As another year comes to a close we’d like to look back at the fascinating research breakthroughs and inspiring patient stories from 2011. ScienceLife ran 168 posts this year, and while we wish we could highlight all of them, here are a handful of our favorites from each month.

January

Patrick Wilson found out that the H1N1 virus could end up helping us fight all types of flu. Stephen Pruett-Jones studied how some male birds mimic the sounds of predators to pick up the ladies (with an audio clip). We interviewed David Gozal about his study on the link between childhood obesity and lack of sleep, and took a look at NCAA regulations mandating sickle cell testing for athletes.

February

Harold Pollack gave a lecture on why violent crime in urban, minority communities should be considered a public health epidemic. Siri Atma Greeley studied the actual medical benefit of widespread genetic testing. Stacy Lindau wanted to know why so few women get help for sexual problems after surviving cancer. We talked to Bana Jabri about the causes of celiac disease, and Sliman Bensmaïa showed us how the brain processes the basic elements of touch very much like it handles visual information.

March

Sola Olopade educated women in Nigeria about using clean-burning stoves to prevent indoor pollution. Stefano Allesina and Jonathan Levine looked at how rock-paper-scissors helps explain evolution. Joshua Miller went to Yellowstone Park to see what stories the ghostly bones of animals can tell, and Scott Eggener questioned the wisdom of indiscriminate prostate cancer screening.

Photo by Gerald Waddell

Andrea King studied the wide range of responses to drinking alcohol, and why it can be fun for some people and a bummer for others. Cheryl Reed took a ride in a helicopter with our UCAN nurses. Kamal Sharma looked at the genes that control animals’ gait, and Ningqi Hou studied how urban environments can dictate how much exercise people get.

May

Daniel McGehee looked at the long-term effects of nicotine on the brain. Habibul Ahsan went to Bangladesh to study the health impacts of accidental exposure to arsenic in drinking water. The brain’s overlooked supporting cells got their due at a conference on neuroscience, and we remembered a landmark discovery about a once popular drug taken during pregnancy that we now know can cause cancer.

June

As we headed into summer, Diana Lauderdale used Google to track MRSA. We learned about an extraordinary transplant where a man received a new heart, liver AND kidney. Daniel Geynisman gave us the rundown on whether or not cell phones are killing us (they’re not, as long as you don’t use them in the car), and some UChicago undergrads studied what happens to gorillas on the birth control pill.

July

We spoke to Donald Jensen and Andrew Aronsohn about the new outlook for patients with hepatitis C. Igor Schneider made a time machine to find the genetic switch for limb development. Farr Curlin led a study about the benefits of addressing spiritual needs alongside medical care, and Adam Cifu looked at the phenomenon of scientific study reversals.

August

Stefano Allesina dug into the long, shady history of nepotism in academia in Italy. John Schneider talked about his work addressing sexual health and stigma in India. Michael Becker discovered a new treatment for the Royal Disease, and we had the rare chance to name check a Spiderman villain in a post.

September

Martha McClintock and Suzanne Conzen studied the connection between social isolation, stress and breast cancer. Gallego Romero traveled to India to search for the origins of lactose intolerance. Stephanie Dulawa developed a mouse model for OCD, and Paul Vezina looked at a different kind of obsession, compulsive gambling.

October

Arshiya Baig started a pilot project to help people learn about life with diabetes through pictures. Manyuan Long found that some of the youngest genes are in the brain. Jens Ludwig and Stacy Lindau published a landmark study about the connection between neighborhood poverty and health, and Issam Awad studied a rare brain disease that soon could be treated with a drug instead of surgery.

November

Cathy Pfister and Tim Wootton figured out how to use seashells to track climate change over the years. Lianne Kurina found a link between loneliness and sleep quality. Shantanu Nundy, Monica Peek and Marshall Chin developed a program to send text message reminders to people with diabetes, and Pan Chen looked at the links between childhood abuse and aggressive behavior in adults.

December

Inbal Ben-Ami Bartal, Jean Decety and Peggy Mason discovered that rats can show empathy for their fellow rats in distress. Maciej Lesniak performed a scary but amazing brain surgery on a patient who was awake. Cathryn Nagler searched for the source of food allergies within our bodies, while Stafano Guandalini uncovered the challenges in educating doctors about one of those allergies, celiac disease.

Whew. Hope you were able to click through at least a few of those. We look forward to another great year of research in 2012. We’re taking a break next week, but we’ll be back on January 5. Happy holidays!

By John Easton

Molecular markers found in cancer cells that have spread from a primary tumor to a limited number of distant sites can help physicians predict which patients with metastatic cancer will benefit from aggressive, targeted radiation therapy.

In a study published online Dec. 13, 2011, in the journal PloS One, researchers from the University of Chicago and the University of Illinois at Chicago show that if cells from metastatic tumors have high levels of a particular type of microRNA — a tool cells use to silence certain genes– not even aggressive treatment of those tumors would help. But if the cells have lower levels of that biological marker, then focused local treatment could be effective, even curative.

“We previously demonstrated that we could provide lasting disease-free survival to a percentage of patients with metastatic disease,” said study author Ralph Weichselbaum, MD, professor and chair of radiation and cellular oncology and Director of the Ludwig Center for Metastasis Research at the University of Chicago. “This finding means we can have a pretty good sense in advance of which patients we can help. Patients unlikely to benefit from focused, local therapy can receive systemic treatment immediately.”

Yves Lussier, MD, professor of medicine at the University of Illinois at Chicago and co-senior author of the study, added that “the biological differences between locally curable metastases or potentially fatal widespread metastases can also be targeted for drug development.”

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By Matt Wood

Each day people make decisions about how much effort they’re willing to put into various tasks. The decision about how much effort to invest in an activity is influenced by the reward for doing something and the probability of actually getting it. You might be willing to work hard at your job because the reward—a paycheck—is both valuable and fairly certain. But you might not be willing to try a complicated new recipe for dinner, even though it sounds delicious, because of the chance that it won’t turn out well.

Animal studies suggest that the neurotransmitter dopamine plays an important role in this type of decision-making, especially the decision to expend effort. In rats, dopamine levels influence tolerance for effort and probability costs. Rats with higher levels of dopamine are more willing to press levers and climb over barriers to reach better food, whereas those with lower levels will settle for food that’s less tasty but within easy reach.

Little is known about how dopamine affects effort-based decision-making processes in humans. But a new study published in The Journal of Neuroscience by Margaret Wardle, a post doctoral researcher in the Department of Psychiatry and Behavioral Neuroscience at the University of Chicago, her mentor Harriet de Wit, Professor and Director of the Human Behavioral Pharmacology Laboratory, and colleagues at Vanderbilt University shows for the first time that people behave in much the same way. Their research, sponsored by the National Institute on Drug Abuse, not only sheds light on how dopamine influences decision-making in humans, but also points toward possible treatment for psychiatric disorders like depression.

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By Rob Mitchum

A surgical procedure is a daunting experience for any patient, though thanks to general anesthesia, it’s not typically a memorable one. That’s not the case for patients who go through an awake craniotomy — a unique procedure that allows surgeons to react based on feedback from the patient during removal of a brain tumor.

“I remember them waking me up using a flashlight and talking to me,” Anna Litchfield, a 49-year-old patient who was operated on by Maciej Lesniak, MD, Professor of Surgery and Neurology, said in August. “I remember Dr. Lesniak saying ‘Anna, are you OK?’ and I remember saying ‘Great, Dr. L!’ out of nowhere. I never thought I’d call him Dr. L! In retrospect, I feel like my brain was thrilled that he was there operating.”

Awake craniotomies are unique, complex procedures typically used to remove tumors nestled close to functional areas of the brain. Though the macabre nature of the surgery might induce shudders, the benefits for the patient are great. As the tumor is carefully removed by the surgeon, a neurologist can continuously monitor the patient’s language, motor and sensory function to make sure critical parts of the brain suffer minimal damage.

“When tumors are in what we call eloquent, functional areas, the margin of error is a millimeter,” Lesniak said. “You have to ask yourself whether you feel comfortable with a patient being asleep, potentially missing that millimeter while taking out the tumor and having them wake up devastated, or minimizing that risk.”

Lesniak and his team at the University of Chicago Medical Center perform more awake craniotomies than any other group in the Chicago area — more than 30 each year. Each surgery utilizes a truly interdisciplinary and experienced team of neurosurgeons, neurologists, anesthesiologists and operating room nurses who must collaborate to ensure the unusual surgery’s success. Often, craniotomy candidates are referred to Lesniak from hospitals around the area and country, as the surgery can be performed only by individuals with significant expertise and experience.

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All of the animal life on Earth, including human beings, can be traced back to a unicellular ancestor somewhat similar to the modern-day protozoa. In one sense, the hundreds of millions of years of evolution is the story of how organisms became more and more complex, growing from a single cell to trillions of highly specialized cells forming different organs and tissues in a single body. Yet while you could easily tell a protozoa from a human in a police lineup, cells from the two species are made up of many of the same proteins, performing similar jobs. What changed to produce these profound differences in complexity?

One potential area where this complexity may have bloomed is tyrosine phosphorylation, a key cellular signal for pathways that control cell growth, proliferation, and structure. Enzymes called tyrosine kinases add a phosphate group to a wide range of cellular targets, which can act like a light switch, turning their function on or off. The phosphorylated proteins are recognized by another group of proteins with a special “sensor” called the SH2 domain. Because tyrosine kinases will promiscuously phosphorylate many targets in the cell, the very picky SH2 domain proteins are responsible for sorting out the noise.

“Tyrosine kinases tend to be not that selective,” said Piers Nash, assistant professor in the Ben May Department of Cancer Research at the University of Chicago who studies this system. “They’ll phosphorylate a lot of things, and that creates all of these docking sites for SH2-domain-containing proteins. It’s really up to the SH2 domains to interpret those signals and convert them into downstream signaling pathways.”

The more complex the cell, the more unique types of SH2 domains that are needed to perform this important sorting function. In the unicellular cousins of animals, organisms can get by with just a single SH2 domain. But in humans, some 121 SH2 domains are known to exist, managing many different pathways in many different cells. In two recent papers, Nash’s laboratory studied how these SH2 domains manage their impressive selectivity and the evolutionary pathway that they took from simple protozoa to complicated human.

It’s essential that SH2 domains only bind to the right phosphorylated protein — repeatedly screwing up and activating the wrong pathway could lead to diabetes, cancer, or worse. But scientists have struggled to figure out how SH2 domains choose their appropriate target, with some even concluding that they aren’t so selective at all, merely in the right part of the cell at the right time to only bind the correct protein. However, that wasn’t what a research team led Bernard Liu from Nash’s laboratory found when they looked at how SH2 domains bind actual cell targets such as the insulin receptor.

“It turned out that the SH2 domains were exquisitely selective, much more selective than the general motifs for the SH2 domains that had previously been mapped,” Nash said. “So it was clear there was additional information encoded in the peptide that the SH2 domain makes use of.”

The researchers then deduced that the SH2 domains select their target through a kind of language, looking for the exact sequence of amino acids - or “word” - that marks the appropriate match. Because each amino acid (akin to the letters of the word) will either attract a particular SH2 domain or reject its peers, changing only one amino acid can completely change the meaning, like altering the word “light” to “fight.”

“For SH2 domains, that makes all the difference in the world. They can sense incredibly subtle differences,” Nash said. “It’s looking at the entire peptide and seeing both the permissive and the non-permissive residues, integrating that and making this collective decision about what to bind.”

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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, an auto-immune disorder that prevents the digestion of gluten in the small intestine and inhibits absorption of nutrients, is gaining awareness in the United States. Gluten-free options are popping up on restaurant menus, television stars such as Elisabeth Hasselbeck and Jennifer Esposito are going public with their diagnoses, and major food companies including General Mills are developing more gluten-free products and market directly to the celiac community.

A 2003 study estimated that 1 in 133 people in the United States have celiac disease. That means at least 3 million people in this country are living with celiac, but screening studies show that identification of patients lags behind the actual prevalence of the disease. Up to 97 percent of those cases are undiagnosed.

Concerned that a lack of physician awareness of celiac could be contributing to a delay of up to 11 years in the diagnosis of adults in North America, Stefano Guandalini, MD, Medical Director of the University of Chicago Celiac Disease Center, co-authored a study that looks at how well gastroenterologists adhere to established diagnostic and treatment guidelines for celiac disease.

Guandalini and his colleagues at the Celiac Disease Center and the NorthShore University Health System conducted a survey of gastroenterologists who attended the annual Digestive Disease Week conference in 2009. A total of 169 doctors answered questions about vignettes that described cases of possible celiac disease. Guandalini’s team compared the responses to those of 22 experts on celiac disease, and found that very few of the non-expert physicians were able to follow correct diagnostic approaches. “This is a bit alarming because if you think of it, the people who were there were already screened in a way because they are those who actually want to attend a national meeting, so they are seeking an education,” Guandalini said. “Not only that, but they received this paper requesting to participate in this survey, so it means that they already thought themselves to be familiar with celiac disease.”

Until very recently, Guandalini said, basic medical education didn’t teach that celiac disease was widespread in the United States. “Nobody really was ready to accept the 1 percent prevalence of celiac disease,” he told the New York Times recently. In that article he pointed out the example of a medical textbook that put the prevalence of celiac in the United States at 1 in 10,000 as recently as 1999. And when doctors did have any familiarity with celiac, it was with the “classical presentation” of a small child with chronic digestive problems, instead of the myriad symptoms in both children and adults that can lead to a celiac diagnosis, from muscle cramps to an itchy skin rash, especially around the elbows.

As one of the country’s leading authorities, the Celiac Disease Center is doing its part to close this gap in medical education. It recently hosted its sixth annual Preceptorship Program, an on-site, intensive two-day training course for medical professionals who want to learn about diagnosing and treating celiac disease. This year more than 30 doctors, nurses and dieticians attended seminars, got hands-on training and sampled gluten-free foods. While the center offers a comprehensive approach to caring for patients and research toward finding a cure, Guandalini says that medical education is a primary goal. As demonstrated by this latest study, he said, “Clearly there is a lot of education that needs to be done.”

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Parakkal D, Du H, Semer R, Ehrenpreis ED, & Guandalini S (2011). Do Gastroenterologists Adhere to Diagnostic and Treatment Guidelines for Celiac Disease? Journal of clinical gastroenterology PMID: 21959324

Have you ever cheated on a test by glancing over at someone else’s work? Or relied on a fellow student to carry the load on a group project while you coast along with minimal effort? While few will admit to these forms of cheating, they have long been fixtures of the classroom. However, a lazy individual benefiting from the hard work of a colleague is not a trick exclusive to humans. In a recent study of bacterial infections in plants, the laboratory of evolutionary biologist Joy Bergelson demonstrated that these unsavory practices can also be found in pathogens - and that may be a good thing for us.

In the bacterial world, the goal is survival. What we perceive as an infection is merely colonization for the bacterial population, who are establishing a new home where they can happily feed off the host’s nutrients and reproduce. Bacteria build and release virulence factors to achieve this settlement and evade immune system defenses. But because these factors spread out, benefiting an individual bacterium’s neighbors as well as itself, a sneaky bacterium can get by without producing its own virulence factors. In laboratory dish experiments, scientists observed that bacteria engineered without the ability to release factors can still thrive so long as they are paired with normal, pathogenic partners.

Though scientists described this “cooperator-cheater model” in the artificial environment of the dish, nobody had yet observed it in a natural setting. For a study published in September by the journal Ecology Letters, a team led by postdoctoral fellow Luke Barrett discovered the model in action within the cells of the popular genetic model plant Arabidopsis thaliana.

“We’re showing that cheating actually happens in nature, and that the cheaters persist,” Bergelson said. “You can make cheaters that do well in the lab, and you can show that these systems may be stable in theory, but to show that it is actually happening in nature is novel.”

Recently, researchers discovered that Arabidopsis carried two strains of the bacteria Pseudomonas syringae, a common plant pathogen. While one strain had all the normal pathogenic activity, another was a kind of bacterial pacifist, with a broken system for secreting virulence factors. Surprisingly, these two strains appear with almost equal frequency in Arabidopsis, suggesting that the non-pathogenic strains are far more successful in nature than previously thought.

To test the nature of this relationship, researchers took the two natural strains and experimentally infected plants with only one or the other. When grown alone, the “cheater” strain was not nearly as successful without its more aggressive partner around to unwittingly “donate” virulence factors. Additional modeling suggested that the more aggressive the virulent strain, the more likely it was that cheaters would be found nearby eager to exploit the hard work of their pathogenic peers. The cheater strains are also harder for the host immune system to spot, since the machinery that produces and releases virulence factors is a frequent target of those defenses.

“When you go into the field, it’s kind of a curiosity: why would non-pathogenic cheaters be almost as common as pathogens inside the host?” Bergelson said. “It turns out that the cheaters can do really well as long as they’re with the pathogenic variety, and they don’t pay the price of having to actually make a secretion system or effectors. They also don’t run any risk of being recognized because it is the presence of secreted effectors that causes the recognition events in the first place. So, these non-pathogens have some good things going for them.”

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If you are an avid reader of food packaging materials or a parent of an elementary school student, you might get the feeling that food allergies are on the rise. Statistics back up this notion, with the CDC reporting an 18 percent increase [pdf] in child food allergies between 1997 or 2007. That puts current estimates of food allergy prevalence at 4 percent for children and 2 percent for adults, with allergies to peanuts (3.3 million Americans) and shellfish (6.9 million) leading the way.

The factors driving this surge remain a scientific mystery, and answers are even more scarce when it comes to treating or preventing dangerous allergic reactions. Currently, the only way to prevent anaphylaxis caused by a food allergy is avoidance, a strategy that can be very cumbersome for parents raising small children who cannot be exposed to basic food groups. Dave and Denise Bunning faced this challenge with their two children, both of whom were allergic to milk and eggs, leading to “several emergency room visits before the age of 5,” Dave Bunning said. Those experiences inspired the family’s philanthropy for research into the science of food allergies, which included this year’s founding of the Bunning Food Allergy Professorship at the University of Chicago Medical Center.

At the official naming ceremony for the new position, the inaugural Bunning Food Allergy Professor Cathryn Nagler presented her latest research to a large crowd including the Bunning family themselves. Nagler’s intriguing theory about food allergies looks within, at the bacterial universes that exist inside the human body. In parallel with other laboratories on campus looking at the impact of the human “microbiome” upon diseases such as inflammatory bowel disease and diabetes, Nagler is focused on the trillions of bacterial tenants that occupy each of our bodies.

“It’s becoming clear that we are outnumbered,” Nagler said. “There are 10 trillion human cells encoding 20,000 genes [in an individual], but 100 trillion bacterial cells encoding an estimated 2 to 20 million genes. So there are as many E. coli in each of our digestive tracts as there are people on Earth…and that’s not even one of the more popular species.”

All those bacteria, sometimes called the “commensal microbiota” to distinguish them from disease-causing pathogens, could play the environment role in the genes + environment recipe for food allergies. Many of the trappings of modern life, including high-fat diets, antibiotic treatments, and the use of baby formula instead of breastfeeding, can affect the census of our bacterial inhabitants. In food allergies, where the immune system mistakenly treats innocuous dietary proteins as harmful invaders, these microbiota changes might tip the balance towards over-sensitivity to components of peanuts or shrimp.

“An increase in disease prevalence in 10 to 15 years’ time can’t be explained by genetics, so there’s got to be other factors that are driving this increase in disease prevalence,” Nagler said. “All of these environmental variables lead to alterations of the commensal microbiota, which in genetically susceptible individuals could drive allergic responses to food and other antigens.”

To study this model, Nagler’s laboratory gave a long-term treatment of antibiotics to lab mice, finding that this prolonged exposure did indeed trigger an allergic response to peanuts. Using genetic identification methods, her group compared the gut microbiomes of mice treated with antibiotics versus mice who did not receive the drugs, finding several differences in the bacterial populations colonizing their digestive system. One bacterial family, called Clostridia, were reduced in the mice treated with antibiotics, while another was increased — suggesting that reducing or decreasing different species of bacteria might affect the chances of developing food allergy.

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By Dianna Douglas

The goal of World AIDS Day 2011 is not to make the public aware of the disease. That was the goal in 1988, back when the international health threat was still new, infections were rising every year, and there was no hope of a treatment in sight. This year, World AIDS Day marks the sunset of the public panic about the virus. The stated goal this year is “getting to zero” — or bringing the number of AIDS-related deaths and new HIV infections down to zero and ending all discrimination against people living with the virus.

The University of Chicago has various ways of reaching that goal here in Chicago. There’s the STI/HIV Intervention Network (SHINE) based at the School of Social Service Administration, which brings interventions to neglected groups such as men who have sex with men, people in the criminal justice system, minority youth, and young couples. There’s also the Medical Center’s Living Positively program, in which HIV-positive young people act as advocates to their peers who are at risk.

Now, in honor of World AIDS Day, the Medical Center is trying an innovative approach to this public health issue. Instead of doing what he calls the “typical academic thing for World AIDS Day” — a panel of researchers talking about AIDS in Africa in an auditorium full of other researchers — John Schneider, MD, MPH, has organized a ball. “This year, we want to collaborate and fully engage with the community,” he said. In gay culture, a ball is where people dress in drag to show off their moves, a lot like a fashion show. The community he hopes to reach with this ball is the young GLBTQ (gay, lesbian, bisexual, transgender, and queer) minorities who have the highest HIV infection rates in the city.

While the tide may have turned in the AIDS epidemic, the infection rates of several groups remain stubbornly high. Around 22,000 people in Chicago live with HIV or AIDS, and the infection rates among African Americans and gay men are particularly sobering. Since 2005, 57 percent of new HIV infections in men have been a result of men having sex with infected men. Among African Americans, the HIV infection rate since 2005 is more than double the general population’s infection rate.

A partnership with the young people striking a pose at underground balls may seem unusual, but it may also be the best way to reach Chicago’s most vulnerable populations. “We know where the epidemic is, and we have the tools to take care of it. What is needed now is hard work using traditional case-finding methods to reach these vulnerable groups with health services,” Schneider said.

The ball tradition, subject of the award-winning documentary Paris is Burning, has long been a safe place for young black gay and transgendered people to express their creativity and build communities. The World AIDS Day mini-ball will celebrate the support that the members of this subculture offered each other during the worst days of the AIDS epidemic in the 1980s and ’90s.

“These are the people most impacted by AIDS in the United States,” said Keith Green, MSW, co-director for the Chicago Black Gay Men’s Caucus and a co-sponsor for the event.

Everyone at the ball will see their peers promoting safe sex and healthy behavior.

Contestants — many of whom are gay, transgender or bisexual — will compete against one another in the lobby of the School of Social Service Administration this Friday night. Participants will display their dance skills, costumes and attitude in a variety of events, similar to a runway show. In some events, they will be judged on the “realness” of their drag. In others, on the beauty of their clothing and overall style. Each of the seven walk competition categories has a cash prize for the winner.

“Every category requires the creative integration of the AIDS ribbon, the color red, or latex,” said Matt Richards, outreach program manager for pediatric infectious diseases at the University of Chicago Medical Center.

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