With public satisfaction in the NHS just 21%, one area has a plan to shake up its services that could reduce GP waiting lists, as well as unblock hospital beds – but can it really work nationwide?
Grace Davidson gave birth to a baby girl two years after her sister’s womb was transplanted into her body.
Olivia Knowles noticed something “wasn’t quite correct” while competing in an ironman competition.
Health Secretary Robert F Kennedy Jr is reportedly headed to the state, which has recorded 480 cases.
Health bosses are accused of keeping resident doctors in the dark about their first position.
Men are more likely to die prematurely than women – and worse at seeking care when they need it.
Louise Gleadell died aged 38 after she was wrongly told her cervical screening tests were negative.
Fast-charging lithium-ion batteries are ubiquitous, powering everything from cellphones and laptops to electric vehicles. They’re also notorious for overheating or catching fire.
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.
It’s no coincidence that our bodies feel a little creakier as we age. The trillions of cells that make up our skeleton age too, and some change in ways that weaken the very structure of our bones.
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.
An NHS trust has paid compensation after a woman, now in her 70s, discovered she had been swapped at birth.
