Brains Mean Higher Video Game Scores. That’s not a false headline, but it does miss the subtle point. The authors, from 4 different schools including the University of Illinois and MIT, trained people without video game experience to play the vintage game Space Fortress. In those who learned the game faster (i.e. had achieved higher scores by the end of the training day), a brain area called the striatum was found to be larger on average than the slower learner’s striatum.

The striatum is actually a pretty interesting area, implicated in both movement (and movement disorders such as Parkinson’s and Huntington’s diseases) and addiction. The ventral striatum, including a region called the nucleus accumbens, is the focus of many addiction studies because it is the “reception area” for dopamine, the neurotransmitter increased by all drugs of abuse. With video games, the size of the ventral striatum correlated with early stages of learning, lending support to the idea that learning is enhanced by activities that are rewarding - or to put it more simply, fun.

That could explain why video games are powerful tools for improving a person’s attention and pereception, a phenomenon that researchers such as Daphne Bavelier at the University of Rochester are trying to corral to facilitate education. The study’s findings also may explain the limitations of that approach - some people appear to be resistant to the beneficial effects of video games, a fact that could be explained by brain architecture limiting their ability to learn the game. So next time I’m cursing these new-generation games for being so much harder to play than Super Mario Bros., perhaps I should blame my striatum instead of the developers.

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One of the major goals of the health care reform effort that has dominated political discussion for the past year has been reining in medical spending. Oft quoted is the fact that U.S. health care expenditures have tripled since 1990, that the health care industry comprises a whopping 16% of U.S. GDP, and that each American citizen spends over $7,000 per year on health care, higher than any other country, all despite ranking merely 50th in the worldwide competition for life expectancy. To many, these spiraling figures are a cause for concern, a runaway train that needs to be slowed down through government intervention and industry reforms. But to Robert Fogel, University of Chicago economist and 1993 Nobel laureate, these figures were not worrying omens, but positive signs of a healthier world and a thriving health care industry.

Fogel expressed these views during his talk to a packed room of doctors and ethicists Wednesday as part of the MacLean Center for Clinical Medical Ethics lecture series. Titled “Forecasting the Cost of U.S. of Health Care in 2040,” Fogel’s predictions and figures seemed to feed people’s worst fears about rising costs of health care - for example, during the Q&A portion following his talk, he estimated that health care will comprise 29 percent of the U.S. GDP by 2040, drawing gasps from the crowd. But uniquely, Fogel stressed that such an increase was not a bad thing, taking the minority position (albeit a very University of Chicago economics one) that there is no need to restrict health care spending because it’s what the people demonstrably want.

The key statistic that informed Fogel’s conclusion was that American households, when they gain an extra 1 percent of income, spend an average of 1.6 percent more on health care. Americans have a demand for higher quality health care, and as basics like food and shelter cost less, they choose to spend more of their income on attaining that medical quality - “the long-term inelasticity of the demand for health care,” as he put it in economicsese.

“Consequently, there is no need to suppress the demand for healthcare,” Fogel said. “Expenditures on health care are driven by demand, which is spurred by income and by advances in biotechnology that make health interventions increasingly effective…health care is the great growth industry of the 21st century.”

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Photo from haitiorphansproject.org

One of the unfathomably tragic numbers to come from last week’s earthquake in Haiti last week is the estimate about the number of orphans the disaster created. As many as tens of thousands of children may have been orphaned by the earthquake, according to United Nations estimates, a total that becomes even more shocking when it’s added to the approximately 380,000 orphaned children in the country before last week’s disaster. Some efforts have sprung up quickly to try and find homes for these children, but so far it’s only a trickle, restricted both by logistical difficulties from the earthquake and pre-existing legal obstacles to international adoption.

That real-time crisis lingered over a timely event held Saturday at Comer Children’s Hospital on the University of Chicago Medical Center campus. Organized by the hospital’s International Adoption Clinic as an informational and networking session for about a dozen families who have adopted or are on the verge of adoption, presentations and conversations kept veering back to the topic of Haiti.

“It’s hard today not to talk about international adoption and at the same time keep those images of Haiti out of your head,” clinic founder Larry Gray, assistant professor of pediatrics, told the room at the start of the event. “It’s sort of overwhelming at times.”

The International Adoption Clinic, which started in 2002, was set up to help children from countries such as the Ukraine, Ethiopia and China medically and developmentally transition to a new life with a new family. Gray and nurse practitioner Linda Walsh screen newly adopted children for a wide range of diseases and conditions that can be brought on by living in poverty or an overcrowded orphanage, directing them toward the treatment they need to recover. Many of the children are literally shrunken by the stressful environment they endured, charting as significantly shorter (stunting) or less heavy (wasting) than other children their age. In extreme cases, the child’s brain will even shrink from malnourishment, a condition called microencephaly.

Finding and addressing the causes of these medical issues requires extensive screening, Gray said.

“We think that to pull out a successful adoption transition, it needs to be a very multi-focused effort,” Gray said. “When a family arrives in the United States, it’s just the beginning of a network of processes that come into play.”

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Myelin is the secret weapon of the nervous system, the insulation that allows neurons to transmit electrical signals at the speed of thought. Wrapping itself around the long projecting axons of neurons, myelin acts like the insulation on a power cable, allowing electricity to travel more efficiently down nerve cells that can stretch for several feet. The importance of this function is revealed by diseases such as multiple sclerosis, where the loss of myelin causes severe movement difficulties and seizures.

The myelinating machines of the central nervous system have been known for decades: cells called oligodendrocytes, which produce myelin sheets that wrap around axons. But what genes and signals drive oligodendrocytes to do their work properly - and which of those factors go wrong in diseases like MS - remains a mystery. But the laboratory of Brian Popko, professor of neurology at the University of Chicago Medical Center, recently found a key piece of the myelination puzzle thanks to an odd, shivering mouse.

Published last week in the journal Genes & Development, Popko and his team used a method called forward genetics to launch an unbiased hunt for genes that had not previously been identified as important for myelination. Unlike reverse genetics, where researchers choose a gene of interest and make a knockout mouse lacking that gene, forward genetics relies upon the spontaneous creation of an interesting mutant. In this case, Popko and colleagues were looking for a mouse with the muscle tremors and seizures you would expect from deficient myelination.

“There were a number of knockout mutants available to us that disrupted the myelination process. They all resulted in mice that had a tremor, with names like shiverer, jumpy, trembler - you can get an idea of what the phenotype is,” Popko said. “Our screen was about as unsophisticated as you can imagine; we just selected for mice that have a tremor.”

Soon, Jackson Laboratory, a company that breeds and distributes mice for lab studies, came up with just such a mouse, who in its brief life (only about 3-1/2 weeks) has a chronic tremor in its hind legs, like it is constantly shivering in the cold.

Sure enough, when the brain and spinal cord of this mouse was dissected, it had little to no white matter, the informal term for myelinated neurons. Even more promising, the oligodendrocytes of this mutant were present, and appeared mature, but were frozen in the state just before actually initiating myelination - an interruption that resembles the malfunctioning oligodendrocytes in MS.

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If you’ll forgive the light posting today, I’d like to direct you to an article that appeared this week on the website of New Scientist magazine by Peter Aldhous, “Poor Neighborhoods Can Kill.” Aldhous gives a broad overview of a collaboration here at the University of Chicago that we’ve only barely nibbled at here on the blog, a team of biologists, clinicians, sociologists and epidemiologists that are grappling with a sobering statistic - breast cancer death rates of black women in Chicago are a shocking 68 percent higher than the rates for white women.

A frequent theme here has been the simultaneous promise and difficulty of translating animal research and laboratory findings to the real world, but this project offers a pretty remarkable example of how different types of research can be united. The effort builds bridges from Martha McClintock’s studies of social isolation worsening breast cancer in rats, to Suzanne Conzen’s studies of the genes that show increased expression in stressful or isolated conditions, to Funmi Olopade’s research on differences in breast tumors in populations of African-American and West African women.

Results from the collaboration indicate that social isolation and a fear of crime cause an overload of stress hormones that can change cell biology, sending tumours into overdrive. “We’re showing that your social environment can affect your health directly,” says Suzanne Conzen of the University of Chicago. “It goes into gene expression. That concept is really new.”

What’s more, sociologist Sarah Gehlert (now at Washington University in St. Louis) has taken those results out into the community, collecting surveys and hormonal measurements from South Side Chicago women diagnosed with breast cancer.

Gehlert suggests that the fear that comes with living in high-crime areas combined with scant social support causes overproduction of cortisol, similar to that seen in McClintock’s isolated rats. This eventually erodes the body’s ability to release the stress hormone, creating the flatline effect. Similar “burnout” patterns have been seen in patients with post-traumatic stress disorder.

It’s a great article on a great project, do check it out.

Elsewhere…

- The coolest science story of the week may have been the discovery that the Y chromosomes of humans and chimpanzees are much different than previously thought, suggesting dramatic evolution for both species on the chromosome that carries male-sex genes.

- While donations flood in to aid the people of Haiti after this week’s tragic earthquake, science writer Jonah Lehrer contributes a timely post on how the value of a charitable donation is reflected in the brain.

- The science blog NCBI ROFL moves to Discover magazine’s website, and given that their angle is one of my favorite time-wasters (searching for weird and funny articles on PubMed, the online library of scientific journals), it’s definitely going to be a regular visit. For a taste, enjoy the Onionesque “getting babies drunk” study, or the study that uses Pink Floyd-induced hallucinations to screen for a neurological disease.