Scientists at the University of Chicago have developed a new pacemaker that’s thinner than a human hair, wireless and operated entirely by light from an optic fiber. The non-invasive device could help regulate heart activity or even stimulate neurons in a set pattern to treat symptoms of conditions like Parkinson’s.
The heart pumps thanks to a series of very carefully timed electrical signals, but if those signals fall out of time, they can lead to all sorts of issues, such as strokes, heart attacks or even a fatal failure of the organ. Pacemakers monitor and correct these abnormal rhythms, but they require invasive surgeries and bring their own risks.
The new device is much less invasive – it’s a thin film just one micrometer thick, which is about 100 times thinner than a human hair, or a recent similar device made of graphene which was also 100 micrometers thick. It tips the scales at just one 50th of a gram, making it 250 times lighter than a regular pacemaker. And rather than needing a battery, it’s powered by light.
More than 80% of stroke survivors experience walking difficulty, significantly impacting their daily lives, independence, and overall quality of life. Now, new research from the University of Massachusetts Amherst pushes forward the bounds of stroke recovery with a unique robotic hip exoskeleton designed as a training tool to improve walking function.
This invites the possibility of new therapies that are more accessible and easier to translate from practice to daily life compared to current rehabilitation methods.
Following a stroke, people often experience walking asymmetry, where one step is shorter than the other. The study, published in IEEE Transactions on Neural Systems and Rehabilitation Engineering, reveals that the robotic hip exoskeleton has the potential to effectively train individuals to modify their walking asymmetry, presenting a promising avenue for stroke rehabilitation.
Myocarditis game-changer: We've blamed the wrong culprit
By Paul McClure
March 07, 2024
Inflammation resulting from a viral infection has traditionally been thought to cause acute myocarditis, which can lead to fatal heart arrhythmias in otherwise healthy young adults. Now, a new study has shown for the first time that the virus itself damages heart cells before inflammation sets in, challenging traditional assumptions.
Viral infections are the most frequent cause of acute inflammation of the heart muscle or myocarditis, a condition linked to up to 42% of sudden cardiac deaths in young adults. The common cold (adenovirus), hepatitis B and C, and parvovirus have all been associated with myocarditis.
The traditional explanation for what causes myocarditis focuses on inflammation, triggered by the body’s immune response to a virus, which leads to potentially fatal rapid or irregular heart rhythms called arrhythmias. However, a new study led by researchers at the Fralin Biomedical Research Institute at Virginia Tech may have just turned tradition on its head, finding that the virus itself damages heart muscle before the onset of inflammation.
Heparin, the world's most widely used blood thinner, is used during procedures ranging from kidney dialysis to open heart surgery. Currently, heparin is derived from pig intestines, but scientists at Rensselaer Polytechnic Institute (RPI) have discovered how to make it in the lab. They have also developed a path to a biomanufacturing process that could potentially revolutionize how the world gets its supply of this crucial medicine.
"In recent years, with disease and contamination issues disrupting the global supply chain of pig heparin and potentially putting millions of patients at risk, it's clear we need to diversify the way we make this drug," said Jonathan Dordick, Ph.D., Institute Professor of Chemical and Biological Engineering, and vice president of Strategic Alliances and Translation at RPI. "Our work will make it possible to manufacture heparin that is both consistently available and safe."
A team of engineers led by the University of Massachusetts Amherst and including colleagues from the Massachusetts Institute of Technology (MIT) recently announced in Nature Communications that they had successfully built a tissue-like bioelectronic mesh system integrated with an array of atom-thin graphene sensors that can simultaneously measure both the electrical signal and the physical movement of cells in lab-grown human cardiac tissue.
In a research first, this tissue-like mesh can grow along with the cardiac cells, allowing researchers to observe how the heart's mechanical and electrical functions change during the developmental process. The new device is a boon for those studying cardiac disease as well as those studying the potentially toxic side effects of many common drug therapies.
University of Virginia School of Medicine researchers have discovered a gene on the Y chromosome that contributes to the greater incidence of heart failure in men. The work is published in the journal Nature Cardiovascular Research.
Y chromosome loss in men occurs progressively throughout life and can be detected in approximately 40% of 70-year-old men. UVA's Kenneth Walsh, Ph.D., discovered in 2022 that this loss can contribute to heart muscle scarring and lead to deadly heart failure. That finding was the first to directly link Y chromosome loss to a specific harm to men's health; Y chromosome loss is increasingly thought to play a role in diseases ranging from Alzheimer's to cancer.
In an important follow-up finding, Walsh and his team have discovered how Y chromosome loss triggers changes in heart immune cells that make the cells more likely to cause scarring and heart failure.
Further, the researchers found they could reverse the harmful heart changes by giving lab mice a drug that targets the process of fibrosis that leads to the heart scarring, which could lead to a similar treatment for men.
"Our previous work identified that it was loss of the entire Y chromosome that contributed to heart disease in men," said Walsh, the director of UVA's Hematovascular Biology Center. "This new work identified a single gene on the Y chromosome that can account for the disease-promoting effects of Y chromosome loss."
Taking a single pill that combines medications targeting cardiovascular disease-related conditions was shown long ago to lower the risk of death from such causes, including heart attacks and strokes.
The concept of using such "polypills" to prevent and treat atherosclerotic cardiovascular disease was introduced nearly 25 years ago. Shortly thereafter, the strategy was the focus of a seminal modeling study that promoted polypills to reduce cardiovascular disease at the population level. Still, many years and a body of supportive research later, use of such pills remains low throughout the world.
Now, a new study from researchers at Washington University School of Medicine in St. Louis published in Nature Medicine bolsters previous findings and provides additional evidence that polypills are beneficial in preventing heart attacks and strokes and reducing deaths among people with cardiovascular risk factors, including high blood pressure and high cholesterol.
