Major review finds vaping likely causes lung and oral cancer

 A comprehensive new review led by UNSW Sydney has concluded that nicotine-based e-cigarettes are likely to cause cancers of the lungs and oral cavity.

Published in the journal Carcinogenesis, the study evaluated a broad range of international research and brought together experts from several institutions, including The University of Queensland, Flinders University, The University of Sydney, Royal North Shore Hospital, The Prince Charles Hospital, and Sunshine Coast University Hospital.

The research team included specialists from multiple fields such as pharmacy, epidemiology, thoracic surgery, and public health. By examining evidence from a variety of scientific disciplines, they sought to determine whether vaping itself may contribute to cancer development.

"To our knowledge, this review is the most definitive determination that those who vape are at increased risk of cancer compared to those who don't," Prof. Stewart says.

The review focused on carcinogenicity, or cancer causation, and argues that while vaping has often been studied as a pathway to cigarette smoking, far less attention has been paid to the possibility that e-cigarettes could directly cause cancer on their own.

Researchers describe the work as one of the most extensive evaluations yet of whether vaping can increase cancer risk independently of traditional tobacco smoking. The analysis combined findings from clinical research, animal studies, and laboratory investigations involving chemicals generated by e-cigarettes.

"Considering all the findings -- from clinical monitoring, animal studies and mechanistic data -- e-cigarettes are likely to cause lung cancer and oral cancer," Prof. Stewart says.

Although the results were highly consistent across different areas of research, Prof. Stewart notes that the exact number of cancer cases attributable to vaping remains unknown.

"Our assessment is qualitative and does not involve a numerical estimate of cancer risk or burden. We'll only be able to determine the precise risk once longer-term studies are available."

Growing Concerns About Vaping and Public Health

E-cigarettes first entered the market in the early 2000s and became available in Australia around 2008. They were initially promoted as a potentially safer alternative to conventional cigarettes and as a tool to help people quit smoking.

Since then, brightly colored and flavored vaping products have become increasingly popular, especially among younger users. Despite tighter regulations introduced by the Australian Government in 2023, vaping remains common outside schools, bars, and train stations throughout the country. Current rules prohibit disposable and non-therapeutic vapes, while therapeutic vaping products can only be sold through pharmacies and only for smoking cessation purposes.

"E-cigarettes are known to be a gateway to smoking and hence cancer," says co-author UNSW Associate Professor Freddy Sitas.

"But the extent to which they may cause cancer in their own right has not received as much attention in research," he says.

"The evidence was remarkably consistent across fields," he says. "It dictated an unequivocal finding now, though human studies that estimate the risk will take decades to accumulate."

Evidence Points in the Same Direction

Scientists have spent more than a century studying the health effects of smoking. Although e-cigarettes are much newer, exposure to nicotine containing aerosols has already been associated with addiction, poisoning, inhalation injuries, and burns.

Because long-term population studies are still underway, researchers must currently rely on other forms of evidence to assess potential cancer risks from vaping.

The review identified multiple cancer-causing substances in e-cigarette aerosols, including volatile organic compounds and metals released by heating coils.

Researchers also examined several other lines of evidence. These included biomarkers in people that indicate DNA damage, oxidative stress, and inflammation in tissues; mouse studies that resulted in lung tumors; and laboratory experiments showing cellular injury and disruptions to biological processes linked to cancer development.

According to the authors, the collective findings consistently point toward the same conclusion.

Dual Use May Increase Lung Cancer Risk

The researchers also highlight growing evidence that many smokers who switch to vaping continue using conventional cigarettes as well.

"Most of those who use e-cigarettes to quit smoking end up in 'dual-use-limbo', unable to shake off either habit," says A/Prof. Sitas.

"What we do know from recent epidemiological evidence from the USA is that those who both vape and smoke are at an additional four-fold increased risk of developing lung cancer."

Source: ScienceDaily

Scientists discover neurons must break their DNA to build the brain

 As the brain develops, newly formed neurons must travel through tightly packed tissue to reach their final destinations in the cerebral cortex, where they become part of the brain's communication network. This journey forces the cells through narrow gaps between fibers and neighboring cells.

A new study published in Nature has revealed an unexpected consequence of that process. Researchers from Kyoto University's Institute for Integrated Cell-Material Sciences (WPI-iCeMS) and collaborating institutions found that migrating neurons routinely experience significant DNA damage. Specifically, the cells develop double-strand breaks, a severe form of DNA damage in which both strands of the DNA double helix are cut.

Although double-strand breaks are typically associated with mutations, cell dysfunction, and even cell death, the researchers discovered that they are a normal part of brain cortex development. In healthy brains, the damage is rapidly repaired before it can cause lasting problems.

"The developing brain appears to have evolved to tolerate and repair the neuronal damage efficiently," says Professor Mineko Kengaku, of WPI-iCeMS, who led the study. "But understanding the limits of that tolerance -- and what happens when repair is incomplete -- brings us closer to understanding a range of neurological conditions."

DNA Damage During Neuronal Migration

To investigate how this damage occurs, the researchers recreated the physical challenges faced by developing neurons. They guided neurons through tiny microchannels designed to mimic the confined spaces found in growing brain tissue.

Using fluorescent markers, the team observed double-strand DNA breaks appearing as neurons moved through the channels. Once the cells emerged from the other side, the damage gradually disappeared. Most of the breaks were repaired within 24 hours, and the neurons continued functioning normally.

The researchers identified the source of the damage as Topoisomerase IIβ, an enzyme that normally helps cells manage stress within DNA. Under ordinary conditions, the enzyme temporarily cuts DNA strands to relieve twisting and tension generated by routine cellular activity before reconnecting them.

The process can be compared to cutting a tangled cable to remove twists and then reconnecting it. However, when neurons are subjected to mechanical stress while squeezing through tight spaces, the enzyme can become trapped midway through the process, leaving sections of DNA broken. The cell then relies on a repair mechanism called non-homologous end joining to reconnect the damaged DNA ends.

Why Neurons Recover While Other Cells Do Not

The team found that neuronal DNA damage differs from the damage seen in certain cancer cells moving through the same microchannels. In cancer cells, DNA damage tends to occur more randomly and can disrupt normal cellular activity or trigger cell death.

In contrast, the DNA breaks in neurons were concentrated mainly in regions of the genome that are not actively involved in critical gene functions. Because essential genes are largely spared, the cells are able to maintain normal function despite the temporary damage.

When DNA Repair Falls Short

To explore the consequences of failed repair, the researchers engineered mice whose newly formed cerebellar neurons lacked Ligase 4, an enzyme required for repairing DNA breaks.

The mice developed normally and showed no obvious early abnormalities. However, as they reached adulthood, they began to experience mild but gradually worsening balance problems. These symptoms resemble those seen in certain human disorders linked to genome instability that affect the cerebellum.

Clues to Brain Diversity and Disease

The findings suggest that DNA breakage and repair may play a larger role in brain biology than previously recognized. Researchers now want to understand whether these early DNA changes contribute to differences between individual neurons and whether they influence neurodevelopmental or neurodegenerative diseases later in life.

"It shifts how we think about the neuronal genome," says Professor Kengaku. "All neurons originate from the same DNA, but DNA damage and repair can introduce small genetic differences between individual neurons through a small mechanical journey. Some of that history may be written into the genome itself."

Source: ScienceDaily

Think human anatomy is finished? Scientists say think again

 Leaf through a textbook, watch a wellness influencer or listen in at the gym, and it can feel as though the human body has already been mapped to exhaustion. Every muscle named, every nerve traced. Everything understood and readily available.

Most people recognize at least a few anatomical terms – “traps,” “glutes,” “biceps.” After centuries of dissection, microscopy and medical imaging, it seems reasonable to assume the work is done. Surely anatomy, as a discipline, must be complete?

It isn’t. Not even close.

Since the publication of De Humani Corporis Fabrica by Andreas Vesalius in 1543 – the first comprehensive anatomy book based on direct observation of human dissection – anatomy has carried an air of authority. Vesalius famously corrected centuries of inherited error, challenging the ancient physician Galen through direct observation of the human body. His work helped establish anatomy as an evidence-based science.

Three hundred years later, Gray’s Anatomy by Henry Gray reinforced the impression that the body had finally been catalogued, indexed and neatly organized – a system mapped and fully explained.

But textbooks create a misleading sense of certainty. They present the body as stable, universal and fully agreed upon. Real anatomy is messier than that.

The illusion of completeness

Much of early topographical anatomy – the careful mapping of structures in relation to one another – depended on cadavers obtained through grave robbery.

“Resurrectionists” – body snatchers – exhumed the recently buried, disproportionately targeting the poor, the institutionalized and those without family protection or the financial means to guard graves. These bodies were then sold to anatomists, who relied on them for dissection and teaching.

Working conditions for early anatomists were difficult, and the limitations considerable.

Lighting was poor. Bodies were often malnourished or diseased. Post-mortem change had already altered tissue planes. Sample sizes were small and opportunistic. Demographic information was largely absent, beyond what could be inferred from appearance. The bodies of women were sometimes dissected but rarely reported.

Yet it was under precisely these conditions that anatomists produced the observations that became the foundation of classical anatomical topography.

The anatomical “norm” that emerged from these studies was therefore constructed from a narrow and socially stratified sample.

None of this diminishes the extraordinary technical skill of early anatomists. Their observational ability was remarkable. But the conditions under which they worked inevitably shaped what they saw – and what they missed.

So when we ask whether anatomy is finished, we might also ask a more uncomfortable question: was it ever truly complete in the first place? This question matters scientifically as well as ethically.

For much of the 20th century, anatomical investigation slowed dramatically. By the 1960s, relatively few cadaveric studies were being published worldwide. The assumption was simple: the human body had already been mapped.

Medical education continued, of course, but much of it focused on teaching established knowledge rather than generating new anatomical observations. That apparent stability masked a deeper problem: much of the knowledge had been inherited rather than tested.

Improved imaging techniques, renewed cadaveric research and a growing awareness of anatomical variation have triggered something of a renaissance in anatomical study. Structures once overlooked or poorly described are being re-examined.

Far from being finished, anatomy is rediscovering just how incomplete its map of the human body may be.

Beyond the ‘standard’ human body

One of the most important shifts in modern anatomy has been recognizing that variation is the rule rather than the exception. Textbooks present a “typical” body for teaching, but real human anatomy sits along a spectrum.

Human anatomy varies across several dimensions at once. Differences exist between males and females, across the lifespan as the body develops and ages, and between populations shaped by genetics and environment.

Beyond these broad patterns lies enormous individual variation: blood vessels may follow different routes, muscles may be absent or duplicated, and even the folding patterns of the brain differ from person to person. The “standard” anatomy shown in textbooks is therefore best understood not as a universal blueprint, but as a simplified reference point within a wide biological range.

Source: ScienceDaily

Tubulin prevents toxic brain protein clumps linked to Alzheimer’s and Parkinson’s

 Scientists at Baylor College of Medicine have identified a potential new approach for tackling Alzheimer's and Parkinson's diseases. Both conditions are associated with the buildup of harmful clumps formed by the proteins Tau and alpha synuclein in the brain.

In a study published in Nature Communications, the researchers found that tubulin, a protein that serves as the building block of microtubules, may help prevent these toxic accumulations. Microtubules act as the cell's internal 'railway tracks,' helping transport materials and maintain structure. According to the findings, tubulin can keep Tau and alpha synuclein from forming damaging aggregates and instead encourage them to perform their normal functions inside healthy neurons.

Toxic Protein Clumps and Brain Disease

"Tau and alpha synuclein are well known for their roles in neurodegenerative diseases like Alzheimer's and Parkinson's. In these conditions, these proteins can misfold, stick together and form harmful aggregates that damage neurons and contribute to memory loss, movement problems and other symptoms," said first author Dr. Lathan Lucas, postdoctoral associate of biochemistry and molecular pharmacology in Dr. Allan Ferreon's lab.

"But Tau and alpha synuclein also fulfill essential functions in healthy neurons - they help maintain cell structure and support communication by interacting with tubulin and contributing to microtubule assembly and stabilization."

Tau and alpha synuclein carry out both their beneficial and harmful activities within tiny cellular droplets known as condensates. Because these droplets are involved in disease-related processes, scientists have considered preventing their formation as a possible treatment strategy. However, condensates also play important roles in normal brain function, raising concerns that eliminating them could disrupt healthy neuronal activity.

Redirecting Proteins Toward a Healthy Role

"This led us to the following idea: what if instead of preventing the formation of droplets, we created conditions that would drive Tau and alpha synuclein inside the droplets toward their healthy path, discouraging them from taking the disease path?" said Ferreon, associate professor of biochemistry and molecular pharmacology and co-corresponding author of the work.

Lucas offered an analogy to explain the concept.

"I think of Tau and alpha synuclein as troublemaker kids in school. You can keep them in the classroom with little to do but to act out or keep them engaged with schoolwork, sports or theater so they do not get in trouble," Lucas said. "We found that tubulin can drive Tau and alpha synuclein troublemakers down a healthy path."

To investigate the idea, the researchers combined biochemical and biophysical methods with high-resolution microscopy and neuron-based assays. Their goal was to determine whether tubulin could influence the behavior of Tau and alpha synuclein and prevent the formation of toxic aggregates within condensates.

Tubulin Acts as a Protective Factor

"When tubulin levels are low, as it has been found in Alzheimer's disease, microtubules are less abundant and Tau and alpha synuclein can form toxic aggregates," Lucas said.

"But when tubulin is present, Tau and alpha-synuclein shift away from harmful aggregates and instead promote the assembly of healthy microtubules," Lucas said. "Tubulin redirects the activity of these proteins by giving them something productive to do."

The findings suggest that tubulin may play a much more active role in protecting the brain than previously recognized.

"Our findings significantly shift tubulin's role in neurodegeneration, from a passive casualty of disease to an active protector against toxic protein aggregation," Ferreon said. "Boosting the tubulin pool, rather than blocking droplet formation, can curb toxic aggregation while preserving the healthy roles of Tau and alpha synuclein, offering a potential selective therapeutic strategy."

Other contributors to the study include co-first author Phoebe S. Tsoi, My Diem Quan, Kyoung-Jae Choi and co-corresponding author Josephine C. Ferreon, all at Baylor College of Medicine.

Source: ScienceDaily

This DNA repair gene went rogue and exposed a cancer weakness

 Tumor suppressor genes are often viewed as the body's built-in defense system against cancer. They produce proteins that help maintain and repair DNA, reducing the chances that harmful mutations will accumulate. When these genes stop working properly or are present at low levels, cancer risk can rise.

But new research suggests that having too much of one DNA repair protein can also be a problem.

Researchers at Penn State College of Medicine found that excessive activity of the gene EXO1 can damage DNA rather than protect it. Instead of repairing genetic material, too much EXO1 can break down DNA and destabilize the genome, a key feature of cancer.

The findings, published in Nature Communications, show that EXO1 is overexpressed in 20% to 30% of breast and ovarian cancers, as well as in melanoma, testicular, cervical and hepatobiliary cancers, which occur in the liver, gall bladder and bile duct.

The team also discovered that cancer cells with unusually high levels of EXO1 behave much like cells carrying BRCA mutations, which are well known for increasing the risk of hereditary breast and ovarian cancers. Importantly, these BRCA-like behaviors occurred even when no BRCA mutation was present.

EXO1 May Help Identify Patients for Targeted Therapies

The researchers found that tumors with elevated EXO1 responded to treatments in ways that closely resembled BRCA-mutant cancers.

"EXO1 doesn't predict cancer risk, but it could potentially serve as a biomarker to help predict which patients are more likely to respond to certain chemotherapy treatments, leading to more personalized therapies," said George-Lucian Moldovan, professor of molecular and precision medicine and senior author on the study. "The same drugs that are reserved for treating BRCA-mutant tumors and that have fewer side effects could potentially be used to treat EXO1 overexpressing tumors, which don't have BRCA mutations. It would expand the applicability of those drugs."

To investigate the role of EXO1, the researchers analyzed tumor data from The Cancer Genome Atlas, a National Cancer Institute cancer genomics program. They found evidence of EXO1 overproduction in multiple cancer types, including tumors of the breast, skin, liver and cervix, consistent with earlier research. Elevated EXO1 levels were especially associated with basal-like breast cancer, an aggressive form of the disease.

How Excess EXO1 Damages DNA

The team then performed laboratory experiments using commercially available human cancer cells.

Researchers artificially increased EXO1 production in the cells to determine how excess amounts of the protein affected DNA. They also created a disabled version of EXO1 that produced protein but lacked its normal biochemical activity. This allowed them to confirm that any observed DNA damage was caused by the protein's activity rather than simply its presence.

Under normal conditions, EXO1 functions like a pair of molecular scissors, helping trim and repair damaged DNA. However, when too much EXO1 is present, those scissors begin cutting DNA structures that should remain intact.

The researchers found that excess EXO1 destabilizes newly formed DNA through two main mechanisms, expanding single-stranded DNA gaps and degrading reversed replication forks. Both processes erode DNA and result in localized loss of genetic material, Moldovan explained.

"Regardless of which pathway, EXO1 overexpression leads to the generation and accumulation of toxic lesions in DNA, such as double strand breaks, which we ultimately think is what makes the tumor more sensitive to chemotherapy and increases cell death," said Alexandra Nusawardhana, the lead author of the study and who earned her doctorate in biomedical sciences this year from Penn State College of Medicine.

Why EXO1 Mimics BRCA Mutations

BRCA genes normally produce proteins that help protect vulnerable DNA structures during replication. When BRCA genes are mutated, cells lose part of this protective function, which can contribute to cancer development.

In the current study, however, researchers found that excessive EXO1 activity was able to overwhelm those protective mechanisms even when BRCA genes were functioning normally and carried no mutations.

The team also discovered that EXO1 works alongside another protein called MRE11 to enlarge DNA gaps and generate dangerous DNA breaks.

"Mechanistically, this overexpression does exactly what the loss of the BRCA pathway does in BRCA-mutant tumor cells," Moldovan said.

He noted that EXO1 overexpression differs from BRCA mutations in an important way. It is not inherited, and researchers do not yet know whether it directly causes cancer.

Potential Impact on Cancer Treatment

Because EXO1-overexpressing tumors behaved so much like BRCA-mutant tumors, the researchers investigated whether they would also respond similarly to treatment.

They tested olaparib, a drug commonly used against BRCA-mutant cancers that targets cellular DNA repair pathways. Tumors with elevated EXO1 were highly sensitive to the treatment and responded in a manner similar to BRCA-mutant cancers.

The results suggest that patients whose tumors overexpress EXO1 could potentially benefit from the same repair-targeted therapies, even if they do not carry BRCA mutations.

The researchers also found that EXO1-overexpressing tumors responded to cisplatin, a widely used chemotherapy drug. Their findings raise the possibility that lower doses of cisplatin might achieve comparable tumor shrinkage while reducing side effects.

Because EXO1 overexpression appears in a wider range of tumors than BRCA mutations, Moldovan said it could become a valuable biomarker for guiding treatment decisions.

"We shouldn't treat cancers based on what tissue they come from but based on the landscape of the genetic mutations present in the tumors," Moldovan said. "That would result in high efficiency treatment. That's the future of cancer treatment."

The research team plans to continue studying EXO1 with the long-term goal of launching clinical trials involving patients whose tumors overexpress the gene.

Claudia Nicolae, assistant professor of molecular and precision medicine at Penn State College of Medicine, also contributed to the study.

Source: ScienceDaily

As lakes turn brown, trout and bass decline while pike and walleye thrive

 The lakes, streams and ponds you’ve visited for years are likely looking more brown than they used to. And people who are fishing those waters are likely catching different species and sizes of fish than in the past.

Our research has identified a link between those two developments, which means that trout, bass, perch and whitefish may become less common in unstocked lakes. But pike and walleye anglers may be in for a trophy-sized surprise.

In the past several decades, across much of northeastern North America and northern Europe, many freshwater ecosystems are getting darker, and they are changing in other ways as a result.

What is freshwater browning?

The specific phenomenon of darkening water, called “freshwater browning,” is driven by a few factors. Among the reasons are climate change, as higher temperatures and increased runoff are combining to increase the amount and types of carbon compounds that move from soil and land into bodies of water.

Similarly, as people have taken steps to reduce acidic emissions coming from smokestacks and other sources, less acid has fallen as precipitation, changing the chemistry of soils. Those chemical changes are also increasing the flow of carbon to bodies of water.

Higher levels of carbon make water look brown because it’s basically dissolved plant matter that stains the water like tea leaves would.

Underwater visibility

It’s harder to see in browner waters, which makes it harder for fish to locate prey, escape from predators and find suitable habitat to live in.

Our recent study combined a review of past research with some new analyses to examine how different kinds of fish do in darker water. Working with a large team of experts, we tallied findings from previous studies that looked at the relationship between the darkness of a body of water and fish growth rates in that same body of water.

We found that in browner waters, fish often grow more slowly. The decreased growth rate in individual fish appears to reduce the population sizes of these fish, which may, in turn, change the quantities and proportions of different kinds of fish in a lake.

But freshwater browning doesn’t affect all species of fish equally.

Unsurprisingly, we found that vision appeared to be quite important for navigating browner waters. When we studied fish communities in 303 Canadian lakes, we found that in lakes with darker water, fish species with larger eyes were more common.

When we looked at data on populations of eight economically important fish in 871 lakes across North America and Europe, we found that browning was associated with smaller populations of several species, including lake trout, lake whitefish, yellow perch, largemouth bass and smallmouth bass. Brook trout abundance was not affected by freshwater browning.

Browning was associated with larger populations of northern pike and walleye.

We believe that’s because walleye, for example, have a specialized retina that helps them see in browner waters with poorer visibility. Similarly, pike have a well-developed lateral-line sensory system that allows them to sense vibration, movement and pressure changes in the water.

A change for anglers

People fishing in browner lakes may consider appealing to the senses of the fish that are likely to be in the water. For example, rather than using colorful or shiny lures to attract their visual attention, when fishing in darker water, consider using vibrating lures that a fish’s lateral line system can detect, or scented lures that trigger an olfactory response.

By examining what’s happening to the water and in it, both scientists and people who enjoy fishing can understand the changes we’re seeing and what they mean in practical terms. 

Source: ScienceDaily

Chinese sodium battery surprised scientists by matching key Tesla benchmarks

 A widely used sodium-ion battery developed by Chinese manufacturer Hina has achieved performance and manufacturing quality levels comparable to Tesla's lithium-ion batteries, according to research published in the Cell Press journal Cell Reports Physical Science.

The findings suggest sodium-ion technology could become a lower-cost alternative for future electric vehicles and large-scale energy storage systems. To reach that goal, however, the battery will need further improvements in low-temperature charging and energy density. Unlike lithium, sodium is abundant and readily available, making it an attractive material for reducing battery costs and supply chain concerns.

"The combination of good uniformity, high power capability, and strong low-temperature performance makes these cells attractive for stationary storage, grid services, and shorter-range or commercial vehicles where potential lower cost and resource availability matter more than maximum driving range," says Moritz Schütte, a battery researcher at RWTH Aachen University in Germany.

Comparing Sodium-Ion Batteries With Tesla Technology

To evaluate the Hina battery, Schütte and colleagues examined 120 sodium-ion cells using impedance spectroscopy, a non-destructive method that measures battery uniformity.

The researchers then tested the cells under a variety of real-world operating conditions. Performance was measured across different current levels and temperatures ranging from −20 °C to 45 °C. The team also used X-rays to examine the batteries internally before disassembling them to analyze electrode dimensions, material composition, and microscopic structural features.

One notable discovery was the battery's tabless, double-aluminum current collector design. This configuration helps reduce electrical resistance and promotes more even temperature distribution throughout the cell. The researchers noted that this design closely resembles the architecture currently used in Tesla batteries.

"We were positively surprised by how uniform the cells are," says Schütte.

Strengths and Remaining Challenges

Despite the encouraging results, the researchers identified several areas where the sodium-ion battery still trails leading lithium-ion technologies.

"The high-power performance was better than one might expect from an early commercial sodium-ion product," says Schütte. "However, for applications that require frequent charging at low ambient temperatures, appropriate thermal management or operating strategies will be important because low-temperature charging remains a clear weakness."

The team also detected unexpectedly high concentrations of copper in certain regions of the battery's cathode. In addition, the copper was unevenly distributed throughout those areas.

According to Schütte, this finding "raises interesting questions about its role in performance and aging.""It will be exciting to see future sodium-ion technologies that are free of nickel and copper, as well, while achieving competitive energy density," he said.

Why Sodium Could Matter for Future Batteries

Because sodium is far more abundant and widely available than lithium, manufacturers could potentially lower raw material costs while reducing long-term supply chain risks.Sodium-ion batteries also maintain strong performance under load in cold conditions, making them attractive for stationary energy storage systems and mobile applications operating in colder climates."However, today's commercial sodium-ion cells generally have lower energy density than the best lithium-ion cells, and the technology is less mature overall," said Schütte.

Next Steps for Sodium-Ion Research

The researchers plan to focus on improving charging performance at low temperatures, with the goal of enabling safer and more efficient charging below 0°C.

Additional work will also explore ways to optimize the materials used in sodium-ion batteries "Advances in hard-carbon anodes and electrolyte formulations may be especially promising," he said.The study was supported by the Federal Ministry of Research, Technology, and Space and the Federal Ministry for Economic Affairs and Energy.

Source: ScienceDaily