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.

But more common viral diseases also contribute to global health challenges and economic costs. For example, seasonal influenza epidemics occur annually, causing a substantial global disease burden and economic losses exceeding $11.2 billion each year in the United States alone. Meanwhile, herpes simplex virus-1 (HSV-1), spread primarily through oral contact, infects over two-thirds of the global population and is the leading cause of infectious blindness in Western countries.

Low vaccination rates for influenza viruses and the lack of an HSV vaccine underscore the need for a new approach — one that targets reducing viral loads at the sites where transmission occurs. And for viruses like these, which are transmitted more efficiently through the mouth than the nose, this means focusing on the oral cavity.

Now, in a study published in Molecular Therapy, researchers at the School of Dental Medicine at the University of Pennsylvania and collaborators in Finland, have done just that.

Building on their previous work — now in clinical trial — showing that a similar approach was able to reduce SARS-CoV-2 in COVID-19 patient saliva or swab samples by more than 95%, Henry Daniell, W.D. Miller Professor in Penn’s School of Dental Medicine, and collaborators tested the ability of a chewing gum made from lablab beans, Lablab purpureus — that naturally contain an antiviral trap protein (FRIL) — to neutralize two herpes simplex viruses (HSV-1 and HSV-2) and two influenza A strains (H1N1 and H3N2). The chewing gum formulation allowed for effective and consistent release of FRIL at sites of viral infection.

They demonstrated that 40 milligrams of a two-gram bean gum tablet was adequate to reduce viral loads by more than 95%, a reduction similar to what they saw in their SARS-CoV-2 study.

Importantly, the researchers prepared the gum as a clinical-grade drug product to comply with the FDA specifications for drug products and found the gum to be safe. Daniell notes, “These observations augur well for evaluating bean gum in human clinical studies to minimize virus infection/transmission.”

Daniell and his colleagues are now looking to use lablab bean powder to tackle bird flu, which is currently having a significant impact in North America. In the previous three months, 54 million birds have been affected by H5N1, and several human infections have been reported in the U.S. and Canada.

Previously, bean powder was shown by others to effectively neutralize H5N1 and H7N9 — two strains of influenza A known to cause bird flu in humans as well as in birds. Daniell and colleagues are currently looking to test its use in bird feed to help control bird flu in birds.

“Controlling transmission of viruses continues to be major global challenge. A broad spectrum antiviral protein (FRIL) present in a natural food product (bean powder) to neutralize not only human flu viruses but also avian (bird) flu is a timely innovation to prevent their infection and transmission,” says Daniell.

Henry Daniell is the W.D. Miller Professor in the Department of Basic & Translational Sciences at the School of Dental Medicine at the University of Pennsylvania.

Other authors include Gary H. Cohen, Yuwei Guo, Uddhab Karki, Rachel J. Kulchar, Rahul Singh, and Geetanjali Wakade of Penn Dental Medicine, Hamid Khazaei of the Natural Resources Institute Finland (Luke) and the University of Finland and Juha-Matti Pihlava of the University of Finland.

Research performed in the Daniell lab is supported by NIH grant R01 HL 107904.

University of Maryland biologists offer new insights into this mysteriously universal pattern in a study published in the journal Proceedings of the National Academy of Sciences on April 4, 2025. The new study on baby plants shows that fighting disease at a young age often comes at a steep cost to growth and future evolutionary fitness — or their ability to reproduce.

“It’s a mystery why young organisms don’t evolve stronger disease resistance because getting sick early in life can be deadly,” said study co-author Emily Bruns, an assistant professor of biology at UMD. “Our findings suggest that a hidden trade-off is involved, stopping them from being able to completely fight off a disease.

The researchers studied a wild plant called Silene latifolia (commonly known as white campion) and its relationship with a fungal disease called anther-smut that infects it. This disease doesn’t kill the plants but prevents them from producing pollen, making them unable to reproduce — much like a “plant STD,” as Bruns describes it.

By testing 45 different genetic variations of the Silene plant under controlled settings, the team discovered that plants with stronger disease resistance as seedlings produced significantly fewer flowers and seeds over their lifetime when grown in a disease-free field. Meanwhile, plants with stronger resistance as adults showed no such penalty.

“We found that young plants paid a higher ‘cost’ for fighting the disease compared with adult plants,” Bruns said. “Trying to fight off the fungus was more difficult and resource-consuming for these baby plants. They only have so much energy to spend. If baby plants spend it on disease defense, they can’t put it toward future growth.”

Using their findings, the researchers created a mathematical model showing that these costs of fighting off pathogens are high enough to prevent the evolution of stronger disease resistance in younger plants. Without these costs, plant families with stronger juvenile resistance would theoretically be able to eliminate the disease entirely. But because developing resistance is so impactful for young plants, they remain vulnerable to infection.

“Some young plants ‘pay the cost’ and survive into adulthood, but they make fewer flowers, meaning they’re less able to reproduce,” Bruns explained. “But most remain susceptible as babies, allowing the disease a toehold.”

The team was surprised that these costs didn’t show up right away. Plants that invested in disease resistance as seedlings looked fine at first but produced dramatically fewer flowers in their second year when reproduction would normally peak.

Interestingly, the researchers also found that male plants suffered much higher costs for disease resistance than female plants. Bruns noted that this may be because male plants produce many more flowers than females to spread their pollen as widely as possible — making the cost of diverting resources to disease resistance especially steep for males.

Bruns believes that the team’s findings have implications beyond wild plants. Because juvenile susceptibility drives disease epidemics across many species, understanding the evolutionary mechanisms behind this pattern could inform disease management strategies in agriculture, conservation and public health.

Next, Bruns and the team hope to investigate whether disease resistance costs can be reduced by introducing pathogens to plants slightly later in life when plants establish their first true leaves and no longer rely on stored energy. They also plan to explore whether adult plants with higher disease resistance might protect nearby seedlings by reducing the overall presence of disease presence in a specific area.

“Nature is full of infectious diseases,” Bruns said. “Understanding the different checks and balances between hosts and pathogens helps us understand how evolution has shaped these relationships over millions of years.”

Published in the academic journal Aquaculture, the research compares two scallop farming methods, ear-hanging and lantern net culture, over a complete grow-out cycle to determine which approach yields the best results for commercial growers. The study, led by UMaine postdoctoral researcher Christopher Noren, provides new insights into how each method influences scallop size and adductor muscle weight, a key factor in market value.

Evaluating Two Common Farming Methods

Maine’s scallop aquaculture industry is still in its early stages, and growers are looking for efficient ways to scale up production. Suspended culture is the most common approach, with farmers typically using multi-tiered lantern nets to grow scallops to a harvestable size. However, this method requires frequent maintenance to manage biofouling — an unwanted accumulation of microorganisms, plants and animals — and to optimize growth conditions.

Ear-hanging, a technique adapted from Japanese scallop farming, offers a potential alternative. This method involves drilling a small hole in the scallop’s shell and suspending it on a line, allowing for better water flow and potentially reducing maintenance needs.

To evaluate the effectiveness of each method, researchers partnered with two commercial scallop farms in Maine’s Penobscot Bay and Frenchman Bay. Over four years, they measured scallop growth and the weight of their adductor muscles, the primary product from scallops that are sold in U.S. seafood markets.

Findings to inform Maine’s aquaculture industry

The study found that scallops grown with ear-hanging culture had slightly larger shell heights, about 1-4% greater than those in lantern nets. More significantly, ear-hanging scallops had up to 12% more adductor muscle weight, which is the primary product sold in U.S. seafood markets and commands a higher price per pound when larger. This suggests a potential advantage for growers aiming to maximize profitability within that market.

“We wanted to provide growers with data they could actually use on the water,” said Christopher Noren, doctoral researcher at UMaine and lead author of the study. “By comparing these two methods across a full grow-out cycle, we were able to identify where the biological advantages lie and how they might translate to better yields and more efficient operations.”

The results also highlight the role of temperature in scallop growth. Ear-hanging scallops grew more quickly in optimal conditions, which are between 50 and 59 degrees Farhenheit, but were more affected by colder winter temperatures than those in lantern nets.

“These findings give scallop farmers a clearer picture of how different methods impact growth and harvest timing. Understanding the trade-offs between techniques will help inform decisions about production strategies.” says co-author Damian Brady, a professor of oceanography at UMaine.

Supporting a sustainable, domestic seafood supply

The U.S. imports the majority of its seafood, including scallops, from foreign markets. As interest in domestic scallop aquaculture grows, studies like this can help Maine farmers refine their operations and improve profitability.

“This research gives us real-world numbers to work with,” said Andrew Peters, owner of Vertical Bay LLC and co-author on the study. “Understanding how small changes in gear choice impact growth and market value helps us make smarter decisions as we scale up scallop farming in Maine.”

By identifying methods that balance growth efficiency with labor demands, UMaine researchers are contributing to the development of a sustainable scallop aquaculture industry in the Gulf of Maine.