Thursday, 23 July 2026

New Metal Alloy Is up to 10 Times Stronger Than Structural Steel

By Purdue U., July 20, 2026

This image displays inverse pole figures of cobalt aluminum and a framework of amorphous interfaces after deformation, showing the crystal orientation of a cobalt aluminum intermetallic material. 
Credit: Purdue University

A cobalt aluminum nanolaminate has shattered the usual tradeoff between strength and flexibility, emerging up to 10 times stronger than structural steel without becoming dangerously brittle.

Jet engines demand materials that can survive tremendous heat and force without bending, cracking, or slowly losing their shape. The strongest candidates, however, often come with a major weakness: they are too brittle to deform safely.

Purdue University engineers have now found a way to overcome that tradeoff in cobalt aluminum (CoAl), an intermetallic compound with potential uses in high-performance turbines. By redesigning the material at the nanoscale, the researchers created a form of CoAl that is exceptionally strong but can still undergo substantial deformation at room temperature.

The advance, reported in Science Advances, could point toward a broader strategy for making notoriously brittle intermetallic compounds more practical for aerospace, energy, and defense technologies.

Why Intermetallics Fracture

Intermetallics contain two or more metallic elements arranged in a highly ordered crystal structure. That atomic order can give them remarkable strength, high melting temperatures, and resistance to creep, the slow deformation that occurs when a material remains under stress for long periods.

These qualities are valuable in jet engines, gas turbines, energy storage systems, and automotive components. Yet the same ordered structures that make intermetallics strong can also prevent them from deforming easily. Instead of bending under force, many fracture, particularly at room temperature.


Purdue University postdoctoral researcher Ke Xu performs in situ nanomechanical testing on a scanning electron microscope at the Purdue Electron Microscopy Center. In these tests, Purdue researchers observed how they achieved both high strength and plasticity in typically brittle materials called cobalt aluminum intermetallics. 
Credit: Purdue University

CoAl illustrates this problem. The compound is strong enough to be considered for demanding turbine components, but its brittleness makes it difficult to manufacture into complex shapes and limits its ability to withstand sudden mechanical stress.

“Bulk CoAl intermetallics are a high-strength compound,” said corresponding author Xinghang Zhang, a professor in Purdue’s School of Materials Engineering. “Among other applications, they can potentially be used in the next-generation materials of turbine blades for aeroengines, which are gas turbine engines that generate thrust for aircraft propulsion. High-strength, plastically deformable CoAl alloys could allow an engine or turbo to spin faster while sustaining higher centrifugal force, improving their performance.”

Engineering Helpful Crystal Defects

The researchers approached the problem by deliberately introducing imperfections into the material.

In a crystal, atoms normally follow a repeating geometric pattern. A dislocation is a microscopic disruption in that pattern. Although defects are often associated with weakness, dislocations can give metals a way to change shape by allowing layers of atoms to move rather than break apart.

CoAl typically lacks enough mobile dislocations to deform substantially at room temperature. Previous efforts to improve its plasticity by changing its composition or combining it with other materials had only limited success.

Micropillar compression tests on cobalt aluminum intermetallic nanocomposities fabricated by Purdue University researchers revealed that the team had enabled these nanocomposities to achieve a high-yield strength exceeding 6 GPa, a sustained work hardening to approximately 8.5 GPa, and a compressive plastic strain exceeding 15%. 
Credit: Purdue University

Flexible Interfaces Unlock Plasticity

The Purdue team instead built dislocations directly into CoAl as it formed. They also created a network of amorphous interfaces, thin boundaries where atoms lack the ordered arrangement found in a crystal.

“In this study, we show that CoAl can exhibit significant plasticity at room temperature, offering a new, alternative approach to improve the plastic deformation capability in CoAl,” said Ke Xu, a Purdue postdoctoral researcher and the study’s first author.

These flexible internal boundaries act as more than passive separators. During deformation, parts of the interfaces crystallize and help generate additional dislocations, giving the surrounding CoAl layers more ways to absorb force.

“We directly introduced dislocations in CoAl during sputtering deposition,” Zhang said. “More importantly, we designed the framework of amorphous interfaces (FAIs)—flexible boundaries in the materials for structural flexibility, which partially crystallize during deformation and promote the nucleation of the dislocations in CoAl intermetallics.”

Stronger Than Structural Steel

The resulting nanolaminate reached a yield strength of 6 GPa (gigapascal, a stress measurement), roughly six to 10 times that of high-strength structural steel. Yield strength measures the amount of stress a material can endure before it begins to deform permanently.

Despite that extreme strength, the material sustained 15% plastic strain under compression at room temperature. In other words, it could undergo significant permanent deformation without immediately fracturing.

“This combination of ultrahigh mechanical strength and outstanding plasticity makes the current CoAl nanolaminate system one of the best intermetallic systems reported to date,” Xu said.

Building the Alloy From Vapor

The team produced the material using magnetron sputtering deposition. During this process, atoms are released from a source material and deposited as a thin film on another surface. Unlike conventional casting, which solidifies molten metal, sputtering allows a material to form directly from alloy vapor.

That unconventional route helped trap large numbers of dislocations inside the CoAl while creating the amorphous aluminum-cobalt interfaces.

“This nonequilibrium fabrication approach enables us to fabricate materials from alloy vapor to a solid, introducing a significant number of dislocations in CoAl,” Zhang said. “We were able to achieve significant strength and plasticity in CoAl, which can’t be realized via traditional casting.”

Watching Deformation at the Atomic Scale

The researchers compressed the material while observing it inside a scanning electron microscope. This in situ testing allowed them to track how the microscopic structure changed as the CoAl deformed.

University of Houston professor Yashashree Kulkarni and PhD student Anand Mathew also performed molecular dynamics simulations to examine the process at the atomic level. Their models showed parts of the amorphous interfaces crystallizing under pressure and releasing dislocations into neighboring CoAl layers.

Together, the experiments and simulations suggest that the interfaces function as active sources of plastic deformation. Rather than weakening the material, they help it respond to stress without sacrificing its exceptional strength.

From Nanolayers to Turbine Components

The current material is a nanoscale layered system produced through thin-film deposition, not yet a bulk turbine component. The researchers’ next challenge is to transfer the same structural concept into larger CoAl nanocomposites that could be manufactured at an industrial scale.

“We will also be testing the concept using other intermetallics, with the goal of establishing the general applicability of FAIs for improving plasticity in this metal class,” Xu said.

If the approach works across other compounds, it could provide engineers with a new way to design materials for environments where conventional metals struggle. Instead of choosing between strength and deformability, researchers may be able to engineer both by controlling where defects form and how internal boundaries respond to force.

“Ductile intermetallics will significantly boost our capabilities for designing advanced materials for aerospace and outer space, energy, and defense applications,” Zhang said.


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Orcas Keep Punching Giant Sunfish to Smithereens, And Scientists Are Mesmerized

23 July 2026, By M. Starr

A still from footage of an orca smacking headlong into a giant sunfish, which was smashed up on impact.
 (creaturesofbaja/Instagram)

Well, sea shenanigans are once again afoot – and the culprit is very much the usual suspect.

Orcas (Orcinus orca) are already renowned for their elaborate and effective hunting techniques, from generating waves to wash seals off ice floes to surgically divesting fearsome white sharks of their juicy livers.

Now, in the Gulf of California, orcas are turning their powerful strength and cunning to a strange new pursuit: smacking headlong into giant sunfish to shatter their bodies into smithereens.

"The first time I witnessed this behavior was in December 2021, and in that moment, the sheer energy of the impact was stunning – seeing an apex predator hit a massive fish with that much velocity was breathtaking," marine biologist Erick Higuera Rivas of Conexiones Terramar in Mexico told ScienceAlert.

"We immediately knew we were witnessing something highly unusual because of the scale of the tissue explosion."

It wasn't an isolated incident, either.

Since then, the behavior has been documented at least twice more, once in 2024 and again in 2025, allowing scientists to analyze it in detail.

What they found is a highly coordinated routine that raises more questions than it answers – what, exactly, are these orcas trying to accomplish?

The two later encounters played out in almost exactly the same way, as Higuera Rivas, marine scientist Kathryn Ayres of the non-profit Beneath The Waves, and colleagues described in a new Frontiers in Ethology paper.

A pod of orcas approaches a sharptail mola (Masturus lanceolatus), or sunfish, apparently just hanging out, minding its own business.

One of the orcas grabs hold of the mola to immobilize it; another swims a distance away to gain momentum, and slams into the mola at full speed – punching it into shreds.

"I never imagined this could be the hunting method orcas would use against defenseless prey that posed little risk to the predator." – marine biologist Erick Higuera Rivas.

Then, in one event, a juvenile orca moved in and started hoovering up the shreds with relish.

Here's where it gets even weirder, though. That impact didn't kill the sunfish in either scenario.

"Initially, upon seeing a high-speed ram, our instinct leads us to assume it is the killing blow intended to incapacitate a moving target," Higuera Rivas said.

"But upon careful analysis of the images, we discovered that the sunfish were most likely already dead and that their nutrient-rich internal organs (viscera) had been removed before impact."

The first event was recorded on 29 July 2024.
 (Ayres et al., Front. Ethol., 2026)

Instead, the researchers found, the immense burst of energy is possibly being used for butchery – smashing the carcass into bite-sized pieces.

Why expend so much energy pulverizing prey that is already dead? Part of the answer may lie in the peculiar anatomy of the sharptail mola.

Molas are slow and large – in other words, easy prey that poses little danger to an orca. But their bodies are extraordinarily difficult to pull apart.

"Sunfish skin cannot be cleanly unzipped. It is an incredibly dense, waterlogged shield of collagen," Higuera Rivas explained.

"Instead of using tension to rip it, the orcas use massive kinetic energy. While one orca immobilizes the prey, the hitting orca uses its multi-ton body as a high-speed projectile, delivering an impact that shatters the dense collagen framework into manageable fragments."

The second incident was recorded on 7 September 2025.
 (Héctor Franz/Ayres et al., Front. Ethol., 2026)

Rather than trying to tear through that dense, rubbery skin with their teeth, the orcas are using force and physics to do the hard work.

It's also a tightly choreographed team effort.

"Through a 'stabilization-and-ram' model, two orcas combine their physical attributes to compensate for the lack of appendages for tearing," Higuera Rivas told ScienceAlert.

"One acts as the anvil (the anchor), and the other as the hammer (the burst)."

Orcas are wily and resourceful. They seek prey that might daunt other predators, in both size and defenses, that require skill, intelligence, patience, and endurance to bring down – high risk, high reward.

Molas don't seem to fit that pattern. They're enormous, certainly, but they're also famously sluggish and almost entirely defenseless, except for their incredibly dense collagenous skin.

That, combined with their odd shape, presents a challenge of a different kind – or perhaps a learning opportunity for young orcas.

Higuera Rivas believes sunfish ramming may serve a dual purpose: breaking the sunfish into bite-sized chunks, and assisting the youngsters' physical and social development.

"Orcas are highly encephalized predators that frequently engage in object manipulation and play behavior with their prey," he explained.

"Because sunfish are slow-moving and defenseless, they present a low-risk opportunity for the pod – especially subadults – to practice strike precision and reinforce social bonds."

More observations will be needed to confirm it – but if that interpretation is correct, the behavior would join a growing catalog of region-specific hunting traditions passed between generations of orcas.

The researchers weren't able to identify the exact pod of orcas in these hunting incidents, but they suspect the ramming behavior may be a strategy the orcas devised for devouring this particular species of mola.

It joins a growing list of ways these incredible animals continue to surprise even the scientists who know them best.

"I never imagined this could be the hunting method orcas would use against defenseless prey that posed little risk to the predator," Higuera Rivas said.


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Could tomatoes protect brain cells? Scientists uncover an unexpected clue in a familiar kitchen staple

July 13, 2026, written by S. Tribedi, edited by S. Harley, reviewed by A. Zinin
https://sciencex.com/news/2026-07-tomatoes-brain-cells-scientists-uncover.html

Credit: Pixabay/CC0 Public Domain

Envision a world where an ordinary part of your daily diet acts as a robust protector against one of humanity's most devastating neurological diseases. The search for effective treatments for conditions including Parkinson's disease has been a long journey, with scientists exploring several intricate directions for many years. However, breakthroughs can emerge in the most ordinary places, pointing to nature's own pharmacies.

In a recent publication in the journal Nutrients, scientists report a remarkable discovery: Lycopene—a red pigment that gives tomatoes, watermelons and even pink grapefruits their typical color—is a potent neuroprotector.

In a study of mice with induced Parkinson's disease, animals fed lycopene daily displayed enhanced motor skills compared with those that had no lycopene in their diet. Specifically, they showed steadier steps and better balance, as well as preserved dopamine-secreting neurons in the midbrain.

The mice got better—but what changed inside the brain?

Researchers used a common mouse model of Parkinson's disease in which animals are treated with MPTP—a toxin that selectively injures dopamine neurons to mimic the disease. Over three weeks, one group of mice ate lycopene mixed into their food, while a control group did not.

When the team tested the mice on balance beams and open-field mazes, the lycopene group outperformed the controls. They walked more steadily, explored more and showed fewer signs of anxiety- or low-mood-related behavior that Parkinson's can cause.

In the brains of these mice, biochemical tests confirmed that lycopene had preserved many more dopamine neurons in the midbrain. In effect, the pigment appeared to slow the disease process: Treated mice had higher dopamine levels and a more normal balance of related chemicals in brain tissue than untreated mice.

A surprising clue points to dopamine's recycling system

Scientists have identified something essential about lycopene and its mechanisms of action. One of the main components of dopamine-producing neurons is the dopamine transporter (DAT). DAT can be thought of as a miniature recycling truck located on the outer surface of neurons. It recycles dopamine by taking it back inside the neuron to be reused. As the number of dopamine-producing neurons decreases in patients with Parkinson's disease, the amount of DAT also decreases.

Remarkably, the lycopene-treated mice showed significantly higher levels of DAT in their midbrain cells than untreated mice. This means lycopene appears to help maintain the brain's natural dopamine recycling system. Further experiments, including computer simulations and lab tests, suggested that lycopene can directly bind to the DAT protein.

As one of the study's authors explained, "We found that LYC increased the expression of DAT/SLC6A3 and formed direct physical binding with the DAT/SLC6A3 protein." This suggests that lycopene might stabilize dopamine signaling by helping these crucial recycling trucks do their job more effectively.

Side-by-side illustration showing how Parkinson's disease impairs movement and balance in mice during behavioral tests commonly used in neuroscience research. Credit: Generated using AI tools for illustrative purposes

At the cellular level, lycopene acted as a protective agent, "relieving motor impairment and reducing midbrain pathological injury" in the Parkinson's mice. This suggests the antioxidant pigment doesn't just mask symptoms but actively shields delicate brain cells.

If a compound can be identified that reliably stimulates this natural recycling system—or similarly protects dopamine neurons—it could represent a significant stride toward halting the progression of Parkinson's disease.

Why aren't scientists calling it a treatment yet?

But experts caution that these lab findings are just a first step. Mice treated with MPTP develop symptoms much faster than humans do, and a single animal study does not guarantee the same effect in humans. The researchers tested only one dose of lycopene for a few weeks; it's unknown whether long-term intake or different amounts would help or hurt.

Importantly, it's not yet clear how much dietary lycopene actually reaches human brains after a meal. And while this work links lycopene, more DAT and better mouse outcomes, it doesn't prove that DAT is the sole cause of those gains. In fact, the authors admit, "further functional experiments are still required to clarify the precise regulatory mechanism."

Where could this discovery lead next?

Nevertheless, the research opens new possibilities. It will be interesting to conduct additional research to see whether inhibiting the DAT protein would stop lycopene from protecting neurons. Additionally, researchers are looking forward to finding out how lycopene stimulates DAT production and whether these effects are long-lasting. Finally, tests are needed to determine what doses of lycopene would be beneficial to humans.

For now, these findings should be viewed with cautious optimism. It's fascinating that a familiar food pigment might hold neuroprotective potential—a concrete example of how diet-derived antioxidants sometimes show effects in animals. But this is not a green light to swap your medication for tomato juice. There's a long road from a mouse experiment to a human therapy. For now, lycopene remains a promising lead in the lab, not a proven remedy.


The Life of Earth
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Wednesday, 22 July 2026

Ultimate Limit of The Human Lifespan May Be Identified, Study Suggests

22 July 2026, By M. Starr

Long-lived neurons in the brain are among the cells most vulnerable to the gradual accumulation of somatic DNA mutations, according to the new model.
 (Ruslanas Baranauskas/Science Photo Library/Getty Images)

When the iconic rock band Queen asked, "Who wants to live forever?" the question was rhetorical, but for many people, the answer was "Yes".

Well, a new study suggests immortal life may be scientifically impossible, even if we somehow found the perfect anti-aging medicine.

If scientists managed to overcome every other aspect of aging, humans still couldn't live forever, the new research shows. Random DNA mutations would continue accumulating in our cells until the body could no longer function.

Simulations conducted by a team at the Skolkovo Institute of Science and Technology in Russia suggest this process could impose a fundamental limit on human lifespan, with most people living no longer than about 150 to 190 years under this optimistic scenario.

That's roughly double humans' current longevity, of about 79 years in fortunate circumstances, but it's still a hard limit on the human lifespan.

But rather than predicting how long humans might live, the researchers say their framework offers a new way to measure the contribution of different biological processes to aging.

"We thus present a robust framework for evaluating the impact of somatic mutations on aging and propose a novel approach to modeling aging," they write in a paper published in npj Aging.

https://www.youtube.com/watch?v=GV5m1wNCJRg

The researchers say this framework could help scientists estimate how much different biological processes contribute to aging, potentially helping identify which mechanisms should be prioritized in efforts to slow it.

As we age, our risk of certain diseases escalates exponentially. Cancer, heart disease, and dementia are some of the most common ailments – and causes of death – among the elderly.

Aging isn't just about disease, though. Over the course of a lifetime, our DNA gradually accumulates random mutations. Every time a cell divides, tiny mistakes can arise in our DNA. Our bodies are great at repairing this damage – but not perfect.

Over time, these somatic mutations build up. Most are harmless, while a few can contribute to diseases such as cancer.

But even if cancer and every other age-related disease could somehow be prevented, the mutations would continue accumulating, gradually impairing how well our cells function, according to the new analysis.

Led by computational biologist Dmitrii Kriukov, the researchers asked a deceptively simple question: If every other hallmark of aging could somehow be removed, would random DNA mutations alone still limit how long humans can live?

The model assumes somatic mutations accumulate throughout life and estimates how much they contribute to declining survival, independent of other hallmarks of aging.
 (Efimov et al., npj Aging, 2026)

This wasn't a prediction of how long people will live in the future.

Instead, it was a thought experiment designed to estimate the upper limit that somatic mutations alone might impose to improve our approach to understanding aging.

The researchers built a mathematical model that systematically quantified how the DNA mutation rate impacts the body's major organs, and used this information to calculate the lifespan of a human population free of age-related disease.

The answer was surprisingly optimistic – at least compared to current human longevity.

Depending on the model, the median lifespan ranged from 146 to 194 years.

A few exceptional individuals might theoretically live much longer, but no one would live forever.

https://www.youtube.com/watch?v=mlFUJ-0Rb8Y

"This is a mathematical estimate (though careful), not experimental data," Kriukov notes.

The maximum lifespans calculated are "not a verdict of inevitability", he says, "but it does highlight that somatic mutations, while surprisingly weak as a standalone aging driver, may become critical when combined with other mechanisms".

Interestingly, the researchers found that some cells are more hardy than others. Many tissues, such as the skin and liver, constantly replace old cells with new ones, and can theoretically continue this replenishment for a very long time.

Other vital organs are less resilient. Cells in the heart and brain are largely irreplaceable, so they continue to accumulate mutations as the years mount up. It's these long-lived cells that impose the strictest limitations on lifespan, the team found.

The research made another interesting observation.

The idea that accumulating DNA mutations might be the fundamental cause of aging has been debated for decades and forms the basis of the somatic mutation theory of aging.

Previous studies have shown that mutations build up throughout life, but the question of whether they alone could explain aging has remained controversial.

The work of Kriukov and his team suggests that somatic mutations are likely only part of the aging story. If mutations alone set a median lifespan of around 156 years, and humans currently live much shorter lifespans, then other factors must be imposing limits too.

The finding reinforces an increasingly common view that aging is complicated, with many contributing factors – and that identifying and understanding those individual factors could be key to happy, healthy later lives.

The researchers are careful to note that their work is only part of the overall picture, and solving this problem will likely require collaboration across many fields.

"Our work provides a critical first step towards dissecting aging into quantifiable mechanistic components," they write.

"Ultimately, incorporating other major aging factors could pave the way to a comprehensive, mechanistic theory of aging. Achieving it would require coordinated efforts across multiple research groups – a challenging but increasingly attainable prospect in the near future."


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Moss Is Generating Electrical Waves That Look Startlingly Like a Neural Network

22 July 2026, By J. Cockerill

A different type of moss to the one studied.
 (Oliver Strewe/Getty Images Plus)

Mosses are some of the earliest plants that appeared in the fossil record, but they're anything but simple.

A new study, published in Royal Society Open Science, reveals that moss cushions produce surprisingly complex electrical activity, with patterns that undulate across the velvety patch in dynamic waves.

The study's sole author, Andy Adamatzky, is actually a computer scientist, whose fascination with unconventional 'computing' systems like slime molds, crowds, and mycelium networks has now led him to a new subject: the humble moss, Brachythecium rutabulum.

Brachythecium rutabulum is a common species of moss.
 (dr Barmely/iStock/Getty Images Plus)



"Plants and bryophytes display diverse forms of electrical activity, yet the organization of endogenous signals in mosses has received little attention," Adamatzky writes in his new paper.

His findings suggest that "moss cushions behave as spatially distributed excitable systems potentially capable of coordinating and integrating electrical signals across both space and time."

Moss cushions are actually many individual clones of the same teensy tiny plant.

If you look really, really closely at a mat of moss, you can see it is made up of simple, minute leaves on stems, similar to those of their larger plant relatives.

But the stems of mosses are actually much less useful at moving water and nutrients around the body of the plant.

Mosses actually never developed the vascular systems that we see in other more complex plants, which is why they cannot grow much taller than a few centimeters. Their leaf-like structures are just one cell thick; they don't even have roots.

But that doesn't mean they're not potentially capable of transmitting information across the colony by other means.

For the study, Adamatzky collected cushions of the common moss species B. rutabulum from natural outdoor environments in North Somerset in the UK.

Back in the lab, he poked electrodes into the moss clumps to track any electrical activity that might be passing across this soggy green matrix.

Figures a) and b) show the experimental setup, with electrodes inserted into moss on a wet substrate.
 Figure c) shows the moss's electrical activity, with recordings from each electrode pair represented by a distinct color.
 (Adamatzky, R. Soc. Open Sci., 2026)

Like many plants, moss lives life in slow motion, so to get on its level, Adamatzky recorded its electrical behavior across multiple days.

This revealed "a rich repertoire of electrical events, including components consistent with both physiological activity and slower drift-related processes: fast oscillatory spikes, slower rhythmic fluctuations and very slow depolarization waves," he reports.

"In addition to these described classes, we also observed spikes resembling high-amplitude action potentials and neuron-like spike trains."

Some of the moss's electrical waves were rapid, while others undulated slowly. They tended to spread across the entire cushion rather than remaining confined to a particular region, and followed patterns across different timescales.

These findings suggest that "moss behaves as a dynamic, interconnected system rather than a collection of independent cells."

There are a few limitations here.

For one, there were no negative control recordings, using the same electrode method on an inert substrate (rather than living moss) to rule out electrical signals being the result of something other than the moss – the instruments, for example.

Secondly, using moss collected from nature also brings an element of chaos: it's unclear in this study whether some contamination, mixed levels of hydration, or other factors might have influenced the flow of electricity.

Much more detailed research is needed before we will know whether mosses could actually act as "responsive sensory networks or distributed biocomputing substrates", as Adamatzky proposes in his paper.

"This multi-layered organization supports the emerging view that moss can serve as a naturally evolved, energy-efficient living substrate for biohybrid
sensing and unconventional computation."

But even just knowing more about what these little green plants are getting up to, in the cracks and crevices of the world around us, is cause for wonder.


The Life of Earth
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A Single Human Neuron Is Far More Powerful Than Scientists Thought

By The Hebrew U. of Jerusalem, July 21, 2026

A new study suggests that the human brain’s extraordinary abilities may depend not only on its vast number of neurons, but also on the unusual computational power of each individual cell. 
Credit: Shutterstock

Individual human neurons may be far more powerful computing units than previously understood.

Inside the human cortex, a single neuron may be doing far more than simply deciding whether to send a signal. New research suggests that one brain cell can carry out computations complex enough to rival the work of a deep artificial neural network.

That possibility changes where scientists might look for the origins of human abilities such as language, mathematics, imagination, and invention. Intelligence may depend not only on the enormous scale of the brain, but also on what each of its individual cells can accomplish.

For decades, researchers largely explained the brain’s power through its size and connectivity. The human brain contains close to 100 billion neurons, linked through a vast network. Research published in the Proceedings of the National Academy of Sciences (PNAS), however, indicates that the exceptional abilities of the human brain may also arise from the unusually sophisticated processing performed within individual neurons.

Intelligence may begin inside single neurons

Neurons from the human cortex, the brain’s outer layer involved in advanced thought, appear to function as unusually complex information processing units (“microchips”). Rather than merely collecting signals and producing a simple response, they can combine incoming information through intricate internal processes.

This possibility could help explain how the human cortex supports cognitive abilities that exceed those of other mammals. If each cell performs more computation, the brain gains additional processing power before information even moves through its wider network.

Human cortical neurons are remarkably powerful computing devices. A single human cortical neuron has computational capabilities comparable to those of a deep neural network.
 Credit: Daniela Yoeli / Hebrew University of Jerusalem

The research was led by Hebrew University Profs. Idan Segev and Mickey London, along with PhD students Ido Aizenbud and Daniela Yoeli at the Edmond and Lily Safra Center for Brain Sciences (ELSC). Prof. Chris de Kock of the Free University, Amsterdam, also collaborated on the work.

“People often think of a neuron as a simple switch that either turns on or off,” said Segev. “What we show is that a single human neuron is itself an extraordinarily sophisticated computing device.”

AI reveals each neuron’s computing power

The researchers first needed a consistent way to compare the computational abilities of neurons from different mammals. Simply examining a cell’s size or shape would not reveal how much information it could process.


Daniela Yoeli.
 Credit: Hebrew University



They approached the problem by building a digital imitator for each neuron. Using computer modeling and artificial intelligence, they tested how difficult it was for an artificial neural network (ANN) to learn the relationship between the signals entering a biological neuron and the response coming out.

A relatively simple neuron could be copied by a small artificial model. A more capable biological cell required a deeper and more elaborate network before the artificial version could reproduce its behavior accurately.

This imitation test gave the researchers a practical measure of neuronal complexity. The more difficult the neuron was to reproduce, the greater its apparent computational power.

Human neurons outperform other mammals

Human cortical neurons consistently required more complex artificial networks to imitate their behavior than neurons from other mammals. Their advantage appears to arise partly from their richly branched dendritic trees, the structures that receive signals from neighboring cells, and from their distinctive electrical characteristics.

Those features allow a neuron to analyze combinations of incoming signals instead of simply adding them together. In principle, this could support demanding distinctions within sensory information (e.g., distinguishing between images of cats versus dogs).

The results portray a human cortical neuron as much more than an “on-off” component. One cell can operate as a layered computing system with capabilities comparable to those of a deep neural network.


Ido Aizenbud. 
Credit: Hebrew University



That conclusion challenges the long-standing assumption that human intelligence depends mainly on neuron count and the number of connections among cells. The sophistication built into individual neurons may also have contributed to the evolution of human cognition.

Smarter artificial neurons could reshape AI

The researchers also introduced a general framework for connecting the physical features of a neuron with the computations it can perform. That approach could help scientists investigate how cellular structure contributes to learning, thought, and other forms of cognition.

The findings may also influence the design of brain-inspired AI. Most current systems are assembled from highly simplified artificial units, even when the resulting networks contain many layers.

Future models could instead use artificial components with more processing ability inside each unit. Such systems would more closely resemble biological neurons and could offer a different path for developing state-of-the-art machine-learning technology.


The Life of Earth
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Tuesday, 21 July 2026

The Sunlight on Your Face Took 8 Minutes to Reach Earth. But First, It Spent 170,000 Years Escaping The Sun.

21 July 2026, By M. Starr

(ESA & NASA/Solar Orbiter/EUI Team)

Imagine you're at a party.

All your friends are crammed into a room, you're having a blast – but it's time to head home.

You start to make your way to the door, but every few steps you have to stop for just one more goodbye chat. One friend wants a hug. Another needs to tell you about a band she's discovered. By the time you're free, it's taken you an hour to get from the couch to the door.

Welcome to the life of energy inside the Sun.

It famously takes sunlight just over 8 minutes to travel the 150 million kilometers (93 million miles) from the Sun to Earth.

Before it can get there, though, the energy produced in the Sun's core has to fight its way through the Sun's densely packed interior.

https://www.youtube.com/watch?v=-a9cmyY-qZ8

It's repeatedly passed from particle to particle so many times that traveling the 695,700-kilometer distance from the Sun's center to its surface can take around 170,000 years.

That's according to a 1992 paper by astrophysicists Romas Mitalas and Kenneth R. Sills of the University of Western Ontario.

The pair had noticed that an assumption used to calculate the travel time of energy out of the Sun was incorrect.

It would be easy to imagine the energy simply streaming straight out from the core, but that would also be very wrong. A photon traveling in a straight line would take about 2.3 seconds to travel from the core to the surface.

Instead, it takes something physicists delightfully refer to as a "random walk".

https://www.youtube.com/watch?v=stgYW6M5o4k

In the dense plasma in the solar interior, a gamma-ray photon can only travel a short distance before interacting with a charged particle. It may be absorbed and re-emitted, or scattered off in a new, random direction.

That short distance – known as the step length – is the key ingredient in calculating how long sunlight takes to escape the Sun.

Previously, scientists assumed that the step length was roughly constant throughout the Sun's interior, and based their calculations on an estimated value of 0.5 to 1 centimeter. That gives a diffusion time of 3,000 to 30,000 years.

The problem with that, according to Mitalas and Sills, was that it did not accurately account for the much higher density of the star's inner layers.

OK, so we're back at the party.

You've left the house and walk to your car parked on the street.

A scientist sees only that final part of your journey. Watching from across the street, they measure how long it takes you to walk from the front door to your car, then use that speed to estimate how long it must have taken you to get from the couch to the door.

That scientist has not accounted for all the friends who stopped you along the way.

When the researchers recalculated the step length using a realistic model of the Sun's changing density, they discovered that it would be less than 0.1 centimeters for more than 50 percent of the Sun's radius.

That tiny correction stretched the Sun's photon diffusion time from tens of thousands of years to around 170,000 years.

Once you've finally reached your car, getting home is easy. You simply drive away.

That's kind of like what happens to sunlight.

Once the energy finally reaches the Sun's surface, it no longer has billions of particles blocking its path. It races across the vacuum of space, covering the remaining 150 million kilometers to Earth in just over 8 minutes.

So, next time you raise your face to the warmth of the Sun, spare a thought for how long that energy has spent getting to you.

It likely began its journey before the ancient Egyptians began building the pyramids – and maybe even before the start of the last Ice Age.


The Life of Earth
https://chuckincardinal.blogspot.com/

Ancient Dog Skulls Rewrite the Story of Canine Evolution

By K. M. Cairns, UNSW Sydney & M. Fillios, U. of New England, July 20, 2026

Photograph of an archaeological canid skull used for the photogrammetric reconstruction of 3D models in the study. 
Credit: C. Ameen (University of Exeter)

Ancient bones and DNA reveal that dog diversity and their close relationship with migrating humans developed thousands of years ago.

Place a village dog beside a toy poodle and a mastiff, and the extraordinary physical range of a single species becomes obvious. An estimated 700 million dogs now live alongside or near humans worldwide.

Dogs serve as companions, working animals, and members of the family – and their history is closely bound to our own. Yet the origins of their remarkable variety, and the true age of their relationship with people, have remained difficult to trace.

Two studies published today in Science approach those questions from different directions. Allowen Evin of the University of Montpelier led an investigation of ancient skeletal remains, while Shao-Jie Zhang of the Kunming Institute of Zoology examined DNA from ancient dogs across Eastern Eurasia.

Taken together, the findings indicate that canine diversity and the connection between dogs and humans reach farther into the past, and developed through a more complicated history, than researchers once understood.


Photograph of a modern dog skull used for the photogrammetric reconstruction of 3D models in the study.
 Credit: C. Ameen (University of Exeter)



Dog diversity began thousands of years ago

Evin and her colleagues examined 643 dog and wolf skulls covering a period of 50,000 years to investigate when the physical diversity seen in modern dogs began to emerge.

Their results indicate that the characteristic “dog-like” skull first appeared about 11,000 years ago during the Holocene epoch, the period following the most recent ice age. Dog skulls from that same era already displayed considerable variation in form.

This means the wide range of shapes and sizes dogs have today isn’t solely a product of the intense selective breeding programs that became popular in the last few centuries. Some of that variation emerged millennia earlier.

Early dogs still looked like wolves

The team reanalyzed the skull shapes of all 17 known dog or wolf skulls from the Late Pleistocene, a geological period from 129,000 to 11,700 years ago. Some skulls were 50,000 years old.

They found all of these Pleistocene skulls were essentially wolf-like in shape, including some previously identified as early dogs.

Importantly, this suggests that while the split between wolves and dogs likely occurred during the Pleistocene, the skull shape of early dogs didn’t start to change until closer to the Holocene – that is, 11,000 years ago. However, some Holocene dog skulls still retained wolf-like features.

This research suggests early dogs were much more diverse than previously thought. This diversity may have laid the groundwork for the extreme variations in size and shape of the dogs we have today.

Earlier genomic studies have uncovered four major dog lineages that likely originated about 20,000 years ago: Eastern (East Asian and Arctic) and Western (Europe and Near East) dogs.

The origins of these ancient dog lineages are still being untangled. However, studying shifts in the ancestry of dogs through time and between different regions can help us better understand both the origins of dogs and the movement of Neolithic (new stone-age) humans.

Dog DNA traces human migrations

The new study by Zhang and his colleagues used 73 ancient dog genomes spanning the last 10,000 years to explore how humans and dogs moved across Eastern Eurasia through time.

Analysis of these ancient dogs identified multiple shifts in the ancestry of dogs in Eastern Eurasia at times that correlate with the movement of specific human groups (hunter-gatherers, farmers, and pastoralists). This suggests that as different human cultural groups moved across Eurasia, their dogs often moved with them, carrying their unique genetic signatures.

There was some discrepancy between human and dog population ancestry in some parts of Asia. For example, Eastern hunter-gatherers from Veretye and Botai, who were more closely related to Western Eurasian humans, had largely Eastern (Arctic) dogs rather than the Western dogs observed with other Western Eurasian cultures at the time.

This means dogs may have been a key part of cultural exchange or trade between different human cultures or communities. It may also illustrate complexities in the evolution of dogs that we are yet to understand.

The work by Zhang and his team presents compelling evidence that in Eastern Eurasia thousands of years ago dogs played an indispensable role in human societies as crucial “biocultural packages” that moved with humans. In other words, humans took their companions with them on their journeys (and perhaps traded them), rather than simply acquiring new dogs after moving.

Dogs preserve a shared human history

These findings highlight the long-term, complex, and intertwined relationship between dogs and humans that spans more than 10,000 years.

The genetic ancestry of dogs can act as a living record of ancient human migrations, trade networks, and cultural exchanges. Studies on ancient dogs may also help us understand the environmental factors that contributed to the evolution of dogs, and their relationship with humans.

Together, these new studies profoundly reshape our understanding of how dogs became so diverse and how they have related to humans along the way.

Both studies underscore that the incredible diversity in modern dogs is not an entirely recent phenomenon. The genetic and morphological foundations for this variation were laid thousands of years ago, shaped by natural selection, human selection, and diverse environments, long before the structured breeding of the past few centuries.

Future studies investigating the physical diversity and ancestry of dogs through time could deepen our understanding of the complex origins and spread of dogs across the globe. Whatever their origins, this research deepens our appreciation for the unique and ancient bond between humans and dogs that was almost as diverse as canines themselves.


The Life of Earth
https://chuckincardinal.blogspot.com/

Why Are Bees Struggling To Survive This Summer?

By A. Dittrich, Nottingham Trent U., July 21, 2026

Dead bumblebees on summer pavements may reflect more than their naturally short lives. Extreme heat, disrupted foraging, and colony hygiene can all contribute, while wider environmental pressures make the pattern more concerning. 
Credit: Shutterstock

Multiple environmental pressures are harming bees whose pollination supports crops and flowering plants worldwide.

You may be spotting bodies of dead bumblebees lying across pavements near you in the summer months.

There are several reasons for this, some to do with the weather and some very much due to humans.

Bumblebees live in social colonies supported by highly active worker bees, which typically survive for only 4-6 weeks. As older workers die, younger bees carry their bodies away from the nest to reduce the risk of disease spreading through the colony.
Extreme heat pushes bees beyond limits

Weather can add another source of danger. June 2026 was the warmest June recorded in England (and the second hottest across the whole UK), with more high temperatures expected during the summer.

Such extreme conditions can cause thermal stress in bees. Extended exposure to heat can interfere with their development and threaten the long-term stability of their populations.

Heatwaves can also impair reproduction, flight, and the ability to find food. Bees and other social insects try to cool their colonies by behaviors such as fanning their wings, but these defenses can only provide limited protection when temperatures become extreme.

As it gets hotter bee foraging activity may increase, and they may cover greater distances. Bees can thermoregulate themselves by moving heat around their body while in flight, but extremes of temperature can affect their health.

Chemicals and habitat loss compound deaths

Other elements play a part in bee deaths. Pesticide and herbicide use is commonplace, and these chemicals affect the fitness of bees, causing them to die off. However, not only do these chemicals affect the bees directly, but they can also remove important plants that they rely on for food, causing them to starve. Dandelions, for example, are a massively important nectar source for bees, but also a plant commonly controlled with herbicides. So don’t weed your garden and pull them out.

Pesticide use is one of the historical key causes for the loss of bees. Pesticides applied to reduce the insects feeding on crops – is some what ironically – responsible for harming a group of animals responsible for their pollination.

The EU and the UK have banned the use of the most harmful neonicotinoids; however, pesticides are still routinely used, with harmful knock-on effects on pollinators. Insecticides such as organophosphates, synthetic pyrethroids and phenylpyrazoles cause paralysis and death of these insects, as well as disrupting the bees’ ability to navigate.

Habitat loss is another key issue for bees, with land use changing for housing developments, intensive agriculture and other human structures such as roads. Without these habitats to support the bees, their populations suffer.

Climate change is causing other problems.

Phenological mismatch is when two organisms that are dependent upon each other appear at the wrong time. With a changing climate, this is happening. An example of this is that plants that the bees are dependent upon are in flower when the bees aren’t around. Essentially, they are flowering at a time of year when the bees aren’t there. They could come out of hibernation too early and not have any nectar to feed on, or conversely, the flowers could come out before the bees appear. This, of course, is a disaster for both flowers and the bees.
Bee declines threaten food security

Insects are the most diverse and abundant group of animals on the planet, but in spite of this dominance, they are the most threatened.

We are losing our bees at an alarming rate. In Europe, the number of wild bee species considered at risk of extinction has more than doubled from 77 in 2014 to at least 172 today (around 10% of assessed species).

But we really need them. They provide so much support for our planet, as decomposers, pest controllers, food for other animals and generally for keeping our systems clean and tidy. Scientists call these roles ecosystem services. However, one such service they provide is directly very important for us, and disproportionately carried out by one group of insects, the bees, and that is pollination of our crops.

Bees are one of the most diverse insect groups. They support an estimated 75% of global crop pollination, and nearly 90% of all flowering plants. The rest can be pollinated by other animals, or by the wind and weather.

If we lose that food security afforded by our pollinators we could have a global food crisis on our hands.

Everyday choices can support bees

When it comes to pesticide use, be a thoughtful and informed consumer. Support local, sustainably produced food where possible and, if feasible, buy from farmers who use nature-friendly practices. This does not necessarily mean choosing organic products, but rather considering how food is produced and the environmental impact of different farming systems. As a homeowner, explore non-chemical alternatives first, and apply any treatments sparingly and responsibly to minimize harm to beneficial insects and other wildlife.

One of the simplest ways to address habitat loss for bees is to make room for native species. Plant a diverse range of native flowering species, and leave some areas of lawn unmown. This can help create safe havens for bees.

In the short term, there is one thing that people can do to help bees in distress. Providing sugary water to a bee you see struggling on the pavement on a hot summer’s day can help revive it. A mixture of sugar and water will do the trick at a two-to-one ratio of sugar to water..

Moving the bee, if safe to do so, to a flower or a shady spot too is also advised. But please do not do this if you have allergies, or are likely to get stung.


The Life of Earth
https://chuckincardinal.blogspot.com/

Monday, 20 July 2026

39 Sweeteners Put to the Test Produced Surprising Gut Changes

By U. of Cambridge, July 19, 2026


Cambridge scientists found that many widely used sweeteners can directly change how gut bacteria grow, especially when mixed with other substances found in foods, drinks, and medications. 
Credit: Shutterstock



Scientists found that sweeteners can behave unexpectedly inside a simulated gut, especially when combined with common medications.

Cambridge researchers have found that many widely used sweeteners can directly slow or alter the growth of bacteria found in the human gut. The strongest effect appeared when isosteviol, a sweetener used in foods and beverages, was combined with the antidepressant duloxetine.

In laboratory experiments, that combination sharply reduced two important bacterial species associated with digestive health and blood sugar regulation. It also produced changes that could influence inflammation and immune activity.

The researchers caution that the findings come from controlled laboratory tests, not studies involving people. More work will be needed to determine whether the same interactions occur inside the human body and whether they have meaningful health consequences.

Sweeteners May Not Be Biologically Inactive

Sweeteners are found in a wide range of everyday products, including soft drinks, candy, desserts, snacks, cereals, and some medications. They are often promoted as alternatives that provide sweetness with less sugar or fewer calories.

However, growing evidence has linked the consumption of some sweeteners with conditions including type 2 diabetes, obesity, and cancer. These associations do not necessarily prove that sweeteners directly cause those diseases, but they have raised questions about how the compounds behave inside the body.

One possible link is the gut microbiome, the enormous community of bacteria and other microorganisms living throughout the digestive tract. These microbes help break down food, produce useful compounds, support the intestinal barrier, and communicate with the immune system.

Despite the widespread use of sweeteners, relatively few studies have examined whether they interact directly with individual gut bacteria.

Professor Kiran Patil from the Medical Research Council (MRC) Toxicology Unit at the University of Cambridge said: “Most of what we know about the potential impact of sweeteners on our health comes from animal research or from population studies. While these studies have indicated involvement of the microbiome in mediating the effect of sweeteners, it’s difficult to know how sweeteners act in the body – is it through direct interactions with our gut bacteria?”

“Answering this is further complicated by the fact that we rarely ever take sweeteners by themselves – we take them with drinks, in snacks, or even in medication to mask bitterness,” added Dr. Sonja Blasche, a lead author of the study, also the MRC Toxicology Unit.

Researchers Tested 39 Common Sweeteners

For the study, published in Molecular Systems Biology, Dr. Blasche and her colleagues investigated how artificial and low-calorie sweeteners affect gut bacteria under laboratory conditions. They also examined whether those effects changed when the sweeteners were mixed with other substances commonly consumed at the same time.

The team grew 25 bacterial species individually. The collection included microbes considered beneficial, neutral, or potentially harmful.

Each bacterial culture was then exposed to 39 commercially used sweeteners, including both natural and artificial varieties. The researchers measured whether the bacteria continued multiplying normally, grew more slowly, or stopped growing.

About three-quarters of the sweeteners altered the growth of at least one bacterial species. Some significantly slowed or completely halted the growth of microbes associated with a healthy gut.

More Than 100 Hidden Interactions

People rarely consume sweeteners in isolation, so the scientists next combined them with other common compounds. These included caffeine, vanillin (vanilla extract), advantame (an artificial sweetener), and eight widely used medications.

The results revealed more than 100 interactions in which a sweetener affected bacteria differently when another compound was present. In 34 cases, the second substance strengthened the sweetener’s effect. In 68 cases, it weakened the effect.

This suggests that the biological impact of a sweetener may depend partly on what is eaten, drunk, or taken with it.

One Sweetener and Antidepressant Stood Out

The most dramatic response involved isosteviol and duloxetine. Isosteviol is used in the food and beverage industry, while duloxetine is prescribed for depression and several other conditions.

Together, the two compounds strongly suppressed Roseburia intestinalis and Parabacteroides merdae. Both bacteria are associated with functions that help maintain digestive and metabolic health.

Duloxetine is also widely prescribed. In the US in 2023, more than 4.2 million patients received the medication.

Studying bacteria individually can reveal direct effects, but the gut is a crowded ecosystem in which many species constantly interact. A change affecting one organism may therefore spread through the wider microbial community.

To better approximate those conditions, the researchers built a synthetic community containing all 25 bacterial species. They allowed the community to develop and then exposed it to different combinations of sweeteners and medications.

The scientists tracked which species became more or less abundant and whether the diversity of the community changed.

Gut Microbial Diversity Declined

The combination of isosteviol and duloxetine reduced microbial diversity in the simplified gut community. Greater microbiome diversity is generally considered a feature of a healthy and resilient digestive system, although the precise meaning of diversity can vary from person to person.

The combination also changed the balance of the community, allowing some bacterial species to thrive while others declined.

Additional experiments found that the altered microbial community became more toxic to certain host cells. It also interfered with cells involved in inflammation and immune responses.

These findings suggest that interactions between sweeteners and medications may influence more than bacterial growth alone. They could potentially affect how microbial communities communicate with the body.

Dr. Blasche said: “Sweeteners are often marketed as metabolically neutral, but our study challenges this idea. We found that they can directly affect gut bacteria, particularly when mixed with other compounds such as medication and food additives. These common combinations could have unintended effects on our gut microbiome.”

Human Health Effects Remain Unclear

The researchers emphasize that the experiments were conducted in laboratory cultures rather than in people. The human digestive system is much more complex and includes hundreds of microbial species, changing chemical conditions, food components, and interactions with organs and immune cells.

The concentrations of sweeteners and medications reaching the gut may also differ from those used in laboratory testing. As a result, the study cannot show that consuming a particular sweetener while taking duloxetine will cause harm.

Instead, the findings identify combinations that deserve closer investigation in animals and humans.

Professor Patil, the study’s senior author, added: “Our study suggests that artificial sweeteners don’t just pass through the body passively — they can interact with gut microbes, and these effects can be amplified or altered by other substances like medications. These findings can help guide new studies towards understanding how sweeteners might influence health in unexpected ways.”


The Life of Earth
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