Electronic skin for prosthetics senses temperature and pressure

An electronic skin with a sensing system that can detect pressure and temperature could someday be used to help amputees gain feeling in their prosthetics.

The work led by Washington State University researchers and published in the journal Cell Reports Physical Science, can sense at ten times a finer scale than current commercial glove sensors.

“This approach democratizes the production of medical-grade e-skins, making advanced tactile feedback viable for widespread clinical adoption,” says Hongyi Shen, graduate student in the School of Mechanical and Materials Engineering and first author on the paper.

“This work lays a crucial foundation for a full bionic skin with both sensing and haptic stimulation functions on prosthetics.”

Haptic stimulation replicates the sense of touch. Providing even partial sensation for amputees could greatly improve their ability to perform tasks. While there are electronic skins available now, they are expensive and have low sensing resolution. They also often don’t fit people well and only cover small regions. In fact, the more that e-skins are made to a custom shape, the worse they perform in sensing ability. Furthermore, the large amount of data generated from the sensing arrays mean that they don’t work well in real-time.

“Often these devices are forced to compromise between comfort and mechanical reliability,” says Shen.

The WSU researchers developed a customizable sensing system for prosthetics that conforms to the freeform shape of limbs and better mimics real human skin in its sensing abilities. The sensor modules they created are thin-layered sandwiches that incorporate temperature and pressure sensors. The elements allow human-like tactile sensing, enabling reliable identification of surface texture and material properties.

The researchers used a “scan-model-print” manufacturing method that allows for high-density sensing at the same time as the personalized, 3D fabrication.

“The scanner basically scans the prosthetic and then, based on the geometry, we map our sensors as a multimodal sensing system with that geometry,” says Kaiyan Qiu, an assistant professor in the School of Mechanical and Materials Engineering and corresponding author on the paper.

“This enables our sensing system to have seamless coverage over the freeform region on the prosthetics.”

The sensors are accurate and reliable and can measure both pressure and temperature at a high density across a flat or curved surface. Rather than requiring adhesives, modules of sensors snap together like Legos.

“Our main manufacturing method using 3D printing and laser cutting is relatively simple, so it could be relatively low cost and convenient,” says Qiu.

The project was partially supported by WSU’s National Science Foundation Research Traineeship in Next-Generation Robotics (NRT-LEAD), led by Prashanta Dutta, professor and director in the School of Mechanical and Materials Engineering. Dutta is also a corresponding author on the paper. Additional support was provided by Qiu’s WSU startup and Cougar Cage funds.

The researchers have submitted an invention disclosure for a provisional patent with the WSU Office of Research Innovation and Entrepreneurship team. They are also working on an actuator that will eventually convert the sensing signals of the e-skin to let an amputee know what they’re touching. That would entail converting the sensing signals to stimulation and signaling of nearby nerves.

Source: Washington State University

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The brain has a switch that shuts off chronic pain

Scientists have identified a switch in mice brains that shuts off chronic pain.

Deep at the base of the brain, a tiny cluster of nerve cells serves as the body’s natural pain reliever, dialing down pain signals traveling up the spinal cord. But nerve damage can flip this system into a hyperactive engine for chronic pain.

Now, researchers at Washington University School of Medicine in St. Louis have figured out why that switch flips and how to shut it off.

They identified, in mice, that certain receptors that reside on the surface of cells in the brain’s main alert and stress center act as biological brakes on pain. Previously known to influence stress in this region of the brain, these receptors also can turn off the pain engine to relieve chronic neuropathic pain following nerve injury.

The study in Current Biology opens new doors for developing therapies that specifically target this region of the brain, known as the locus coeruleus, to reduce chronic pain.

“Millions of adults live with chronic neuropathic pain caused by nerve damage,” says Jordan McCall, an associate professor in the Center for Clinical Pharmacology in the WashU Medicine anesthesiology department and the study’s senior author.

“The pain is difficult to treat, and traditional opioid medications bind to receptors throughout the entire body and brain, often leading to side effects, tolerance and addiction risk. Understanding how localized receptors in the locus coeruleus act as gatekeepers could lead to more targeted, effective pain therapies with fewer risks.”

Neuropathic pain occurs when damaged nerve fibers send relentless, misfired signals to the brain, causing shooting, stabbing or burning sensations. The condition frequently stems from diabetes, viral infections, or nerve compression, among other factors.

To understand how to stop these signals, McCall’s team, including co-first authors Chao-Cheng Kuo, a postdoctoral research associate, and Makenzie R. Norris, a former graduate student, focused on the locus coeruleus, a part of the brain that has been shown to play a role in pain regulation.

First, they confirmed that nerve injury turns this region into an active driver of pain. When they temporarily turned off locus coeruleus brain cells in mice, they observed reduced sensitivity to touch and heat among animals modeling neuropathic pain compared with healthy mice.

Next, they turned their attention to receptors on locus coeruleus brain cells that respond to opioids, and in particular, a type of opioid receptor known as mu. Mu opioid receptors are scattered throughout the brain and spinal cord. When the body’s naturally produced opioids or synthetic ones such as morphine and fentanyl land in the receptors’ pockets, pain throughout the nervous system lessens. Because the locus coeruleus is packed with these receptors, the researchers wondered if they play an important role in pain regulation.

They deleted the mu opioid receptors on only the locus coeruleus brain cells in mice with neuropathic pain. Without the receptors, the mice were even more sensitive to touch and heat compared with mice with mu opioid receptors still present in the locus coeruleus. Restoring the receptors to those same neurons reversed the hypersensitivity, effectively turning the pain off.

The result indicates that chronic pain may be impairing the ability of mu opioid receptors to tamp down the activity of brain cells in the locus coeruleus. Building on these findings, the researchers are exploring how to manipulate the locus coeruleus without affecting receptors across the rest of the nervous system. By designing therapies that specifically engage mu opioid receptors in this brain region, the researchers says they hope to pave the way for treatments that offer powerful relief for chronic neuropathic pain.

This work was funded by the National Institutes of Health; the National Science Foundation, the McDonnell Center for Systems Neuroscience, a Collaboration Support initiative for Translational Anesthesiology Research (COSTAR) award from the anesthesiology department at Washington University School of Medicine, and the Rita Allen Foundation with added financial help from the Open Philanthropy Project.

The content is solely the responsibility of the authors and does not necessarily represent the official view of the NIH.

Source: Washington University in St. Louis

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Team finds way to ‘wake up’ tired immune cells

Researchers have found a way to wake up tired immune cells..

It’s like a shot of espresso for “exhausted” immune systems—a discovery that could restore the body’s defenses against cancer and infection.

For decades, scientists have accepted that the immune system naturally weakens with age. Georgia Tech biomedical engineer Ankur Singh wasn’t convinced.

Then the COVID-19 pandemic made the stakes impossible to ignore.

Singh says that as older adults struggled to recover from COVID, he recognized the same pattern he had been studying for years in cancer: an aging immune system that could no longer respond the way it once had.

“It pointed us back to the immune system,” says Singh, a faculty member in the Parker H. Petit Institute for Bioengineering and Bioscience and director of the Center for Immunoengineering at Georgia Tech.

“Looking at the number of people who suffered from Covid, and how poorly the immune system was prepared to fight a new infection, it became clear this was a fundamental problem.”

A lot of aging research, he notes, “focuses on the brain or physical health. But immune aging is central to so many of these problems, and there are far fewer solutions. Now we’re asking whether we can repair some of its root causes.”

In a study published in Cell Biomaterials, Singh and his collaborators, led by PhD student Zhonghao Dai, set out to answer that question.

The team focused on T cells, the immune system’s frontline defenders against viruses, abnormal cells, and the earliest signs of cancer.

T cells protect us by responding to new infections and eliminating dangerous cells before they can take hold. As we age, the body produces fewer fresh T cells, and older ones become less effective.

“They’re exhausted,” Singh says.

He wanted to know whether aging immune cells could recover some of what they had lost. To restore aging immune cells, researchers first have to deliver new biological instructions into T cells. Existing methods have made that difficult, often damaging fragile cells or failing to reach enough of them to be effective.

Using microscopic silicon nanowires, Singh and his team delivered the instructions into more than 90% of aging T cells without damaging them. The goal wasn’t to reverse aging. It was to restore enough of the cells’ lost function to allow them to behave more like younger immune cells.

“These signals act like instructions,” Singh says. “They help reset the cells’ internal programs.”

A scanning electron micrograph from the laboratory of Ankur Singh and Zhonghao Dai shows aged human T cells resting on top of a bed of microscopic silicon nanowires, which are engineered to interact directly with the cells and restore their youthful function.

Much like a cup of coffee, the treatment invigorated exhausted immune cells, helping them respond more like younger ones. The treated cells became more active. They multiplied and regained their ability to attack infected and cancerous cells.

“What surprised me most was that we only needed to fix four or five of these genes to bring T cells closer to a younger state,” Singh says.

The team then tested immune cells from healthy older adults, cancer survivors, and patients living with cancer. “We started seeing improvement in their T cell function,” Singh says. “That’s when we knew this could work across different conditions and across different people.”

The results held across each group, giving him confidence that the approach could work far more broadly than the team first imagined.

“This technique has wide applications: cancer, infection, inflammatory bowel disease, autoimmunity,” Singh says. “They’re ready to fight whatever is invading your body. You’ll respond better to vaccines. You’ll simply live a healthier life and get sick less often.”

For now, the effects last about two weeks. Singh and his team are working to make them last longer.

The body’s cells still grow older. But they may not have to act like it.

Additional coauthors are from Georgia Tech and Emory University.

This research was supported by the National Institutes of Health, the National Science Foundation, the Curci Foundation, and the Carl Ring Family Endowment.

Source: Georgia Tech

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New system captures seizures in real time

A new study is among the first to provide a high-resolution 3D video of a seizure event.

A seizure is a sudden, overwhelming wave of electrical energy passing through the brain in a matter of seconds—so fast, in fact, that it’s been nearly impossible to fully capture where these electrical bursts originate, how they move and where they stop.

That’s why University of Georgia researchers developed a new high-resolution light-sheet imaging system that is fast enough to document seizures in 3D in real-time.

Using zebrafish larvae, the go-to animal model for neuroscience research, the researchers captured images of a seizure making its way through the brain.

The images show that the seizure began toward the back of the brain and moved forward toward the part of the midbrain that processes visual information known as the optic tecta. This region controls eye movement and manages responses to what the animal is seeing. The electrical activity gradually subsides over several seconds.

The study is among the first to provide a high-resolution 3D video of a seizure event from start to finish.

“The brain is obviously three dimensional, so when you have 2D imaging, not everything is going to be visible on that single 2D plane,” says Peter Kner, corresponding author of the study and a professor in UGA’s College of Engineering.

“Seeing where something is going or where something happens, if you’re looking at a 2D plane, you start to wonder, ‘Did I actually capture the whole thing?'”

Examining those images in 3D could offer new insights into how seizures form and how they propagate. Seizure propagation is how seizure activity starts in one part of the brain and moves through other parts of the brain. This, in turn, helps researchers understand how the brain operates.

A better understanding of how the brain operates could inform new treatments of brain diseases and disorders, Kner says.

Light sheet microscopy uses a thin sheet of light to illuminate a single slice of a sample at one time. It works well on living organisms because it provides clear images at high-speed with low background, enabling fast tracking of complex processes like brain activity.

The new microscope also relies on adaptive optics, a technology originally developed for use in astronomy.

“When you look at the stars in the night sky, they sort of twinkle because the atmosphere is making the image wobble around,” Kner explains.

“It looks nice, but it’s not great for astronomers because they don’t get a good, sharp image. Adaptive optics technology corrects that.”

A similar problem is present in brain imaging caused by the tissues the light travels through. As the light travels through the tissue, its path gets bent, and the images get blurred. Using adaptive optics enables researchers to get a sharper image.

“You always want the sharpest image you can get,” Kner says. “The whole field of imaging is really exciting right now. Microscopes have been around since roughly 1650, so you think what could possibly be new?

“But there are a lot of places left for the field to go.”

The research appears in Biomedical Optics Express.

The study was funded by a grant from the National Institutes of Health.

Source: University of Georgia

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Prolonged exposure to wildfire smoke raises heart health risks

Repeated and cumulative exposure to wildfire smoke is linked to a higher risk of being hospitalized for cardiovascular disease in older adults in the US, a new study finds.

As the climate warms, wildfires are becoming larger, more frequent, and more intense. The smoke now routinely travels hundreds of miles, as was seen when Canadian wildfires this month sent heavy smoke across the Midwest and Northeastern US, triggering dangerous air quality across the region.

But the health risks of wildfire smoke goes beyond the short-term threat to your lungs.

In the new study, Yale researchers found that repeated and cumulative exposure to the fine particles in wildfire smoke is linked to a higher risk of being hospitalized for cardiovascular disease in older adults in the United States.

Looking at more than 65 million Medicare beneficiaries across the continental US,the researchers saw that exposure to even relatively modest levels of smoke, built up over a few years, was associated with more hospitalizations for conditions like ischemic heart disease, irregular heart rhythms, stroke, and heart failure.

“In other words, the cardiovascular toll of wildfire smoke reaches well beyond the fire lines and well beyond the day the sky turns orange,” says Kai Chen, associate professor of epidemiology (environmental health sciences) at the Yale School of Public Health and corresponding author of the study.

The study appears in the Journal of the American College of Cardiology.

So far, much of the research into wildfire-related smoke has focused on the immediate effects of breathing in smoke over a few days or weeks, Chen says. And it has mostly looked at the respiratory system, including the lungs. On smoky days, there are more emergency department (ED) visits and hospitalizations, especially for breathing problems like asthma, studies have shown.

In the longer term, a small but growing number of studies have also started to connect prolonged wildfire smoke exposure to cardiovascular death and, more recently, to new cases of heart failure and stroke.

But those earlier studies largely didn’t include incidents from more recent years, which is when wildfire activity and smoke exposure has really intensified. And they didn’t look across the full range of heart and blood-vessel conditions, the authors say. So, the long-term cardiovascular picture—especially for specific subtypes like ischemic heart disease and arrhythmias, and for the older adults who are most at risk—was still very much an open question.

Because heart disease is the leading cause of death in this country, the researchers decided to look into what that repeated, long-term exposure does to cardiovascular health—and whether some groups of people carry more of that burden than others.

To do that, they built a large population-based study using Medicare records for everyone aged 65 and older in the contiguous US from 2017 through 2022—about 65 million people. Then, for the exposure side, they used a validated model that estimates fine particulate matter related to smoke—what they call “smoke PM2.5″—on a 10-by-10-kilometer grid across the country, using satellite imagery, smoke-plume tracking, and ground monitors.

They then assigned those smoke levels to each person based on the ZIP code where they lived. Because the researchers were more concerned with long-term exposure than exposure during a single bad day, they calculated each person’s cumulative average smoke level over the prior three years, deliberately leaving out the year of hospitalization so they were capturing chronic buildup, not a short-term spike, Chen says.

On the health side, they tracked for relevant individuals the first hospitalization for overall cardiovascular disease and for specific subtypes: ischemic heart disease, stroke and other cerebrovascular disease, heart failure, and arrhythmias.

Finally, they used statistical models to estimate how risk of hospitalization changed across increasing levels of smoke exposure, carefully accounting for other factors that affect heart health like other kinds of air pollution, temperature, humidity, and a wide range of community-level social and economic factors. They also checked whether risk differed by age, sex, race, and socioeconomic status, and they ran several sensitivity and falsification tests to make sure the findings held up.

Through this process, the researchers found that long-term wildfire smoke exposure was clearly associated with a higher risk of cardiovascular hospitalization. Heart failure showed the strongest association, with risk more than 20% higher at higher exposure levels. And for stroke, particularly ischemic stroke, the risk just kept rising as exposure went up.

Two additional findings stood out to the researchers, Chen says. First, they saw elevated long-term risk even at fairly modest smoke levels, which means communities that are only lightly touched by smoke—not just those near the fires—may still face real cardiovascular risk. Second, the burden wasn’t shared equally: people of lower socioeconomic status were potentially more vulnerable, which points to a real equity problem in how this exposure plays out, they found.

“Wildfire smoke should be treated as more than a temporary respiratory nuisance,” says Harlan Krumholz, a professor of medicine at Yale School of Medicine (YSM) and coauthor of the study.

“This study finds that cumulative exposure is linked to a higher risk of cardiovascular hospitalization in older adults. Clinicians should help high-risk patients prepare for smoke events, and public health leaders should expand timely alerts, clean-air spaces, and access to effective filtration, especially for communities with fewer resources.”

These findings suggest that “the same steps that protect your lungs also help protect your heart,” says Yuan Lu, associate professor of medicine at YSM and co-senior author of the study. That includes checking local air quality, staying indoors when pollution levels are high, running air purifiers or creating what have become known as “clean-air rooms” (a designated space in any building where air quality is maintained), limiting strenuous outdoor activities, and using a well-fitting N95 or KN95 mask when outdoors.

Source: Yale

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Why do your pupils dilate when you’re surprised?

New research digs into why people’s pupils dilate when they’re surprised.

When people encounter new information that challenges their expectations, their pupils are likely to dilate. This physiological response is a sign that something is happening in the brain to help the person adapt to the new situation, according to a new study.

“Pupil dilation signals a spike in arousal, and our findings support the idea that these rapid fluctuations in arousal are doing something useful in the brain,” says study author Matt Nassar, an associate professor of neuroscience and of cognitive and psychological sciences at Brown University.

“They’re enabling us to deal with a world that often changes from one context to another context.”

Nassar is part of a research team at Brown’s Carney Institute for Brain Science that studied the function and purpose of spikes in physical alertness. Their findings in Nature Human Behaviour show that the spikes are a signal of the brain’s transition into a new mode, instantly changing how the person perceives and learns from what is happening around them.

Surprising events elicit activity in the part of the brain known as the locus coeruleus, which is the primary source of norepinephrine, the chemical messenger that drives the body’s flight-or-flight stress response. This activity is correlated with a change in pupil diameter as well as with specific brain waves measured by electroencephalography (EEG). Despite many studies showing spikes in norepinephrine and other markers of arousal in response to surprising events, the function of these physical signals and how they might shape behavior has been unclear, Nassar says.

The team designed an experiment, involving colored squares on a screen, during which participants repeatedly make predictions about what they are about to see. Then participants are shown a new set of squares, report what they see and make new predictions about what they’d see next. During this time, the researchers collect physiological data including changes in pupil diameter as well as EEG signals.

“We wanted to capture the phenomenon associated with two overarching ideas about how the arousal system affects behavior,” says study coauthor Harrison Marble, who earned a bachelor’s degree in neuroscience from Brown in 2023 and is now a research assistant and manager in Nassar’s lab.

“One of them is related to learning, and the other is related to perceptual bias.”

The experiment included 63 participants, which resulted in 57 EEG datasets and 60 pupil measurement datasets.

The researchers found that surprising colors—those that didn’t match predictions—elicited pupil dilation and amplified certain brain waves. They also found that these measurements related to reductions in bias and adjustment in learning: When images looked like what the participants thought they were going to see, participants were biased toward their expectations. Yet pupil and brain measurements showed that participants were also able to learn from unexpected results and adjust their subsequent prediction accordingly.

In surprising situations, the researchers found, the norepinephrine spike is almost like a refresh mechanism—it’s a sign the brain is adjusting to new information that changes expectations.

“The brain holds on to some mental context, and then when it recognizes that you’re in a new situation, you replace that context,” Nassar says.

“Changes in pupil diameter, as well as specific EEG readings, are external markers of the brain that shows it’s loading that new context. This both limits the effect that the previous context had on perception and also provides a clean slate, unencumbered by previous expectations, thereby allowing one to learn faster.”

Funding for was provided by the National Institute of Mental Health.

Source: Brown University

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Team uncovers environmental cues behind bear hibernation

New research provides fresh insight into how environmental conditions influence black bear hibernation.

The findings have implications for wildlife management in today’s environment.

The study, led by Brogan Holcombe, a doctoral student in the Department of Fish and Wildlife Conservation in the Virginia Tech College of Natural Resources and Environment, and coauthored by Professor Marcella Kelly and Bernardo Mesa-Cruz, examines how ambient temperature and day length interact to shape hibernation behavior in American black bears.

“As temperatures rise, bears may become more active during times when they would traditionally remain dormant,” Holcombe wrote in the study.

This increased activity could lead to mismatches between bear behavior and seasonal food availability, potentially driving bears to seek out human-associated resources.

Using more than 22,000 hours of continuous video footage collected at Virginia Tech’s Black Bear Research Center during Mesa-Cruz’s original study, Holcombe tracked the activity of four wild, pregnant female bears across multiple stages of the hibernation cycle. The analysis categorized 45 distinct behaviors and linked them to environmental cues such as temperature and photoperiod—the seasonal pattern of daylight—as well as physiological changes during hibernation.

The team found that both temperature and day length play important and interacting roles in driving bear activity, particularly during critical periods such as pre-hibernation feeding and den emergence. While temperature alone influenced behavior during the onset of hibernation, the combined effects of temperature and photoperiod were key drivers of activity in other stages.

These findings challenge the long-standing assumption that hibernation timing in black bears is driven primarily by temperature. Instead, the results suggest a more complex relationship between environmental signals, one that could be disrupted as climate patterns shift.

Because photoperiod remains constant while temperatures fluctuate, the researchers highlight the risk that climate change could decouple these environmental cues. Such mismatches may alter hibernation timing, with cascading effects for ecosystems and increases in human-wildlife interactions.

The study in the Proceedings of the Royal Society B: Biological Sciences, represents one of the first to directly examine the combined influence of temperature and photoperiod in bear hibernation ecology, offering new data to inform conservation strategies.

By improving understanding of how black bears respond to environmental change, the research provides wildlife managers with better tools to anticipate behavioral shifts and plan for future conditions.

Source: Virginia Tech

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