“If you frame it as an either/or question, it’s too simplistic,” says Utah State University evolutionary biologist Zachariah Gompert. “The answer isn’t ‘completely random’ or ‘completely deterministic and predictable.’ And yet, examining short time scales, we can find predictable, repeatable evolutionary patterns.”

Gompert and colleagues report evidence of repeatable evolution in populations of stick insects in the May 24, 2024, online edition of the American Association for the Advancement of Science’s journal Science Advances. Collaborating authors on the paper include Gompert’s long-time collaborator Patrik Nosil and other researchers from France’s University of Montpelier, Brazil’s Federal University of São Paulo, the University of Nevada, Reno and Notre Dame University. The research is supported by the National Science Foundation and the European Research Council.

The team examined three decades of data on the frequency of cryptic color-pattern morphs in the stick insect species Timema cristinae in ten naturally replicate populations in California. T. cristinae is polymorphic in regard to its body color and pattern. Some insects are green, which allows the wingless, plant-feeding insect to blend in with California lilac (Ceanothus spinosus) shrubs. In contrast, green striped morphs disappear against chamise (Adenostoma fasciculatum) shrubs.

Hiding amongst the plants is one of T. christinae’s key defenses as hungry birds, such as scrub jays, are insatiable predators of the stick insects.

“Bird predation is a constant driver shaping the insects’ organismal traits, including coloration and striped vs. non-striped,” says Gompert, associate professor in USU’s Department of Biology and the USU Ecology Center. “We observed predictable ‘up-and-down’ fluctuations in stripe frequency in all populations, representing repeatable evolutionary dynamics based on standing genetic variation.”

He says a field experiment demonstrates these fluctuations involved negative frequency-dependent natural selection (NFDS), where cryptic color patterns are more beneficial when rare rather than common. This is likely because birds develop a ‘search image’ for very abundant prey.

“At short time scales, evolution involving existing variations can be quite predictable,” says Gompert, who received a National Science Foundation CAREER grant in 2019 to support his research. “You can count on certain drivers always being there, such as birds feeding on the insects.”

But at longer time scales, evolutionary dynamics become less predictable.

“The populations might experience a chance event, such as a severe drought or a flooding event, that disrupts the status quo and thus, the predictable outcomes,” Gompert says.

On long time scales, a new mutation in the species could introduce a rare trait, he says. “That’s about as close to truly random as you can get.”

“Rare things are easily lost by chance, so there’s a strong probability a new mutation could disappear before it gains a stronghold,” he says. “Indeed, another species of Timema stick insect that also feeds on chamise either never had or quickly lost the mutations making the cryptic stripe trait. Thus, the evolution of stripe is not a repeatable outcome of evolution at this long scale.”

Gompert notes replicated, long-term studies from natural populations, including research on the famous Darwin’s finches, are rare.

“Because most of this work is restricted to one or few populations, it is difficult to draw inferences on repeatability among multiple evolutionary independent populations,” he says. “Such studies are challenging to implement not only because they take concerted effort, but also because you can’t rush time.”

Gompert, who is designated a High Ranked Scholar by ScholarGPS, has developed, with USU colleagues, a research-intensive, interactive introductory biology laboratory class to introduce undergraduates to research. He and colleagues also developed an interactive presentation about evolution for all ages, called “Nabokov’s Butterflies,” that was presented at the USU College of Science’s Science Unwrapped public outreach program in 2022.

In a new study of 11 affected individuals, researchers from Newcastle University, the Wellcome Sanger Institute, the Great North Children’s Hospital, and their collaborators were able to link mutations in the NUDCD3 gene to Severe Combined Immunodeficiency and Omenn syndrome¹ – rare and life-threatening immunodeficiency disorders. These mutations prevented the normal development of diverse immune cells needed to combat different pathogens².

The findings, published today (24 May) in Science Immunology, open opportunities for early diagnosis and intervention for this condition.

Severe Combined Immunodeficiency (SCID) and Omenn syndrome are both rare genetic disorders that leave children without a functional immune system and at risk of life-threatening infections. Without urgent treatment, such as stem cell transplants to replace the faulty immune system, many affected will not survive their first year.

While newborn screening methods can flag T cell deficiency, knowledge of the specific genetic cause increases confidence in the diagnosis of SCID and informs the choice of curative therapy. Currently this remains out of reach for at least 1 in 10 affected families.

In this new study, researchers from Newcastle University, the Wellcome Sanger Institute and their collaborators studied 11 children across four families, two of whom had SCID while the other nine had Omenn syndrome. All had inherited mutations that disrupted the function of the NUDCD3 protein, which had not previously been linked to the immune system.

Using detailed studies of patient-derived cells and mouse models, the team demonstrated that NUDCD3 mutations impair a crucial gene-rearranging process called V(D)J recombination, essential for generating the diverse T cell receptors and antibodies needed to recognise and fight different pathogens.

While mice engineered with the same NUDCD3 mutations had milder immune problems, the human patients faced severe, life-threatening consequences. Two patients did survive, however, after receiving a stem cell transplant — reinforcing the importance of early diagnosis and intervention.

Dr Gosia Trynka, author of the study at the Wellcome Sanger Institute and science director at Open Targets, said: “For babies born with high-risk immunodeficiencies, early detection can mean the difference between life and death. These diseases leave newborns essentially defenceless against pathogens that most of us can easily fend off. The identification of this new disease gene will help clinicians to make a prompt molecular diagnosis in affected patients, meaning they can receive life-saving treatments more quickly.”

Professor Sophie Hambleton, senior author of the study at Newcastle University and practicing paediatric immunologist at the Great North Children’s Hospital, said: “SCID and Omenn syndrome are devastating disorders, requiring complex and timely treatments. The more we can understand about its underlying causes, the better we can look after affected babies. Our research is aimed at filling in the gaps so that families can achieve a molecular diagnosis while we continue learning more about how the immune system works in health and disease. We are deeply grateful to the families whose invaluable participation in this study will help future generations.”

Notes

1. Children with severe combined immunodeficiency disorder completely lack the T cells needed to combat infections, while those with Omenn syndrome have abnormal T cells that not only fail to combat infections but also mount attacks on the body’s own tissues. They require urgent infection management and treatment.

2. Specifically, the mutant NUDCD3 could not regulate RAG1, a key enzyme needed in V(D)J recombination. This caused RAG1 to get trapped within cell nucleoli instead of facilitating the gene rearrangements that build immune diversity.

While not possible yet, new research by a team of CU Boulder scientists could potentially lead to such advances.

Published today in the Proceedings of the National Academy of Sciences, researchers in Ankur Gupta’s lab discovered how tiny charged particles, called ions, move within a complex network of minuscule pores. The breakthrough could lead to the development of more efficient energy storage devices, such as supercapacitors, said Gupta, an assistant professor of chemical and biological engineering.

“Given the critical role of energy in the future of the planet, I felt inspired to apply my chemical engineering knowledge to advancing energy storage devices,” Gupta said. “It felt like the topic was somewhat underexplored and as such, the perfect opportunity.”

Gupta explained that several chemical engineering techniques are used to study flow in porous materials such as oil reservoirs and water filtration, but they have not been fully utilized in some energy storage systems.

The discovery is significant not only for storing energy in vehicles and electronic devices but also for power grids, where fluctuating energy demand requires efficient storage to avoid waste during periods of low demand and to ensure rapid supply during high demand.

Supercapacitors, energy storage devices that rely on ion accumulation in their pores, have rapid charging times and longer life spans compared to batteries.

“The primary appeal of supercapacitors lies in their speed,” Gupta said. “So how can we make their charging and release of energy faster? By the more efficient movement of ions.”

Their findings modify Kirchhoff’s law, which has governed current flow in electrical circuits since 1845 and is a staple in high school students’ science classes. Unlike electrons, ions move due to both electric fields and diffusion, and the researchers determined that their movements at pore intersections are different from what was described in Kirchhoff’s law.

Prior to the study, ion movements were only described in the literature in one straight pore. Through this research, ion movement in a complex network of thousands of interconnected pores can be simulated and predicted in a few minutes.

“That’s the leap of the work,” Gupta said. “We found the missing link.”

A University of Washington team has developed an artificial intelligence system that lets a user wearing headphones look at a person speaking for three to five seconds to “enroll” them. The system, called “Target Speech Hearing,” then cancels all other sounds in the environment and plays just the enrolled speaker’s voice in real time even as the listener moves around in noisy places and no longer faces the speaker.

The team presented its findings May 14 in Honolulu at the ACM CHI Conference on Human Factors in Computing Systems. The code for the proof-of-concept device is available for others to build on. The system is not commercially available.

“We tend to think of AI now as web-based chatbots that answer questions,” said senior author Shyam Gollakota, a UW professor in the Paul G. Allen School of Computer Science & Engineering. “But in this project, we develop AI to modify the auditory perception of anyone wearing headphones, given their preferences. With our devices you can now hear a single speaker clearly even if you are in a noisy environment with lots of other people talking.”

To use the system, a person wearing off-the-shelf headphones fitted with microphones taps a button while directing their head at someone talking. The sound waves from that speaker’s voice then should reach the microphones on both sides of the headset simultaneously; there’s a 16-degree margin of error. The headphones send that signal to an on-board embedded computer, where the team’s machine learning software learns the desired speaker’s vocal patterns. The system latches onto that speaker’s voice and continues to play it back to the listener, even as the pair moves around. The system’s ability to focus on the enrolled voice improves as the speaker keeps talking, giving the system more training data.

The team tested its system on 21 subjects, who rated the clarity of the enrolled speaker’s voice nearly twice as high as the unfiltered audio on average.

This work builds on the team’s previous “semantic hearing” research, which allowed users to select specific sound classes — such as birds or voices — that they wanted to hear and canceled other sounds in the environment.

Currently the TSH system can enroll only one speaker at a time, and it’s only able to enroll a speaker when there is not another loud voice coming from the same direction as the target speaker’s voice. If a user isn’t happy with the sound quality, they can run another enrollment on the speaker to improve the clarity.

The team is working to expand the system to earbuds and hearing aids in the future.

Additional co-authors on the paper were Bandhav Veluri, Malek Itani and Tuochao Chen, UW doctoral students in the Allen School, and Takuya Yoshioka, director of research at AssemblyAI. This research was funded by a Moore Inventor Fellow award, a Thomas J. Cabel Endowed Professorship and a UW CoMotion Innovation Gap Fund.

The team’s research findings, representing the genomic analyses of over 280 specimens from 17 countries and six continents, show that this species evolved some 2,100 years ago from an outside species in Asia and were released this week in the Proceedings of the National Academy of Sciences journal.

One may think by its name that its origins are in Germany. But it is not native to any wilderness in that country. In fact, it doesn’t seem to have any home in the wild anywhere in the world. To date, populations have never been found outside of structures.

Following its evolution, the German cockroach spread from Southeast Asia, hitchhiking around the world in association with humans. In addition to rapid spread, it evolved a resistance to a variety of insecticides, making it extremely difficult to control using over-the-counter products.

According to Booth, the German cockroach is a major public health issue due to its links to disease spread, the contamination of food, and its role in triggering asthma and allergies.

About Booth

Warren Booth is an associate professor of urban entomology in the Department of Entomology in the College of Agriculture and Life Sciences. He is also an affiliated faculty of the Fralin Life Sciences Institute at Virginia Tech.

His research interests include:

• Population and evolutionary genomics of indoor urban pest insects
• Insecticide resistance evolution
• Influence of socioeconomic disparity on urban pest population dynamics
• Mitochondrial heteroplasmy and recombination
• Invasion biology and ecology
• Urban pest management
• Urban evolutionary biology/genomics

The work was led by Joseph Karpie, a postdoctoral associate in the Center for Theoretical and Computational Physics (Theory Center) at the U.S. Department of Energy’s Thomas Jefferson National Accelerator Facility.

He said that this decades-old mystery began with measurements of the sources of the proton’s spin in 1987. Physicists originally thought that the proton’s building blocks, its quarks, would be the main source of the proton’s spin. But that’s not what they found. It turned out that the proton’s quarks only provide about 30% of the proton’s total measured spin. The rest comes from two other sources that have so far proven more difficult to measure.

One is the mysterious but powerful strong force. The strong force is one of the four fundamental forces in the universe. It’s what “glues” quarks together to make up other subatomic particles, such as protons or neutrons. Manifestations of this strong force are called gluons, which are thought to contribute to the proton’s spin. The last bit of spin is thought to come from the movements of the proton’s quarks and gluons.

“This paper is sort of a bringing together of two groups in the Theory Center who have been working toward trying to understand the same bit of physics, which is how do the gluons that are inside of it contribute to how much the proton is spinning around,” he said.

He said this study was inspired by a puzzling result that came from initial experimental measurements of the gluons’ spin. The measurements were made at the Relativistic Heavy Ion Collider, a DOE Office of Science user facility based at Brookhaven National Laboratory in New York. The data at first seemed to indicate that the gluons may be contributing to the proton’s spin. They showed a positive result.

But as the data analysis was improved, a further possibility appeared.

“When they improved their analysis, they started to get two sets of results that seemed quite different, one was positive and the other was negative,” Karpie explained.

While the earlier positive result indicated that the gluons’ spins are aligned with that of the proton, the improved analysis allowed for the possibility that the gluons’ spins have an overall negative contribution. In that case, more of the proton spin would come from the movement of the quarks and gluons, or from the spin of the quarks themselves.

This puzzling result was published by the Jefferson Lab Angular Momentum (JAM) collaboration.

Meanwhile, the HadStruc collaboration had been addressing the same measurements in a different way. They were using supercomputers to calculate the underlying theory that describes the interactions among quarks and gluons in the proton, Quantum Chromodynamics (QCD).

To equip supercomputers to make this intense calculation, theorists somewhat simplify some aspects of the theory. This somewhat simplified version for computers is called lattice QCD.

Karpie led the work to bring together the data from both groups. He started with the combined data from experiments taken in facilities around the world. He then added the results from the lattice QCD calculation into his analysis.

“This is putting everything together that we know about quark and gluon spin and how gluons contribute to the spin of the proton in one dimension,” said David Richards, a Jefferson Lab senior staff scientist who worked on the study.

“When we did, we saw that the negative things didn’t go away, but they changed dramatically. That meant that there’s something funny going on with those,” Karpie said.

Karpie is lead author on the study that was recently published in Physical Review D. He said the main takeaway is that combining the data from both approaches provided a more informed result.

“We’re combining both of our datasets together and getting a better result out than either of us could get independently. It’s really showing that we learn a lot more by combining lattice QCD and experiment together in one problem analysis,” said Karpie. “This is the first step, and we hope to keep doing this with more and more observables as well as we make more lattice data.”

The next step is to further improve the datasets. As more powerful experiments provide more detailed information on the proton, these data begin painting a picture that goes beyond one dimension. And as theorists learn how to improve their calculations on ever-more powerful supercomputers, their solutions also become more precise and inclusive.

The goal is to eventually produce a three-dimensional understanding of the proton’s structure.

“So, we learn our tools do work on the simpler one-dimension scenario. By testing our methods now, we hopefully will know what we need to do when we want to move up to do 3D structure,” Richards said. “This work will contribute to this 3D image of what a proton should look like. So it’s all about building our way up to the heart of the problem by doing this easier stuff now.”

This peptide originates from within a long non-coding RNA (lncRNA) called LOUP. According to the researchers, the human genome encodes over 20,000 lncRNAs, making it the largest group of genes produced from the genome. But despite this abundance, scientists know little about why lncRNAs exist or what they do. This is why lncRNA is sometimes referred to as the “dark matter of the genome.”

The study, published May 23 in the Proceedings of the National Academy of Sciences (PNAS), is one of the very few in the existing literature to chip away at the mysteries of lncRNA. It also presents a new strategy for conducting high-throughput screening to rapidly identify functional lncRNAs in immune cells. The pooled-screen approach allows researchers to target thousands of genes in a single experiment, which is a much more efficient way to study uncharacterized portions of the genome than traditional experiments which focus on one gene at a time.

The research was led by immunologist Susan Carpenter, a professor and Sinsheimer Chair of UC Santa Cruz’s Molecular, Cell, and Developmental Biology Department. She studies the molecular mechanisms involved in protection against infection. Specifically, she focuses on the processes that lead to inflammation to determine the role that lncRNAs play in these pathways.

“Inflammation is a central feature of just about every disease,” she said. “In this study, my lab focused on trying to determine which lncRNA genes are involved in regulating inflammation.”

This meant studying lncRNAs in a type of white blood cell known as a monocyte. They used a modification of the CRISPR/Cas9 technology, called CRISPR inhibition (CRISPRi), to repress gene transcription and find out which of a monocyte’s lncRNAs play a role in whether it differentiates into a macrophage — another type of white blood cell that’s critical to a well-functioning immune response.

In addition, the researchers used CRISPRi to screen macrophage lncRNA for involvement in inflammation. Unexpectedly, they located a region that is multifunctional and can work as an RNA as well as containing an undiscovered peptide that regulates inflammation.

Understanding that this specific peptide regulates inflammation gives drugmakers a target to block the molecular interaction behind that response in order to suppress it, Carpenter said. “In an ideal world, you would design a small molecule to disrupt that specific interaction, instead of, say, targeting a protein that might be expressed throughout the body,” she explained. “We’re still a long way from targeting these pathways with that level of precision, but that’s definitely the goal. There’s a lot of interest in RNA therapeutics right now.”

Co-authors of the study from UC Santa Cruz include Haley Halasz, Eric Malekos, Sergio Covarrubias, Samira Yitiz, Christy Montano, Lisa Sudek, and Sol Katzman, along with researchers at UCSF and MIT. The research was supported with funding from the National Institute of General Medical Sciences (R35GM137801 to Carpenter) and the National Institute of Allergy and Infectious Diseases (F31AI179201 to Malekos).

Innovative methods have also been bolstered with new tools, and a growth in the use of robotics since the 1980s has moved health care forward significantly. Assistant Professor Zhenhua Tian has pressed forward another step in the march of progress using robotics and noninvasive acoustics, and his team’s work has been published in Science Advances.

Robot-assisted surgery

Surgery using robots has been invasive since its invention because cutting is involved and often other instruments are inserted into the incision. However, because robotic-assisted tools can be smaller, the cuts also tend to be smaller than traditional surgeries, making robotics a preferred choice. This form of surgery has proven its benefits and has grown in use over time, with advantages to patients including

• Less discomfort and bleeding
• Less time in the hospital
• Faster recovery periods

In fact, according to the American College of Surgeons, 1.8 percent of surgeries included a robot in 2012. By 2018, that percentage had risen to 15.1 percent and continues to rise through advancements in robotics. Some of the most common procedures involving robotics include appendectomies, hysterectomies, and gastric bypasses.

Noninvasive sound treatment

While robotic-assisted surgery has its share of advantages, Tian’s team has taken that idea a step beyond its current state: Team members are developing a method of moving small targets, such as cells and medicine, within a body that is noninvasive. That means the method requires no cuts.

The secret is found in acoustic energy emitters that Tian’s team uses to surround and capture particles, working like invisible tweezers. The emitters create 3D acoustic vortex fields that can pass through barriers such as bone and tissue, crossing over one another to form tiny ring-shaped acoustic traps. Micro- to millimeter-sized objects caught at the center of an acoustic trap can be moved and rotated. Tian received a 2024 National Science Foundation Faculty Early Career Development Program (CAREER) award for the acoustic vortex development.

“The ability to move cells and drugs around inside veins without breaking the skin creates new opportunities in medicine,” said Tian. “As we continue the work on this research, I anticipate we will find a host of new applications.”

By mounting an acoustic vortex emitter onto a robotic platform, the acoustic vortex beam can be moved at the micrometer scale. Accordingly, the particle trapping area can be precisely set in a 3D space, and moving a particle after its capture can be engineered. When moving a tiny object along the winding path of a blood vessel, this can be a critical feature.

More than medicine

While Tian’s team is able to move a small object behind a solid structure, the acoustic vortex beams can move particles within both gases and liquids as well. Although the current approach targets small particles within those substances, integrating the acoustic energy emitters together with robotics has applications beyond surgery and very small particles. Contactless, robotic manipulation has potential in many other applications across engineering, biology, and chemistry research. Some of those include

• Controlling microrobots
• Handling delicate bioparticles, such as exosomes and cells
• Transporting hazardous reagent droplets
• Controlling self-assembly of colloidal materials
• Arranging nanomaterials for composite fabrication

“When we were recently participating in a STEM expo, the children who visited us enjoyed putting small beads into the invisible acoustic fields generated by our devices, but we would like to offer the opportunity for them to move larger objects,” said Tian. “Next year, we hope to have a larger emitter that can hold a ping pong ball. It will be interesting to see how we plug that approach into our other research.”

Healthier lives and improved well-being are among the United Nations’ global Sustainable Development Goals. Positively, a recent study shows that life expectancy worldwide is projected to increase by about 4.5 years by 2050. Much of this is thanks to public health efforts to prevent disease and improved survival from illnesses, such as cardiovascular disorders. However, heart disease is still the leading cause of death worldwide, with 26 million people estimated to be affected by heart failure.

Once heart failure has occurred, it has a tendency to reoccur along with other health issues, such as kidney and muscle problems. Researchers in Japan wanted to understand what causes this recurrence and the deterioration of other organs, and whether it can be prevented.

“Based on our earlier research, we hypothesized that recurrence may be caused by stress experienced during heart failure accumulating in the body, particularly in hematopoietic stem cells,” explained Project Professor Katsuhito Fujiu from the Graduate School of Medicine at the University of Tokyo. Hematopoietic stem cells are found in bone marrow and are the source of blood cells and a type of immune cell called macrophages, which help to protect heart health.

By studying mice with heart failure, the researchers found evidence of stress imprinting on the epigenome, that is, chemical changes occurred to the mice’s DNA. An important signaling pathway, called the transforming growth factor beta, which is involved in regulating many cellular processes, was suppressed in the hematopoietic stem cells of mice with heart failure, leading to the production of dysfunctional immune cells.

This change persisted over an extended period of time, so when the team transplanted bone marrow from mice with heart failure into healthy mice, they found that the stem cells continued to produce dysfunctional immune cells. The latter mice later developed heart failure and became prone to organ damage.

“We termed this phenomenon stress memory because the stress from heart failure is remembered for an extended period and continues to affect the entire body. Although various other types of stress might also imprint this stress memory, we believe that the stress induced by heart failure is particularly significant,” said Fujiu.

The good news is that by identifying and understanding these changes to the TGF-β signaling pathway, new avenues are now open for potential future treatments. “Completely new therapies could be considered to prevent the accumulation of this stress memory during hospitalization for heart failure,” said Fujiu. “In animals with heart failure, supplementing additional active TGF-β has been shown to be a potential treatment. Correcting the epigenome of hematopoietic stem cells could also be a way to deplete stress memory.”

Now that it has been identified, the team hopes to develop a system that can detect and prevent the accumulation of stress memory in humans, with a long-term goal of being able to not only prevent the recurrence of heart failure, but also catch the condition before it can fully develop.