Now, with an innovative computational model, a University of Wisconsin-Madison mechanical engineer has gained new understanding of a phenomenon that causes lithium-ion batteries to fail.

Developed by Weiyu Li, an assistant professor of mechanical engineering at UW-Madison, the model explains lithium plating, in which fast charging triggers metallic lithium to build up on the surface of a battery’s anode, causing the battery to degrade faster or catch fire.

This knowledge could lead to fast-charging lithium-ion batteries that are safer and longer-lasting.

The mechanisms that trigger lithium plating, until now, have not been well understood. With her model, Li studied lithium plating on a graphite anode in a lithium-ion battery. The model revealed how the complex interplay between ion transport and electrochemical reactions drives lithium plating. She detailed her results in a paper published on March 10, 2025, in the journal ACS Energy Letters.

“Using this model, I was able to establish relationships between key factors, such as operating conditions and material properties, and the onset of lithium plating,” Li says. “From these results, I created a diagram that provides physics-based guidance on strategies to mitigate plating. The diagram makes these findings very accessible, and researchers can harness the results without needing to perform any additional simulations.”

Researchers can use Li’s results to design not only the best battery materials — but importantly, charging protocols that extend battery life.

“This physics-based guidance is valuable because it enables us to determine the optimal way to adjust the current densities during charging, based on the state of charge and the material properties, to avoid lithium plating,” Li says.

Previous research on lithium plating has mainly focused on extreme cases. Notably, Li’s model provides a way to investigate the onset of lithium plating over a much broader range of conditions, enabling a more comprehensive picture of the phenomenon.

Li plans to further develop her model to incorporate mechanical factors, such as stress generation, to explore their impact on lithium plating.

Scientists and researchers around the globe are investigating a series of mysteries about what happens to our bones over time. In a new study, a team led by The University of Texas at Austin, in collaboration with Mayo Clinic and Cedars-Sinai Medical Center just made a major break in the case. New research found that osteocytes undergo dramatic structural and functional changes with age that impair their ability to keep our bones strong. Their findings, published in Small and Aging Cell, offer new insights that could pave the way for better treatments for osteoporosis and age-related bone loss.

Aging and stress can induce cellular senescence in osteocytes, resulting in cytoskeletal and mechanical changes that impair their ability to sense mechanical signals, ultimately weakening bone.

Osteocytes are the master regulators of bone health, sensing mechanical forces and directing when to build or break down bone. But when exposed to senescent cells — damaged cells that stop dividing but don’t die — osteocytes themselves begin to stiffen. This cytoskeletal stiffening and altered plasma membrane viscoelasticity undermine their ability to respond to mechanical signals, disrupting healthy bone remodeling and leading to bone fragility.

“Imagine the cytoskeleton as the scaffolding inside a building,” said Maryam Tilton, assistant professor in the Cockrell School of Engineering’s Walker Department of Mechanical Engineering and principal investigator of the study. “When this scaffolding becomes rigid and less flexible, the building can’t adapt to changes and stresses, leading to structural problems. Similarly, stiffened osteocytes can’t effectively regulate bone remodeling, contributing to bone loss.”

Senescent cells release a toxic brew of molecules, called senescence-associated secretory phenotype (SASP), which triggers inflammation and damage in surrounding tissues. They’ve been linked to the development of cancer and many other chronic diseases. Until now, most research has focused on detecting senescence through genetic markers, a notoriously challenging task because these markers vary widely across cell types.

Tilton and her collaborators approach the issue from a different perspective, focusing on cell mechanics. Combining genetic and mechanical approaches could lead to improved treatments for aging cells.

“Much like physical therapy helps restore movement when our joints stiffen, we’re exploring how mechanical cues might help reverse or even selectively clear these aging cells,” Tilton said.

“In the future, biomechanical markers could not only help identify senescent cells but also serve as precise targets for eliminating them, complementing or offering alternatives to current drug-based senolytic therapies,” added Dr. James Kirkland, principal investigator of the National Institutes of Health Translational Geroscience Network, director at the Center for Advanced Gerotherapeutics at Cedars-Sinai and a co-leader of the new research.

Improved knowledge about how bones age could improve treatments for osteoporosis. The condition leads to weakened bones and an increased risk of fractures and affects millions of people worldwide, particularly those over the age of 50. As the global population ages, understanding the mechanisms behind bone deterioration becomes increasingly important.

The team plans to expand their research by exploring the effects of different stressors on osteocytes and investigating potential therapeutic interventions.

This project is led by Tilton in collaboration with Kirkland. Other co-authors on the project include Junhan Liao, Domenic J. Cordova, and Hossein Shaygani of the Walker Department of Mechanical Engineering; Chanul Kim of the Department of Biomedical Engineering; Maria Astudillo Potes from Mayo Clinic; and Kyle M. Miller of Emory University.

But the disease has made a troubling comeback in recent years as vaccine coverage declined after the COVID-19 pandemic. In 2024, several outbreaks left public health officials and hospitals scrambling to accommodate a sudden influx of patients, primarily infants, who are often too young to be vaccinated and suffer the most severe symptoms.

Now, new research from The University of Texas at Austin could aid in improving whooping cough vaccines to once again push this disease toward eradication by targeting two key weaknesses in the infection.

A New Target

Against this backdrop, a team of researchers, including members of UT’s McKetta Department of Chemical Engineering and Department of Molecular Biosciences, has made significant strides in understanding and enhancing pertussis immunity. One of the things that makes pertussis infections dangerous is pertussis toxin (PT), a chemical weapon produced by the bacteria that weakens a patient’s immune response and causes many of the severe symptoms associated with whooping cough.

The new research, described in a new study published in the Proceedings of the National Academy of Sciences, focuses on two powerful antibodies, hu11E6 and hu1B7, which neutralize the PT in different ways.

Using cutting-edge cryo-electron microscopy approaches, the researchers identified the specific epitopes on PT where these antibodies bind. Epitopes are chemical targets the immune system can zero in on to fight pathogens. Hu11E6 blocks the toxin from attaching to human cells by interfering with sugar-binding sites, while hu1B7 prevents the toxin from entering cells and causing harm. These findings are the first to precisely map these critical regions, providing a blueprint to improve vaccines.

“There are currently several promising new pertussis vaccines in the research and clinical trial phases,” said Jennifer Maynard, professor of chemical engineering at the Cockrell School of Engineering and corresponding author of the new study. “Our findings could be incorporated into future versions quite easily, improving overall effectiveness and longevity of protection.”

She pointed to innovations like mRNA technology used in the COVID-19 vaccine, as well as breakthroughs in using genetic engineering on pertussis toxin (PT_gen) to generate safer and more potent new recombinant acellular pertussis vaccines as technologies preserving neutralizing epitopes that can combine with her team’s new findings.

“Training the immune system to target the most vulnerable sites on the toxin is expected to create more effective vaccines,” Maynard said. “And the more effective and longer-lasting a vaccine is, hopefully, the more people will take it.”

In addition to helping guide future vaccine designs, the hu1B7 and hu11E6 antibodies themselves hold promise as therapeutic medicines for infected and high-risk infants. Previous work by Maynard and colleagues show that they can prevent the lethal aspects of pertussis infection. UT researchers are actively seeking partnerships to develop ways to prevent lung damage and death in newborns exposed to the disease.

A Persistent Threat

Caused by the bacterium Bordetella pertussis, whooping cough is infamous for its violent coughing fits, which can lead to complications like pneumonia, seizures, and even death, particularly in infants. One nickname for the disease is the 100-days cough because the painful coughing fits can linger for months, even in mild or moderate cases. The disease kills an estimated 200,000 people each year worldwide, most of them infants and children, and survivors of severe illness can be left with brain damage and lung scarring.

While modern vaccines have reduced the toll, their effectiveness wanes over time, with protection only lasting two to five years. Modern pertussis vaccines are acellular, which means they contain portions of the bacteria that train the immune system to recognize the pathogen, including PT.

Recent outbreaks of whooping cough around the world have stunned public health officials. This fall, New York City saw a 169% increase in whooping cough cases since 2023. Cases have increased 500% since 2019. Australia is currently suffering through the largest outbreak of whooping cough since the introduction of the vaccine in the 1940s, with an estimated 41,000 cases reported this year.

Health officials point to missed initial and booster vaccinations as major contributors to the outbreaks.

Overcoming Hesitancy

While advances in fighting pertussis are exciting, they face a dual challenge: overcoming the biological complexity of pertussis and the societal hurdles of vaccine hesitancy. The most effective way to prevent pertussis in vulnerable newborns is for mothers to be vaccinated during pregnancy, which confers protection to the newborn until it is old enough to be vaccinated. According to the CDC, the full vaccination rate against pertussis in kindergarteners is typically over 90% in the US, but under 60% of mothers receive the vaccine during pregnancy. Skepticism about vaccine safety and slow normalization of routine vaccination after the COVID-19 pandemic has led to pockets of under-vaccinated communities and overall low protection of newborns, providing fertile ground for deadly outbreaks. This environment, coupled with the limitations of current vaccines, makes innovation essential.

Co-author Annalee W. Nguyen, a research professor in chemical engineering, emphasized the importance of prevention over treatment. “It’s always easier to prevent disease in a high-risk person,” she said. “Once someone is extremely ill, their immune system isn’t functioning well, and it’s harder to help them recover. Mothers have an incredible opportunity to shield their babies after they are born by getting a pertussis booster vaccination during pregnancy, and parents can continue to protect their families by working with their pediatrician to ensure children and teens are up-to-date on vaccinations.”

By focusing on neutralizing epitopes — areas where antibodies can effectively block the toxin — new vaccines can potentially provide stronger, longer-lasting immunity. This could help bolster public confidence in pertussis vaccines and curb the disease’s resurgence.

Rebecca E. Wilen of the McKetta Department of Chemical Engineering at UT Austin, Jory A. Goldsmith and Jason McLellan of the Molecular Biosciences Department at UT Austin and Wassana Wijagkanalan of BioNet-Asia were also authors on the paper. The research was financially supported by the Cancer Prevention and Research Institute of Texas, Welch Foundation and the National Institutes of Health.

Directive 2010/63/EU laid down restrictions on animal testing for the testing of cosmetics and their ingredients throughout the EU. Therefore, there is an intense search for alternatives to test the absorption and toxicity of nanoparticles from cosmetics such as sun creams. A team of researchers from Graz University of Technology (TU Graz) and the Vellore Institute of Technology (VIT) in India is working on the development of skin imitations that mimic the native three-layer tissue structure and biomechanics of human skin. Such imitations can be produced using 3D printing and consist of hydrogel formulations that are printed together with living cells.

Hydrogels in which skin cells survive and grow

“The hydrogels for our skin imitation from the 3D printer have to fulfil a number of requirements,” says Karin Stana Kleinschek from the Institute of Chemistry and Technology of Biobased Systems. “The hydrogels must be able to interact with living skin cells. These cells not only have to survive, but also have to be able to grow and multiply.” The starting point for stable and 3D-printable structures are hydrogel formulations developed at TU Graz. Hydrogels are characterised by their high-water content, which creates ideal conditions for the integration and growth of cells. However, the high-water content also requires methods for mechanical and chemical stabilisation of the 3D prints.

TU Graz is working intensively on cross-linking methods for stabilisation. Ideally, following nature’s example, the cross-linking takes place under very mild conditions and without the use of cytotoxic chemicals. After successful stabilisation, the cooperation partners in India test the resistance and toxicity of the 3D prints in cell culture. Only when skin cells in the hydrogel survive in cell culture for two to three weeks and develop skin tissue can we speak of a skin imitation. This skin imitation can then be used for further cell tests on cosmetics.

Successful tests

The first tests of 3D-printed hydrogels in cell culture were very successful. The cross-linked materials are non-cytotoxic and mechanically stable. “In the next step, the 3D-printed models (skin imitations) will be used to test nanoparticles,” says Karin Stana Kleinschek. “This is a success for the complementary research at TU Graz and VIT. Our many years of expertise in the field of material research for tissue imitations and VIT’s expertise in molecular and cell biology have complemented each other perfectly. We are now working together to further optimise the hydrogel formulations and validate their usefulness as a substitute for animal experiments.”

In a recent study published in the journal Proceedings of the Royal Society B, an international team of researchers tested a new hypothesis for why some Lepidoptera have very specific diets, feeding on only a few types of plants, while others are far less picky.

The new idea, called the Salient Aroma Hypothesis, suggests that the smells plants release play a crucial role in determining how specialized a butterfly or moth’s diet becomes. The researchers found that greater availability of plant aromas during the day provides more chemical information for day-active insects to use to locate and specialize on particular host plants, while the decrease in plant aromas at nighttime means night-active Lepidoptera have to take what they can get and have a more varied diet.

“This idea provides a new perspective on why some butterflies and moths are picky eaters while others are not,” said Po-An Lin, an assistant professor at the National Taiwan University who launched the research while earning his doctoral degree from Penn State and continued the work as a postdoc in Taiwan. “It also highlights the critical role of plant volatiles, or scents, in shaping insect-plant interactions and evolutionary adaptations.”

To determine whether plant scent may have driven adaptation, the researchers looked at the insects’ primary organs for smelling — the antennae — and compared the antennal size of 582 specimens from 94 species of butterflies and moths.

The Penn State team collaborated with a team at Harvard that found that female Lepidoptera that are active during the day tend to have larger antennae relative to their body size than those active at night.

This might suggest that having better “smelling” equipment is more beneficial when there are more smells to detect, explained Gary Felton, the Ralph O. Mumma Professor of Entomology at Penn State, co-author on the paper and Lin’s research adviser. Similarly, specialist female Lepidoptera — those that feed from only a few types of plants — often have larger antennae than generalist females, possibly because they need to be very good at detecting the specific aromas of their host plants.

“The relationship between antennal size and host plant breadth was very strong,” Felton said. “Larger antennal sizes have been associated with a greater number of sensilla, the sensory structures involved in the sense of smell, thereby increasing the surface area for sensory receptors. The enhanced capacity may be a key adaptation for how certain Lepidoptera have evolved to feed on a limited and specific range of plants.”

The findings suggest a potential link between the availability of plant aromas during the day and an evolutionary investment in olfactory structures in the insects, particularly in females that engage in host plant selection by laying their eggs on the plant, Lin explained.

“This finding demonstrates how the availability of chemical signals influences the evolution of sensory organs in insects,” he said. “It provides a fascinating example of how plants, through their chemical emissions, have played a direct role in shaping the evolution of the insects that rely on them.”

Lin and colleagues at Penn State used a combination of approaches to investigate the link between plant aromas and Lepidoptera diets. They first conducted a meta-analysis of existing scientific literature to confirm that plants generally release more diverse and abundant volatile organic compounds, or aromas, during the day versus the night. Then they studied the Lepidoptera family tree to analyze the relationship between the insects’ activity patterns — day or night active — and their preferred host plants, using statistical models that account for evolutionary relationships.

“Our analyses showed a significant correlation between being active during the day or night and the diversity of host plant species that Lepidoptera consume,” said Naomi Pierce, professor of biology at Harvard University and co-author on the paper.

The researchers found that day-active Lepidoptera, like monarch butterflies, have more opportunities and more specialized organs to detect plant aromas and, as such, have evolved to be picky eaters. On the other hand, night-active species, like the Polyphemus Moth, encounter fewer and less diverse plant aromas. With less clear chemical information available, it might be harder for them to be so selective, potentially leading them to have more generalized diets, feeding on a wider range of plants.

“Insect herbivores, such as butterflies and moths, must find the right plants to feed on and, in the case of females, to lay their eggs,” Lin said. “This is a crucial decision because caterpillars depend entirely on the selected plant for survival. Unlike humans, who eat a wide variety of foods to stay healthy, many insect herbivores specialize in feeding on only a few plant species. The Salient Aroma Hypothesis helps explain why some insects are highly specialized while others are more flexible in their diet.”

The other authors on the paper are Wei-Ping Chan and Even Dankowicz of Harvard University; Liming Cai of the University of Texas Austin; Yun Hsiao of National Taiwan University; and Kadeem Gilbert of Michigan State University.

The U.S. National Science Foundation, Taiwan’s National Science and Technology Council and the Yushan Fellowship Program from the Ministry of Education of Taiwan funded this work.

The aptamers — short single-strand snippets of DNA that can target molecules like larger antibodies do — not only deliver cancer-fighting drugs, but also are themselves toxic to the cancer stem cells, the researchers said.

Led by Xing Wang, a U. of I. professor of bioengineering and of chemistry, the researchers documented their findings in the journal Advanced Functional Materials.

“This work demonstrates a way to get to the root of leukemia,” Wang said. “Targeted cancer treatments often have problems with toxicity or efficacy. Our aptamers seek out these stem cells specifically and kill them effectively.”

Leukemia and other cancers of the blood are more difficult to target than cancers that produce localized tumors because the cancerous cells circulate throughout the body and can’t be surgically removed, said postdoctoral researcher Abhisek Dwivedy, first author of the paper. Leukemia has a high rate of relapse due to its evasive stem cells. Though they make up a tiny fraction of cancerous cells, leukemia stem cells have the ability to evade chemotherapy by retreating to the bone marrow, since they share markers and properties, Dwivedy said. The cancerous cells can lurk, sometimes for years, and later proliferate and migrate.

“It’s important in leukemia, lymphoma or other blood cancers that we actually target and eliminate these stem cells, because as long as any are remaining, they can cause relapse and secondary cancers,” Dwivedy said.

The researchers began by finding DNA aptamers that seek out markers found on the surface of acute myeloid leukemia stem cells. They wanted to target not just the cancer, but the stem cells specifically.

“A big thing we showed in this study is that having two targets is better than one in terms of selectivity,” Wang said. “There are known antibody-drug conjugates for blood cancers that target one marker, but that marker is also found on a lot of healthy cells. So there is a lot of toxicity associated with antibody conjugates. But we used two targets: a combination often found in leukemia cancer cells and leukemia stem cells. The two together give a very specific target.”

The researchers then paired their aptamers with the leukemia-fighting drug daunorubicin. The drug-laden aptamers carry the drug to their target, then release the drug once inside the cell so the drug can act.

“This is especially important for drugs like daunorubicin, because the drug on its own cannot cross the cell membrane easily. But aptamers can carry it in,” Dwivedy said.

The researchers tested the drug-delivering aptamers in leukemia cell cultures as well as in live mice with leukemia.

After 72 hours, the aptamer alone had reduced the cancer cells in culture by 40 percent, demonstrating the aptamer’s toxicity to the cancer, the researchers report. When the aptamers carried the leukemia-fighting drug, the cells were wiped out with a dose 500 times smaller than the standard dosage of the drug. In mice with leukemia, delivering the drug via aptamer yielded the same efficacy at a dose 10 times smaller than the clinical standard, showing that the one-two punch of the aptamer and drug is more effective than either alone.

“This was exciting to us, because in cancer research, what we see in vitro is not always what we see in the body. Yet we saw excellent survivability and tumor reduction in the mice treated with our aptamer-drug conjugates, at one-tenth of the therapeutic dose, and no off-target effects,” Wang said.

The researchers said they hope to expand their suite of drug-delivering aptamers by identifying key marker combinations for other cancers, as well as coupling the aptamers with other drugs.

“Every cancer cell has a signature in its surface biomarkers. If we can find markers that are present uniquely in cancer cells, we can target other cancer types as well. Also, in my experience, it’s much easier to pair a drug with the DNA molecules than proteins, so that opens possibilities for delivering more drugs this way,” Dwivedy said.