Research Roundup |
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February 17, 2015, Volume 61, No. 23 |
How ‘Spontaneous’ Social Norms Emerge
Wearable Tracking Devices Alone Won’t Drive Health Behavior Change
Why Wound Healing Is Impaired in Diabetics
Penn-led Team Pieces Together Signaling Pathway Leading to Obesity How ‘Spontaneous’ Social Norms Emerge
A new study led by the University of Pennsylvania’s Damon Centola provides a scientific explanation for how social conventions—everything from acceptable baby names to standards of professional conduct—can emerge suddenly, seemingly out of nowhere, with no external forces driving their creation. The research used an original Web-based experiment to test whether and how large populations come to consensus. The findings have implications for everything from understanding why different regions of the country have distinct words for the same product—soda versus pop, for example—to explaining how norms regarding civil rights gained widespread traction in the United States.
The paper, “The Spontaneous Emergence of Conventions,” appeared in the Early Edition of the Proceedings of the National Academy of Sciences. “Our study explains how certain ideas and behaviors can gain a foothold and, all of a sudden, emerge as big winners,” Dr. Centola said. “It is a common misconception that this process depends upon some kind of leader, or centralized media source, to coordinate a population. We show that it can depend on nothing more than the normal interactions of people in social networks.”
Dr. Centola is an associate professor in Penn’s Annenberg School for Communication and the School of Engineering & Applied Science and is director of the Network Dynamics Group at Penn. He partnered on the work with physicist Andrea Baronchelli, an assistant professor at City University London.
To understand how social norms arise, Dr. Centola and Dr. Baronchelli invented a Web-based game, which recruited participants from around the World Wide Web using online advertisements. In each round of the “Name Game,” participants were paired, shown a photograph of a human face and asked to give it a name. If both players provided the same name, they won a small amount of money. If they failed, they lost a small amount and saw their partner’s name suggestion. The game continued with new partners for as many as 40 rounds. Though the basic structure of the game remained the same throughout the experiment, the researchers wanted to see whether changing the way that players interacted with one another would affect the ability of the group to come to consensus.
Wearable Tracking Devices Alone Won’t Drive Health Behavior Change
New Year’s weight loss resolutions are in full swing, but despite all the hype about the latest wearable tracking devices, there’s little evidence that this technology alone can change behavior and improve health for those that need it most, according to a new online-first viewpoint piece in JAMA. The paper, written by researchers at the Perelman School of Medicine, the Penn Medicine Center for Health Care Innovation and the LDI Center for Health Incentives and Behavioral Economics at the University of Pennsylvania, points out that even though several large technology companies are entering this expanding market, there may be a disconnect between the assumed benefits and actual outcomes.
“The notion is that by recording and reporting information about behaviors such as physical activity or sleep patterns, these devices can educate and motivate individuals toward better habits and better health,” wrote authors Mitesh S. Patel, David A. Asch and Kevin G. Volpp, all of whom are faculty at Penn and attending physicians at the Philadelphia VA Medical Center. “The gap between recording information and changing behavior is substantial, however, and while these devices are increasing in popularity, little evidence suggests that they are bridging the gap.”
Instead, the authors suggest that applying behavioral economics concepts—such as lotteries or telling individuals what they would have won had they achieved a goal—could help achieve behavioral change. “Building new habits may be best facilitated by presenting frequent feedback… and by using a trigger that captures the individual’s attention at those moments when he or she is most likely to take action.”
The authors believe that there are four challenges that need to be addressed for wearable devices—available as bracelets, watches and even necklaces from high-end designers—to effectively promote health behavior change. First, a person must be motivated enough to want a device and be able to afford it. Second, once a device is acquired, a person must remember to wear it and occasionally recharge it. Third, the device must be able to accurately track its targeted behavior. And fourth, the information must be presented back to the user (using a feedback loop) in a way that can be understood, that motivates action and that sustains the motivation towards improved health.
Why Wound Healing Is Impaired in Diabetics
One of the most troubling complications of diabetes is its effect on wound healing. Roughly 15 percent of diabetics will suffer from a non-healing wound in their lifetime. In some cases, these open ulcers on the skin lead to amputations. For years, researchers have investigated the reasons for problems with wound healing in diabetics. And while many factors contribute, the specific molecular events responsible have remained unclear and therapies to treat these stubborn wounds are few.
Now, scientists at the University of Pennsylvania School of Dental Medicine have identified a critical molecule that helps explain why diabetics suffer from this problem and pinpoints a target for therapies that could help boost healing. The research was led by Dana T. Graves, professor in Penn Dental Medicine’s department of periodontics and vice dean for scholarship and research. The team found that a molecule called Foxo1 played an unexpected role in wound healing (Foxo1 refers to the protein and FOXO1 refers to the gene.) While earlier findings had suggested its presence might be detrimental to healing, their team showed that it in fact promoted healing by “doing two things that are beneficial: protecting cells against oxidative stress and inducing TGF-β1, a molecule critical to the healing process,” Dr. Graves said. Yet the team members wondered if the same factor might be responsible for the poor healing seen in people with diabetes.
To find out, they compared mice with diabetes to normal mice, creating small wounds on their tongues under anesthesia. As expected, the diabetic mice healed more slowly than normal mice. But, when the researchers performed the same experiment in diabetic mice that had been bred to lack Foxo1 in their keratinocytes, the primary cells comprising the outer layer, wound healing was significantly improved. Surprisingly, the effect of deleting the FOXO1 gene in keratinocytes was opposite in diabetic compared to normal mice. To drill down more precisely on how reducing Foxo1 improved healing, the researchers examined various aspects of healing, focusing on the movement of keratinocytes to fill in the hole left by the injury and the proliferation of cells to close the gap, in this case, in the layer of cells on the tongue’s surface known as the mucosal epithelium.
“A critical aspect of wound healing is to cover the wound to limit its exposure to the environment and prevent it from being colonized by a microbial biofilm,” Dr. Graves said. Looking at mice with diabetes, the team observed that both cell movement and, to a lesser extent, cell proliferation were suppressed in diabetic mice, unless the keratinocytes of the mice lacked Foxo1, in which case the negative impact of diabetes was largely reversed. The same response was seen in cells in culture: cells grown in a high-sugar media had an impaired ability to move and proliferate compared to cells grown in standard solution. This impairment was reduced when Foxo1 was silenced.
Penn-led Team Pieces Together Signaling Pathway Leading to Obesity
As scientists probe the molecular underpinnings of why some people are prone to obesity and some to leanness, they are discovering that weight maintenance is more complicated than the old “calories in, calories out” adage. A team of researchers led by the University of Pennsylvania School of Veterinary Medicine’s Kendra K. Bence have now drawn connections between known regulators of body mass, pointing to possible treatments for obesity and metabolic disorders. Their work also presents intriguing clues that these same molecular pathways may play a role in learning and perhaps even in some forms of brain cancer.
Previous research highlighted the important role of the enzyme protein tyrosine phosphatase 1B (PTP1B) in regulating body weight. They showed that PTP1B acts to counter the action of the hormone leptin, which is produced by fat cells and suppresses appetite. When mice have been bred to lack PTP1B, they remain lean even when they have unlimited access to high-fat food. Yet other work has shown that mice lacking both leptin and PTP1B are trimmer than mice that lacked just leptin.“That nagged at us because it clearly indicates that there are other targets than just leptin signaling for this phosphatase,” Dr. Bence said.
That sparked a search for these theoretical targets. The team knew that PTP1B has an affinity to recognize a particular sequence of amino acids. Looking for other proteins with this sequence, they turned up tropomyosin receptor kinase B (TrkB), a receptor in the brain that binds to a molecule called brain-derived neurotrophic factor (BDNF).“That was interesting because mutations in the BDNF gene have been found in study after study to be strongly correlated with body mass index in humans,” Dr. Bence said.
To see if PTP1B does in fact act upon TrkB, the researchers first performed a series of experiments on neuronal cells in culture. They found that boosting expression of PTP1B suppressed BDNF and TrkB activity. Conversely, inhibiting PTP1B activity enhanced the activity of the BDNF-TrkB signaling pathway. The researchers also used biochemical assays to confirm that PTP1B physically interacts with TrkB.
Moving to mice, the team gave animals bred to lack PTP1B a dose of BDNF in their brains, an action that, in normal mice, reduces appetite. Lacking PTP1B didn’t change this fact. But these mice did differ from normal mice in one important way: their core temperature. The genetically altered mice had higher core temperatures after a dose of BDNF than normal mice, an effect that correlates with increased energy expenditure — calories out — and thus causes weight loss. “This is the first time that anyone has linked PTP1B with BDNF and TrkB in vivo,” Dr. Bence said. “And it was interesting to see that the effect on weight regulation seems to be through impacting core temperature and not food consumption.” |