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A photo of Michelle Craske.

Michelle Craske to share how research can inform anxiety and depression treatment

A photo of Michelle Craske.

Michelle Craske and colleagues are studying how to integrate virtual reality into treatment for anxiety and depression. Photo Credit: Reed Hutchinson/UCLA

For more than three decades, Michelle Craske has been trying to understand what makes some people prone to anxiety and depression. She’s studied what biomarkers, behaviors and thinking patterns contribute to these conditions, and how to use that knowledge to develop better treatments.

At the 128th Faculty Research Lecture, Craske, distinguished professor of psychology in the UCLA College, will describe some of her findings and talk about how virtual reality has begun playing a role in changing patients’ mindsets for the better. The talk will be held at 3 p.m. on Wednesdsay, Feb. 19.

“Anxiety and depression are dramatically increasing in prevalence,” said Craske, who is also a professor of psychiatry and biobehavioral sciences at the David Geffen School of Medicine at UCLA and holder of the Joanne and George Miller and Family Endowed Chair. “We need to understand the engine that’s driving these conditions so we can improve our treatments.”

In the U.S., only about half of people with symptoms of anxiety or depression receive treatment. And when they do get help, treatments are only effective about half the time, said Craske, also an executive committee member for the UCLA Depression Grand Challenge, a campus-wide initiative that aims to cut the global burden of depression in half by 2050.

Much of Craske’s work on anxiety centers on the idea that people prone to anxiety disorders, which affect an estimated 18% of U.S. adults each year, anticipate threat more often than others and have difficulty inhibiting this fear. Most people feel fearful when faced with a real threat — say, a bear in front of us in the woods. But people most at risk for anxiety disorders are more likely to respond to an uncertain situation — feeling afraid in the woods even when there’s no bear, for instance.

The challenge for clinicians like Craske is to decrease this anticipation of threat. Craske uses a technique known as exposure therapy, in which a person is exposed to a situation or setting that makes them anxious, in an attempt to train their brain that it’s safe. Craske utilizes prediction error learning to explain the effects of exposure therapy and attempts to optimize such learning. The greater the element of surprise, the more the learning sticks.

“We want to design a treatment where a person says, ‘Oh, I was wrong! I really expected this to be unmanageable or even risky and it wasn’t at all,’” Craske said.

Craske’s research aims to make people with depression — or those prone to depression — more motivated to work toward and to savor rewards. This “reward sensitivity” is often dampened by depression and Craske thinks it’s an avenue for potential treatments to target. For example, in her studies of the effects of kindness and compassion on depression, she has found that training people how to more regularly engage in acts of kindness can ease their symptoms.

Craske and colleagues also are studying how to integrate virtual reality into treatment for anxiety and depression.

“We use virtual reality to help people face the situations they fear and avoid, and at other times we use virtual reality to increase their capacity for positive emotions,” she said. “By immersing themselves in positive scenes we can teach them how to anticipate and savor rewarding events and then transfer that to real life.”

In her talk, titled “Anxiety and Depression: Risk Factors and Treatment,” Craske wants to convey a sense of her scientific approach, which builds off her background as a clinical psychologist to improve psychotherapies. It will take many different perspectives, however, to solve anxiety and depression, she said. In her role with the Depression Grand Challenge, she helps build collaborations between researchers like herself and those that study psychological diseases from a genetic, molecular or neurological point of view.

Craske looks forward to presenting her research, and hopes the audience comes away from her lecture feeling hopeful about the progress that science is making on anxiety and depression.

“I am deeply honored to have been selected to give this lecture which represents the true pinnacle of my career at UCLA,” Craske said.

The Faculty Research Lecture — a UCLA tradition since 1925 — is free and open to the public and will be held at 3 p.m. on Feb. 19 in the Schoenberg Music Building. Please RSVP here if you’d like to attend.

This article originally appeared in the UCLA Newsroom.

Photo of a computer-generated 3D rendering of a flu virus.

First childhood flu helps explain why virus hits some people harder than others

Photo of a computer-generated 3D rendering of a flu virus.

A computer-generated 3D rendering of a flu virus. Photo Credit: Dan Higgins/Courtesy of CDC/Douglas Jordan

Why are some people better able to fight off the flu than others? Part of the answer, according to a new study, is related to the first flu strain we encounter in childhood.

Scientists from UCLA and the University of Arizona have found that people’s ability to fight off the flu virus is determined not only by the subtypes of flu they have had throughout their lives, but also by the sequence in which they are been infected by the viruses. Their study is published in the open-access journal PLoS Pathogens.

The research offers an explanation for why some people fare much worse than others when infected with the same strain of the flu virus, and the findings could help inform strategies for minimizing the effects of the seasonal flu.

In addition, UCLA scientists, including Professor James Lloyd-Smith, who also was a senior author of the PLoS Pathogens research, recently completed a study that analyzes travel-related screening for the new novel coronavirus 2019-nCoV. (The research is under review; a preprint is online.)

The researchers report that screening travelers is not very effective for the 2019 coronavirus — that it will catch less than half of infected travelers, on average — and that most infected travelers are undetectable, meaning that they have no symptoms yet, and are unaware that they have been exposed. So stopping the spread of the virus is not a matter of just enhancing screening methods at airports and other travel hubs.

“This puts the onus on government officials and public health officials to follow up with travelers after they arrive, to isolate them and trace their contacts if they get sick later,” said Lloyd-Smith, a UCLA professor of ecology and evolutionary biology. Many governments have started to impose quarantines, or even travel bans, as they realize that screening is not sufficient to stop the spread of the coronavirus.

One major concern, Lloyd-Smith said, is that other countries, especially developing nations, lack the infrastructure and resources for those measures, and are therefore vulnerable to importing the disease.

“Much of the public health world is very concerned about the virus being introduced into Africa or India, where large populations exist that do not have access to advanced medical care,” he said.

The researchers, including scientists from the University of Chicago and the London School of Tropical Hygiene and Medicine, have developed a free online app where people can calculate the effectiveness of travel screening based on a range of parameters.

“Our finding concerning the effectiveness of screening for the coronavirus is not a criticism of screening practices being done by public health officials in the United States or elsewhere,” Lloyd-Smith said.

He said that the biology and epidemiology of the virus itself makes infection extremely difficult to detect in its early stages, because the majority of cases show no symptoms for five days or longer after exposure.

“My colleagues and I know there is a lot of speculation online about the coronavirus and how it spreads,” Lloyd-Smith said “People should look to trusted sources for accurate information, such as the Centers for Disease Control and Prevention, the Los Angeles County Department of Public Health, and the peer-reviewed scientific literature.”

Solving a decades-old question

The PLoS Pathogens study may help solve a problem that had for decades vexed scientists and health care professionals: why the same strain of the flu virus affects people with various degrees of severity.

A team that included some of the same UCLA and Arizona scientists reported in 2016 that exposure to influenza viruses during childhood gives people partial protection for the rest of their lives against distantly related influenza viruses. Biologists call the idea that past exposure to the flu virus determines a person’s future response to infections “immunological imprinting.”

The 2016 research helped overturn a commonly held belief that previous exposure to a flu virus conferred little or no immunological protection against strains that can jump from animals into humans, such as those causing the strains known as swine flu or bird flu. Those strains, which have caused hundreds of spillover cases of severe illness and death in humans, are of global concern because they could gain mutations that allow them to readily jump not only from animal populations to humans, but also to spread rapidly from person to person.

In the new study, the researchers investigated whether immunological imprinting could explain people’s response to flu strains already circulating in the human population and to what extent it could account for observed discrepancies in how severely the seasonal flu affects people in different age groups.

To track how different strains of the flu virus affect people at different ages, the team analyzed health records that the Arizona Department of Health Services obtains from hospitals and private physicians.

Two subtypes of influenza virus, H3N2 and H1N1, have been responsible for seasonal outbreaks of the flu over the past several decades. H3N2 causes the majority of severe cases in high-risk elderly people and the majority of deaths from the flu. H1N1 is more likely to affect young and middle-aged adults, and causes fewer deaths.

The health record data revealed a pattern: People first exposed to the less severe strain, H1N1, during childhood were less likely to end up hospitalized if they encountered H1N1 again later in life than people who were first exposed to H3N2. And people first exposed to H3N2 received extra protection against H3N2 later in life.

The researchers also analyzed the evolutionary relationships between the flu strains. H1N1 and H3N2, they learned, belong to two separate branches on the influenza “family tree,” said James Lloyd-Smith, a UCLA professor of ecology and evolutionary biology and one of the study’s senior authors. While infection with one does result in the immune system being better prepared to fight a future infection from the other, protection against future infections is much stronger when one is exposed to strains from the same group one has battled before, he said.

The records also revealed another pattern: People whose first childhood exposure was to H2N2, a close cousin of H1N1, did not have a protective advantage when they later encountered H1N1. That phenomenon was much more difficult to explain, because the two subtypes are in the same group, and the researchers’ earlier work showed that exposure to one can, in some cases, grant considerable protection against the other.

“Our immune system often struggles to recognize and defend against closely related strains of seasonal flu, even though these are essentially the genetic sisters and brothers of strains that circulated just a few years ago,” said lead author Katelyn Gostic, who was a UCLA doctoral student in Lloyd-Smith’s laboratory when the study was conducted and is now a postdoctoral fellow at the University of Chicago. “This is perplexing because our research on bird flu shows that deep in our immune memory, we have some ability to recognize and defend against the distantly related, genetic third cousins of the strains we saw as children.

“We hope that by studying differences in immunity against bird flus — where our immune system shows a natural ability to deploy broadly effective protection — and against seasonal flus — where our immune system seems to have bigger blind spots — we can uncover clues useful to universal influenza vaccine development.”

Around the world, influenza remains a major killer. The past two flu seasons have been more severe than expected, said Michael Worobey, a co-author of the study and head of the University of Arizona’s department of ecology and evolutionary biology. In the 2017–18 season, 80,000 people died in the U.S., more than in the swine flu pandemic of 2009, he said.

People who had their first bout of flu as children in 1955 — when the H1N1 was circulating but the H3N2 virus was not — were much more likely to be hospitalized with an H3N2 infection than an H1N1 infection last year, when both strains were circulating, Worobey said.

“The second subtype you’re exposed to is not able to create an immune response that is as protective and durable as the first,” he said.

The researchers hope that their findings could help predict which age groups might be severely affected during future flu seasons based on the subtype circulating. That information could also help health officials prepare their response, including decisions about who should receive certain vaccines that are only available in limited quantities.

The research was funded by the National Institutes of Health, the National Science Foundation, DARPA and the David and Lucile Packard Foundation. In 2018, the NIH’s National Institute of Allergy and Infectious Diseases announced a strategic plan to develop a universal flu vaccine.

The study’s co-authors are Rebecca Bridge of the Arizona Department of Health Services and Cecile Viboud of the Fogarty International Center at the NIH.

This article originally appeared in the UCLA Newsroom.

A photo of images of fruit flies’ eyes, wings and lymph glands.

Hundreds of UCLA students publish paper analyzing 1,000 genes involved in organ development

A team of 245 UCLA undergraduates and 31 high school students has published an encyclopedia of more than 1,000 genes, including 421 genes whose functions were previously unknown. The research was conducted in fruit flies, and the genes the researchers describe in the analysis may be associated with the development of the brain, eye, lymph gland and wings.

The fruit fly is often the object of scientific research because its cells have similar DNA to that of human cells — so knowledge about its genes can help researchers better understand human diseases. The UCLA study should be useful to scientists studying genes involved in sleep, vision, memory and many other processes in humans.

The research is published in the journal G3: Genes, Genomes, Genetics. The study’s senior authors include researchers Cory Evans and John Olson, who taught UCLA’s Biomedical Research 10H, the course in which the studies were conducted.

“I expect this will be a highly cited paper and a valuable resource to life scientists,” said Tracy Johnson, director of UCLA’s biomedical research minor, which offers the course the students all took. “It’s inspiring to know all of this really important research came from freshmen and sophomores. It’s beautiful, high-quality research.”

A photo of images of fruit flies’ eyes, wings and lymph glands.

Visible on this page are images of fruit flies’ eyes (top), wings and lymph glands, showing which genes are active (red) or were previously active (green). (Download the full image to also see scans of the brain.) Photo credit: Cory Evans

The students studied short DNA sequences to learn how specific genes are turned on and off and understand how those genes control the functions of various cell types. Although all cells have essentially the same collection of genes, specific genes are turned on or off depending on the cells’ needs, Evans said.

Each student studied several genes, ultimately producing a total of more than 50,000 microscopic images; the researchers then posted their analysis on an online database where other scientists can study the genes’ roles.

“This shows not only which genes are turned on, but the history of which genes have been turned on,” Johnson said.

The research was conducted as part of a UCLA life sciences course that was developed in the early 2000s by Utpal Banerjee, a UCLA distinguished professor of molecular, cell and developmental biology, a Howard Hughes Medical Institute Professor and a senior author of the paper. The course received initial funding from the HHMI.

“Research on science education says that one of the best way to teach science is by having authentic research experiences embedded in a course,” said Johnson, who holds the Keith and Cecilia Terasaki Presidential Endowed Chair in the Division of Life Sciences and is an HHMI Professor. “Professor Banerjee understood years ago when he envisioned the class that students learn more by doing science. They learn how to design experiments, how to think like scientists, how to write about science and how to present their research.”

Johnson said the approach is analogous to teaching a sport. “If a kid wants to play soccer, you don’t say, ‘Don’t touch the soccer ball yet. You have to first learn all of the rules, watch other people play and read about the soccer greats, and maybe in a couple of years, we’ll let you kick the ball.’ No, bring out the soccer balls! So we need to get science students in the lab.”

The students completed two other research projects, one of which Evans expects will be published this year. In that study, the undergraduates studied the effects of turning off specific genes in fruit flies using a scientific technique called RNA interference. They then determined which of those 4,000 genes, when turned off, affect the proper development of blood cells.

“We teach students how to do research, not fly biology,” said Evans, who is now an assistant professor of biology at Loyola Marymount University. “Their science literacy is high, and they know how to evaluate evidence.”

This article originally appeared in the UCLA Newsroom.

Photo of Anthony and Jeanne Pritzker.

UCLA psychology department receives $30 million from Anthony & Jeanne Pritzker Family Foundation

Photo of Anthony and Jeanne Pritzker.

Anthony and Jeanne Pritzker at the Hammer gala in 2019. (Photo credit: Courtesy of the Pritzkers)

UCLA has received a $30 million commitment from the Anthony and Jeanne Pritzker Family Foundation to support a major renovation of the Psychology Tower on the UCLA campus. In recognition of the gift, the building has been named Pritzker Hall.

Tony Pritzker served as co-chair of the Centennial Campaign for UCLA, which concluded in December. The campaign exceeded its original $4.2 billion fundraising goal 18 months ahead of schedule.

“Tony’s visionary leadership and unwavering support has inspired unprecedented philanthropy to UCLA throughout the campaign, helping cement a strong foundation for our second century,” UCLA Chancellor Gene Block said. “Now, thanks to Tony and Jeanne’s latest extraordinary gift, UCLA Psychology will be primed for decades of trailblazing research and exceptional teaching.”

The $30 million commitment is the second largest in the history of the UCLA College’s life sciences division, which is home to the psychology department. Of the total amount, $10 million will create the Anthony and Jeanne Pritzker Endowment for Excellence, which will provide faculty and student support and fund ongoing infrastructure needs.

Photo of an architect’s rendering of Pritzker Hall from above.

An architect’s rendering of Pritzker Hall from above. (Photo courtesy of CO Architects)

“We have tremendous confidence in UCLA, as a public university, to move society and the world forward, which is why we invest our time and resources there,” Tony Pritzker said. “We are pleased to build upon our foundation’s earlier commitments to UCLA, while strengthening the extraordinary reputation that the psychology department’s research and scholarship have rightfully earned.”

The donation bookends the Anthony and Jeanne Pritzker Family Foundation’s Centennial Campaign giving to the UCLA College; the foundation also gave $15 million to the UCLA Institute of the Environment and Sustainability in 2013, before the campaign’s public launch. The Pritzker Foundation’s total giving to UCLA, which also includes major gifts to athletics, law, medicine, neuroscience, education, public policy and programs to support foster youth on campus, now stands at just under $100 million.

“We are immensely grateful to Tony and Jeanne Pritzker for taking the lead in investing in a new era for UCLA Psychology,” said Victoria Sork, dean of life sciences. “I am especially heartened by this gift, because the values the Pritzkers espouse align with our own values of service and investment in our communities.”

“Their generous gift will help us transform Pritzker Hall into a space for breakthroughs — a collaborative, modern teaching and research space befitting one of the top psychology departments in the United States.”

The tower was designed by celebrated Los Angeles architect Paul Revere Williams and completed in 1967. Work on seismic upgrades began in 2018 and the full renovation is expected to be completed this year.

Sork said the endowment created by the Pritzkers’ gift will strengthen the department’s ability to recruit and retain top-notch faculty and students, a crucial factor in maintaining its excellence. UCLA Psychology faculty are pursuing research in a wide range of areas, including anxiety and depression; substance abuse and addiction; human relationships; stress, resilience and health; neuroscience; and cognition and consciousness, all focusing on how to improve people’s daily lives.

“This gift will be of incalculable benefit to faculty, students and members of the community for many decades to come,” Sork said.

This article originally appeared in the UCLA Newsroom.

Photo of group of volunteers at first mobile health clinic.

Student launches mobile health clinic to increase access to care

Photo of group of volunteers at first mobile health clinic.

Ahmad Elhaija, center, with International Collegiate Health Initiative medical staff, volunteers and student team members at the organization’s first mobile health clinic. Photo: Reed Hutchinson/UCLA

On a sunny autumn Saturday at the Southeast-Rio Vista YMCA in the city of Maywood, kids colored drawings and played Jenga while their parents and other family members underwent basic health screenings conducted by volunteer nurses.

After their bloodwork and other tests were done, the people met with doctors from medical centers in southeast Los Angeles County to discuss their results. Aided by Spanish-language translators, the doctors also gave advice about everything from medications to old injuries — anything the patients wanted to know.

The free event, attended by about 40 community members plus their children, was the first mobile community health clinic hosted by the International Collegiate Health Initiative. Founded two years ago by UCLA junior psychobiology major Ahmad Elhaija, the initiative aims to increase access to affordable, high-quality medical care in low-income and refugee communities in Los Angeles through mobile community health clinics and social advocacy.

“I thought, what can we do here that’ll make a big impact, where we can affect the statistics of a community, their health outcomes?” he said.

Elhaija drew inspiration for the project from two aspects of his youth in Anaheim — growing up frequently sick without consistent health insurance and his volunteer work assisting Arab and Muslim refugees.

Given the need for this kind of service, Elhaija applied for the annual Donald A. Strauss Foundation scholarship to help implement his vision. Each year, the Strauss Foundation awards 10 to 15 students from across 14 California colleges a $15,000 scholarship which is divided between the student’s educational costs and a grant for the public service project they propose in their application.

Elhaija was the only UCLA student to win the $15,000 scholarship in 2019. In 2018, two UCLA students won the Strauss scholarship; their projects helped transfer students prepare for doctoral programs, and provided therapy and support for K-12 students who stutter.

Photo of Ahmad Elhaija

Ahmad Elhaija Photo: Reed Hutchinson/UCLA

As part of the scholarship, Elhaija was assigned a mentor to advise him on his project. Elhaija’s mentor, Marc Anthony Branch, is a program officer for sustainable development for the United Methodist Committee on Relief and an expert in grant writing. Elhaija relied on Branch’s knowledge to improve his grant writing skills.

“I set him up with my grant-writing team, and he was really pivotal in actually getting us moving forward,” Elhaija said. “Before him, we didn’t really have much progress in grant writing, so having him on board and him giving his expertise was really cool. He knows what grant-giving organizations are looking for and he has some good contacts in that realm as well.”

Growing up in a low-income neighborhood in Anaheim, Elhaija was frequently sick from asthma and a rare blood disorder called cyclic neutropenia. His family didn’t always have health insurance, and although they worked hard to support and care for him, they were often left with high hospital bills.

While his family’s difficulty navigating his health care opened his eyes to the importance of providing affordable care, as a teenager Elhaija also volunteered at the nonprofit Access California Services, which provides support and resources to Arab and Muslim refugees in Anaheim. He said that volunteering with the organization and seeing the services for refugees that were still lacking inspired him to think of ways he could help.

So when Elhaija got to UCLA in 2017, he formed the International Collegiate Health Initiative with the goal to provide medical care to refugees in countries like Syria and Palestine. Through his volunteer work and visiting his own family in the Middle East, Elhaija learned that college campuses would be the safest places to provide medical services in the region.

However, finances and logistics made it more productive for Elhaija to focus his efforts on refugee and low-income communities closer to home. So he switched the initiative’s focus to offering mobile community health clinics in southeast Los Angeles.

The initiative is managed by a team of 20 students, a board of directors and professional advisers who offer guidance and medical services for the clinics. The clinic in Maywood, held on Nov. 16, was the organization’s first mobile health clinic. Another is planned for the city of Bell in February.

The ICHI’s ultimate goal is to raise enough money for a mobile clinic van, and to expand to other cities in California or even overseas.

“The idea is that we could have our full blown mobile clinic running in the fall of next year, where we can provide basically every type of care that a standard clinic can provide,” Elhaija said.

This article originally appeared in the UCLA Newsroom.

Chronic opioid treatment may raise risk of post-traumatic stress disorder, study finds

Senior author Michael Fanselow said the research suggests that chronic opioid use increases susceptibility to developing anxiety disorders. Photo credit: Reed Hutchinson/UCLA

While opioids are often prescribed to treat people with trauma-related pain, a new UCLA-led study suggests doctors should use caution before prescribing the drug to those they believe may experience severe stress in the future, in order to reduce the risk the patient will develop PTSD.

In the study, researchers administered doses of the opioid morphine to a group of 22 mice for one week, then gave the mice relatively strong foot shocks. After the morphine wore off, the mice were given mild electric foot shocks. These mice showed a substantially longer “freezing response” than a second, control group of 24 mice that had not been given morphine. When mice recall a frightening memory, they freeze. Their heart rates and blood pressure go up, and the more frightening the memory, the more they freeze.

“While we are generally aware that drug use, such as that in the current opioid crisis, has many deleterious effects, our results suggest yet another effect — increased susceptibility to developing anxiety disorders,” said senior author Michael Fanselow, UCLA distinguished Staglin family professor of psychology and director of UCLA’s Staglin Family Music Festival Center for Brain and Behavioral Health. “As opioids are often prescribed to treat symptoms such as pain that may accompany trauma, caution may be needed because this may lead to a greater risk of developing PTSD, if exposed to further traumatic events, such as an accident, later on.”

“The foot shocks produced lasting fear and anxiety-like behaviors, such as freezing,” Fanselow said.

“Our data are the first to show a possible effect of opioids on future fear learning, suggesting that a person with a history of opioid use may become more susceptible to the negative effects of stress,” Fanselow said. “The ability of opioids to increase PTSD-like symptoms far outlasted the direct effects of the drug or withdrawal from the drug, suggesting the effect may continue even after opioid treatment has stopped.”

Fanselow’s view is if there is reason to believe a patient is likely to experience severe emotional stress after opioid treatment, then doctors should use caution about prescribing an opioid. If opioid use is medically called for, then the patient should be kept away from potentially stressful situations. So, for example, a soldier treated with opioids for pain should not be sent back into combat for a period of time, he said. The development of post-traumatic stress disorder requires some stressful experience after opioid use, he said.

The researchers also gave some of the mice morphine after the initial trauma had occurred but before exposing them to the second, mild stressor. They found that mice treated with morphine after the initial trauma did not show enhanced fear learning following exposure to the mild stressor. This finding suggests that chronic use of opioids before — but not after — a traumatic event occurs affects fear learning during subsequent stressful events.

The researchers concluded the mice given morphine were more susceptible to post-traumatic stress disorder than the control group of mice not given any opioids, and inferred that people with a history of using opioids are more susceptible to PTSD than the general population.

The study is published in Neuropsychopharmacology, an international scientific journal focusing on clinical and basic science research that advances understanding of the brain and behavior.

The research was funded by the National Institute on Drug Abuse and National Institute of Mental Health.

An opiate is a drug naturally derived from the opium poppy plant, such as heroin, morphine and codeine. Opioid is a broader term that includes opiates and any substance, natural or synthetic, that binds to the brain’s opioid receptors — which play a key role in controlling pain, rewards and addictive behaviors. Synthetic opioids include the prescription painkillers Vicodin and OxyContin, as well as fentanyl and methadone.

Substance abuse and PTSD often go hand-in-hand, Fanselow said, and people with PTSD often take drugs to self-medicate. Nearly 40% of people with PTSD also have a drug disorder.

Fanselow and colleagues reported last month that a traumatic brain injury causes changes in a brain region called the amygdala; and the brain processes fear differently after such an injury.

This article originally appeared in the UCLA Newsroom.

Photo of student smiling.

Meet UCLA Student Researcher Julia Nakamura

Photo of student smiling.

Fourth-year UCLA student researcher Julia Nakamura

Meet fourth-year UCLA student researcher Julia Nakamura!

Julia majors in Psychobiology with a minor in Gerontology and is in our Undergraduate Research Scholars Program. The title of her research project is “The Role of Social Support in the Association between Early Life Stress, Depression, and Inflammation in Older Adults.”

 

How did you first get interested in your research project?

UCLA’s Cluster course “Frontiers in Human Aging” initially sparked my interest in aging populations. Through a service learning project at ONEgeneration Adult Day Care Center, I directly witnessed the burden of chronic disease in later-life adults and realized the pressing need to understand the mechanisms underlying these adverse health outcomes. Through my coursework in psychology, I became interested in the psychological factors that influence biological mechanisms and have the potential to positively impact the trajectory of chronic disease outcomes.

I began research in psychology in Dr. Julienne Bower’s Mind-Body Lab under the direction of Dr. Kate Kuhlman. We study the effects of childhood adversity on biological and behavioral responses to psychological stress. My experiences in this lab led me to wonder what factors could mitigate adverse physical and mental health outcomes from stressful experiences, specifically in older adults. My honors research project examines if social support moderates the relationship between early-life stress, depressive symptoms, and inflammation in older adults using data from the Health and Retirement Study.

What has been the most exciting aspect of your research so far?

Getting to test my own research questions has been the best part of this project. Specifically, it has been really exciting for me to run my own data analyses for the first time with Dr. Kuhlman’s guidance. Experiencing the “behind-the-scenes” of research and systematically moving through the steps of conducting an independent project has been really informative. This project has helped me to feel that I am truly developing the skill set of an independent researcher, which is very exciting!

What has surprised you about your research or the research process?

The immensely collaborative nature of research in academia was quite surprising to me when I first started on this project. Through my research, I’ve had the privilege of working with several scientists and professors who are experts in their respective areas of study. They have all welcomed me and helped to make my project as scientifically sound and comprehensive as possible. Research really builds on itself. Learning from other people’s projects and ideas, even if they are outside of your immediate area of study, can result in high levels of collaboration and really interesting research!

What is one piece of advice you have for other UCLA students thinking about doing research?

I would advise students interested in research to actively pursue research opportunities. There are plenty of amazing opportunities to be involved in research at UCLA, but you have to seek them out. It can be intimidating to take the initial steps to reach out to professors and discuss their research interests, but it is so worthwhile to find a lab and professor that are a good fit! I would recommend that students find an area of study that they are really passionate about. I think that your passion for your area of study and your continued curiosity will drive your research questions and help you get the most out of each research experience.

What effect do you hope your research has in your field, at UCLA, in your community, or in the world?

I hope to spend my life contributing to our understanding of the biobehavioral processes that promote mental and physical health across the lifespan. As the number of older adults (a majority of whom have at least one chronic disease) increase in our society, it is now more important than ever to identify potential intervention targets that can improve the trajectory of chronic disease outcomes.

This article originally appeared on the Undergraduate Research Center website.

Picture of a valley oak tree.

One of California’s iconic tree species offers lessons for conservation

Picture of a valley oak tree.

The valley oak, the largest oak in California, grows to over 100 feet tall and provides habitat and food for a variety of animals. Photo credit: Victoria Sork/UCLA

 

With increasing regularity, Californians are witnessing firsthand the destructive power of wildfires. But not everyone sees what happens after the flames die down, when debris is cleared, homes and lives rebuilt — and trees replanted to help nature recover.

New research led by UCLA evolutionary biologist Victoria Sork examines whether the trees being replanted in the wake of California’s fires will be able to survive a climate that is continuing to warm.

The study, which is published in the Proceedings of the Natural Academy of Sciences, focuses on California’s iconic valley oak. The research is among the first to demonstrate the potential of using genomics to inform conservation strategies — essentially giving species an evolutionary boost. The study showed that planting trees that are genetically better suited to higher temperatures makes them more likely to survive and grow to maturity.

“When we think about managing ecosystems under rapidly changing climates, we have to realize trees need to be able to survive past 50 years,” Sork said.

The paper also discovered something surprising: The valley oak, an essential component of many ecosystems in California, is already poorly adapted to its environment — even considering climate conditions in 2019.

“They actually seem to grow better in cooler climates than they’re in right now,” said Luke Browne, a postdoctoral scholar at the UCLA La Kretz Center for California Conservation Science and the study’s lead author. “They might grow better if climates were more like they were 21,000 years ago, during the last ice age.”

During the peak of the last ice age, summer temperatures were about 4 to 5 degrees Celsius colder, and ice covered most of Canada and mountainous areas of the U.S.

In the fields of conservation and land management, it is a common assumption that plants and animals are adapted to their environments — that’s how evolution and natural selection are supposed to work. The new research casts doubt on that assumption.

The study is part of an ongoing project initiated by Sork and Jessica Wright, an expert in conservation genetics at the USDA Forest Service, more than 10 years ago.

Researchers gathered 11,000 seeds from 94 locations throughout the trees’ range, which stretches from the Santa Monica Mountains to the Cascade foothills in the northern part of the state. They grew them to saplings in a greenhouse and planted them in two large experimental gardens, in Chico and Placerville, California. They tracked how well trees from different locations grew, and sequenced the genomes of their mother trees to link genetic information and growth rates.

The researchers then identified which genetic variants would be more likely to thrive as climate change continues to warm California. They predicted that, under predicted future warmer temperatures, trees containing beneficial genetic variations would have 11% higher growth rates than the average for all of the trees in the experiment, and 25% higher growth rates than the trees without the beneficial variations.

Information like that could help the U.S. Forest Service, for example, in its efforts to restore forests with species that have the best chance for long-term survival.

“Studies like this one provide valuable insights that help land managers make informed decisions on reforestation projects,” Wright said. “When planting trees in a particular location, managers have to decide where to collect the acorns.”

By 2070, average temperatures in the state are projected to be up to 4.8 degrees warmer than they were during the mid- to late 20th century.

“That’s going to have consequences for how fast these trees grow,” Browne said. “We’re at a challenging time to figure out the best way to do conservation science. This paper shows one approach we could use that takes advantage of modern genomics.”

The study did not determine why valley oaks are not well adapted to their environment. It might be because the climate has already warmed up so much, the trees’ long lifespans — up to 500 years — or some other, unknown factor.

The valley oak is the largest oak in California; it grows to over 100 feet tall, and has dark green leaves and a deeply grooved trunk. It is considered a foundational species because it provides habitat and food for a variety of animals, including squirrels, birds, deer and insects. In parts of the state, it is one of the only species of tree that exists. Valley oaks provide benefits to humans, too: filtering water and providing shady places to escape the heat.

Although it focuses on the oak, the paper has broader implications for conservation science in a changing climate — especially for species that evolve and adapt slowly. That’s what Sork and Wright were thinking when they initiated the project.

At the time, they hoped to find conservation strategies that could eventually be implemented using genetic information alone — without extensive field experiments.

“Not everyone in the world is going to be able to collect 11,000 seeds and plant them in a common garden,” Sork said.

This article originally appeared in the UCLA Newsroom.

What wolves’ teeth reveal about their lives

Biologist Blaire Van Valkenburgh has spent more than three decades studying the skulls of large carnivores. Here she displays a replica of a saber-toothed cat skull. At left are the skulls of a spotted hyena (in white) and a dire wolf (the black skull). Photo credit: Christelle Snow/UCLA.

UCLA evolutionary biologist Blaire Van Valkenburgh has spent more than three decades studying the skulls of many species of large carnivores — including wolves, lions and tigers —  that lived from 50,000 years ago to the present. She reports today in the journal eLife the answer to a puzzling question.

Essential to the survival of these carnivores is their teeth, which are used for securing their prey and chewing it, yet large numbers of these animals have broken teeth. Why is that, and what can we learn from it?

In the research, Van Valkenburgh reports a strong link between an increase in broken teeth and a decline in the amount of available food, as large carnivores work harder to catch dwindling numbers of prey, and eat more of it, down to the bones.

“Broken teeth cannot heal, so most of the time, carnivores are not going to chew on bones and risk breaking their teeth unless they have to,” said Van Valkenburgh, a UCLA distinguished professor of ecology and evolutionary biology, who holds the Donald R. Dickey Chair in Vertebrate Biology.

For the new research, Van Valkenburgh studied the skulls of gray wolves — 160 skulls of adult wolves housed in the Yellowstone Heritage and Research Center in Montana; 64 adult wolf skulls from Isle Royale National Park in Lake Superior that are housed at Michigan Technological University; and 94 skulls from Scandinavia, collected between 1998 and 2010, housed in the Swedish Royal Museum of Natural History in Stockholm. She compared these with the skulls of 223 wolves that died between 1874 and 1952, from Alaska, Texas, New Mexico, Idaho and Canada.

Yellowstone had no wolves, Van Valkenburgh said, between the 1920s and 1995, when 31 gray wolves were brought to the national park from British Columbia. About 100 wolves have lived in Yellowstone for more than a decade, she said.

In Yellowstone, more than 90% of the wolves’ prey are elk. The ratio of elk to wolves has declined sharply, from more than 600-to-1 when wolves were brought back to the national park to about 100-to-1 more recently.

In the first 10 years after the reintroduction, the wolves did not break their teeth much and did not eat the elk completely, Van Valkenburgh reports. In the following 10 years, as the number of elk declined, the wolves ate more of the elk’s body, and the number of broken teeth doubled, including the larger teeth wolves use when hunting and chewing.

The pattern was similar in the island park of Isle Royale. There, the wolves’ prey are primarily adult moose, but moose numbers are low and their large size makes them difficult to capture and kill. Isle Royale wolves had high frequencies of broken and heavily worn teeth, reflecting the fact that they consumed about 90% of the bodies of the moose they killed.

Scandinavian wolves presented a different story. The ratio of moose to wolves is nearly 500-to-1 in Scandinavia and only 55-to-1 in Isle Royale, and, consistent with Van Valkenburgh’s hypothesis, Scandinavian wolves consumed less of the moose they killed (about 70%) than Isle Royale wolves. Van Valkenburgh did not find many broken teeth among the Scandinavian wolves. “The wolves could find moose easily, not eat the bones, and move on,” she said.

Van Valkenburgh believes her findings apply beyond gray wolves, which are well-studied, to other large carnivores, such as lions, tigers and bears.

Extremely high rates of broken teeth have been recorded for large carnivores — such as lions, dire wolves and saber-toothed cats — from the Pleistocene epoch, dating back tens of thousands of years, compared with their modern counterparts, Van Valkenburgh said. Rates of broken teeth from animals at the La Brea Tar Pits were two to four times higher than in modern animals, she and colleagues reported in the journal Science in the 1990s.

“Our new study suggests that the cause of this tooth fracture may have been more intense competition for food in the past than in present large carnivore communities,” Van Valkenburgh said.

She and colleagues reported in 2015 that violent attacks by packs of some of the world’s largest carnivores — including lions much larger than those of today and saber-toothed cats — went a long way toward shaping ecosystems during the Pleistocene.

In a 2016 article in the journal BioScience, Van Valkenburgh and more than 40 other wildlife experts wrote that preventing the extinction of lions, tigers, wolves, bears, elephants and the world’s other largest mammals will require bold political action and financial commitments from nations worldwide.

Discussing the new study, she said, “We want to understand the factors that increase mortality in large carnivores that, in many cases, are near extinction. Getting good information on that is difficult. Studying tooth fracture is one way to do so, and can reveal changing levels of food stress in big carnivores.”

Co-authors are Rolf Peterson and John Vucetich, professors of forest resources and environmental science at Michigan Technological University; and Douglas Smith and Daniel Stahler, wildlife biologists with the National Park Service.

The research was funded by the National Science Foundation and National Park Service.

This article originally appeared in the UCLA Newsroom.

Study shows how serotonin and a popular anti-depressant affect the gut’s microbiota

Senior author Elaine Hsiao says researchers hope to build on their current study to learn whether microbial interactions with antidepressants have consequences for health and disease. Photo: Reed Hutchinson/UCLA

A new study in mice led by UCLA biologists strongly suggests that serotonin and drugs that target serotonin, such as anti-depressants, can have a major effect on the gut’s microbiota — the 100 trillion or so bacteria and other microbes that live in the human body’s intestines.

Serotonin — a neurotransmitter, or chemical messenger that sends messages among cells — serves many functions in the human body, including playing a role in emotions and happiness. An estimated 90% of the body’s serotonin is produced in the gut, where it influences gut immunity.

The team — led by senior author Elaine Hsiao and lead author Thomas Fung, a postdoctoral fellow — identified a specific gut bacterium that can detect and transport serotonin into bacterial cells. When mice were given the antidepressant fluoxetine, or Prozac, the biologists found this reduced the transport of serotonin into their cells. This bacterium, about which little is known, is called Turicibacter sanguinis. The study is published this week in the journal Nature Microbiology.

“Our previous work showed that particular gut bacteria help the gut produce serotonin. In this study, we were interested in finding out why they might do so,” said Hsiao, UCLA assistant professor of integrative biology and physiology, and of microbiology, immunology and molecular genetics in the UCLA College; and of digestive diseases in the David Geffen School of Medicine at UCLA.

Hsiao and her research group reported in the journal Cell in 2015 that in mice, a specific mixture of bacteria, consisting mainly of Turicibacter sanguinis and Clostridia, produces molecules that signal to gut cells to increase production of serotonin. When Hsiao’s team raised mice without the bacteria, more than 50% of their gut serotonin was missing. The researchers then added the bacteria mixture of mainly Turicibacter and Clostridia, and their serotonin increased to a normal level.

That study got the team wondering why bacteria signal to our gut cells to make serotonin. Do microbes use serotonin, and if so, for what?

In this new study, the researchers added serotonin to the drinking water of some mice and raised others with a mutation (created by altering a specific serotonin transporter gene) that increased the levels of serotonin in their guts. After studying the microbiota of the mice, the researchers discovered that the bacteria Turicibacter and Clostridia increased significantly when there was more serotonin in the gut.

If these bacteria increase in the presence of serotonin, perhaps they have some cellular machinery to detect serotonin, the researchers speculated. Together with study co-author Lucy Forrest and her team at the National Institutes of Health’s National Institute of Neurological Disorders and Stroke, the researchers found a protein in multiple species of Turicibacter that has some structural similarity to a protein that transports serotonin in mammals. When they grew Turicibacter sanguinis in the lab, they found that the bacterium imports serotonin into the cell.

In another experiment, the researchers added the antidepressant fluoxetine, which normally blocks the mammalian serotonin transporter, to a tube containing Turicibacter sanguinisThey found the bacterium transported significantly less serotonin.

The team found that exposing Turicibacter sanguinis to serotonin or fluoxetine influenced how well the bacterium could thrive in the gastrointestinal tract. In the presence of serotonin, the bacterium grew to high levels in mice, but when exposed to fluoxetine, the bacterium grew to only low levels in mice.

“Previous studies from our lab and others showed that specific bacteria promote serotonin levels in the gut,” Fung said. “Our new study tells us that certain gut bacteria can respond to serotonin and drugs that influence serotonin, like anti-depressants. This is a unique form of communication between bacteria and our own cells through molecules traditionally recognized as neurotransmitters.”

The team’s research on Turicibacter aligns with a growing number of studies reporting that anti-depressants can alter the gut microbiota. “For the future,” Hsiao said, “we want to learn whether microbial interactions with antidepressants have consequences for health and disease.” Hsiao wrote a blog post for the journal about the new research.

Other study co-authors are Helen Vuong, Geoffrey Pronovost, Cristopher Luna, Anastasia Vavilina, Julianne McGinn and Tomiko Rendon, all of UCLA; and Antoniya Aleksandrova and Noah Riley, members of Forrest’s team.

The research was supported by funding from the National Institutes of Health’s Director’s Early Independence Award, Klingenstein-Simons Fellowship Award, and David & Lucile Packard Foundation’s Packard Fellowship for Science and Engineering.

This article originally appeared in the UCLA Newsroom.