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.