Roselinde Kaiser, a clinical psychologist and neuroscientist, is being recognized for her research on the science and treatment of adolescent depression

Roselinde Kaiser, a University of Colorado Boulder associate professor of psychology and neuroscience, has been named a winner, the highest honor bestowed by the U.S. government on outstanding scientists and engineers early in their independent careers.

“PECASE embodies the high priority placed by the government on maintaining the leadership position of the United States in science by producing outstanding scientists and engineers and nurturing their continued development,” according to the National Science and Technology Council (NSTC), which was commissioned in 1996 to create PECASE.

“The awards identify a cadre of outstanding scientists and engineers who will broadly advance science and the missions important to the participating agencies.

In honoring scientists and engineers who are early in their research careers, the PECASE Awards recognize “exceptional potential for leadership at the frontiers of scientific knowledge during the 21st century. The awards foster innovative and far-reaching developments in science and technology, increase awareness of careers in science and engineering, give recognition to the scientific missions of participating agencies, enhance connections between fundamental research and national goals, and highlight the importance of science and technology for the nation's future,” according to the NSTC.

Kaiser is a clinical psychologist and neuroscientist who studies the science and treatment of adolescent depression. With her research group, the Research on Affective Disorders and Development Lab (RADD Lab), she conducts research that asks questions such as: How can brain functioning and behavior help us to understand the experience of depression in adolescence and over the course of human development? Can we use brain or behavioral markers to better predict depression—or to predict resilience? How can we enhance brain and behavioral functioning to promote emotional health and wellness throughout the lifespan?

The mission of the RADD Lab is to gain insight into the brain and behavioral processes that reflect or underlie depression and other mood experiences, with the goal of leveraging research discoveries to foster emotional health. This year, in partnership with an interdisciplinary team of scientists, educators and young people, Kaiser and her team are launching an initiative to scale and translate scientific discovery into high-impact programs aimed at promoting mental health.

“I am delighted and honored to receive the PECASE, which truly reflects the dedicated efforts of our research team and the commitment to innovation at the University of Colorado,” Kaiser says.

“Youth depression is an urgent public health priority; in our research, we are advancing new paths to promote healthy mood through interdisciplinary discovery achieved with and for young people. The PECASE recognizes the promise and innovation of this work and is a launchpad for research that will develop and scale programs for personalized health insight and wellness promotion. We are enthusiastic to begin the next chapter in research discovery and real-world impact.”

Also recognized with a PECASE award was , JILA fellow, National Institute of Standards and Technology physicist and CU Boulder physics professor.

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CU Boulder Professor Jamie Nagle will discuss the quarks and gluons that formed at the Big Bang in his Distinguished Research Lecture Feb. 6

Ten trillion degrees Fahrenheit is unfathomably hot—more than 10,000 times hotter than the Sun’s core—and it’s the temperature of the universe just moments after the Big Bang. At such extreme temperatures, according to nuclear theory, ordinary matter made of protons and neutrons transforms into a plasma of fundamental particles called quarks and gluons.

At the world’s most powerful accelerators, scientists recreate tiny droplets of this early-universe matter by colliding heavy nuclei at near-light speeds. One of these scientists is Jamie Nagle, a University of Colorado Boulder professor of physics who for 20 years has studied these fleeting droplets and, along with his research group, engineered their shapes, sizes and temperatures to better understand their properties.

Nagle will discuss this work in the 125th Distinguished Research Lecture, “10 Trillion Degrees: Unlocking the Secrets of the Early Universe,” at 4 p.m. Feb. 6. in the Chancellor's Hall and Auditorium of the Center for Academic Success and Engagement (CASE).

About Jamie Nagle

Nagle has spent much of his career investigating the early universe through high-energy nuclear physics. His research has focused on understanding the quark-gluon plasma, a state of matter theorized to have existed just microseconds after the Big Bang. 

“As you go back to about six microseconds after the universe started, the temperature was around two trillion Kelvin,” Nagle explains. “It was theorized that protons and neutrons inside of nuclei would melt away, creating a bath of more fundamental particles—quarks and gluons.”

Nagle's work involves recreating droplets of this quark-gluon plasma in a laboratory by colliding large nuclei at nearly the speed of light. These collisions occur at the world’s highest-energy accelerators, including the Relativistic Heavy Ion Collider (RHIC) at Brookhaven National Laboratory in New York and the Large Hadron Collider (LHC) in Geneva, Switzerland. 

“In the world's highest-energy accelerators, we can collide very large nuclei like gold, lead or platinum at such high velocities that we create a tiny droplet of this 2 trillion Kelvin plasma,” he says.

   What: 125th Distinguished Research Lecture, 10 Trillion Degrees: Unlocking the Secrets of the Early Universe

  Who: Professor Jamie Nagle of the Department of Physics

  When: 4-5 p.m. Feb. 6, followed by a Q&A and reception

  Where: Chancellor's Hall and Auditorium, Center for Academic Success and Engagement (CASE)

Reflecting on the award, Nagle expresses gratitude and a sense of accomplishment: “It means a lot to me. You get to a certain middle age and are more self-confident, but this recognition feels rewarding. There's a lot of effort, and much of the hard work goes unnoticed. It’s nice to feel like the fruits of that labor are appreciated.”

The Distinguished Research Lectureship also emphasizes communicating complex scientific concepts to broader audiences. For Nagle, this is a vital part of his work: “This award is very meaningful to me because I often listen to the lectures of past recipients. It's about communicating the broader context of why this scientific research is important, not just within the microcosm of nuclear physics.”

About the Distinguished Research Lectureship

The Distinguished Research Lectureship is among the highest honors given by faculty to a faculty colleague at CU Boulder. Each year, the Research and Innovation Office requests nominations from faculty for this award, and a faculty review panel recommends one or more faculty members as recipients.

The lectureship honors tenured faculty members, research professors (associate or full) or adjoint professors who have been with CU Boulder for at least five years and are widely recognized for a distinguished body of academic or creative achievement and prominence, as well as contributions to the educational and service missions of CU Boulder. Each recipient typically gives a lecture in the fall or spring following selection and receives a $2,000 honorarium.

Read the original article from the Department of Physics

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CU Boulder chemist Niels Damrauer and his research colleagues use visible light to break environmentally persistent carbon-fluorine bonds in PFAS

The strength of the bond between carbon and fluorine can be both a positive and a negative. Because of its seeming unbreakablility, food doesn’t stick to Teflon-coated frying pans and water rolls off rain jackets rather than soaking in.

However, these bonds are also what put the “forever” in “forever chemicals,” the common name for the thousands of compounds that are perfluoroalkyl and polyfluoroalkyl substances (PFAS). PFAS are so commercially abundant that they can be found in everything from candy wrappers to home electronics and guitar strings—to say nothing of their presence in industrial products.

The C-F bond is so difficult to break that the products containing it could linger in the environment for thousands of years. And when these molecules linger in a human body, they are associated with increased risk for cancer, thyroid disease, asthma and a host of other adverse health outcomes.

“There are a lot of interesting things about those bonds,” says Niels Damrauer, a University of Colorado Boulder professor of chemistry and fellow in the Renewable and Sustainable Energy Institute. “(The C-F bond) is very unnatural. There are a lot of chemical bonds in the world that natural systems have evolved to be able to destroy, but C-F bonds are uncommon in nature, so there aren’t bacteria that have evolved to break those down.”

Instead of long-used methods of breaking or activating chemical bonds, Damrauer and his research colleagues have looked to light. , the scientists detail an important finding in their ongoing research, showing how a light-driven catalyst can efficiently reduce C-F bonds.

“What we’re really trying to do is figure out sustainable ways of making transformations,” Damrauer explains. “We’re asking, ‘Can we change chemical reactivity through light absorption that we wouldn’t necessarily be able to achieve without it?’ For example, you can break down PFAS at thousands of degrees, but that’s not sustainable. We’re using light to do this, a reagent that’s very abundant and that’s sustainable.”

A foundation of spectroscopy

An important foundation for this research is spectroscopy, which can use light to study chemical reactions that are initiated with light, as well as the properties of molecules that have absorbed light. As a spectroscopist, Damrauer does this in a number of ways on a variety of time scales: “We can put light into molecules and study what they do in trillionths of a second, or we can follow the paths of molecules once they have absorbed light and what they do with the excess energy.”

Damrauer and his colleagues, including those in his research group, frequently work in photoredox catalysis, a branch of photochemistry that studies the giving and taking of electrons as a way to initiate chemical reactions.

“The idea is that in some molecules, absorption of light changes their properties in terms of how they give up electrons or take in electrons from the environment,” Damrauer explains. “That giving and taking—giving an electron is called reduction and taking is called oxidation—so that if you can put light in and cause molecules to be good reducers or good oxidizers, it changes some things you can do. We create situations where we catalyze transformations and cause a chemical reaction to occur.”

Damrauer and his research colleague Garret Miyake, formerly of the CU Boulder Department of Chemistry and now at Colorado State University, have collaborated for many years to understand molecules that give up electrons—the process of reduction—after absorbing light.

Several years ago, Miyake and his research group discovered a catalyst to reduce benzene, a molecule that’s notoriously difficult to reduce, once it had absorbed light. Damrauer and his graduate students Arindam Sau and Nick Pompetti worked with Miyake and his postdoc and students to understand why and how this catalyst worked, and they began looking at whether this and similar catalysts could activate the C-F bond—either breaking it or remaking it in useful products. This team also worked with Rob Paton, a computational chemist at CSU, and his group.

They found that within the scope of their study, the C-F bond in molecules irradiated with visible light—which could, in principle, be derived from the sun—and catalyzed in a system they developed could be activated. They found that several PFAS compounds could then be converted into defluorinated products, essentially breaking the C-F bond and “representing a mild reaction methodology for breaking down these persistent chemicals,” they note in the study.

Making better catalysts

A key element of the study is that the C-F bond is “activated,” meaning it could be broken—in the case of PFAS—or remade. “C-F bonds are precursors to molecules you might want to make in chemistry, like pharmaceuticals or other materials,” Damrauer says. “They’re a building block people don’t use very much because that bond is so strong. But if we can activate that bond and can use it to make molecules, then from a pharmaceutical perspective this system might already be practical.”

While the environmental persistence of PFAS is a serious public health and policy concern, “organofluorines [containing C-F bonds] have a tremendous impact in medicinal, agrochemical and materials sciences as fluorine incorporation results in structures imparting specific beneficial attributes,” Damrauer and his colleagues write.

By pursuing systems that mitigate the negative aspects of C-F bonds and harness the positive, and using the abundant resources of visible light and organic molecules, Damrauer says he hopes this research is a significant step toward sustainably producing products that use light as a reagent rather than heat or precious metal-based catalysts.

While the catalytic process the researchers developed is not yet at a level that it could be used on PFAS in the environment at a large scale, “this fundamental understanding is really important,” Damrauer says. “It allows us to evolve what we do next. While the current iteration isn’t good enough for practical application, we’re working to make better and better catalysts.”

Xin Liu, Arindam Sau, Alexander R. Green, Mihai V. Popescu, Nicholas F. Pompetti, Yingzi Li, Yucheng Zhao, Robert S. Paton and Garret M. Miyake also contributed to this research.

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CU Boulder researchers find that socioeconomic status is a key indicator of heart health

Cardiovascular disease, the  in the United States, significantly affects those of lower socioeconomic status. In addition, members of historically marginalized groups—including Black, Indigenous and Asian populations—suffer disproportionately. Therefore, public health advocates and policy makers need to make extra efforts to reach these populations and find ways to reduce their risk of cardiovascular disease.

These are the findings of researchers Sanna Darvish and Sophia Mahoney, PhD candidates in the University of Colorado Boulder Department of Integrative Physiology. Their  on socioeconomic status and arterial aging—written with CU Boulder co-authors Ravinandan Venkatasubramanian, Matthew J. Rossman, Zachary S. Clayton and Kevin O. Murray—was published in the Journal of Applied Physiology.

Darvish and Mahoney conducted a literature review of cardiovascular disease, looking specifically at how it affects various demographics. Their focus was on two physiological features that are predictors of cardiovascular issues: endothelial dysfunction—a failure of the lining of blood vessels that can cause a narrowing of the arteries—and stiffening of arteries.

“It’s pretty well established that individuals of lower socioeconomic status have increased risk for many chronic diseases, but our lab focuses on the physiological and cellular mechanisms contributing to that increased risk,” Darvish explains. “We’re looking at what studies have been conducted, looking at blood vessel dysfunction, arterial dysfunction in these marginalized groups that then will predict their risk for cardiovascular disease.”

Exercise as therapy

Beyond the clinical findings, Darvish and Mahoney cite four social determinants of health regarding cardiovascular disease across ethnic and racial groups: environmental factors, like proximity to pollution or access to green spaces; psychological and social factors, such as stress or structural racism; health care access; and socioeconomic status.

While each of the four has different facets that contribute to overall cardiovascular health, the authors found that socioeconomic status was the “cause of causes,” and thus the most important indicator to examine in their goal of recommending effective therapies.

“It became clear to us that socioeconomic status really played a role in every single aspect of social determinants of health,” says Mahoney. “So, our paper naturally centered around socioeconomic status as we realized that it was the most integrated and affected the rest of the determinants of health.”

To help overcome the barriers to better cardiovascular health among those in lower socioeconomic groups, Darvish and Mahoney recommend exercise.

“Exercise is well established as first line of defense, especially aerobic exercise,” says Mahoney. “It’s easy for us to say that in Colorado, but there are plenty of barriers to people everywhere who do not have access to resources.”

One option the researchers propose is high-intensity interval training (HIIT), which packs a robust aerobic effort into workouts as brief as five or 10 minutes. The authors also recommend inspiratory muscle strength training (IMST), during which users breathe into a simple handheld device that inhibits air flow and get a simulated aerobic workout that also strengthens the diaphragm.  that just a few minutes of IMST therapy a day can reduce blood pressure and the risk of cardiovascular disease.

Reducing research barriers

One thing Darvish and Mahoney hope their study will do is galvanize researchers to include more diverse populations in their research. While investigating the existing literature for their review, the two were dismayed to find few studies that included or focused on populations from the lower socioeconomic echelons.

There are structural reasons for that, Darvish explains. Time is an issue, as those lower on the socioeconomic ladder often work more hours and have more demands on their non-work time. In addition, transportation can be an obstacle, as research facilities may not be near neighborhoods with more diverse populations. “We pay our participants an appropriate amount for their participation, but not all clinical trials do,” Darvish says.

“Another thing we are doing is instituting a lift service through our lab, to drive people in from their homes in Denver to our lab in Boulder, and we hope this will help improve access for more people to participate.”

Language barriers can be another impediment, as all release forms and study literature would need to be translated for those who don’t speak English. Darvish and Mahoney say it is important that researchers work to overcome these structural barriers. “Our lab is working to do all we can to reduce biases, and include these diverse populations,” says Mahoney. “We need to practice what we preach and start with ourselves.”

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In a recent study, CU Boulder’s Robert Moulder and colleagues find that individuals with trait neuroticism rarely modify how they respond to negative emotions 

Emotions, like temperatures, go up and down. Yet everyone copes with these ups and downs in his or her own way. Some use the same emotion-regulation strategies over and over—read a book, take a walk, watch a movie—while others change which strategy they use depending on the situation.

Research scientist Robert Moulder of the University of Colorado Boulder Institute of Cognitive Science, along with , ,  and , wanted to know why: Why do some people frequently modify their regulation strategies? Why do others reuse the same strategies? And are there benefits to both approaches?

Difficult questions, these, not least because they seek to identify patterns in what seem like random human behaviors. Which is why Moulder was particularly well-suited to the job of answering them. With a background in both mathematics and psychology, he uses chaos theory and nonlinear dynamics to understand human systems. “The way I like to describe it, I am like  from Jurassic Park, but for people instead of dinosaurs,” he jokes. “I do the ‘mathy math’ behind how psych works.”

Thanks to Moulder’s “mathy math,” he and his fellow researchers  a key distinction between those who rarely change up their emotion-regulation strategies and those who do so often: trait neuroticism.

Trait vs. state

Neuroticism, Moulder says, refers to “someone's overall tendency to engage in and ruminate on negative emotions like getting angry, getting upset, being distrustful. You can think about it as the propensity of an individual to experience and act upon negative emotions.”

There are two categories of neuroticism: state neuroticism and trait neuroticism, the differences between which Moulder illustrates with an analogy to extroversion.

“A state personality would be, say, how extroverted you are right now, or how extroverted you are in two or three days,” he says. “Have you ever gone to a party and felt really engaged but afterwards felt dead? During that party your extroversion was higher than it normally would be, and afterwards, it was probably a little lower.” 

Trait extroversion, on the other hand, takes the average of those individual moments over time. “It's kind of like your stable equilibrium,” says Moulder. “If you were going to describe to someone how extroverted you are, you'd be talking about your trait extroversion.”

The same thing goes for neuroticism. One person may have a high degree of neuroticism at any given moment but a low degree overall—high state, low trait—whereas another person may be exactly the opposite.

What Moulder and his colleagues found was that subjects with high levels of trait neuroticism tend not to experiment with their regulation strategies. “That means someone who is very high in neuroticism will consistently use the same tools over and over again, whether they’re working or not.”

A new mathematical model

Moulder and his colleagues arrived at these findings with the help of transition matrices, an analytical tool Moulder and Daniel developed in a . 

“Why people do the things they do after a negative event has thousands of components,” Moulder says. “There was not a good method for measuring that. So, we made one.”

Transition matrices are rectangular grids of rows and columns that enable study subjects to keep track of which emotion-regulation strategies they use and when they use them.

A subject who got into an argument with her boss at noon and then took a walk, for example, would put a “1” in the box in her matrix associated with taking a walk. If she received an angry email from her boss an hour later and chose this time to call a friend, she would put a “1” in the box associated with that regulation strategy.

“If someone used the exact same strategy all the time, you would just see one number in the matrix, and all the rest of the matrix would be ‘0,’” Moulder says, whereas someone who constantly switched from one regulation strategy to the next would have numbers all over his or her matrix.

These transition matrices provide two key metrics, Moulder explains: stability and spread. Higher stability means fewer regulation strategies; higher spread, more strategies. Subjects with high levels of trait neuroticism are therefore likely to have high stability. 

Just-in-time interventions

With this information about their own emotion-regulation behaviors, subjects can see which strategies they use and reuse; they get a snapshot of their own stability and spread. If they find they’re putting the same strategies on repeat, they can decide to change things up—play pickleball instead of binge-eating pickles, for instance.

“There are some times when it makes sense to choose the same strategy,” Moulder says, “but we know from prior research that there are some times when it makes sense to become more adaptive—to increase, to spread, to try other things.”

Moulder adds that the knowledge gleaned from transition matrices can also be turned toward potentially more effective approaches to emotion regulation. He and Daniel call one idea “just-in-time interventions.” 

“If we are, let’s say, giving individuals telehealth, which is a really big space right now for therapy, we want to do something called just-in-time interventions,” he says. By understanding a person’s regulation practices, “we can say to that person, ‘Hey, you keep going to drink almost every time something negative happens. Maybe this time go read a book or a call a friend.’ We can offer alternatives that research shows will lead to better outcomes.”

The power of such interventions lies in their precision. They’re based not purely on statistics, Moulder says, but on “person-specific analysis, which we can use to give people personalized messaging that would ideally best help them in the long run.”

There’s no guarantee that switching strategies will bring the desired outcome, Moulder admits, but experimentation is part of the process. “We’re never going to know what works until we try.” 

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University of Colorado Boulder scientists review the evidence for the bacterial origin of eukaryotic immune pathways

Scientists generally agree that eukaryotes, the domain of life whose cells contain nuclei and that includes almost all multicellular organisms, originated from a process involving the symbiotic union of two prokaryotes: an archaeon and a bacterium. It is unsurprising, then, that prokaryotes (single-celled organisms lacking nuclei and organelles) share many basic features—such as DNA genomes, cell membranes and cytoplasm—with eukaryotes; they developed these traits first and passed them down.

However, if the situation is this (relatively) simple, then the different kingdoms of eukaryotic life—animals, plants and fungi—should all have some variation of the same essential traits.

By reviewing the research on this subject, two University of Colorado Boulder scientists have demonstrated that this is not the case with respect to elements of the innate immune system that come from bacteria. Rather, some of the eukaryotic kingdoms have these elements while others do not. This is suggestive of a more obscure phenomenon known as horizontal gene transfer.

As authors of a , Aaron Whiteley, the principal investigator of the Aaron Whiteley Lab and an assistant professor of biochemistry, and postdoctoral fellow Hannah Ledvina were not involved in most of the research used to draw this conclusion, and were not the first to come to it, but write to summarize the state of the field and provide clarity by aggregating sources.

Categories of immune system

There are two categories of immune systems: innate and adaptive. Both exist within an individual because they serve distinct purposes. The adaptive immune system is more effective at eliminating viruses than the innate immune system, Whiteley says, but the innate immune system also plays an important role.

“We all know that you start feeling sick maybe one or two days after you were exposed to most viruses,” he says. “In the beginning, part of the reason you feel sick is because your first line of defense, the innate immune system, is trying to buy as much time as possible for the adaptive immune system.”

It is hard to successfully fight a virus without the antibodies and other virus-specific cells created by the adaptive immune system, Whiteley explains, but the generalized response of the innate immune system is necessary to slow the progression of disease during the time it takes for the adaptive immune system to respond.

By studying the innate immune system, scientists have found connections between the immune systems of bacteria and those of humans.

“We only started sequencing large numbers of genomes about 20 years ago,” Whiteley says, “and before we sequenced any genome, it was very hard to compare two organisms.” When some genomes became available, rudimentary comparisons were possible, “but as of maybe 10 years ago, our detection techniques for similarities of genes have skyrocketed,” and this has made comparisons like the ones in Whiteley and Ledvina’s review possible in combination with the sequencing of many more genomes.

Conserved immune pathways

“What we’ve been finding is the way that bacteria stop phages is very similar to the ways that humans fight off their pathogens,” Ledvina says. “The same proteins, as well as the same types of signaling pathways, are being used.”

"We know that the world of the immune system is so much bigger than viruses. Our immune system controls cancer, our immune system is important for wound healing and our immune system also restricts bacterial pathogens.”

Ledvina and Whiteley highlight four such types of signaling pathways of the innate immune system that are conserved between bacteria and either humans or humans and plants: cGAS-STING, NACHT and STAND NTPases, viperins and TIR.

A signaling pathway is a series of chemical reactions between a group of molecules in a cell that collectively control a cell function. The two basic elements of a signaling pathway are sensor and effector proteins: sensors detect the presence of a virus or phage and start the signaling cascade that ends with the activation of an effector, which is responsible for some form of immune response.

In the first type of signaling pathway, bacteria use the same sensor and effector proteins, cGAS and STING, to respond to phages as humans use to respond to DNA viruses (e.g., smallpox-like viruses).

In the second type of signaling pathway, Whiteley says, bacteria sometimes use the exact same protein domain, NACHT, as humans. NACHT is a subtype of STAND NTPase, a class of protein. In other cases, bacteria use different STAND NTPase subtypes, and plants use this protein class too.

A third type of signaling pathway found in eukaryotes and bacteria uses an effector protein called viperin. Similarly, in the fourth type of signaling pathway, the signaling domain TIR is used by plants, humans and bacteria.

Horizontal gene transfer

The relationships between the immune systems of humans and bacteria are especially interesting, Whiteley says, because these four pathways are likely to have been passed to eukaryotes by horizontal rather than vertical gene transfer.

Eukaryotes have many genetic similarities to bacteria, including in terms of the immune system. This, Whiteley explains, is because “things like the mitochondria, which is a really important organelle within all our cells, look like they came from a bacterium that started living inside the cell and then became a permanent resident.”

In other words, bacteria are ancestors of eukaryotes, and therefore many of the genes from bacteria were passed down to eukaryotes through vertical gene transfer, which is the transfer of genes from ancestors to progeny. However, shared genes can also be transferred horizontally.

The exact mechanism for this type of transfer is unknown, Whiteley says, but the formation of mitochondria may provide a model: “You can imagine something similar, where a bacterium went into a cell, only rather than taking up residence, it broke open and released its genome. DNA is DNA, so it can be incorporated from exotic sources, albeit rarely.”

It is hard to be certain about this because of how long ago it would have happened, according to Whiteley. Eukaryotes lacking a given immune pathway may have used it at one point but then lost it through an evolutionary process like stabilizing selection, which removes traits that are no longer useful in order to free up resources (the classic example being fish or other animals that lose their eyes because they live in dark places like caves).

There is, however, significant evidence for horizontal gene transfer, Whiteley says. “If you find that a gene is in animals, but it's not in all the cousins of animals like plants or fungi,” as was the case with these immune pathways, “then the simplest explanation is that it was transferred in.”

This is all to say that these pathways evolved in bacteria after the creation of the first eukaryotes and were introduced to some of the eukaryotic kingdoms after the last eukaryotic common ancestor, which was about 2 billion years ago.

That kind of interaction is important because it’s how antibiotic resistance forms, Whiteley explains. “Bacteria in the hospital talk to other bacteria and they swap genes. We think about that all the time between bacteria, but we rarely think about it between different domains of life, like going from bacteria into, in this case, some ancestor of a human cell from a billion years ago, and that has real impacts.”

Immune evasion and drug development

According to Ledvina, there are at least four different ways for viruses to prevent immune systems from sensing and inhibiting them. These include preventing critical enzymes from functioning, destroying the products of such enzymes, blocking protein sensors by mimicking whatever activates them, and physically shielding the features that immune systems look for to identify viruses. This is true of both the viruses that make us sick and the viruses that infect bacteria.

One question that people always ask, Whiteley says, is “if our immune system is so great, why are we still getting sick? And it's because viruses find every way possible to maintain the upper hand.

“The wild thing is, I guess because the immune system of humans and bacteria looks so similar, the viruses of humans and bacteria have come up with shared strategies for that immune evasion. So, we can discover things in bacteria, but then go to human viruses and understand, are they also using this mimic strategy? And if so, that becomes a great antiviral strategy for drug development.”

Bacteria are particularly useful for testing, he explains, because they grow fast and because scientists have already developed genetic and biochemical tools with which to study them. These advantages and the similarities between bacterial and human immune systems mean that bacteria could inspire drugs to treat human viruses.

However, Whiteley says, “we know that the world of the immune system is so much bigger than viruses. Our immune system controls cancer, our immune system is important for wound healing and our immune system also restricts bacterial pathogens.”

This is what makes Hannah Ledvina’s research on ubiquitin-like proteins interesting. As demonstrated in , bacteria have ubiquitin pathways resembling those in eukaryotes, and ubiquitin is broadly important in humans according to , such that its failure is associated with the development of cancer, immune disorders, and neurodegenerative diseases, among other things. As that article points out, this means there may be new therapeutic opportunities within the ubiquitin system.

“I think with Hannah's work,” Whiteley says, “we've shown the sky's the limit in terms of understanding the ways bacteria defend themselves, and then hopefully informing the way that human cells defend themselves.”

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Wildfire smoke’s health risks can linger in homes that escape burning—as Colorado’s Marshall Fire survivors discovered

On Dec. 30, 2021, a raced through two communities just outside Boulder, Colorado. In the span of about eight hours, and businesses burned.

The fire left entire blocks in ash, but among them, , seemingly untouched. The owners of these homes may have felt relief at first. But fire damage can be deceiving, as many soon discovered.

When wildfires like the Marshall Fire reach the , they are burning both vegetation and human-made materials. Vehicles and buildings burn, along with all of the things inside them—electronics, paint, plastics, furniture.

Research shows that when human-made materials like these burn, from what is emitted when just vegetation burns. The smoke and ash can blow under doors and around windows in nearby homes, bringing in chemicals that stick to walls and other indoor surfaces and continue off-gassing for weeks to months, particularly in warmer temperatures.

In a , my colleagues and I looked at the health effects people experienced when they returned to still-standing homes. We also created a in the future to help them protect their health and reduce their risks when they return to smoke-damaged homes.

Tests in homes found elevated metals and VOCs

In the days after the Marshall Fire, residents quickly reached out to nearby scientists who study wildfire smoke and health risks at the University of Colorado Boulder and area labs. People wanted to know what was in the ash and .

In homes we were able to test, my colleagues found . We also found elevated VOCs – volatile organic compounds – in airborne samples. Some VOCs, such as , , and , can be toxic to humans. Benzene is a .

People wanted to know whether the chemicals that got into their homes that day could harm their health.

At the time, we could find no information about physical health implications for people who have returned to smoke-damaged homes after a wildfire. To look for patterns, we affected by the fire six months, one year and two years afterward.

Symptoms six months after the fire

Even six months after the fire, we found that that aligned with health risks related to smoke and ash from fires.

More than half (55%) of the people who responded to our survey reported that they were experiencing at least one symptom six months after the blaze that they attributed to the Marshall Fire. The most common symptoms reported were itchy or watery eyes (33%), headache (30%), dry cough (27%), sneezing (26%) and sore throat (23%).

All of these symptoms, as well as having a strange taste in one’s mouth, were associated with people reporting that their home smelled differently when they returned to it one week after the fire.

Many survey respondents said that the smells decreased over time. Most attributed the improvement in smell to the passage of time, cleaning surfaces and air ducts, replacing furnace filters, and removing carpet, textiles and furniture from the home. Despite this, many still had symptoms.

We found that living near a large number of burned structures was associated with these health symptoms. For every 10 additional destroyed buildings within 820 feet (250 meters) of a person’s home, there was a 21% increase in headaches and a 26% increase in having a strange taste in their mouth.

These symptoms align with what could be expected from exposure to the chemicals that we found in the ash and measured in the air inside the few in depth.

Lingering symptoms and questions

There are a still a lot of unanswered questions about the health risks from smoke- and ash-damaged homes.

For example, we don’t yet know what long-term health implications might look like for people living with lingering gases from wildfire smoke and ash in a home.

We found a significant reporting symptoms one year after the fire. However, 33% percent of the people whose homes were affected still reported at least one symptom that they attributed to the fire. About the same percentage also reported at least one symptom two years after the fire.

We also could not measure the level of VOCs or metals that each person was exposed to. But we do think that reports of a change in the smell of a person’s home one week after the fire demonstrates the likely presence of VOCs in the home. That has health implications for people whose homes are exposed to smoke or ash from a wildfire.

Tips to protect yourself after future wildfires

Wildfires are as the wildland-urban interface, and fire seasons lengthen.

It can be confusing to know what to do if your home is one that survives a wildfire nearby. To help, my colleagues and I put together a if your home is ever infiltrated by smoke or ash from a wildfire.

Here are a few of those steps:

• When you’re ready to clean your home, start by protecting yourself. Wear at least an N95 (or KN95) mask and gloves, goggles and clothing that covers your skin.
• Vacuum floors, drapes and furniture. But avoid harsh chemical cleaners because they can react with the chemicals in the ash.
• Clean your HVAC filter and ducts to avoid spreading ash further. Portable air cleaners with carbon filters can help remove VOCs.

documents how within a home can reduce reservoirs of VOCs and lower indoor air concentrations of VOCs.

Given that we don’t know much yet about the health harms of smoke- and ash-damaged homes, it is important to take care in how you clean so you can do the most to protect your health.

Colleen E. Reid is an associate professor in the  Department of Geography.

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We developed a way to use light to dismantle PFAS ‘forever chemicals’–long-lasting environmental pollutants

, have earned the nickname of from their extraordinary ability to stick around in the environment long after they’ve been used.

These synthetic compounds, commonly used in consumer products and industrial applications for their water- and grease-resistant properties, are now found practically everywhere .

While many chemicals will degrade after they’re disposed of, PFAS for up to 1,000 years. This durability is great for their use in firefighting foams, nonstick cookware, waterproof clothing and even food packaging.

However, their resilience means that they persist in soil, water and even living organisms. They can accumulate over time and of both ecosystems and humans.

Some initial research has shown potential links between PFAS exposure and various — including cancers, immune system suppression and hormone disruption. These concerns have led scientists to search for these stubborn chemicals.

We’re a team of researchers who developed a chemical system that uses light to break down bonds between carbon and fluorine atoms. These strong chemical bonds help PFAS resist degradation. We in November 2024, and we hope this technique could help address the widespread contamination these substances cause.

Why PFAS compounds are so hard to break down

PFAS compounds have carbon-fluorine bonds, one of the strongest in chemistry. These bonds make PFAS incredibly stable. They resist the degradation processes that usually break down industrial chemicals – , and microbial breakdown.

Conventional water treatment methods , but these processes merely concentrate the contaminants instead of destroying them. The resulting PFAS-laden materials are typically sent to landfills. Once disposed of, they can still leach back into the environment.

for breaking carbon-fluorine bonds depend on use of metals and very . For example, can be used for this purpose. This dependence makes these methods expensive, energy-intensive and challenging to use on a large scale.

How our new photocatalytic system works

The new method our team has developed uses a . A photocatalyst is a substance that speeds up a chemical reaction using light, without being consumed in the process. Our system harnesses energy from cheap blue LEDs to drive a set of chemical reactions.

After absorbing light, the photocatalyst to the molecules containing fluorine, which breaks down the sturdy carbon-fluorine bonds.

By directly targeting and dismantling the molecular structure of PFAS, photocatalytic systems like ours hold the potential for complete mineralization. Complete mineralization is a process that transforms these harmful chemicals into harmless end products, like hydrocarbons and fluoride ions, which degrade easily in the environment. The degraded products can then be safely reabsorbed by plants.

Potential applications and benefits

One of the most promising aspects of this new photocatalytic system is its simplicity. The setup is essentially a small vial illuminated by two LEDs, with two small fans added to keep it cool during the process. It operates under mild conditions and does not use any metals, which are to handle and can sometimes be explosive.

The system’s reliance on light – a readily available and renewable energy source – could make it economically viable and sustainable. As we refine it, we hope that it could one day operate with minimal energy input, outside of the energy powering the light.

This platform can also transform other organic molecules that contain carbon-fluorine bonds into valuable chemicals. For instance, thousands of are commonly available as industrial chemicals and laboratory reagents. These can be transformed into building blocks for making a variety of other materials, including medicines and everyday products.

Challenges and future directions

While this new system shows potential, challenges remain. Currently, we can degrade PFAS only on a small scale. While our experimental setup is effective, it will require substantial scaling up to tackle the PFAS problem on a larger level. Additionally, large molecules with hundreds of carbon-fluorine bonds, like Teflon, do not dissolve into the solvent we use for these reactions, even at high temperatures.

As a result, the system currently can’t break down these materials, and we need to conduct more research.

We also want to improve the long-term stability of these catalysts. Right now, these organic photocatalysts degrade over time, especially when they’re under constant LED illumination. So, designing catalysts that retain their efficiency over the long term will be essential for practical, large-scale use. Developing methods to regenerate or recycle these catalysts without losing performance will also be key for scaling up this technology.

With our colleagues at the , we plan to keep working on light-driven catalysis, aiming to discover more light-driven reactions that . SuPRCat is a -funded nonprofit Center for Chemical Innovation. The teams there are working to develop reactions for more sustainable chemical manufacturing.

The end goal is to create a system that can remove PFAS contaminants from drinking water at purification plants, but that’s still a long way off. We’d also like to one day use this technology to clean up PFAS-contaminated soils, making them safe for farming and restoring their role in the environment.

Arindam Sau is a Ph.D. candidate in the  Department of Chemistry; is a postdoctoral associate in chemistry at Colorado State University; is a postdoctoral scholar in chemistry at Colorado State University.

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In a study she conducted while she was a CU Boulder postdoctoral researcher, Elizabeth Holzhausen and colleagues find a link between night-shift work and prostate-cancer risk

More workers than ever before can take advantage of flexible schedules. But some in health care, emergency services, manufacturing and other occupations are often constrained to regular overnight shifts. Epidemiologist Elizabeth Holzhausen had questions about the serious health risks associated with night shift work, specifically regarding prostate cancer.

Holzhausen, who worked as a postdoctoral associate in the University of Colorado Boulder Department of Integrative Physiology before recently becoming an assistant research professor at the Johns Hopkins Bloomberg School of Public Health, is coauthor—along with Jinyoung Moon of the College of Natural Sciences, Seoul National University, and Yongseok Mun of the Hallym University Kangnam Sacred Heart Hospital in Seoul—of in men who regularly work the night shift.

They also examined whether the number of years on that shift increased the risk to employees. Their paper was recently published in the journal Heliyon.

For the study, Holzhausen and her colleagues conducted a meta-analysis, examining a large number of studies that looked at prostate cancer incidence and its possible relationship to night-shift work. One motivation for the meta-analysis was that there had been mixed results regarding any correlation between prostate cancer and night-shift workers in past studies. Holzhausen and the research team hoped to settle the matter with a rigorous meta-analysis.

Previous research has shown that working the night shift can present numerous health hazards. Along with heightened cancer risk, night shifts can increase the probability of heart disease, stroke, type 2 diabetes and sleep disorders in workers.

According to the Centers for Disease Control, 13% of men will get prostate cancer, and approximately 3% of men die from the disease, which is more likely to strike older men. Definitive current figures are difficult to find, but the U.S. Bureau of Labor Statistics reported that in 2018, close to 4% of employees worked the night shift, including approximately 2.5 million men.

Prostate cancer and the night shift

In their study, Holzhausen and her co-authors found that there was a link between increased incidence of prostate cancer and night-shift work. They also determined that the longer men worked the night shift, the higher the risk became. The study showed that workers on the night shift for just one year had a 1% increase in prostate cancer risk, but for workers who had 30 years of overnight shifts, that risk jumped to 39%.

“I was surprised about the magnitude of the findings,” says Holzhausen. “There are a lot of people who work the night shift, so this is especially impacting people who work this shift over a long period of time.”

As Holzhausen explains, the disruptions to the body from shift work are significant: “There are several cancers that have been associated with night-shift work, and one of the big things is that we know lack of sleep and circadian misalignment can reduce the functioning of the immune system,” she says. “As a result, [the body’s] surveillance for cancer cells could be impacted if someone is doing chronic night-shift work.”

One of the challenges of the study was controlling for outside factors across a number of different studies that used different methods. A large chunk of the paper describes how the researchers achieved that.

"There are several cancers that have been associated with night-shift work, and one of the big things is that we know lack of sleep and circadian misalignment can reduce the functioning of the immune system."

“We were very rigorous about what studies we included," says Holzhausen. "Studies where the exposure was maybe nursing or some occupation that could be night-shift work, but they didn't explicitly identify if they were doing night-shift work, were excluded. We only looked at studies where specifically night-shift work was the exposure.”

The researchers also included studies that controlled for socioeconomic status to remove it as a variable in the study. "Nearly all of the studies included in our meta-analysis considered socioeconomic status. We did not analyze socioeconomic status explicitly and aren’t able to make inferences about different socioeconomic strata," says Holzhausen.

"However, the aim in adjusting for socioeconomic status is to estimate the impact of night-shift work on risk of prostate cancer independent of socioeconomic status. In other words, the results we observed are unlikely to be due to differences in socioeconomic status between day- and night-shift workers."

Holzhausen says that since night-shift work is probably not going away anytime soon, night-shift workers should be proactive in mitigating the potential risks: “Get additional screenings for prostate cancer, and take other measures that we know can help prevent prostate cancer, like eating a healthy diet, maintaining a healthy weight, limiting alcohol and not smoking.”

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Apparently, herbivores are not fond of chewing sandpaper

Sand verbena, Abronia fragrans, has a moth pollination syndrome, or a suite of floral characters modified by natural selection driven by moth pollination. Its flowers are open all night but closed all day, and long corolla tubes prevent bees from taking nectar but are ideal for moths with long tongues.

Moths follow plumes of floral fragrance from sand verbena until they are within sight of the bright, conspicuous white globes of 25 to 80 flowers, where they sip a nectar reward.

Although sand verbena has a large geographic range, it is limited to sandy habitats in Texas, New Mexico, Arizona, Utah, Colorado, Oklahoma, Kansas, Wyoming, Montana, Nebraska, South Dakota and North Dakota. While sand verbena is described as having white flowers that open only at night, populations in northern Texas and southwestern Oklahoma have a range of flower colors from light pink through fuchsia, and they also differ from most populations in the times that flowers open and close.

The plants with pink or fuchsia flowers remain open until late morning, and they reopen in early evening, allowing considerable visitation by bees and butterflies. Measurements of pollination success in the pink and fuchsia populations showed that diurnal or daytime pollination contributed 18% of the pollination success, in contrast to nothing at all in the remainder of the geographic range of the species.

These data are consistent with the hypothesis that diurnal pollinators were a selective force producing and maintaining novel flower color and diurnal presentation of open flowers in the mornings and late afternoons. The long corolla tubes frustrate bee efforts to collect pollen or nectar but hold nectar available to virtually all butterflies.

Butterflies are visiting diurnally—the most common among them is the skipper Lerodea eufala, the Eufala skipper. These data and other observations suggest the hypothesis that the Eufala skipper applied selective pressure to change flower color from white to pink or fuchsia and to modify the times that flowers open and close.

How could a butterfly apply selection pressure? This terminology unintentionally suggests that the butterflies had a plan and the organization to apply it. But that was not the case. If some flowers did not close exactly at sunrise and if a small butterfly pollinated them, enhancing their seed set, the genes that influenced tardy closing of flowers would become more common in the next generation.

The butterfly did nothing more than sip nectar from a large globe of flowers, nor did the sand verbena do anything to achieve an intended goal. The metric of natural selection is the relative number of offspring produced by competing genotypes of sand verbena. Genes that had been rare produce more seeds, making those genes more common.

Sand verbena is in the genus Abronia, which has about 20 species, all in North and Central America. All thrive in sandy environments, and it is known that 14 of the 20 species have psammophory, a defense to herbivory that is more commonly called sand armor. The armor is assembled when wind-blown sandy grit adheres to sticky exudates on stems and leaves.

I first encountered psammophory when photographing dwarf lupine in the Maze in Canyonlands National Park, and since then I thought it was a rare defense. But a scientific article whose title begins with "Chewing sandpaper" lists more than 200 psammophorous species in 88 genera in 34 families.

Sand armor is not a rare defense; it is geographically widespread and has evolved many times. Experimental studies show that sand armor reduces herbivory—remove it from stems and leaves, and the plant suffers more herbivory than when the armor was intact. Add more sand, and the plant suffers less herbivory.

While sand verbena has a large geographic range, some species of Abronia have tiny geographic distributions. One example is Yellowstone sand verbena, A. ammophila, which is adapted to and endemic (found nowhere else) to the lake shores in Yellowstone National Park.

An obligate relationship was found recently when a new species of moth, Copablepharon fuscum, was discovered in 1995 on the shores of the Salish Sea between Georgia Straight and Puget Sound. The sand-verbena moth was found on just a few beaches and spits on Vancouver Island and Whidbey Island, and it only occupies sites with windblown sand and large and dense populations of A. latifolia, yellow sand verbena, which is found along Pacific Shores from Baja to British Columbia.

The sand-verbena moth uses yellow sand verbena as its host plant, meaning that it is the site of oviposition and the sole food consumed by the caterpillars. The caterpillars have specialized mouth parts allowing them to manipulate around grains of sand.

I know I will never see a sand verbena nor a dwarf lupine without the phrase "chewing sandpaper" popping into my thoughts.

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