When most people think about global warming, they envision rising temperatures and sea levels. Robert Agnew, a professor of sociology at Emory, thinks about rising crime rates.
It was in the early 1990s, while focusing on the causes of crime and delinquency, that he began to see that certain strains, or stressors, increase the likelihood of crime – including economic deprivation, discrimination, criminal victimization, harsh or erratic discipline, child abuse and neglect. These strains can foster a range of negative emotions such as anger, frustration and depression that put people under pressure to take corrective action. Some of those actions are criminal.
During the last few decades, Agnew’s research on general strain theory has become one of the leading explanations for crime, and he has become its chief architect. He is among the most frequently cited criminologists in the world, and was recently elected president of the American Society of Criminologists.
Agnew believes the pressures caused by climate change will become “one of the major forces – if not the major force – driving change as the century progresses.” He lists strains such as increased temperatures, heat waves, natural disasters, serious threats to livelihood (think farming, herding, fishing), forced migrations on a massive scale and social conflicts arising as nations and groups compete for increasingly scarce food, fresh water and fuel. Especially in the developing world, he believes crime will become a critical issue, making it more difficult to keep the peace in megacities heavily populated by immigrants.
Agnew’s background in criminology isn’t purely academic. He grew up in the Atlantic City of the 1950s and 60s, before casinos brought tourist dollars and jobs. “There was a lot of race and ethnic conflict a lot of crime and delinquency in high school, and I drew very much on those experiences when I came to criminology.”
The Supreme Court ruling that largely supports President Obama’s health care overhaul will not end the contentious debate over health care in the United States.
Health care reform is more complicated than a single piece of legislation, said Kenneth Thorpe, chair of the Department of Health Policy Management at Emory’s Rollins School of Public Health, in an interview shortly before the court’s decision.
"A lot of the increase in health care spending over the last two decades is because we've had an explosion in the number of people who have chronic health conditions like diabetes, high blood pressure, pulmonary disease, and more," says Thorpe.
"We need to have a better prevention system in this country," says Thorpe, "but we also need to do a better job of caring for chronically ill patients, to keep them out of hospitals, nursing homes and clinics. Three quarters of what we spend in health care is on chronically ill patients. We need to do a better job of engaging them to keep them healthy."
Bees, termites and ants are all social, group-minded insects or "superorganisms" but "honey bees are the only ones I love," says Cindy Hodges. Photo by Kay Hinton.
In honor of National Pollinator Week, we bring you Emory alum Cindy Ransom Lewis Hodges, a master beekeeper and vice president of the Metro Atlanta Beekeepers Association.
“Honeybees are vital to the sustainability of the food supply all the way down to the neighborhood garden,” Hodges says. “They are the only pollinator that ‘gives back’ with honey, wax, pollen, and propolis.”
In fact, Hodges’s honey won best in show from the Georgia State Beekeepers Association last fall. “And that’s with urban honey!” she says.
Her hives include a research colony on a fifth-floor patio of Emory’s Math and Science Center that is used for foraging studies in the Department of Environmental Studies. “We took the bees up in the elevator,” she says, laughing. Her bees need regular tending: on a recent rainy spring day, she was planning to deliver a swarm hive (also known as a bait hive) to one of her existing hives. “In the spring, honeybees swarm, which is their form of colony reproduction and is actually a healthy sign, but as urban beekeepers we try to prevent it,” she says. Sometimes the bees will relocate to bait hives, which smell like old wax, when they are placed nearby.
Part beekeeper, part bee evangelist, Hodges and husband Mike Hodges, another Emory alum, decided they needed an avocation once their children left the house (daughter Maggie will receive an MD/MPH from Emory in 2013). So Cindy tends her hives and Mike makes mead from the honey. “When we attend beekeeper conventions, I go for the bees and he goes for the microbreweries,” she jokes.
Honeybees in the U.S. are in trouble, although not endangered, and the need for agricultural pollinators has increased exponentially. Although Hodges admits to being stung about once a week, she is constantly recruiting others into the fold. “I am proud to be taking an active part in the repopulation of Atlanta’s urban corridor,” she says. “Urban bees are helping to pollinate trees, shrubs, fruits, vegetables, and, of course, flowers in the oasis areas of the city between the concrete deserts.”
Scientists at Emory's Yerkes National Primate Research Center have achieved some insight into how fleeting experiences become memories in the brain.
Their experimental system could be a way to test or refine treatments aimed at enhancing learning and memory, or interfering with troubling memories.
The researchers set up a system where rats were exposed to a light followed by a mild shock. A single light-shock event isn't enough to make the rat afraid of the light, but a repeat of the pairing of the light and shock is, even a few days later.
"I describe this effect as 'priming'," says the first author of the paper, postdoctoral fellow Ryan Parsons. "The animal experiences all sorts of things, and has to sort out what's important. If something happens just once, it doesn't register. But twice, and the animal remembers."
Parsons worked with Michael Davis, Robert W. Woodruff professor of psychiatry and behavioral sciences at Emory's School of Medicine, who studies the molecular basis for fear memory.
Even though a robust fear memory was not formed after the first priming event, at that point Parsons could already detect chemical changes in the amygdala, part of the brain critical for fear responses. Long-term memory formation could be blocked by infusing a drug into the amygdala. The drug inhibits protein kinase A, which is involved in the chemical changes Parsons observed.
It is possible to train rats to become afraid of something like a sound or a smell after one event, Parsons says. However, rats are less sensitive to light compared with sounds or smells, and a relatively mild shock was used.
Fear memories only formed when shocks were paired with light, instead of noise or nothing at all, for both the priming and the confirmation event. Parsons measured how afraid the rats were by gauging their "acoustic startle response" (how jittery they were in response to a loud noise) in the presence of the light, compared to before training began.
Scientists have been able to study the chemical changes connected with the priming process extensively in neurons in culture dishes, but not as much in live animals. The process is referred to as "metaplasticity," or how the history of the brain's experiences affects its readiness to change and learn.
"This could be a good model for dissecting the mechanisms involved in learning and memory," Parsons says. "We're going to be able to look at what's going on in that first priming event, as well as when the long-term memory is triggered."
The research was supported by the National Institute of Mental Health
It’s not easy for a theoretical physicist and an ophthalmologist to see eye-to-eye. But a collaboration between the two at Emory University proved worth the effort, sparking a new insight into the leading cause of blindness in adults.
“We looked at a problem from different angles, and came up with a whole new way of seeing choroidal neovascularization – a major eye disease,” says Hans Grossniklaus, a clinical ophthalmologist who is the F. Phinizy Calhoun Jr. Professor of Ophthalmology and Professor of Pathology at Emory’s School of Medicine.
Their results include the first biophysical computer model of how choroidal neovascularization, or CNV, develops. “We can use this model to test new drugs at specific sites and stages during the progression of CNV, which could lead to more effective treatments,” says Fereydoon Family, Samuel Candler Dobbs Professor of Physics at Emory.
CNV vision loss changes the above scene into the one below.
CNV is the most serious form of age-related macular degeneration. In the early stages of CNV, blood vessels begin to sprout abnormally beneath the center of the retina. These abnormal vessels can leak fluid or blood and scar the layer of tissue on the inside back wall of the eyeball. If untreated, CNV can cause a blind spot in the central field of vision, which is crucial for reading, driving and recognizing faces.
Photos by National Eye Institute/NIH.
Age-related macular degeneration affects about 1.75 million people in the U.S., mainly aged 50 and over. Due to the rapidly aging population, that number is expected to increase to 3 million annually by 2020, according to the National Institutes of Health.
In addition to lowering the quality of life for those afflicted, CNV costs a significant amount of Medicare dollars, says Grossniklaus, a leading expert on the pathology of the disease.
Injections of anti-angiogenic drugs into the eye can block the development of new blood vessels but cannot cure CNV, so patients often must continue to receive injections to prevent vision loss.
Grossniklaus turned to Fereydoon Family in an effort to find better methods of treatment. Family’s lab is well-known for using simulation and computational models to decode systems like fractals – seemingly random forms in nature that actually repeat in predictable patterns. Family had previously modeled the branching patterns for the normal growth of blood vessels in the retina.
“I asked him if he could create predictive models for abnormal growth of these vessels,” Grossniklaus recalls of their initial conversation, in 2004.
Blood vessels in the human retina. (NIH)
Over the years, Family and Grossniklaus published several papers on various aspects of macular degeneration while trying to develop a realistic computer simulation model on what makes the choroidal blood vessels grow and cause CNV. For the most recent PLoS paper, they joined forces with Yi Jing, from the Los Alamos National Laboratory and Georgia State University; and Abbas Shirinifard, James Glazier and Maciej Swat from Indiana University in Bloomington.
One of the biggest challenges of the collaboration was communicating between specialties, Grossniklaus says. “They were talking physics, and I was talking medicine and biology, and we had to find a common language. That was half the battle.”
Grossniklaus would draw pictures on a white board to show how the blood vessels grew between the center of the retina and the underlying membrane in cases of CNV. The physicists peppered him questions: On what parts of the tissue do the blood vessels grow? How fast do they grow? What are the dimensions? What are the molecules involved?
“It was an iterative process, with a lot of back and forth,” Grossniklaus says. “It was difficult at times, but fun to develop a mutual understanding with people who have a much different perspective.”
Grossniklaus served as “the reality check,” Family says, “as we developed quantitative ways of measuring changes in the eye.”
A serendipitous accident led to the big breakthrough: A retina sent from Emory to Indiana was damaged by shaking during shipment. The researchers noticed that regions of the retina with overgrown blood vessels had separated from their underlying membrane, while the parts of the retina with no abnormal blood vessel growth remained attached. That suggested that lack of adhesion might be a key factor in the progression of CNV.
“We began focusing on weakness in adhesion in retinal cells and the underlying retinal pigment epithelium cells. That tactic led to simulations of invading blood vessel growth that agreed with many known clinical cases of CNV,” Family says.
“No one had looked at cell adhesion in relation to CNV before,” Grossniklaus says. “Before, it was thought that the invasive growth of blood vessels caused the tissue to weaken. Now we realize that the weakened tissue is what allows the blood vessels to invade. It’s like the little boy holding his finger in the dike: The blood vessels are ready and wanting to grow. They’re just waiting for the retinal tissue to weaken and allow them to break through.”
Grossniklaus and Family are now teaming up with molecular biologists to conduct more research, focused on retinal pigment epithelium cells. “By better understanding the physical properties of RPE, we may be able to develop drugs designed to strengthen this tissue and keep adhesion strong,” Grossniklaus says.
“We also hope to develop models to predict whether someone may be at greater risk for CNV,” Family added.
