These tiny soil microbes could rescue crops from salty farmland

 Researchers have uncovered an unexpected natural ally that could help farmers tackle one of agriculture's fastest growing challenges: salty soil.

A team including scientists from the University of East Anglia (UEA), led by Chinese researcher Dr. Yanfen Zheng, found that naturally occurring soil bacteria can significantly improve plants' ability to survive in saline conditions.

The study also uncovered a previously unknown way these microbes protect crops such as maize, tomato, and rapeseed from salt stress. The discovery could eventually help farmers grow food on land that has become too salty for conventional agriculture.

Soil salinity threatens global agriculture

Salt buildup in farmland is becoming an increasingly serious problem because of climate change, irrigation practices, and rising sea levels. As salt accumulates in soil, it stunts plant growth, damages roots, and can sharply reduce crop yields.

Prof Jonathan Todd, from UEA's School of Biological Sciences and the Quadram Institute on the Norwich Research Park, said: "The build-up of salt in farmland is a major and worsening problem -- driven by climate change, irrigation and rising sea levels.

"Salt chokes plant growth, damages roots and severely impact entire harvests -- putting global food supplies at risk.

"We know that plants rely on communities of microbes around their roots, called the root microbiome, to help them cope with environmental stress. But exactly how these relationships work, and whether they are consistent across crops and soils, has remained largely unclear.

"We found that plants appear to recruit beneficial bacteria in salty soil conditions, which in turn trigger internal changes that strengthen their physical structure and resilience.

"If scientists can harness this natural process, it could mark the beginning of a new era in climate-resilient agriculture."

Root microbes drawn to salt stressed plants

To better understand these plant and microbe partnerships, the researchers examined root microbiomes from multiple crop species grown in different soil types.

They discovered that a group of naturally occurring bacteria known as pseudomonads consistently gathered around plant roots exposed to salt stress. The same pattern appeared across several crops, including maize, tomato, and rapeseed, suggesting this is a widespread biological response rather than something unique to a single plant.

Source: ScienceDaily

These fat-filled brain cells may be making multiple sclerosis worse

 Researchers led by Daan van der Vliet, working with teams from the Netherlands Institute for Neuroscience, Leiden University, and Utrecht University, have identified a biological process that may help explain why multiple sclerosis (MS) becomes especially severe in some patients. Examining brain tissue from people with rapidly progressing MS, they found large numbers of unusual immune cells packed with fat droplets. The findings could point to new treatment strategies and future biomarkers that help predict how quickly the disease will worsen.

MS damages myelin, the fatty protective coating that surrounds nerve fibers in the brain and spinal cord. As this insulation breaks down, patients can develop neurological problems such as difficulty walking or vision impairment.

The disease does not follow the same path in everyone. Some individuals experience relatively mild symptoms for many years, while others develop serious disability and paralysis at a young age. Understanding why these outcomes differ has been a longstanding goal for researchers.

To investigate, the team focused on microglia, specialized immune cells in the brain that remove debris and support tissue repair. In patients with MS, however, these cells can undergo dramatic changes. They become filled with fat droplets, giving them a distinctive foamy appearance. Scientists refer to them as "foamy microglia."

"We found that patients with large numbers of these foamy microglia had a more severe disease course more frequently," says researcher Daan van der Vliet.

When Brain Cleanup Cells Become Overloaded

Normally, microglia help maintain brain health by clearing away damaged material. In MS, researchers believe that these cells may take in so much damaged myelin that they eventually exceed their capacity to process it.

"These cells are probably trying to do something good: clearing up damage," Van der Vliet explains. "But they become overloaded, so to speak. As a result, they can no longer effectively contribute to repair."

The study also revealed important molecular differences between MS lesions containing foamy microglia and those without them. Areas containing these cells were enriched with specific fats linked to long lasting inflammatory activity.

A More Complex View of Multiple Sclerosis

Inflammation has long been considered a major force driving MS progression. However, the new findings suggest the disease may involve a more complicated chain of events.

"It does not appear to be simply about the inflammatory response alone," says Van der Vliet. "These cells are probably attempting to clear damage and promote repair, but that process fails, worsens inflammation, and counteracts recovery."

According to the researchers, the results highlight how a mechanism that initially aims to protect the brain may eventually contribute to ongoing damage when it stops functioning properly.

Source: ScienceDaily

This simple twist could bring quantum computers closer to reality

 Researchers at the University of Technology Sydney have demonstrated a new way to control tiny sources of quantum light by twisting atomically thin layers of hexagonal boron nitride.

The advance provides scientists with a new method for tuning quantum emitters, which are microscopic light sources that could play an important role in future technologies such as quantum computing, secure communications, and ultra-sensitive sensors.

Lead author Dr. Angus Gale said the work offers researchers a valuable new tool for making these quantum systems more practical.

"You can measure these quantum emitters and see that they exist, but it's hard to make them work in practice. This gives us a lever to get closer to that -- a step towards the realization of quantum technologies," said Dr. Gale.

Twisting Layers Changes Quantum Light

During the experiments, Gale and his team found that twisting the material could significantly alter both the color and wavelength of the light emitted by the quantum emitters. The magnitude of the change was especially noteworthy.

Most studies create a device at a specific twist angle and leave it unchanged. In contrast, the researchers were able to repeatedly lift, rotate, and restack the material, allowing them to continuously modify its properties.

"We're leveraging the fact that this material, hexagonal boron nitride (hBN), is layered. We can pick it up, stack it, twist it, and use that twist to modify the emitters. You can't really do that with traditional materials like diamond or silicon carbide."

"The benefit is that we used this twistable platform to shift the emission by a very significant amount," said Gale. "Often when you control these systems, the amount of manipulation is very limited, but in this case the shift was much larger than expected.

"Rather than trying to make hBN defects behave like a traditional solid-state hosts, we took advantage of hBN's own strength: its thin, layered, twistable structure."

Why Hexagonal Boron Nitride Is Different

Gale compared the material's structure to slices of cheese rather than a solid block.

"With a block of cheese, you can't really get to the flavor in the middle. But with slices, you can peel away layers, put them back together and change how they interact," he said.

Because hBN is made of extremely thin layers, researchers can separate and reassemble those layers in ways that are not possible with more conventional quantum materials.

New Possibilities for Quantum Technologies

Supervising author Professor Igor Aharonovich said the ability to twist layered materials is particularly exciting because it can reveal entirely new physical behavior.

"You can take two layers that don't do much on their own, put them together at a specific angle, and suddenly you have a completely different system," said Professor Aharonovich.

According to Aharonovich, the findings could help advance several emerging quantum technologies.

"These materials could eventually be used for quantum computing communications and quantum sensing, which would help for applications such as healthcare, cybersecurity and improved GPS; and gives us more control over the building blocks needed to get there."

Source: ScienceDaily

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