Wednesday, July 21, 2021

Emory team makes finals in Amazon's Alexa Prize for artificial intelligence

The Emory team is led by faculty advisor Jinho Choi (center) and graduate students James Finch (left) and Sarah Finch.

A team of six Emory computer science students made it to the final round for Amazon’s Alexa Prize Socialbot Grand Challenge, a global competition among universities to create a chatbot that advances the field of artificial intelligence. The winner of the 2021 Alexa Prize will be announced in mid-August. At stake is a $500,000 first prize. In addition, $1 million in research funds will be awarded to the winning team if it meets the “grand challenge” criteria, including the ability of its chatbot to engage the judges in conversation for at least 20 minutes. 
 
In addition to Emory, the finalists are Czech Technical University, Prague; SUNY at Buffalo, New York; Stanford University and the University of California Santa Cruz. 
 
The Emory team is headed by graduate students Sarah Finch and James Finch, along with faculty advisor Jinho Choi, assistant professor in the Department of Computer Sciences. Last year, the trio headed a team of 14 Emory students that took first place, winning $500,000 for their chatbot named Emora. They chose the name because it sounds like a feminine version of “Emory” and is similar to a Hebrew word for an eloquent sage. 

This year, they are turning up the heat with an even more advanced version of Emora and new team members, including graduate student Han He and undergraduates Sophy Huang, Daniil Huryn and Mack Hutsell. All the students are members of Choi’s Natural Language Processing Research Laboratory

“I’m extremely proud to have such a talented team of students,” Choi says. “It’s a group of strongly motivated people with the right combination of diverse skills coming together at the right time. They’re working on changing the paradigm for conversational artificial intelligence.” 

“We’re using some established technology but taking a groundbreaking approach in how we combine and execute dialogue management so a computer can make logical inferences while conversing with a human,” adds Sarah Finch. “Ultimately, we’re making Emora even more flexible in how she can interact with people.”


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Monday, July 12, 2021

Using big data to zero in on a mosquito menace

"The ultimate goal is to give public health officials the power to do more effective and efficient mosquito control — even before an epidemic beings," says Gonzalo Vazquez-Prokopec, right, shown with public health technicians in Merida, Mexico.

Scientists from Emory University are leading a new strategy in humanity’s long-running war with the mosquito, using big data to target one species of this tiny disease vector. They have studied the behavior of the Aedes aegypti mosquito, pinpointing where it hangs out in homes. They are mapping cases over time of viral infections that this species can transmit when it bites a human — including dengue fever, Zika, chikungunya and yellow fever. They are zeroing in on high-risk neighborhoods for outbreaks of these diseases in sprawling urban areas of the tropics. 

“We’re working on some of the boldest and biggest changes in decades for the surveillance and control of this mosquito,” says Gonzalo Vazquez-Prokopec, associate professor in Emory's Department of Environmental Sciences
 
The National Institutes of Health’s Division of Microbiology and Infectious Diseases awarded Vazquez-Prokopec a $6.5 million grant to lead a consortium in a randomized clinical trial in Merida, Mexico, as part of the quest to reduce Aedes-borne viral infections. The trial is testing a novel intervention that previous Emory research finds promising: Indoor residual spraying of insecticide, targeted to the places in homes where this mosquito tends to rest. 
 

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Wednesday, July 7, 2021

Mapping dengue hot spots pinpoints risks for Zika and chikungunya

A female Aedes aegypti mosquito takes a blood meal from a human. "The ultimate goal is to give public health officials the power to harness big data and do more effective and efficient mosquito control — even before an epidemic begins," says Emory disease ecologist Gonzalo Vazquez-Prokopec. (Photo by James Gathany / CDC).

By Carol Clark

Data from nine cities in Mexico confirms that identifying dengue fever “hot spots” can provide a predictive map for future outbreaks of Zika and chikungunya. All three of these viral diseases are spread by the Aedes aegypti mosquito. 

Lancet Planetary Health published the research, led by Gonzalo Vazquez-Prokopec, associate professor in Emory University’s Department of Environmental Sciences. The study provides a risk-stratification method to more effectively guide the control of diseases spread by Aedes aegypti

“Our results can help public health officials to do targeted, proactive interventions for emerging Aedes-borne diseases,” Vazquez-Prokopec says. “We’re providing them with statistical frameworks in the form of maps to guide their actions.” 

The study encompassed data for 2008 through 2020 from cities in southern Mexico with a high burden of dengue fever cases during that period, along with cases of the more recently emerged diseases of Zika and chikungunya. The cities included Acapulco, Merida, Veracruz, Cancun, Tapachula, Villahermosa, Campeche, Iguala and Coatzacoalcos. 

The results found a 62 percent overlap of hot spots for dengue and Zika and 53 percent overlap for cases of dengue and chikungunya. In addition, dengue hot spots between 2008 and 2016 were significantly associated with dengue hotspots detected between 2017 and 2020 in five of the nine cities. 

The work builds on a previous study of the spatial-temporal overlap of the three diseases, focused on Merida, a city of one million located in the Yucatan Peninsula. That study showed that nearly half of Merida’s dengue cases from 2008 to 2015 were clustered in 27 percent of the city. These dengue hot spots contained 75 percent of the first chikungunya cases reported during the outbreak of that disease in 2015 and 100 percent of the first Zika cases reported during the Zika outbreak of 2016. 

“In this latest paper, we’ve expanded our analysis in scope and geography and shown that the findings are consistent across these nine cities of different sizes and in different regions,” Vazquez-Prokopec says. “We’ve confirmed that dengue, Zika and chikungunya outbreaks tend to concentrate in small areas of a city, and that these hot spots are predictive of where future cases will concentrate.” 

Mosquito control efforts generally involve outdoor spraying that covers broad swaths of a city, but the Aedes aegypti mosquito has adapted to live inside houses. Work by Vazquez-Prokopec and collaborators has shown that the best way to control these mosquitos and the diseases they spread is by spraying a long-lasting pesticide indoors — on the ceilings, along the bases of walls, and in other areas of homes where the mosquitos tend to cluster. This approach — known as targeted indoor residual spraying — is too expensive and time-consuming to apply across a city. 

The statistical framework in the current paper, however, allows public health officials to concentrate their efforts on previous hot spots for Aedes-borne diseases to better control — and even prevent — outbreaks. 

“The ultimate goal is to give public health officials the power to harness big data and do more effective and efficient mosquito control — even before an epidemic begins,” Vazquez-Prokopec says. 

Vazquez-Prokopec is currently leading a consortium in a randomized clinical trial in Merida to test targeted indoor residual spraying as an intervention against Aedes-borne diseases. The five-year trial, launched in 2020, is funded by a $6.5 million grant from the National Institutes of Health. 

Dengue fever is sometimes called “break-bone fever” due to the excruciating pain that is among its symptoms. More than one third of the world’s population lives in areas at high risk for infection with the dengue virus, a leading cause of illness and death in the tropics and subtropics. Dengue is endemic through most of Mexico, where between 75,000 and 355,000 cases occur annually, translating into an economic cost of between about U.S. $150 million and $257 million annually. 

Chikungunya is rarely fatal but the symptoms can be severe and debilitating. Zika can cause symptoms similar to those of dengue and chikungunya, such as joint pains and fever. While Zika tends to be less debilitating, or even asymptomatic, if a pregnant woman contracts the virus it can have a catastrophic impact on her unborn child, including severe brain defects. 

Co-authors of the Lancet Planetary Health paper include researchers from Mexico’s Ministry of Health; the Autonomous University of the Yucatan; the Autonomous University of Nuevo Leon; Yucatan Health Services; the Mexican Society of Public Health; the National Institute of Public Health in Cuernavaca; the Undersecretary of Prevention and Health Promotion in Mexico City; the Pan American Health Organization; and the U.S. Centers for Disease Control and Prevention. 

The work was funded by USAID, the U.S. Centers for Disease Control and Prevention, the Canadian Institute of Public Health, the state of Yucatan, the National Institutes of Health and Emory University.

Related:

Zeroing in on a mosquito menace

Contact tracing, with indoor spraying, can curb dengue outbreak

Wednesday, June 30, 2021

Genetic risks for nicotine dependence span a range of traits and diseases

"Genetic studies may help reduce some of the stigma society has against substance use disorders, while also making treatment more accessible," says Victoria Risner, first author of the new study on nicotine dependence, who did the work as an Emory undergraduate.

By Carol Clark 

Some people casually smoke cigarettes for a while and then stop without a problem, while others develop long-term, several packs-per-day habits. A complex mix of environmental, behavioral and genetic factors appear to raise this risk for nicotine dependence. 

Studies of groups of twins suggest that 40 to 70 percent of the risk factors are heritable. Until recently, however, studies have only explained about 1 percent of the observed variation in liability to nicotine dependence, using a genetic score based on how many cigarettes a person smokes per day. 

A study led by psychologists at Emory University offers a new model for examining this genetic risk. It leveraged genome wide association studies for a range of different traits and disorders correlated with nicotine dependence and explained 3.6 percent of the variation in nicotine dependence. 

The journal Nicotine & Tobacco Research published the finding. 

Higher polygenetic scores for a risk for schizophrenia, depression, neuroticism, self-reported risk-taking, a high body mass index, alcohol use disorder, along with a higher number of cigarettes smoked per day were all indicators of a higher risk for nicotine dependence, the study found. And polygenetic scores associated with higher education attainment lowered the risk for nicotine dependence, the results showed. 

“If you look at the joint effect of all of these characteristics, our model accounts for nearly 4 percent of the variation in nicotine dependence, or nearly four times as much as what we learn when relying solely on a genetic index for the number of cigarettes someone smokes daily,” says Rohan Palmer, senior author of the study and assistant professor in Emory’s Department of Psychology, where he heads the Behavioral Genetics of Addiction Laboratory. 

“What we’re finding,” Palmer adds, “is that to better leverage genetic information, we need to go beyond individual human traits and disorders and think about how risk for different behaviors and traits are interrelated. This broader approach can give us a much better measure for whether someone is at risk for a mental disorder, such as nicotine dependence.” 

Rohan Palmer heads the Department of Psychology's Behavioral Genetics of Addiction Laboratory that is developing new methods to better understand what makes people vulnerable to substance use disorders.

“All of the traits and diseases we looked at are polygenic, involving multiple genes,” adds Victoria Risner, first author of the study, who did the work as an Emory undergraduate majoring in neuroscience and behavioral biology. “That means that millions of genetic variants likely go into a complete picture for all of the heritable risks for nicotine dependence.” 

The researchers hope that others will build on their multi-trait, polygenetic model and continue to boost the understanding of the risk for such complex disorders. “The more we learn, the closer we can get to one day having a genetic test that clinicians can use to inform their assessment of someone’s risk for nicotine dependence,” Palmer says. 

Although the hazards of smoking are well established, about 14 percent of Americans report daily use of tobacco. Around 500,000 people die each year in the United States from smoking or exposure to smoke, and another 16 million live with serious illnesses caused by tobacco use, including cancer, cardiovascular disease and pulmonary disease. While the toxic chemicals produced during smoking and vaping are what cause harmful health effects, it’s the addictive component of nicotine that hooks people on these habits. 

Risner worked on the current paper for her honors thesis. “Nicotine dependence was interesting to me because the vaping scene was just arriving while I was an undergraduate,” she says. “I saw some of my own friends who were into vaping quickly becoming dependent on it, while some others who were using the same products didn’t. I was curious about the genetic underpinnings of this difference.” 

The project leveraged genome-wide association studies for a range of traits and disorders. The researchers then looked for matching variants in genetic data from a national representative sample of Americans diagnosed with nicotine dependence. The results showed how polygenetic scores for the different traits and disorders either raised or lowered the risk for that dependence. The number of cigarettes smoked per day, self-perceived risk-taking and educational attainment were the most robust predictors. 

The multi-variant, polygenetic model offers a road map for future studies. A clearer picture of heritability for nicotine dependence, for instance, may be gained by adding more risk associations to the model (such as nicotine metabolism) and clusters of polygenic traits (such as anxiety along with neuroticism). 

“As we continue to zero in on who is most at risk for becoming nicotine dependent, and what inter-related factors, whether genetic or environmental, may raise their risk, that could help determine what intervention might work best for an individual,” Palmer says. 

“Just a few decades ago, it was not well understood that nicotine dependence could have a genetic component,” Risner says. “Genetic studies may help reduce some of the stigma society has against substance use disorders, while also making treatment more accessible.” 

Risner graduated from Emory in 2019 and is now in medical school at the University of North Carolina, Chapel Hill. This summer, she’s applying the coding and analytical skills she learned at Emory to conduct research into genetic factors that may raise the risk for pre-term births. 

Emory co-authors of the Nicotine & Tobacco Research article include graduate student Lauren Bertin; post-doctoral fellow Chelsie Benca-Bachman; and Alicia Smith, associate professor in the School of Medicine. Additional authors include researchers from the University of Helsinki; Brown University; the Providence VA Medical Center; the Jackson Laboratory in Bar Harbor, Maine; Purdue University; and the University of Colorado at Boulder. 

The work on the Nicotine & Tobacco Research article was funded by the National Institute on Drug Abuse and the Academy of Finland.

Related:

Heritable traits that appear in teen years raise risk for adult cannabis use

New research aims to understand how genetic differences contribute to addiction

Monday, June 28, 2021

New molecule found in chestnut leaves disarms dangerous staph bacteria

"We're laying the groundwork for new strategies to fight bacterial infections at the clinical level," says Emory ethnobotanist Cassandra Quave, shown gathering samples of chestnut leaves in Italy. "We urgently need these new strategies."

By Carol Clark

Scientists isolated a molecule, extracted from the leaves of the European chestnut tree, with the power to neutralize dangerous, drug-resistant staph bacteria. Frontiers in Pharmacology published the finding, led by scientists at Emory University. 

The researchers dubbed the molecule Castaneroxy A, after the genus of the European chestnut, Castanea. The use of chestnut leaves in traditional folk remedies in rural Italy inspired the research. 

“We were able to isolate this molecule, new to science, that occurs only in very tiny quantities in the chestnut leaves,” says Cassandra Quave, senior author of the paper and associate professor in Emory’s Center for the Study of Human Health and the School of Medicine’s Department of Dermatology. “We also showed how it disarms Methicillin-resistant Staphylococcus aureus by knocking out the bacteria’s ability to produce toxins.” 

Methicillin-resistant Staphylococcus aureus (MRSA) causes infections that are difficult to treat due to its resistance to antibiotics. It is one of the most serious infectious disease concerns worldwide, labeled as a “serious threat” by the Centers for the Disease Control and Prevention. In the United States alone, nearly 3 million antibiotic-resistant infections occur each year, killing more than 35,000 people. 

Antibiotics work by killing staph bacteria, which can lead to greater resistance among those few bacteria that survive, spawning “super bugs.” The Quave lab has identified compounds from the Brazilian peppertree, in addition to the European chestnut tree, that simply neutralize the harmful effects of MRSA, allowing cells and tissue to naturally heal from an infection without boosting resistance. 

“We’re trying to fill the pipeline for antimicrobial drug discovery with compounds that work differently from traditional antibiotics,” Quave says. “We urgently need these new strategies.” She notes that antimicrobial infections kill an estimated 700,000 globally each year, and that number is expected to grow exponentially if new methods of treatment are not found. 

First author of the Frontiers in Pharmacology paper is Akram Salam, who did the research as a PhD student in the Quave lab through Emory’s Molecular Systems and Pharmacology Graduate Program.

The European chestnut, also known as the sweet chestnut, is native to Southern Europe and Asia Minor.

Quave is a medical ethnobotanist, researching traditional plant remedies to find promising leads for new drugs. Although many major drugs are plant-based, from aspirin (the bark of the willow tree) to Taxol (the bark of the Pacific yew tree), Quave is one of the few ethnobotanists with a focus on antibiotic resistance.

The story behind the current paper began more than a decade ago, when Quave and her colleagues researched written reports and conducted hundreds of field interviews among people in rural southern Italy. That pointed them to the European, or sweet, chestnut tree, native to Southern Europe and Asia Minor. “In Italian traditional medicine, a compress of the boiled leaves is applied to the skin to treat burns, rashes and infected wounds,” Quave says. 

Quave took specimens back to her lab for analysis. By 2015, her lab published the finding that an extract from the leaves disarms even the hyper-virulent MRSA strains capable of causing serious infections in healthy athletes. Experiments also showed the extract did not disturb normal, healthy bacteria on skin cells. 

Finally, the researchers demonstrated how the extract works, by inhibiting the ability of MRSA bacteria to communicate with one another, a process known as quorum sensing. MRSA uses this sensing signaling system to make toxins and ramp up its virulence. 

For the current paper, the researchers wanted to isolate these active ingredients from the plant extract. The process is painstaking when done manually, because plant extracts typically contain hundreds of different chemicals. Each chemical must be separated out and then tested for efficacy. Large scale fraction collectors, coupled to high-performance liquid chromatographic systems, automate this separation process, but they can cost tens of thousands of dollars and did not have all the features the Quave lab needed. 

Marco Caputo, a research specialist in the lab, solved the problem. Using a software device from a child’s toy, the LEGO MINDSTORMS robot creator, a few LEGO bricks, and some components from a hardware store, Caputo built an automated liquid separator customized to the lab’s needs for $500. The lab members dubbed the invention the LEGO MINDSTORMS Fraction Collector. They published instructions for how to build it in a journal so that other researchers can tap the simple, but effective, technology. 

The lab's homemade fraction collector.

The Quave lab first separated out a group of molecules from the plant extract, cycloartane triterpenoids, and showed for the first time that this group actively blocks the virulence of MRSA. The researchers then dove deeper, separating out the single, most active molecule from this group, now known as Castaneroxy A. 

“Our homemade piece of equipment really helped accelerate the pace of our discovery,” Quave says. “We were able to isolate this molecule and derive pure crystals of it, even though it only makes up a mere .0019 percent of the chestnut leaves.” 

Tests on mouse skin infected with MRSA, conducted in the lab of co-author Alexander Horswill at the University of Colorado, confirmed the molecule’s efficacy at shutting down MRSA’s virulence, enabling the skin to heal more rapidly. 

Co-author John Bacsa, director of Emory Department of Chemistry’s X-ray Crystallography Center, characterized the crystal shape of Castaneroxy A. Understanding the three-dimensional configuration of the crystal is important for future studies to refine and optimize the molecule as a potential therapeutic.

“We’re laying the groundwork for new strategies to fight bacterial infections at the clinical level,” Quave says. “Instead of being overly concerned about treating the pathogen, we’re focusing on ways to better treat the patient. Our goal is not to kill the microbes but to find ways to weaken them so that the immune system or antibiotics are better able to clear out an infection.” 

Emory co-authors of the paper also include graduate students Caitlin Risener and Lewis Marquez; post-doctoral fellow Gina Porras; and former staff scientist James Lyles. Additional authors from the University of Colorado are Young-Saeng Cho and Morgan Brown. 

The work was funded by the National Center for Complementary and Integrative Health, Emory’s Department of Dermatology, the National Institute of Allergy and Infectious Diseases and the National Institute of General Medical Sciences.

Related:

Brazilian peppertree packs power to knock out antibiotic-resistant bacteria

Major review of plants' role in antibacterial activity clears new paths for drug discovery

Chestnut leaves yield extract that disarms deadly bacteria

Tuesday, June 8, 2021

Study shows adaptive brain response to stress, and its absence in people with depression

"Learning more about how acute stress and chronic stress affect the brain may help in the development of treatment targets for depression," says Jessica Cooper, first author of the study and a post-doctoral fellow in Emory's Department of Psychology.

By Carol Clark

A new study identifies a novel biomarker indicating resilience to chronic stress. This biomarker is largely absent in people suffering from major depressive disorder, and this absence is further associated with pessimism in daily life, the study finds. 

Nature Communications published the research by scientists at Emory University. 

The researchers used brain imaging to identify differences in the neurotransmitter glutamate within the medial prefrontal cortex before and after study participants underwent stressful tasks. They then followed the participants for four weeks, using a survey protocol to regularly assess how participants rated their expected and experienced outcomes for daily activities. 

“To our knowledge, this is the first work to show that glutamate in the human medial prefrontal cortex shows an adaptive habituation to a new stressful experience if someone has recently experienced a lot of stress,” says Michael Treadway, senior author of the study and professor in Emory’s Department of Psychology and Department of Psychiatry and Behavioral Science. “Importantly, this habituation is significantly altered in patients with depression. We believe this may be one of the first biological signals of its kind to be identified in relation to stress and people who are clinically depressed.” 

“Learning more about how acute stress and chronic stress affect the brain may help in the identification of treatment targets for depression,” adds Jessica Cooper, first author of the study and a post-doctoral fellow in Treadway’s Translational Research in Affective Disorders Laboratory

The lab focuses on understanding the molecular and circuit-level mechanisms of psychiatric symptoms related to mood disorders, anxiety and decision-making. 

It’s long been known that stress is a major risk factor for depression, one of the most common and debilitating of mental illnesses. “In many ways, depression is a stress-linked disorder,” Treadway says. “It’s estimated that 80 percent of first-time depressive episodes are preceded by significant, chronic life stress.” 

Around 16 to 20 percent of the U.S. population will meet the criteria for a major depressive disorder during their lifetimes. Experts are predicting rates of depression to climb even further in the wake of the ongoing COVID-19 pandemic. During the pandemic, about four in 10 adults in the United States have reported symptoms of anxiety or depressive disorder, up from one in 10 who reported them in 2019, according to the Kaiser Family Foundation. 

“The pandemic has created more isolation for many people, while also increasing the amount of severe stressors and existential threats they experience,” Treadway says. “That combination puts a lot of people at high risk for becoming depressed.” 

Although the link between stress and depression is clearly established, the mechanisms underlying this relationship are not. Experiments with rodents have shown an association between the response of glutamate — the major excitatory neurotransmitter in the mammalian brain — and stress. The role of glutamate in humans with depression, however, has been less clear. 

The 88 participants in the current study included people without a mental health disorder and unmedicated patients diagnosed with a major depressive disorder. Participants were surveyed about perceived recent stress in their lives before they underwent experiments using a brain scanning technique known as magnetic resonance spectroscopy. 

While in the scanner, participants were required to alternate between performing two tasks that served as acute stressors: Putting their hand up to the wrist in ice water and counting down from the number 2,043 by steps of 17 while someone evaluated their accuracy. 

Brain scans before and after the acute stressor measured glutamate in the medial prefrontal cortex, an area of the brain involved with thinking about one’s state and forming expectations. Previous research has also found that this brain area is involved in regulating adaptive responses to stress. 

Participants submitted saliva samples while in the scanner, allowing the researchers to confirm that the tasks elicited a stress response by measuring the amount of the stress hormone cortisol in the sample. 

In healthy individuals, the brain scans revealed that glutamate change in response to stress in the medial prefrontal cortex was predicted by individual levels of recent perceived stress. Healthy participants with lower levels of stress showed increased glutamate in response to acute stress, while healthy participants with higher levels of stress showed a reduced glutamate response to acute stress. This adaptive response was comparatively absent in the patients diagnosed with depression. 

“The decrease in the glutamate response over time appears to be a signal, or a marker, of a healthy adaptation to stress,” Treadway says. “And if the levels remain high that appears to be a signal for maladaptive responses to stress.” 

The initial result was strong for the adaptation in healthy participants, but was in a modest sample size, so the researchers decided to see if they could replicate it. “Not only did we get a replication, it was an unusually strong replication,” Treadway says. 

The experiment also included a group of healthy controls who underwent scanning before and after performing tasks. Rather than stressful tasks, however, the controls were asked to place a hand into warm water or to simply count out loud consecutively. Their glutamate levels were not associated with perceived stress and they did not show a salivary cortisol response. 

To expand their findings, the researchers followed participants for four weeks after scanning. Every other day, the participants reported on their expected and experienced outcomes for activities in their daily lives. The results showed that glutamate changes that were higher than expected based on an individual’s level of perceived stress predicted an increased pessimistic outlook — a hallmark for depression. 

“We were able to show how a neural response to stress is meaningfully related to what people experience in their daily lives,” Cooper says. “We now have a large, rich data set that gives us a tangible lead to build upon as we further investigate how stress contributes to depression.” 

Emory co-authors of the study include former and current graduate students from the Treadway lab Victoria Lawlor, Shabnam Hossein and Andrew Teer; as well as current and former research assistants Makiah Nuutinen, Brittany DeVries, Daniel Cole, Chelsea Leonard and Emma Hahn. Additional authors include researchers from UCLA, the University of Arkansas, Princeton and McLean Hospital/Harvard Medical School. 

The work was supported by the National Institutes of Mental Health.

Related:

How the brain decides to make an effort

How chronic inflammation may drive down dopamine and motivation

Study reveals how the brain decides to make an effort


Wednesday, June 2, 2021

Flow of slushy sea ice predicts glacier calving

A view of Illusiat Glacier shows the ice melange (in the foreground) and the sheered off edge of the glacier where a massive ice sheet just broke away. (Jason Amundson)

Ice mélange, the mass of floating sea ice that buttresses many tidewater glaciers, plays a major role in the timing of calving icebergs, finds a new study published in Nature Geoscience

Scientists measured how just a tiny shift in the flow of a mélange, from smooth to slightly more chaotic, can predict up to one hour in advance that a massive hunk of ice will break off from a glacier, then crash into the ocean to form a new iceberg. 

“As a gateway to the ocean, ice mélange is critical to predictions of sea-level rise,” says Justin Burton, associate professor of physics at Emory University and co-author of the paper. “We’ve provided what may be the best, most high-resolution data ever on the dynamics of a mélange leading up to a major calving event. That helps us understand the forces determining how much ice melts into the ocean, and how fast it happens.” 

Ryan Cassotto, a glaciologist from the University of Colorado, Boulder, is lead author of the paper. Co-authors include Jason Amundson from the University of Alaska Southeast, Juneau; and Mark Fahnestock and Martin Truffer, both from the University of Alaska Fairbanks. 

The study’s data was drawn from Ilulissat, a World Heritage Site and the most productive tidewater glacier in Greenland, also known as Jakobshavn Glacier. Kilometer-sized icebergs that calve from Ilulissat often capsize, leading to glacial earthquakes and small tsunamis. 


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Monday, May 24, 2021

Even children think money can be 'dirty' money, study finds

Experiments led by Emory psychologist Arber Tasimi found that children prefer non-stolen money offered by a "bad" person over stolen money offered by an "okay" person.

 By Carol Clark

When people deposit a $100 bill into their bank accounts, they don’t imagine that when they later withdraw $100 they will get the same bill. After all, the only thing that matters about money is its amount. A dollar is just like any other dollar — unless it comes with a tainted past. 
 
“People tend to imbue objects with essences,” says Arber Tasimi, assistant professor of psychology at Emory University. “We can be put off by objects that we know have a ‘bad’ essence because of an immoral history, like a sweater worn by Hitler. And money doesn’t appear to be an exception.” 

Tasimi’s latest work finds that children as young as five show an aversion to accepting “dirty” money. The journal Cognitive Science published the research, which Tasimi conducted with Susan Gelman, a psychologist at the University of Michigan. 

“This sensitivity to morality, even in the context of money, seems to emerge early,” Tasimi says. “The fact that children are making these distinctions adds to the evidence showing just how much we care about where things come from, particularly when they come from bad sources.” 

Tasimi heads the Morality and Development Lab at Emory. He’s particularly interested in moral conflict — how we wrestle with our desire for personal benefits versus our interest in the welfare of others. 

In previous research, Tasimi found that even babies prefer to take a single graham cracker offered to them by a “nice” puppet rather than two graham crackers offered by a “mean” puppet. But when the mean puppet offers them eight crackers, most babies “sell out.” 

For the current paper, Tasimi wanted to explore how a sense of morality tied to money develops in children. A series of experiments included participants in two age groups: 5-to-6-year-olds and 8-to-9-year-olds. The children were presented with various hypothetical scenarios: A person offering them a dollar. A person offering them a stolen dollar that they had found. A “bad” person who stole a dollar but was offering them a dollar they did not steal. And a “bad” person offering them a dollar that they had stolen. 

The results showed that the children significantly rejected “dirty” money. They much preferred non-stolen money offered by a “bad” person than stolen money offered by an “okay” person. 

“What we find over and over is that the morality of the money plays a critical role in whether people decide to take it,” Tasimi says. “Why would we imbue money with ‘badness’? I think that’s the million-dollar question.” 

In ongoing work, Tasimi is delving deeper into possible answers to the mystery. Does the source of the money matter because it could be tainted? Is it due to an aversion to profiting at the expense of others? Or is it because accepting the tainted money somehow endorses the immoral activity behind it? 

“I’m also intrigued by individual differences,” Tasimi adds. “Some people do treat a dollar like any other dollar, while others don’t. Why are some people bothered by ‘dirty’ money and others are not?”

Related:

Wednesday, April 28, 2021

Human antibiotic use threatens endangered wild chimpanzees

The number of chimpanzees in Gombe National Park, the site of Jane Goodall's groundbreaking field studies, are down to about 95. "By misusing antibiotics, people can actually harm not only themselves, but also the species they share an environment with," says Emory disease ecologist Thomas Gillespie.

By Carol Clark

It’s well established that infectious disease is the greatest threat to the endangered chimpanzees made famous by the field studies of Jane Goodall at Gombe National Park in Tanzania. Now, new research led by scientists at Emory University shows that nearly half of the fecal samples from wild chimpanzees contain bacteria that is resistant to a major class of antibiotics commonly used by people in the vicinity of the park. 

The journal Pathogens published the findings

“Our results suggest that antibiotic-resistant bacteria is actually spreading from people to non-human primates by making its way into the local watershed,” says Thomas Gillespie, senior author of the study and associate professor in Emory’s Department of Environmental Sciences and Rollins School of Public Health. “People are bathing and washing in the streams, contaminating the water with drug-resistant bacteria where wild chimpanzees and baboons drink.” 

The researchers tested for genes conferring resistance to sulfonamides — drugs often used by people in the region to treat diarrheal diseases — in fecal samples from humans, domestic animals, chimpanzees and baboons in and around Gombe National Park. They also tested stream water used by these groups. 

Sulfonamide resistance appeared in 74 percent of the human samples overall, 48 percent of chimpanzee samples, 34 percent of baboon samples, and 17 percent of the domestic animal samples. Sulfonamide also showed up in 19 percent of the samples taken from streams shared by people, domestic animals and wildlife. 

The researchers also tested all the groups in the study for genes conferring resistance to tetracycline — another class of antibiotics that is used much less frequently by people in the vicinity, likely due to its greater expense and the fact that it is less available in the area. As expected, very few of the fecal samples from any of the groups, and none of the water samples from the streams, showed evidence of tetracycline resistance. 

First author of the study is Michele Parsons, who did the work as an Emory doctoral student in Environmental Sciences. Parsons has since graduated and works at the Centers for Disease Control and Prevention (CDC). Co-authors include researchers from the Jane Goodall Institute, the CDC, the University of Minnesota and Franklin and Marshall College. 

Gillespie is a disease ecologist who helped pioneer the “One Health” approach to protect humans, ecosystems and biodiversity. His projects in Africa, including the collaboration with the Jane Goodall Institute in Tanzania, are focused on helping farmers subsisting amid fragmented forests co-exist with primates and other wildlife in ways that minimize the risk of pathogen exchange between species, known as “spillover.” The virus that causes AIDS, for example, spilled over from chimpanzees to people. 

“It’s important to consider both sides of the story — human health and well-being, as well as conservation of chimpanzees and other species,” Gillespie says. 

Human encroachment has taken a toll on the great apes, due to fragmented habitat and the exchange of pathogens. Today, the number of chimpanzees in Gombe National Park are down to about 95. 

Diarrheal diseases are common in the area and people often turn to cheap sulfonamide antibiotics that are available without a prescription at small stores that act as informal pharmacies, selling drugs, soap and other necessities. Wild chimpanzees also suffer from wasting diseases that can be related to bacterial and other enteric pathogens that affect their ability to maintain calorie intake and absorb nutrients. 

“The majority of people in our sampling harbored bacteria resistant to the sulfonamide medication they are taking,” Gillespie says. “In those cases, they’re spending their money on a drug that is not helping them get better. Overuse of such drugs creates the potential for more lethal, antibiotic-resistant ‘super bugs’ to emerge.” 

The research findings will now support the development of interventions. 

More guidance is needed locally regarding the proper use of antibiotics, Gillespie says. He adds that it is also important to improve hygiene for wash-related activities in area streams, as well as to improve disposal of human waste materials. 

“By misusing antibiotics, people can actually harm not only themselves, but also the species they share an environment with,” Gillespie says. “After drug-resistant bacteria jump into chimpanzees, it can further evolve with the chimpanzees and then spill back into humans. We need to be thinking about infectious diseases within evolutionary and ecological frameworks, something that’s not often done in medicine.” 

The study was funded by the Morris Animal Foundation, the Emory Global Health Institute, the Arcus Foundation, the Leo S. Guthman Foundation and the National Institutes of Health.

Related:

Zoo gorillas contract COVID, raising alarms for great apes in the wild

Valuing 'natural capital' vital to avoid next pandemic, experts warn

Disease poses risk to chimpanzee conservation, Gombe study finds

Wednesday, April 21, 2021

Georgia Aquarium otters join list of animals testing positive for SARS-CoV-2

Otters are Mustelids, a diverse group of carnivorous mammals that includes mink and ferret — two other species that have also become infected with SARS-CoV-2. (Getty Images)

By Carol Clark

The recent positive SARS-CoV-2 tests of Asian small-clawed otters at the Georgia Aquarium add to the mystery of why some animals may be more susceptible than others to the virus that causes COVID-19. 

“In one sense, it’s not surprising to see otters infected, because we’ve already seen infections in mink and ferrets, which are closely related species,” says Thomas Gillespie, associate professor in Emory University’s Department of Environmental Sciences and Rollins School of Public Health. 

Otters, mink and ferrets are all Mustelids, a diverse group of carnivorous mammals, notes Gillespie, a disease ecologist who studies how pathogens jump between wildlife, domestic animals and people.

Most of the research into what animal species may be susceptible to SARS-CoV-2 is based on the genetics of protein binding sites that the virus uses to gain a foothold in a host. People, great apes and some monkeys have the highest susceptibility, according to this research, Gillespie says. 

In January, some members of the gorilla troop at the San Diego Zoo tested positive for SARS-CoV-2, after they exhibited COVID-19 symptoms. 

“What’s surprising,” Gillespie says, “is that Mustelids are at the opposite end of the spectrum in terms of a binding propensity with SARS-CoV-2. In one of the more robust studies to date, they fell into the lower range of binding scores among 400 species of vertebrates. And yet, they keep popping up with infections. That’s where the mystery lies.” 

The Georgia Aquarium announced in an April 18 news release that the otters were tested after showing symptoms such as sneezing, runny noses, lethargy and coughing. The animals were removed from their exhibit for behind-the-scenes care and are expected to make a full recovery, the release stated. 

The virus that causes COVID-19 is zoonotic, meaning that it originated in animals — most likely horseshoe bats — and may have passed through another species before making its way to humans. 

“It’s critical right now for the world to focus on preventing human-to-human transmission of the virus,” Gillespie says. “But it’s also important to consider the longer-term, bigger picture of how pathogens can spill over from animals to people and then back to animals again.” 

Gillespie helped pioneer the One Health approach to protecting humans, ecosystems and biodiversity. The primary risks for future spillover of zoonotic diseases are deforestation of tropical environments and large-scale industrial farming of animals, he says. 

In late 2020, COVID-19 outbreaks were seen in mink around the world, including the United States, at farms that mass-produce the animals for the fur trade. The mink are kept in densely packed conditions that are ideal for spreading pathogens, Gillespie says. 

Denmark culled 17 million mink after the virus spread from the human caretakers to the animals, then mutated and spread back to some of the human caretakers. 

“The good news is that there are relatively few documented cases of animal transmission to humans, and these appear to be restricted to the most ideal conditions for transmission, such as the crowded conditions of industrial mink farming,” Gillespie says. 

Ferrets are a common laboratory model for the study of respiratory diseases, due to their unique respiratory biology. Experimental studies have shown that they can easily be infected with SARS-CoV-2. 

The black-footed ferret is among the most endangered mammals in North America. That prompted researchers at the U.S. National Wildlife Health Center last December to start testing a veterinary vaccine for COVID-19 on a captive population of the animals at the National Black-footed Ferret Conservation Center in Colorado. 

Almost all of the species that have tested positive for SARS-CoV-2, including cats, dogs, tigers, gorillas and a few other mammals, live in close proximity to people — either as pets, in zoos or in laboratories. One exception is a wild mink, found near a mink farm in Utah, that tested positive for SARS-CoV-2, according to the U.S. Department of Agriculture. 

“Testing of wildlife is rare,” Gillespie says. “And most testing of captive animals is done only if they show symptoms, suggesting there may be many more asymptomatic cases. There are a lot of important questions into how SARS-CoV-2 may affect animals that we have not yet started exploring.” 

The questions are important to protect both the health of animals and people, he adds. 

“Widespread infection within a population of a novel virus is the kind of event that could potentially push endangered and critically endangered species over the edge,” Gillespie says. “And any time a virus enters a new species with different selective pressures, that provides more opportunities for new mutants of the virus to evolve and potentially spill over into humans.”

Related:

San Diego Zoo gorillas contract COVID, raising alarms for great apes in the wild

Valuing 'natural capital' vital to avoid next pandemic

Bat ecology in the era of pandemics

Wednesday, April 14, 2021

Physicists develop theoretical model for neural activity of mouse brain

"One of the wonderful things about our model is that it's simple," says Mia Morrell, who did the research as an Emory senior majoring in physics. Morrell graduated last year and is now in New Mexico, above, where she is completing a post-baccalaureate physics program at Los Alamos National Laboratory.

By Carol Clark

The dynamics of the neural activity of a mouse brain behave in a peculiar, unexpected way that can be theoretically modeled without any fine tuning, suggests a new paper by physicists at Emory University. Physical Review Letters published the research, which adds to the evidence that theoretical physics frameworks may aid in the understanding of large-scale brain activity. 

“Our theoretical model agrees with previous experimental work on the brains of mice to a few percent accuracy — a degree which is highly unusual for living systems,” says Ilya Nemenman, Emory professor of physics and biology and senior author of the paper. 

The first author is Mia Morrell, who did the research for her honors thesis as an Emory senior majoring in physics. She graduated from Emory last year and is now in a post-baccalaureate physics program at Los Alamos National Laboratory in New Mexico. 

“One of the wonderful things about our model is that it’s simple,” says Morrell, who will start a Ph.D. program in physics at New York University in the fall. “A brain is really complex. So to distill neural activity to a simple model and find that the model can make predictions that so closely match experimental data is exciting.” 

The new model may have applications for studying and predicting a range of dynamical systems that have many components and have varying inputs over time, from the neural activity of a brain to the trading activity of a stock market. 

Co-author of the paper is Audrey Sederberg, a former post-doctoral fellow in Nemenman’s group, who is now on the faculty at the University of Minnesota. 

The work is based on a physics concept known as critical phenomena, used to explain phase transitions in physical systems, such as water changing from liquid to a gas. 

In liquid form, water molecules are strongly correlated to one another. In a solid, they are locked into a predictable pattern of identical crystals. In a gas phase, however, every molecule is moving about on its own. 

“At what is known as a critical point for a liquid, you cannot distinguish whether the material is liquid or vapor,” Nemenman explains. “The material is neither perfectly ordered nor disordered. It’s neither totally predictable nor totally unpredictable. A system at this ‘just right’ Goldilocks spot is said to be ‘critical.’” 

Very high temperature and pressure generate this critical point for water. And the structure of critical points is the same in many seemingly unrelated systems. For example, water transitioning into a gas and a magnet losing its magnetism as it is heated up are described by the same critical point, so the properties of these two transitions are similar. 

In order to actually observe a material at a critical point to study its structure, physicists must tightly control experiments, adjusting the parameters to within an extraordinarily precise range, a process known as fine-tuning. 

In recent decades, some scientists began thinking about the human brain as a critical system. Experiments suggest that brain activity lies in a Goldilocks spot — right at a critical transition point between perfect order and disorder. 

“The neurons of the brain don’t function just as one big unit, like an army marching together, but they are also not behaving like a crowd of people running in all different directions,” Nemenman says. “The hypothesis is that, as you increase the effective distance between neurons, the correlations between their activity are going to fall, but they will not fall to zero. The entire brain is coupled, acting like a big, interdependent machine, even while individual neurons vary in their activity.” 

Researchers began searching for actual signals of critical phenomena within brains. They explored a key question: What fine tunes the brain to reach criticality? 

In 2019, a team at Princeton University recorded neurons in the brain of a mouse as it was running in a virtual maze. They applied theoretical physics tools developed for non-living systems to the neural activity data from the mouse brain. Their results suggested that the neural activity exhibits critical correlations, allowing predictions about how different parts of the brain will correlate with one another over time and over effective distances within the brain. 

For the current paper, the Emory researchers wanted to test whether fine-tuning of particular parameters were necessary for the observation of criticality in the mouse brain experiments, or whether the critical correlations in the brain could be achieved simply through the process of it receiving external stimuli. The idea came from previous work that Nemenman’s group collaborated on, explaining how biological systems can exhibit Zipf’s law — a unique pattern of activity found in disparate systems. 

“We previously created a model that showed Zipf’s law in a biological system, and that model did not require fine tuning,” Nemenman says. “Zipf’s law is a particular form of criticality. For this paper, we wanted to make that model a bit more complicated, to see if could predict the specific critical correlations observed in the mouse experiments.” 

The model’s key ingredient is a set of a few hidden variables that modulate how likely individual neurons are to be active. 

Morrell wrote the computer code to run simulations and test the model on her home desktop computer. “The biggest challenge was to write the code in a way that would allow it to run fast even when simulating a large system with limited computer memory without a huge server,” she says. 

The model was able to closely reproduce the experimental results in the simulations. The model does not require the careful tuning of parameters, generating activity that is apparently critical by any measure over a wide range of parameter choices. 

“Our findings suggest that, if you do not view a brain as existing on its own, but you view it as a system receiving stimuli from the external world, then you can have critical behavior with no need for fine tuning,” Nemenman says. “It raises the question of whether something similar could apply to non-living physical systems. It makes us re-think the very notion of criticality, which is a fundamental concept in physics.” 

The computer code for the model is now available online, so that anyone with a laptop computer can access it and run the code to simulate a dynamic system with varying inputs over time. 

“The model we developed may apply beyond neuroscience, to any system in which widespread coupling to hidden variables is extant,” Nemenman says. “Data from many biological or social systems are likely to appear critical via the same mechanism, without fine-tuning.” 

The current paper was partially supported by grants from the National Institutes of Health and the National Science Foundation.

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Tuesday, April 6, 2021

Chemists develop tools that may help improve cancer diagnostics, therapeutics

A process known as methylation helps regulate on-and-off switches to keep a host of systems in the body functioning normally. "But the process can get hijacked, creating modifications that may lead to diseases," explains Ogonna Nwajiobi (above), an Emory Ph.D. student in chemistry and first author of the paper.

By Carol Clark

Chemists developed a method to detect changes in proteins that may signal the early stages of cancer, Alzheimer’s, diabetes and other major diseases. Angewandte Chemie published the work, led by chemists at Emory University and Auburn University. The results offer a novel strategy for studying links between unique protein modifications and various pathologies. 

“The knowledge we gain using our new, chemical method holds the potential to improve the ability to detect diseases such as lung cancer earlier, when treatment may be more effective,” says Monika Raj, senior author of the paper and Emory associate professor of chemistry. “A detailed understanding of protein modifications may also help guide personalized, targeted treatment for patients to improve a drug’s efficacy against cancer.” 

The researchers provided a proof of concept for using their method to detect single protein modifications, or monomethylation. Their lab experiments were conducted on the protein lysine expressed from E.coli and other non-human organisms. 

Lysine is one of the nine essential amino acids that is critical to life. After lysine is synthesized in the human body, changes to the protein, known as methylation, can occur. Methylation is a biochemical process that transfers one carbon atom and three hydrogen atoms from one substance to another. Such modifications can occur in single (monomethylation), double (dimethylation) or triple (trimethylation) forms. Demethylation reverses these modifications. 

The small tweaks of methylation and demethylation regulate biological on-off switches for a host of systems in the body, such as metabolism and DNA production. 

“In a normal state, the methylation process creates modifications that are needed to keep your body functioning and healthy,” says Ogonna Nwajiobi, an Emory Ph.D. student in chemistry and first author of the paper. “But the process can get hijacked, creating modifications that may lead to diseases.”

Modifications to lysine, in particular, he adds, have been linked to the development of many cancers and other diseases in humans. 

Sriram Mahesh, from Auburn University is co-first author of the paper. Xavier Streety, also from Auburn, is a co-author. 

The Raj lab, which specializes in developing organic chemistry tools to understand and solve problems in biology, wanted to devise a method to detect monomethylation marks to lysine that have been expressed by an organism. Monomethylation is especially challenging to detect since it leaves negligible changes in the bulk, charge or other characteristics of a lysine modification.

The researchers devised chemical probes, electron-rich diazonium ions, that couple only with monomethlyation sites at certain biocompatible conditions that they can control, including a particular pH level and electron density. They used mass spectroscopy and nuclear magnetic resonance techniques to show that they had selectively hit the correct targets, and to confirm the coupling of atoms at the sites. 

The method is unique because it directly targets the monomethylation sites. Another unique feature of the method is that it is reversible under acidic conditions, allowing the researchers to uncouple the atoms and regenerate the original state of a monomethylation site. 

The Raj lab now plans to collaborate with researchers at Emory’s Winship Cancer Institute to test the new method on tissue samples taken from lung cancer patients. The goal is to home in on differences in lysine monomethylation sites of people with and without lung cancer. 

“It’s like a fishing expedition,” Nwajiobi explains. “The first step is to use our method to find the lysine monomethylation sites in tissue samples, which is difficult to do because of their low abundance. Once we’ve found the sites, our method then allows us to reverse the coupling with our chemical probe, so the functions of the sites can be studied in their intact, original forms.” 

Practical methods for early detection of many diseases, like lung cancer, are needed to help improve patient outcomes. “If we can develop more ways to identify lung cancer earlier, that may open the door for treatments that greatly improve the survival rate,” Raj says. 

The researchers hope to study lysine monomethylation differences between samples taken from patients at different stages of lung cancer, between patients with or without a family history of the disease, and between those who have smoked and those who have not. Knowledge gained from such analyses could set the stage for more personalized, targeted treatments, Raj says. 

Her lab is also developing chemical tools to selectively detect lysine dimethylation and trimethylation sites, in order to help more fully characterize the role of lysine methylation in disease. 

“We hope that other researchers will also apply our methods, and the chemical tools we are developing, to better understand a range of cancers and many other diseases associated with lysine methylation,” Raj says. 

The work was funded by the National Science Foundation.

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Biologists unravel another mystery of what makes DNA go 'loopy'

Tuesday, March 30, 2021

Screams of 'joy' sound like 'fear' when heard out of context

"Our work intertwines language and non-verbal communication in ways that haven't been done in the past," says Emory psychologist Harold Gouzoules, senior author of the study.

By Carol Clark

People are adept at discerning most of the different emotions that underlie screams, such as anger, frustration, pain, surprise or fear, finds a new study by psychologists at Emory University. Screams of happiness, however, are more often interpreted as fear when heard without any additional context, the results show. 

PeerJ published the research, the first in-depth look at the human ability to decode the range of emotions tied to the acoustic cues of screams. 

“To a large extent, the study participants were quite good at judging the original context of a scream, simply by listening to it through headphones without any visual cues,” says Harold Gouzoules, Emory professor of psychology and senior author of the study. “But when participants listened to screams of excited happiness they tended to judge the emotion as fear. That’s an interesting, surprising finding.” 

First author of the study is Jonathan Engelberg, an Emory Ph.D. student of psychology. Emory alum Jay Schwartz, who is now on the faculty of Western Oregon University, is co-author. 

The acoustic features that seem to communicate fear are also present in excited, happy screams, the researchers note. “In fact, people pay good money to ride roller coasters, where their screams no doubt reflect a blend of those two emotions,” Gouzoules says. 

He adds that the bias towards interpreting both of these categories as fear likely has deep, evolutionary roots. 

“The first animal screams were probably in response to an attack by a predator,” he says. “In some cases, a sudden, loud high-pitched sound might startle a predator and allow the prey to escape. It’s an essential, core response. So mistaking a happy scream for a fearful one could be an ancestral carryover bias. If it’s a close call, you’re going to err on the side of fear.” 

The findings may even provide a clue to the age-old question of why young children often scream while playing. 

“Nobody has really studied why young children tend to scream frequently, even when they are happily playing, but every parent knows that they do,” Gouzoules says. “It’s a fascinating phenomenon.” 

While screams can convey strong emotions, they are not ideal as individual identifiers, since they lack the more distinctive and consistent acoustic parameters of an individual’s speaking voice. 

“It’s just speculative, but it may be that when children scream with excitement as they play, it serves the evolutionary role of familiarizing a parent to the unique sound of their screams,” Gouzoules says. “The more you hear your child scream in a safe, happy context, the better able you are to identify a scream as belonging to your child, so you will know to respond when you hear it.” 

Gouzoules first began researching the screams of non-human primates, decades ago. Most animals scream only in response to a predator, although some monkeys and apes also use screams to recruit support when they are in a fight with other group members. “Their kin and friends will come to help, even if some distance away, when they can recognize the vocalizer,” he says. 

In more recent years, Gouzoules has turned to researching human screams, which occur in a much broader context than those of animals. His lab has collected screams from Hollywood movies, TV shows and YouTube videos. They include classic performances by “scream queens” like Jaime Lee Curtis, along with the screams of non-actors reacting to actual events, such as a woman shrieking in fear as aftershocks from a meteor that exploded over Russia shake a building, or a little girl’s squeal of delight as she opens a Christmas present. 

In previous work, the lab has quantified tone, pitch and frequency for screams from a range of emotions: Anger, frustration, pain, surprise, fear and happiness. 

For the current paper, the researchers wanted to test the ability of listeners to decode the emotion underlying a scream, based solely on its sound. A total of 182 participants listened through headphones to 30 screams from movies that were associated with one of the six emotions. All of the screams were presented six times, although never in sequence. After hearing a scream, the listeners rated how likely it was associated with each of six of the emotions, on a scale of one to five. 

The results showed that the participants most often matched a scream to its correct emotional context, except in the case of screams of happiness, which participants more often rated highly for fear. 

“Our work intertwines language and non-verbal communication in a way that hasn’t been done in the past,” Gouzoules says. 

Some aspects of non-verbal vocal communication are thought to be precursors for language. The researchers hypothesize that it may be that the cognitive underpinnings for language also built human capacity in the non-verbal domain. “It’s probably language that gives us this ability to take a non-verbal vocalization and discern a wide range of meanings, depending on the acoustic cues,” Gouzoules says.

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Screams contain a 'calling card' for the vocalizer's identity

What is a scream? The acoustics of a primal human call

Sunday, March 21, 2021

Heritable traits that appear in teen years raise risk for adult cannabis use

Some of the risk for repeated cannabis use into adulthood can be attributed to the genetic effects of neuroticism, risk tolerance and depression, the study found. "While this work marks an important step in identifying genetic factors that can increase the risk for cannabis use, a substantial portion of the factors that raise the risk remain unexplained," says Emory psychologist Rohan Palmer.

By Carol Clark

While some youth experiment with marijuana but don’t go on to long-term use, others develop a problematic pot habit that continues into adulthood. A major new analysis shows that at least a small portion of the risk for developing into an adult marijuana user may be related to inherited behaviors and traits that appear during adolescence. 

The journal Addiction published the findings by researchers at Emory and Brown University. 

“Our analysis suggests that some early adolescent behaviors and traits — like depression, neuroticism and acting out — can be indicative for cannabis use later in life,” says Rohan Palmer, senior author of the paper and assistant professor in Emory’s Department of Psychology, where he heads the Behavioral Genetics of Addiction Laboratory

“Decades of research has shown that behaviors can have a genetic component,” adds Leslie Brick, lead author and assistant professor in the Department of Psychiatry and Human Behavior in Brown’s Alpert Medical School. “And while there is not one genetically-influenced trait that determines whether you’re going to be a long-term cannabis user, our paper indicates that there are polygenic effects across multiple inherited behaviors and traits that show a propensity for increased risk.” 

Brick, a long-time collaborator with Palmer, also holds an adjunct faculty appointment in Emory’s Department of Psychology. 

The Transmissible Liability Index is a well-known measure for a constellation of heritable traits that may appear during the developmental years that are associated with the risk of a substance use disorder. For the current paper, the researchers wanted to tease out which of these heritable characteristics might be associated with repeated marijuana use later in life. 

“Cannabis use has been less studied than tobacco and alcohol,” Palmer says. “For one thing, it’s harder to get people to answer detailed questionnaires honestly about cannabis, since it’s an illegal substance. And it’s also much more difficult to standardize the amount of cannabis consumed, as compared to cigarettes and liquor.” 

Cannabis use, however, is widespread among adolescents and young adults. In 2018, more than 35 percent of high school seniors surveyed reported having used marijuana during the past year and more than 20 percent reported doing so during the past month, according to the National Institute on Drug Abuse (NIDA). 

As cultural norms have shifted, including the legalization of marijuana for adult recreational use in many states, teens’ perceptions of the risks of marijuana use have declined. 

Those risks, however, are real. 

“Adolescence is a major period of brain development,” Brick says. “In fact, our brains don’t stop developing until we are around 25 years old. Research indicates that cannabis has some major impacts on our biology, although its full effects are still not well understood.” 

The researchers drew data from the National Longitudinal Study of Adolescent Health, or Add Health, which includes a nationally representative sample of 20,000 adolescents in grades 7 to 12 in the United States who have been followed into adulthood. Comprehensive data from early adolescence to adulthood was collected on health and health-related behavior, including substance use, personality and genetics. 

For the current paper, the researchers identified a large homogenous subgroup of individuals from the Add Health study, about 5,000 individuals of European ancestry, for their final analytic sample. They then leveraged existing genome-wide association studies to examine whether certain heritable behavioral traits noted during adolescence were associated with the Transmissible Liability Index, and whether any of these traits were also associated with risk for later cannabis use. 

The results showed that a small portion of the risk for repeated cannabis use into adulthood can be attributed to the genetic effects of neuroticism, risk tolerance and depression that can appear during adolescence. 

“While this work marks an important step in identifying genetic factors that can increase the risk for cannabis use, a substantial portion of factors that raise the risk remain unexplained,” Palmer says. “We’ve shown how you can use existing data to assess the utility of a polygenic risk score. More studies are needed to continue to identify unique genetic and other environmental sources for the risk of long-term, problematic use of cannabis.” 

“Better understanding of what behaviors and traits may give someone a pre-disposition for long-term cannabis use gives us a better shot of identifying those most at risk so we can home in on effective interventions,” Brick says. 

A major limitation of the current study, the researchers add, is that it focused on individuals of European ancestry, because no sample size large enough for the genome-wide analysis was available for other ancestral groups. 

Co-authors of the study include the following members of Emory’s Behavioral Genetics of Addiction Laboratory: Graduate students Lauren Bertin, Kathleen Martin and former undergraduate Victoria Risner (now an Emory alum); and Chelsie Benca-Bachman, associate director of research projects in the lab. 

The work was supported by an Avenir grant from the National Institute on Drug Abuse.

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Tuesday, March 9, 2021

Water temperature key to schistosomiasis risk and prevention strategies

Karena Nguyen, a post-doctoral fellow in Emory's Department of Biology, shown with two of the freshwater snails that serve as intermediate hosts for the parasites that cause schistosomiasis. (Photo by Rachel Hartman)

By Carol Clark

About one billion people worldwide are at risk for schistosomiasis — a debilitating disease caused by parasitic worms that live in fresh water and in intermediate snail hosts. A new study finds that the transmission risk for schistosomiasis peaks when water warms to 21.7 degrees centigrade, and that the most effective interventions should include snail removal measures implemented when the temperature is below that risk threshold. 

The Proceedings of the National Academy of Sciences published the results, led by Emory University, the University of South Florida and the University of Florida. 

“We’ve shown how and why temperature matters when it comes to schistosomiasis transmission risk,” says Karena Nguyen, a post-doctoral fellow in Emory University’s Department of Biology and a first author of the study. “If we really want to maximize human health outcomes, we need to consider disease transmission in the context of regional temperatures and other environmental factors when developing intervention strategies.” 

The findings indicate that climate change will increase schistosomiasis risk in regions where surface water moves closer to 21.7 degrees centigrade, or 71 degrees Fahrenheit. The researchers also found, however, that implementing snail control measures decreases transmission but raises the temperature for peak transmission risk to 23 degrees centigrade, or 73 degrees Fahrenheit. 

Co-first author of the paper is Philipp Boersch-Supan, an expert in ecological systems at the University of Florida and the British Trust for Ornithology. 

Nguyen is a member of the lab of David Civitello, Emory assistant professor of biology and a co-author of the PNAS paper. The Civitello lab studies the ecological dynamics of disease, aquatics and agricultural ecology through a combination of experiments, field surveys and models. 

“The control of schistosomiasis currently relies on treating infected people,” Civitello says. “However, there is renewed awareness that the ecological factors surrounding the disease also need to be considered. Our paper is a beautiful example of the potential power of uniting ecology with human disease interventions and control measures.” 


Click on graphic of the life cycle of the schistosomiasis parasite, above, to enlarge.

Schistosomiasis is one of the most devasting water-based diseases in developing countries, with more than 200 million people infected worldwide, leading to around 200,000 deaths annually. It is caused by Schistosoma parasites that have a complex life cycle. Freshwater becomes contaminated by the parasite’s eggs when infected people urinate or defecate in the water. After the eggs hatch, the parasites enter freshwater snails where they develop and multiply. More mature parasites are able to leave the snails and re-enter the water. These free-swimming parasites can then burrow into the skin of people who are wading, swimming, bathing, washing or doing agricultural work in contaminated water.

Children who are repeatedly infected can develop anemia, malnutrition and learning difficulties. Over the long term, the parasites can also damage the liver, intestine, lungs and bladder. 

“Schistosomiasis is treatable — people can take a drug to get rid of the adult parasites in their bodies,” Nguyen says. “But in areas where schistosomiasis is prevalent, people can easily get reinfected by coming in contact with contaminated water. And children, who like to play in water, tend to have the highest burden of the disease.” 

For the current paper, Nguyen focused on how global climate change and rising water temperatures might affect each stage of the schistosomiasis transmission cycle. It was already established that both the parasites and the snails are sensitive to water temperature, with each stage having an optimum temperature. 

“I wanted to build on previous work to see if we could use it to find better predictors for human risk and more effective interventions,” Nguyen says. 

The researchers integrated an epidemiological model of schistosomiasis and temperature-dependent traits of the parasites and their snail hosts to run different computer-simulated interventions. The results showed that interventions targeting snails were most effective at reducing transmission, and pinpointed the water temperature for when the risk of transmission peaks. 

Unexpectedly, the simulations also showed that interventions targeting snail removal actually raised the peak transmission temperature by 1.3 degrees centigrade, while reducing transmission risk. 

“That may not sound like a lot,” Nguyen says, “but we’re talking about water temperature, which takes a lot of energy to warm, so 1.3 degrees is actually a big shift.” 

Snails naturally start to die off at higher water temperatures. The data in the new paper shows how implementing snail control measures, such as through chemical treatment of the water, amplifies snail mortality at all temperatures. This lowers transmission risk overall, but allows peak transmission risk to occur at higher temperatures. 

These insights can guide public health workers to time their interventions, by factoring in regional water temperatures, and how the temperatures fluctuate during different seasons of the year. 

“Our findings don’t mean that we should stop human treatment for schistosomiasis,” Nguyen says. “Instead, it will likely be beneficial to include both the human and ecological components. By combining human drug treatment with snail removal measures, during times when water is below the peak transmission temperature, we may be able to maximize the efficacy of an intervention.” 

Additional authors of the PNAS paper include Jason Rohr (University of Notre Dame), Valerie Harwood (University of South Florida), Rachel Hartman (Emory staff) and Emory graduate student Sandra Mendiola. 

The work was funded by the National Institutes of Health, the National Science Foundation, the Porter Foundation and the U.S. Department of Agriculture.

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Monday, March 8, 2021

Atlanta Science Festival: Life is looking up with science!

This year's festival is a hybrid of more than 80 events, including virtual activities and those held in the outdoors.


By Carol Clark

The Atlanta Science Festival returns March 13-27 stronger than ever. This year’s hybrid of more than 80 events includes virtual activities and those held in safe, socially-distanced environments, aimed to educate, engage and entertain all ages. 

The 2021 festival theme — “Science Always Prevails!” — celebrates the metro area as a powerhouse of scientific research, scholarship, service and innovation, from battling the COVID-19 pandemic to protecting the unique natural resources of Georgia. 

“The pandemic has heightened public awareness of the value of science,” says Meisa Salaita, executive co-director of Science ATL, the non-profit organization that produces the Atlanta Science Festival. “All of our partners, including Emory, have come together to keep the festival going strong, despite the challenges. Everyone is inspired by the knowledge that our mission of service to the community is more important than ever.” 

The Atlanta Science Festival, now in its eighth year, was co-founded by Emory, Georgia Tech and the Metro Atlanta Chamber. 

“We’ll not only continue our celebration of science,” says executive co-director Jordan Rose, “but use it as an opportunity to share knowledge that inspires and empowers others to make the world a better place.” 

Bringing more science to more people

On Friday, March 12, one day before the festival launch, an event called “Imagining the Future” will help set the tone. Local STEM professionals, including many Emory faculty and students, will participate in virtual visits to 100 metro Atlanta K-12 classrooms to give students a sense of how science is done, talk about some major questions that remain unanswered in science, and inspire students to imagine themselves shaping the future as STEM-literate professionals of tomorrow. 

“One of the benefits of having virtual events is that we are able to bring more science, and more science-learning opportunities, to more people,” Salaita says. 

Some of this year’s festival highlights include: 

  • “Atlanta 40,” a celebration of 40 notable organisms of the region explained by videos created by experts and luminaries and mini conservation challenges that the public can complete. 
  • “Discovery Walks,” four family-friendly, self-guided walks through neighborhoods and parks in Atlanta, featuring free maps with cool science facts about each location. 
  • “City Science Quest,” an app-based game that allows participants to use a mobile device to uncover Atlanta’s science contributions and STEM careers by earning prizes through completing interactive “missions,” including many that involve exciting scientific research ongoing at Emory. 

Emory event highlights

While not ignoring the current reality, the tone of this year’s festival is hopeful and encouraging, Salaita says. Emory experts will headline events that showcase how scientists at Emory and around the world came together to produce effective, safe vaccines for the novel coronavirus in record time, and to address concerns of communities that have been especially hard hit by COVID-19. 

Another Emory highlight will be a hands-on, outdoor event to learn how to collect data on Georgia’s air quality. And, not to be missed, Emory chemistry students will engage families in a “Drive-In Demo Show” of dramatic displays of chemistry in action. 

Following is a roundup of some of the festival highlights featuring the Emory community. 

Community scientists and amateur sleuths are invited to a family friendly “Air Quality Scavenger Hunt,” on Saturday, March 13, from 11 a.m. to 3 p.m. in Atlanta’s Historic Fourth Ward Park. Participants will be provided hand-held air sensors and learn to measure the amount of particulate matter, or pollutants, in the air. Their mission will be to use clues to locate different areas around the park to collect air quality data for Eri Saikawa, associate professor of Emory’s Department of Environmental Sciences, and students in her lab. The COVID-19 safety measures for the outdoor event require participants to wear masks and to sign up in advance for half-hour time slots to pick up and return the air sensors. “This event is for anyone who enjoys solving puzzles and wants to be part of the solution when it comes to pollution,” Saikawa says. 

A related at-home or in-class competition led by Saikawa and her students is the “Georgia Air Quality Challenge” for grades 6 to 12. Grade school students will partner with Air Emory, an Emory student-led initiative that began to monitor air quality on campus and is now expanding statewide through a grant from the Environmental Protection Agency and the support of Science ATL and Education Enhanced. Registered grade school students will receive access to lessons and videos to learn about sources of pollution, current data for Georgia, and how air sensors can measure air quality. They will then be challenged to submit a proposal for where air sensors should be placed in local communities in order to fill the gap in air quality data for Georgia. The winners will be invited to present their proposals to an upcoming Georgia STEM day. 

“We want young people to understand the importance of monitoring air quality,” Saikawa says. “We also hope they learn more about sources of air pollution, who may be more vulnerable, and think about ways we might mitigate pollution.” 

Emory physicians will be featured in a series of virtual talks on COVID-19 vaccines.

Emory physician Zanthia Wiley, assistant professor in the School of Medicine’s Division of Infectious Diseases, will give a virtual talk on Saturday, March 13, at 10 a.m., entitled “COVID-19 Vaccines and Disparities in Black Communities: What You Need to Know.” Dr. Wiley, who is also the director of Antimicrobial Stewardship at Emory University Hospital Midtown, will discuss the importance of COVID-19 vaccination and the disproportionate effect that COVID-19 is having in minority communities. She will also take questions submitted directly by those attending the virtual talk. Wiley is a member of the Emory Department of Medicine’s Diversity, Equity and Inclusion Council and the Emory Collaborative Community Outreach and Health Disparities Research Initiative. 

A virtual talk on Tuesday, March 16, at 6 p.m., “COVID-19 Vaccines and Disparities in Latinx Communities: What You Need to Know,” features Emory physician Valeria Cantos, assistant professor in the School of Medicine’s Division of Infectious Diseases and an attending physician at Grady Memorial Hospital and the Grady Infectious Disease Clinic. She will give a bi-lingual talk, in Spanish and English, on vaccine truths, myths and the importance of vaccination. She will also take questions submitted by the audience. Dr. Santos is a lead co-investigator in a study looking at the efficacy of remdesivir in the treatment of hospitalized patients with COVID-19. She is also a co-investigator for the Moderna and Noravax vaccine clinical trials. 

“Vaccine Real Talk,” a virtual panel discussion, is is set for Thursday, March 18, at 7 p.m. The panel will be moderated by Maryn McKenna, a leading infectious disease journalist and a senior fellow in Emory’s Center for the Study of Human Health. The event will take on the topic of how COVID-19 vaccines work and how to best combat misinformation around them. Panelists will include Colleen Kraft, associate professor in Emory School of Medicine’s Division of Infectious Diseases and the director of Emory’s Clinical Virology Research Laboratory. 

At noon on March 18, Deboleena Roy, Emory senior sssociate dean of faculty, will lead a virtual panel discussion about scientists and their social responsibility titled “Citizen Nobel: The Pressure and Power of Winning the Ultimate Scientific Prize.” Roy is professor of neuroscience and behavioral biology with a joint appointment in women’s, gender and sexuality studies. The discussion will be based on the film “Citoyen Nobel,” which will be available free for registrants during the week of March 13 to 20. 

Book your free spot in advance and load your “pod” into the family vehicle for the “Drive-In Demo Show” on Saturday, March 20, at 11 a.m., noon and 1 p.m., in the parking lot of the First Christian Church in Decatur. Instead of a movie, this drive-in will feature live performances by Emory chemistry students, led by Doug Mulford, senior lecturer of chemistry, whose motto is “teaching with a pyrotechnic flair.” Viewers will remain safe in their cars as the masked, socially distanced Emory chemists make sparks fly. They will wrestle with polymers that grow as large as eels, turn gummy bears into flaming dragons, and make a liquid nitrogen cloud. The finale, of course, will feature a safe, but fiery, explosion! 

The Atlanta Science Festival is produced by more than 50 community partners, with major support from founders Emory, Georgia Tech and the Metro Atlanta Chamber, and sponsors UPS, International Paper, Georgia Power, Cox Enterprises, Mercer University and others.