An international team of interdisciplinary researchers, including the Canepa Research Laboratory at the University of Houston, has developed a new type of material for sodium-ion batteries that could make them more efficient and boost their energy performance — paving the way for a more sustainable and affordable energy future.

The new material, sodium vanadium phosphate with the chemical formula Na_xV₂(PO₄)₃, improves sodium-ion battery performance by increasing the energy density — the amount of energy stored per kilogram — by more than 15%. With a higher energy density of 458 watt-hours per kilogram (Wh/kg) compared to the 396 Wh/kg in older sodium-ion batteries, this material brings sodium technology closer to competing with lithium-ion batteries.

“Sodium is nearly 50 times cheaper than lithium and can even be harvested from seawater, making it a much more sustainable option for large-scale energy storage,” said Pieremanuele Canepa, Robert Welch assistant professor of electrical and computer engineering at UH and lead researcher of the Canepa Lab. “Sodium-ion batteries could be cheaper and easier to produce, helping reduce reliance on lithium and making battery technology more accessible worldwide.”

From Theory to Reality

The Canepa Lab, which uses theoretical expertise and computational methods to discover new materials and molecules to help advance clean energy technologies, collaborated with the research groups headed by French researchers Christian Masquelier and Laurence Croguennec from the Laboratoire de Reáctivité et de Chimie des Solides, which is a CNRS laboratory part of the Université de Picardie Jules Verne, in Amiens France, and the Institut de Chimie de la Matière Condensée de Bordeaux, Université de Bordeaux, Bordeaux, France for the experimental work on the project. This allowed theoretical modelling to go through experimental validation.

The researchers created a battery prototype using the new material, Na_xV₂(PO₄)₃, demonstrating significant energy storage improvements. Na_xV₂(PO₄)₃, part of a group called “Na superionic conductors” or NaSICONs, is designed to let sodium ions move smoothly in and out of the battery during charging and discharging.

Unlike existing materials, it has a unique way of handling sodium, allowing it to work as a single-phase system. This means it remains stable as it releases or takes in sodium ions. This allows the NaSICON to remain stable during charging and discharging while delivering a continuous voltage of 3.7 volts versus sodium metal, higher than the 3.37 volts in existing materials.

While this difference may seem small, it significantly increases the battery’s energy density or how much energy it can store for its weight. The key to its efficiency is vanadium, which can exist in multiple stable states, allowing it to hold and release more energy.

“The continuous voltage change is a key feature,” said Canepa. “It means the battery can perform more efficiently without compromising the electrode stability. That’s a game-changer for sodium-ion technology.”

Possibilities for a Sustainable Future

The implications of this work extend beyond sodium-ion batteries. The synthesis method used to create Na_xV₂(PO₄)₃ could be applied to other materials with similar chemistries, opening new possibilities for advanced energy storage technologies. That could in turn, impact everything from more affordable, sustainable batteries to power our devices to help us transition to a cleaner energy economy.

“Our goal is to find clean, sustainable solutions for energy storage,” Canepa said. “This material shows that sodium-ion batteries can meet the high-energy demands of modern technology while being cost-effective and environmentally friendly.”

A paper based on this work was published in the journal Nature Materials. Ziliang Wang, Canepa’s former student and now a postdoctoral fellow at Northwestern University, and Sunkyu Park, a former student of the French researchers and now a staff engineer at Samsung SDI in South Korea, performed much of the work on this project.

According to the Centers for Disease Control and Prevention, heart failure affects nearly 7 million U.S. adults and is responsible for 14% of deaths per year. There is no cure for heart failure, though medications can slow its progression. The only treatment for advanced heart failure, other than a transplant, is pump replacement through an artificial heart, called a left ventricular assist device, which can help the heart pump blood.

“Skeletal muscle has a significant ability to regenerate after injury. If you’re playing soccer and you tear a muscle, you need to rest it, and it heals,” said Hesham Sadek, MD, PhD, director of the Sarver Heart Center and chief of the Division of Cardiology at the U of A College of Medicine — Tucson’s Department of Medicine. “When a heart muscle is injured, it doesn’t grow back. We have nothing to reverse heart muscle loss.”

Sadek led a collaboration between international experts to investigate whether heart muscles can regenerate. The study was funded through a grant awarded to Sadek by the Leducq Foundation Transatlantic Networks of Excellence Program, which brings together American and European investigators to tackle big problems.

The project began with tissue from artificial heart patients provided by colleagues at the University of Utah Health and School of Medicine led by Stavros Drakos, MD, PhD, a pioneer in left ventricular assist device-mediated recovery.

Jonas Frisén, MD, PhD, and Olaf Bergmann, MD, PhD, of the Karolinska Institute in Stockholm, led teams in Sweden and Germany and used their own innovative method of carbon dating human heart tissue to track whether these samples contained newly generated cells.

The investigators found that patients with artificial hearts regenerated muscle cells at more than six times the rate of healthy hearts.

“This is the strongest evidence we have, so far, that human heart muscle cells can actually regenerate, which really is exciting, because it solidifies the notion that there is an intrinsic capacity of the human heart to regenerate,” Sadek said. “It also strongly supports the hypothesis that the inability of the heart muscle to ‘rest’ is a major driver of the heart’s lost ability to regenerate shortly after birth. It may be possible to target the molecular pathways involved in cell division to enhance the heart’s ability to regenerate.”

Finding better ways to treat heart failure is a top priority for Sadek and the Sarver Heart Center. This study builds on Sadek’s prior research into rest and heart muscle regeneration.

In 2011, Sadek published a paper in Science showing that while heart muscle cells actively divide in utero, they stop dividing shortly after birth to devote their energy to pumping blood through the body nonstop, with no time for breaks.

In 2014, he published evidence of cell division in patients with artificial hearts, hinting that their heart muscle cells might have been regenerating.

These findings, combined with other research teams’ observations that a minority of artificial heart patients could have their devices removed after experiencing a reversal of symptoms, led him to wonder if the artificial heart provides cardiac muscles the equivalent of bedrest in a person recovering from a soccer injury.

“The pump pushes blood into the aorta, bypassing the heart,” he said. “The heart is essentially resting.”

Sadek’s previous studies indicated that this rest might be beneficial for the heart muscle cells, but he needed to design an experiment to determine whether patients with artificial hearts were actually regenerating muscles.

“Irrefutable evidence of heart muscle regeneration has never been shown before in humans,” he said. “This study provided direct evidence.”

Next, Sadek wants to figure out why only about 25% of patients are “responders” to artificial hearts, meaning that their cardiac muscle regenerates.

“It’s not clear why some patients respond and some don’t, but it’s very clear that the ones who respond have the ability to regenerate heart muscle,” he said. “The exciting part now is to determine how we can make everyone a responder, because if you can, you can essentially cure heart failure. The beauty of this is that a mechanical heart is not a therapy we hope to deliver to our patients in the future — these devices are tried and true, and we’ve been using them for years.”

Led by Texas A&M University graduate students Samere Zade of the biomedical engineering department and Ting-Ching Wang of the chemical engineering department, an article released by the Lele Lab has uncovered new details about the mechanism behind cancer progression.

Published in Nature Communications, the article explores the influence the mechanical stiffening of the tumor cell’s environment may have on the structure and function of the nucleus.

“Cancer has proven to be a difficult disease to treat. It is extremely complex and the molecular mechanisms that enable tumor progression are not understood,” said Dr. Tanmay Lele, joint faculty in the biomedical engineering and chemical engineering departments. “Our findings shed new light into how the stiffening of tumor tissue can promote tumor cell proliferation.”

In the article, researchers reveal that when a cell is faced with a stiff environment, the nuclear lamina — scaffolding that helps the nucleus keep its shape and structure — becomes unwrinkled and taut as the cell spreads on the stiff surface. This spreading causes yes-associated protein (YAP), the protein that regulates the multiplication of cells, to move to the nucleus.

That localization can cause increased cell proliferation, which may explain the rapid growth of cancer cells in stiff environments.

“The ability of stiff matrices to influence nuclear tension and regulate YAP localization could help explain how tumors become more aggressive and perhaps even resistant to treatment in stiffened tissues,” Zade said.

These findings build on Lele’s previous discovery that the cell nucleus behaves like a liquid droplet. In that work, researchers found that a protein in the nuclear lamina called lamin A/C helps maintain the nucleus’ surface tension. In the most recent study, it was found that reducing the levels of lamin A/C decreases the localization of YAP, in turn decreasing rapid cell proliferation.

“The protein lamin A/C plays a key role here — reducing it made cells less responsive to environmental stiffness, particularly affecting the localization of a key regulatory protein (YAP) to the nucleus,” Zade explained.

Although seemingly complex and specialized, Zade and Lele believe the broader implications of their discovery may guide future treatments for cancer.

“Uncovering how matrix stiffness drives nuclear changes and regulates key pathways, like YAP signaling, opens the door to developing therapies that target these mechanical pathways,” Zade explained. “Drugs or treatments could be designed to soften the tumor environment, disrupting the physical cues that help cancer cells thrive. Lamin A/C and related nuclear mechanics could become targets for cancer treatments.”

Moving forward, the Lele Lab aims to investigate the extent to which their discoveries apply to tumors derived from patients.

For this work, the Lele Lab was funded by the National Institutes of Health, the Cancer Prevention and Research Institute of Texas, and the National Science Foundation. Funding for this research is administered by the Texas A&M Engineering Experiment Station, the official research agency for Texas A&M Engineering.

Extreme longevity is a trait common to the right whales’ cousins, the bowheads.

Scientists working with Indigenous subsistence hunters in Utqiaġvik used chemical analysis of harvested bowhead whales to show they can live more than 200 years. Corroborating the chemical evidence, hunters have recovered 19th-century harpoon tips from bowheads taken in modern hunts.

Right whales, which are much more closely related to bowhead whales than any other species, appear to exhibit similar lifespans. Like bowheads, right whales filter feed through baleen and migrate seasonally to give birth. Whalers considered them the “right” whales to hunt due to their thick blubber, which caused them to float when killed.

The current study examined four decades of data collected by photo identification programs tracking individual whales from two species: the Southern right whale, which lives in the oceans south of the equator, and the critically endangered North Atlantic right whale, found along the Atlantic coast of North America. Researchers used the data to construct survivorship curves — graphs that show the proportion of a population that survives to each age — similar to those used by insurance companies to calculate human life expectancies.

Analysis revealed that Southern right whales, once thought to live only 70 to 80 years, can exceed lifespans of 130 years, with some individuals possibly reaching 150 years. In contrast, the study found the average lifespan of the North Atlantic right whale is just 22 years, with very few individuals surviving past the age of 50.

According to University of Alaska Fairbanks associate professor Greg Breed, the stark contrast in lifespans between these two closely related species is primarily due to human impacts. Breed is the study’s lead author.

“North Atlantic whales have unusually short lifespans compared to other whales, but this isn’t because of intrinsic differences in biology, and they should live much longer,” he said. “They’re frequently tangled in fishing gear or struck by ships, and they suffer from starvation, potentially linked to environmental changes we don’t fully understand.”

Breed has spent years studying marine mammals, including seals, certain species of which can live up to 50 years, and narwhals, with lifespans of a century or more. He noted that a lack of data on whale aging led to significant underestimations of their lifespans in the past.

“We didn’t know how to age baleen whales until 1955, which was the very end of industrial whaling,” Breed said. “By the time we figured it out, there weren’t many old whales left to study. So we just assumed they didn’t live that long.”

The study has important implications for conservation efforts. “To attain healthy populations that include old animals, recovery might take hundreds of years,” Breed said. “For animals that live to be 100 or 150 and only give birth to a surviving calf every 10 years or so, slow recovery is to be expected.”

The study also underscores the importance of cultural knowledge among whale populations.

“There’s a growing recognition that recovery isn’t just about biomass or the number of individuals. It’s about the knowledge these animals pass along to the next generation,” Breed said.

“That knowledge isn’t just genetic — it’s cultural and behavioral. Older individuals teach survival skills. Younger animals learn by observing and copying the strategies of the older ones.”

The loss of older individuals disrupts this critical transfer of knowledge and can impair the survival of the young.

Breed and his colleagues intend to extend their research to other whale populations and predict whether other whale species currently thought to live around 80 years may also have much longer lifespans. They hope to learn more about how whaling affected the number of old individuals in current whale populations and predict when their numbers will recover to pre-whaling levels.

The findings, reported in Nature Communications, also solve a decades-long scientific puzzle that’s prevented drugmakers from successfully using azole antifungal drugs to treat visceral leishmaniasis, or VL.

About 30 years ago, scientists discovered the two species of single-cell parasites that cause VL, Leishmania donovani and Leishmania infantum, made the same lipid sterol, called ergosterol, as fungi proven susceptible to azoles antifungals. These azoles antifungals target a crucial enzyme for sterol biosynthesis, called CYP51.

While not fungi, both Leishmania species have biochemical similarities to fungi in their plasma membrane, where ergosterol helps maintain cellular integrity and supports a host of biological functions, much as cholesterol does in humans.

“People looked into the sterol profile of the parasites and discovered they primarily have ergosterol,” said study corresponding author Michael Zhuo Wang, professor of pharmaceutical chemistry at the University of Kansas School of Pharmacy. “This sterol is the main component of their plasma-membrane sterols. A similar case can be observed in fungi. Fungal organisms also have a high amount of ergosterol in their membranes. There was an original instinct to use antifungal azoles to try to block that pathway.”

However, scientists were unable to effectively use antifungals against VL.

“In the research lab and some of the clinical trials, some azoles worked a little bit, and some other azoles didn’t work at all,” Wang said. “I eventually focused on this sterol pathway a scientific question — if this parasite also uses ergosterol, you’d think all the antifungal azoles would work against this parasite.”

Along these lines, Wang started his independent research career as part of a group at the University of North Carolina-Chapel Hill called the Consortium for Parasitic Drug Development.

“We were interested in developing new drugs against neglected tropical diseases,” he said. “One of these diseases is leishmaniasis. The other one is the African sleeping sickness. Leishmaniasis, spread by a sandfly vector in warmer climates, can cause really devastating infection of internal organs such as the liver and the spleen, as well as the bone marrow.”

In his new scholarly paper, Wang and his collaborators have largely solved that longstanding scientific question. They show the parasites that cause leishmaniasis are vulnerable via a different pathway for biosynthesis of their ergosterol, known as the CYP5122A1 enzyme. Therefore, azole antifungals targeting the CYP5122A1 enzyme as well as the traditional CYP51 pathway should be much more effective at treating leishmaniasis.

“So those azoles don’t work very well against leishmania unless you have an azole that also inhibits the new pathway, the CYP5122A1,” Wang said. “Then, all of a sudden, they’re much more active against leishmania. That’s the main discovery in this study — we figured out the true drug target in leishmania. You really need to hit this new enzyme, 22A1, in order to stop the parasites.”

Wang’s lab at KU demonstrated the CYP5122A1 gene encodes an essential sterol C4-methyl oxidase in the leishmania parasite, through extensive biochemical characterization.

“This involved defining its biochemical function — what this enzyme does in terms of sterol biosynthesis,” he said. “We pinned down its biochemical function, clarifying its role in the ergosterol biosynthesis pathway.”

Already, the researchers are publishing follow-up scholarship and discovery based on their new breakthrough in understanding the sterol synthesis pathway in the parasites. They said drugmakers and researchers should be developing therapies that target CYP5122A1. These should prove more effective at helping people survive leishmaniasis, Wang said.

“This tells us how we should repurpose these existing antifungal azoles through screening against this new target,” said the KU researcher. “The ones that actually inhibit this new target should have a better chance to work against leishmania infection.”

Wang’s co-authors at the KU School of Pharmacy were doctoral students Yiru Jin and Mei Feng, who served as lead authors, and doctoral student Lingli Qin as co-author in the Department of Pharmaceutical Chemistry; Director Chamani Perera and doctoral student Indeewara Munasinghe from KU’s Synthetic Chemical Biology Core Laboratory; Philip Gao, director of KU’s Protein Production Group; and Judy Qiju Wu, associate teaching professor of pharmacy practice.

The KU researchers were joined by Kai Zhang, Somrita Basu, Yu Ning, Robert Madden, Hannah Burks and Salma Waheed Sheikh from Texas Tech University; and Karl Werbovetz, Arline Joachim, Junan Li and April Joice from The Ohio State University.

This study was supported in part by the U.S. National Institute of Allergy and Infectious Diseases, the U.S. Department of Defense and the KU Centers of Biomedical Research Excellence (COBRE).

“When viruses infect cells, they usually create specialized compartments — replication factories — where they form new viruses that infect more cells causing the disease,” said first author Dr. Soni Kaundal, postdoctoral associate in the Verna and Marrs McLean Department of Biochemistry and Molecular Pharmacology at Baylor in the lab of Dr. B.V. Venkataram Prasad, corresponding author of the work. “However, little is known about norovirus’s replication factories.

Increasing evidence shows that some replication factories typically are not separated from their surroundings by a membrane. Instead, they are biomolecular condensates, structures resembling a bubble formed by liquid-liquid phase separation. These condensates selectively incorporate proteins and other materials needed for viral replication. Liquid-like condensates as replication factories have been extensively studied in other viruses, including the rabies and measles viruses. In this study the researchers investigated whether norovirus forms biomolecular condensates that serve as replication hubs.

“We knew that these condensates are often initiated by a single viral protein capable of binding genetic material, having a flexible region and forming oligomers, molecules made of small numbers of repeating units,” Kaundal said.

The team began their investigation by applying bioinformatic analysis to identify norovirus proteins that would present the characteristics most likely leading to the formation of liquid condensates.

“Working with the human norovirus pandemic strain GII.4, the one responsible for causing most cases of gastroenteritis around the world, we found that the RNA-dependent RNA polymerase has the highest propensity to form biomolecular condensates,” Kaundal said. “This protein has a flexible region, can form oligomers, binds RNA, the norovirus’s genetic material, and plays an essential role during viral replication making copies of the viral RNA. All these characteristics prompted us to experimentally test whether the GII.4 RNA polymerase drives the formation of biomolecular condensates conducive to viral replication.”

“Our experimental studies show that GII.4 RNA polymerase indeed forms highly dynamic liquid-like condensates at physiologically relevant conditions in the lab and that the flexible region of this protein is critical for this process,” said Prasad, professor of molecular virology and microbiology and Alvin Romansky Chair in Biochemistryat Baylor. Prasad also is a member of Baylor’s Dan L Duncan Comprehensive Cancer Center. “Furthermore, the condensates are highly dynamic structures: several can merge forming a larger structure or they can divide into smaller ones; they also move inside the cell, exchanging materials with their surroundings.”

Next, the researchers investigated whether these liquid-like condensates are also formed in human norovirus-infected human intestinal cells. Until recently, studying how norovirus replicates inside cells has been difficult because researchers lacked an effective biological system in which to grow the virus in the lab. But in 2016, the lab of Dr. Mary Estes at Baylor and colleagues succeeded at cultivating human norovirus strains in human intestinal enteroid cultures.

Also known as mini-guts, these cultures are a laboratory model of the human gastrointestinal tract that recapitulates its cellular complexity, diversity and physiology. Human enteroids mimic strain-specific host-virus infection patterns, making them an ideal system to dissect human norovirus infection, as in the current study, to identify strain-specific growth requirements and develop and test treatments and vaccines.

“We showed that liquid-like condensates are formed in human norovirus-infected human intestinal enteroid cultures as well as in the HEK293T human cell line grown in the lab. We propose that these condensates are replication hubs for human norovirus, an elegant solution to the puzzling question of how ribosome-assisted translation of the viral genome is segregated from its replication by the viral polymerase in positive-strand RNA viruses,” Prasad said. “Our bioinformatics analysis also showed that the RNA polymerases of almost all the norovirus strains have a high propensity to form these replication factories, suggesting that this may be a common phenomenon of most noroviruses.”

“This is a remarkable paper, and I was glad we could validate the findings in virus-infected cells using our human intestinal enteroids cultivation system for human norovirus,” said Estes, Distinguished Service Professor and Cullen Foundation Endowed Chair of molecular virology and microbiology at Baylor. Estes also is the co-director of the Gastrointestinal Experimental Model Systems core at the Texas Medical Center Digestive Diseases Center and a member of Baylor’s Dan L Duncan Comprehensive Cancer Center.

The findings not only provide new insight into human norovirus replication but also open new targets for designing antivirals for human norovirus infections, which remain a serious threat in children and immunocompromised patients.

Other contributors to this work include Ramakrishnan Anish, B. Vijayalakshmi Ayyar, Sreejesh Shanker, Gundeep Kaur, Sue E. Crawford, Jeroen Pollet and Fabio Stossi. The authors are affiliated with Baylor College of Medicine and the University of Texas, MD Anderson Cancer Center.

Support for this project was provided by NIH grant P01 AI057788, Robert Welch Foundation grant Q1279, the Center for Advanced Microscopy and Image Informatics (Cancer Prevention and Research Institute of Texas (CPRIT) grant RP170719), the Integrated Microscopy Core at Baylor College of Medicine (NIH grants: DK56338, CA125123, ES030285 and S10OD030414), and CPRIT grant RR160029.

But devices that record electrical signals in cell cultures and other liquid environments often use wires to connect each electrode on the device to its respective amplifier. Because only so many wires can be connected to the device, this restricts the number of recording sites, limiting the information that can be collected from cells.

MIT researchers have now developed a biosensing technique that eliminates the need for wires. Instead, tiny, wireless antennas use light to detect minute electrical signals.

Small electrical changes in the surrounding liquid environment alter how the antennas scatter the light. Using an array of tiny antennas, each of which is one-hundredth the width of a human hair, the researchers could measure electrical signals exchanged between cells, with extreme spatial resolution.

The devices, which are durable enough to continuously record signals for more than 10 hours, could help biologists understand how cells communicate in response to changes in their environment. In the long run, such scientific insights could pave the way for advancements in diagnosis, spur the development of targeted treatments, and enable more precision in the evaluation of new therapies.

“Being able to record the electrical activity of cells with high throughput and high resolution remains a real problem. We need to try some innovative ideas and alternate approaches,” says Benoît Desbiolles, a former postdoc in the MIT Media Lab and lead author of a paper on the devices.

He is joined on the paper by Jad Hanna, a visiting student in the Media Lab; former visiting student Raphael Ausilio; former postdoc Marta J. I. Airaghi Leccardi; Yang Yu, a scientist at Raith America, Inc.; and senior author Deblina Sarkar, the AT&T Career Development Assistant Professor in the Media Lab and MIT Center for Neurobiological Engineering and head of the Nano-Cybernetic Biotrek Lab. The research appears today in Science Advances.

“Bioelectricity is fundamental to the functioning of cells and different life processes. However, recording such electrical signals precisely has been challenging,” says Sarkar. “The organic electro-scattering antennas (OCEANs) we developed enable recording of electrical signals wirelessly with micrometer spatial resolution from thousands of recording sites simultaneously. This can create unprecedented opportunities for understanding fundamental biology and altered signaling in diseased states as well as for screening the effect of different therapeutics to enable novel treatments.”

Biosensing with light

The researchers set out to design a biosensing device that didn’t need wires or amplifiers. Such a device would be easier to use for biologists who may not be familiar with electronic instruments.

“We wondered if we could make a device that converts the electrical signals to light and then use an optical microscope, the kind that is available in every biology lab, to probe these signals,” Desbiolles says.

Initially, they used a special polymer called PEDOT:PSS to design nanoscale transducers that incorporated tiny pieces of gold filament. Gold nanoparticles were supposed to scatter the light — a process that would be induced and modulated by the polymer. But the results weren’t matching up with their theoretical model.

The researchers tried removing the gold and, surprisingly, the results matched the model much more closely.

“It turns out we weren’t measuring signals from the gold, but from the polymer itself. This was a very surprising but exciting result. We built on that finding to develop organic electro-scattering antennas,” he says.

The organic electro-scattering antennas, or OCEANs, are composed of PEDOT:PSS. This polymer attracts or repulses positive ions from the surrounding liquid environment when there is electrical activity nearby. This modifies its chemical configuration and electronic structure, altering an optical property known as its refractive index, which changes how it scatters light.

When researchers shine light onto the antenna, the intensity of the light it scatters back changes in proportion to the electrical signal present in the liquid.

With thousands or even millions of tiny antennas in an array, each only 1 micrometer wide, the researchers can capture the scattered light with an optical microscope and measure electrical signals from cells with high resolution. Because each antenna is an independent sensor, the researchers do not need to pool the contribution of multiple antennas to monitor electrical signals, which is why OCEANs can detect signals with micrometer resolution.

Intended for in vitrostudies, OCEAN arrays are designed to have cells cultured directly on top of them and put under an optical microscope for analysis.

“Growing” antennas on a chip

Key to the devices is the precision with which the researchers can fabricate arrays in the MIT.nano facilities.

They start with a glass substrate and deposit layers of conductive then insulating material on top, each of which is optically transparent. Then they use a focused ion beam to cut hundreds of nanoscale holes into the top layers of the device. This special type of focused ion beam enables high-throughput nanofabrication.

“This instrument is basically like a pen where you can etch anything with a 10-nanometer resolution,” he says.

They submerge the chip in a solution that contains the precursor building blocks for the polymer. By applying an electric current to the solution, that precursor material is attracted into the tiny holes on the chip, and mushroom-shaped antennas “grow” from the bottom up.

The entire fabrication process is relatively fast, and the researchers could use this technique to make a chip with millions of antennas.

“This technique could be easily adapted so it is fully scalable. The limiting factor is how many antennas we can image at the same time,” he says.

The researchers optimized the dimensions of the antennas and adjusted parameters, which enabled them to achieve high enough sensitivity to monitor signals with voltages as low as 2.5 millivolts in simulated experiments. Signals sent by neurons for communication are usually around 100 millivolts.

“Because we took the time to really dig in and understand the theoretical model behind this process, we can maximize the sensitivity of the antennas,” he says.

OCEANs also responded to changing signals in only a few milliseconds, enabling them to record electrical signals with fast kinetics. Moving forward, the researchers want to test the devices with real cell cultures. They also want to reshape the antennas so they can penetrate cell membranes, enabling more precise signal detection.

In addition, they want to study how OCEANs could be integrated into nanophotonic devices, which manipulate light at the nanoscale for next-generation sensors and optical devices.

This research is funded, in part, by the U.S. National Institutes of Health and the Swiss National Science Foundation.