Scientists Warn a Silent Oxygen Crisis Is Spreading Through Earth’s Waters

By B. Hook, U. of California San Diego, July 24, 2026

https://scitechdaily.com/scientists-warn-a-silent-oxygen-crisis-is-spreading-through-earths-waters/

Researchers argue that aquatic oxygen loss should be recognized alongside climate change, biodiversity loss, and other planetary boundaries. Its links to warming, pollution, and ecosystem instability suggest it may be more than a regional environmental problem. 

Credit: Shutterstock

New research calls for aquatic deoxygenation to be recognized as a critical planetary process under threat.

Oxygen is declining across oceans, coastal waters, rivers, lakes and streams, threatening the organisms and chemical processes that depend on it. A review led by researchers at UC San Diego’s Scripps Institution of Oceanography warns that this widespread deoxygenation is moving Earth toward an “unsafe space,” with some effects potentially lasting beyond human timescales.

The researchers examined how aquatic deoxygenation, meaning the loss of dissolved oxygen from marine and freshwater environments, interacts with the nine processes included in the Planetary Boundaries framework. Introduced in 2009, the framework identifies major Earth systems and evaluates how human activity is pushing them beyond the conditions that support a stable and resilient planet.

Those nine boundaries cover climate change, ocean acidification, biodiversity loss, atmospheric aerosol loading, stratospheric ozone depletion, freshwater change, land use change, chemical pollution and biogeochemical flows (including the nitrogen cycle). The authors argue that dissolved oxygen should also be included.

Oxygen loss threatens planetary stability

“The health and stability of our planet depends on the health and stability of aquatic ecosystems, which need oxygen to function normally,” said lead author Erica Ferrer, a Scripps Oceanography alumna and current postdoctoral scholar at UC Santa Barbara’s National Center for Ecological Analysis and Synthesis. “This study is designed to elevate the profile of aquatic deoxygenation as a global threat and show that it does not operate in isolation.”

A diagram showing some of the key interactions that exist between aquatic deoxygenation and the other planetary boundaries, including primary and secondary drivers and effects. Here, emphasis is placed on interactions that occur in the marine environment, however, similar interactions are also known to take place in freshwater systems. 

Credit: dataMares

Human-caused warming, excess nutrient pollution and changes in the circulation that carries oxygen into deeper waters are the primary drivers of aquatic deoxygenation. Declining oxygen interferes with biological and chemical processes that help regulate Earth’s climate while threatening organisms ranging from microbes to fish and sharks. Marine mammals can also be affected despite breathing at the surface because oxygen loss changes their habitats, prey, and surrounding food webs.

Scientists call for a new boundary

Ferrer and senior author Lisa Levin, a biological oceanographer at Scripps, developed the idea for the review after attending COP25, the United Nations Climate Change Conference held in Madrid in 2019. They hope the work encourages researchers and policymakers to address aquatic deoxygenation together with the other pressures affecting Earth’s systems.

“Adding aquatic deoxygenation to the Planetary Boundaries framework will help us understand its impacts on Earth system stability,” said Ferrer. “Mitigating its impacts represents a critical component of maintaining biodiversity and climate.”

The Life of Earth

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Watching Too Much TV May Actually Rot Your Brain After All, Study Finds

25 July 2026, By S. J. Vartan

https://www.sciencealert.com/watching-too-much-tv-may-actually-rot-your-brain-after-all-study-finds

(Brasil2/Canva)

If you click on the TV and hear a voice from your childhood saying, "That idiot box is going to rot your brain!" – you're not alone. My grandma said exactly that whenever she walked by me watching cartoons as a kid.

Turns out, grammy wasn't entirely wrong.

It's not just the sitting, which as we've now heard, isn't so great for longevity, or your brain, and may increase the risk of Alzheimer's and other types of dementia.

When it comes to brain health specifically, a new study suggests that spending hours glued to the TV may have a negative effect that's not seen when the same amount of time is spent sitting at a desk solving problems, answering emails, or otherwise putting your gray matter to work.

The research, published in Alzheimer's and Dementia: Journal of the Alzheimer's Association, followed more than 1,700 adults for nearly 24 years.

It found that men (but not women) who frequently watched television in midlife had smaller brain volumes in regions vulnerable to Alzheimer's disease, along with more of the kind of damage to the brain that's associated with cognitive decline and dementia.

Brain regions associated with the frequency of TV watching (left) and sitting during work (right). Red indicates areas associated with lower cortical volumes, while purple indicates volume increases. 

(Feter et al., Alzheimers Dement., 2026)



In contrast, people whose jobs involved sitting for much of the day tended to have healthier-looking brains.

Importantly, when the researchers accounted for differences in overall physical activity, that didn't seem to impact the outcome, so no, exercise didn't impact these findings.

The striking sex difference surprised the researchers.

"We found that the links between TV watching and brain structure were much stronger in men than in women," biological scientist Natan Feter from the University of Southern California told ScienceAlert.

"This could be because men and women accumulate sedentary time differently – for example, women may interrupt their sitting more often – or because of biological differences in how the brain responds to prolonged sedentary behavior."

Previous studies have found that women tend to prefer TV programming in shorter chunks, though they spend more time watching overall, while men's preferences for watching sports and movies are more likely to spend long, uninterrupted periods on the couch.

Hormonal differences, lifestyle factors (such as childcare responsibilities), or differences in how male and female brains age could also play a role.

The striking sex difference surprised the researchers. (pablo_rodriguez1/Canva)



"For years we've focused on how much people sit. Our findings suggest we should also pay attention to what they're doing while they're sitting," says biologist David Raichlen from the University of Southern California.

The data for the study came from 1,712 participants in the long-running Atherosclerosis Risk in Communities (ARIC) study.

Volunteers, who were in their early 50s when they enrolled in the late 1980s, reported how often they watched television during their leisure time and how much they sat at work.

About 24 years later, when they were in their mid-70s, their brains were scanned using an MRI.

Researchers looked specifically at brain areas that are known to show early changes in Alzheimer's disease and related dementias, and areas of increased white matter hyperintensity (WMH) volume, which is "a marker of small vessel cerebrovascular disease associated with cognitive decline and dementia risk," according to the study.

https://www.youtube.com/watch?v=PL5lA2edBwg

Compared to those who reported watching television "very often," people who reported sitting "always" during work had fewer white matter lesions and larger volumes in the frontal, parietal, and occipital cortex.

Importantly, sitting itself wasn't consistently associated with poorer brain health – it depended on the context.

Watching TV is considered a cognitively passive activity.

On the other hand, even sedentary office work often involves planning, reading, writing, decision-making, and problem-solving. Previous research has suggested these kinds of mentally stimulating activities may help build "cognitive reserve", allowing the brain to better cope with age-related changes.

The study has limitations. It used self-reported data from participants who estimated how much TV they watched or how much time they spent sitting at a desk, which is less reliable than objectively measured data.

Research also can't prove that watching TV directly caused the brain differences, and clearly there's a gender element too.

Other unmeasured lifestyle factors, such as snacking, drinking alcohol, or reclining or napping while "watching" TV, could have contributed to the findings.

Still, the study tracked participants for nearly a quarter century, used MRI scans rather than cognitive tests alone, and results were consistent across analyses.

Considering that there's research showing that book-readers live almost 2 years longer than non-readers, it does seem that there's some kind of difference between an active versus passive brain while sitting.

Things like puzzling, crafts, and even texting, which require your brain to work while you are sitting might also change how much sitting negatively impacts your brain, but "more research is needed to confirm," said Natan.

So keep it in mind if you're settling in for another TV marathon tonight. Your brain might appreciate a few breaks – even if your streaming-service-of-choice doesn't provide commercial interruptions anymore.

The birth of modern Man

https://chuckincardinal.blogspot.com/

'Tremendously Grave': The First US City Is on Track to Run Out of Water

25 July 2026, By D. Nield

https://www.sciencealert.com/tremendously-grave-the-first-us-city-is-on-track-to-run-out-of-water

(Nithin PA/Pexels)

It seems inconceivable, even if you're aware of the perilous situation that the world's water supplies are in, but a developed coastal city in Texas that more than 300,000 people call home is now in serious danger of running out of water.

The city is Corpus Christi, and difficulties with water scarcity are now coming to a head after years of concerns over shortages.

There are multiple issues combining here, perhaps most importantly the arrival of major industrial developments, off the back of the unlocking of vast oil and gas reserves that came with the shale revolution.

One plastics chemical complex, built in 2022, uses as much water for cooling every day as all the Corpus Christi residents combined.

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

A planned seawater desalination plant, which was supposed to ease some of the pressure brought on by rising industrial water usage, never materialized, further compounding the problem of supply.

And then there's climate change: Texas has been hit by a series of historical droughts in recent years. It all adds up to a scarcity of water that life and businesses rely on.

"Corpus Christi has come as close to running out of water as practically any city in the United States," says Dylan Baddour, a journalist at Inside Climate News.

"They've rebounded a good bit since the beginning of this year, but they have about one year of water in storage right now, which would already be considered an emergency for any city."

Water levels in Lake Corpus Christi, the second-largest reservoir supplying the city. 

(Water Data for Texas)

While rainfall during 2026 has eased the pressure somewhat, reservoir levels are still precariously low, and it's not clear how much longer the situation can go on for.

The desalination plant plans haven't been completely abandoned.

There's still a proposal on the table to build a huge facility for removing salt and impurities from seawater, which would produce an estimated 378 million liters (100 million gallons) of water a day (twice as much as the biggest desalination plant currently in the US, in San Diego).

However, the plant has been discussed since 2017, and efforts to move forward with it are being caught up in red tape and questions over funding. The bill for the facility is reportedly in the region of $6 billion.

"There were years of fumbling around, of folks trying to get something on the books, other people seeking to stop it, and all the while, water was running out," says Arcelia Martin, also a journalist at Inside Climate News.

Other options being explored are groundwater wells drilled deep underground – already supplying 12 million gallons a day – but these solutions are also vulnerable to drought. Plans to use wastewater for industrial cooling purposes are also being explored, with supplies set to go online this year.

City residents have faced restrictions around watering their gardens or washing their cars since August 2024, but it was expected that emergency measures might have to be introduced as early as December 2026.

Thanks to the rains we've seen this year, that prediction has now been pushed back to September 2027, but there's still very little margin for error. City authorities need to find a solution to the water scarcity problem, and quickly.

Emergency measures might include rolling 'water blackouts', where water is only available for some parts of the day, for example. However, that's not really a solution for industrial uses – these refineries and plants would have to be shut down, bringing subsequent knock-on effects on the economy and communities.

Sadly, as with other natural resources, it seems that we haven't been appreciating what we had until we're dangerously close to running out.

"What this story shows us is that point where we begin to see what it means for a city to run out of water," says Baddour.

"It's never really happened here, or on a large scale in the world, in modern times."

"The possibilities that it raises are tremendously grave, and that's what we're dealing with here."

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https://chuckincardinal.blogspot.com/

A Wild Parasite Makes Ants Live 10x Longer And Tricks Others Into Worshipping Them

24 July 2026, By M. Irving

https://www.sciencealert.com/a-wild-parasite-makes-ants-live-longer-and-tricks-others-into-worshipping-them-scientists-finally-know-how

Temnothorax nylanderi.

 (April Nobile/AntWeb/CC BY 4.0)

Imagine a parasite that makes you live up to 10 times longer than you naturally would – while also inspiring others to treat you like royalty.

It sure seems like a pretty good deal, but of course there's a catch.

The parasite just wants to keep you lazy so you'll be easy pickings for a giant predator – the bowels of which are the parasite's preferred breeding ground.

It might sound like an intriguing setup for an indie horror movie, but that's the reality for Temnothorax nylanderi ants. Now, thanks to a new study in the journal BMC Genomics, we know more about the biology of this bizarre story.

When ant larvae of this species are fed woodpecker droppings, they can become infected with the tapeworm Anomotaenia brevis – and so begins an insidious cycle.

Infected ants start to change color, becoming pale yellow rather than their usual darker brown. They tend not to grow as big as their nest mates, and even start to smell different – in fact, they seem to emit pheromones that other ants interpret as being from a queen.

Infected workers (right) become much lighter in color than uninfected ants (left).

 (©: Susanne Foitzik)



As such, the workers roll out the red carpet for the infected ants. They bring them food, carry them around, and groom them, to the detriment of the rest of the colony.

Infected ants, meanwhile, lean into their new lifestyle. They ignore their chores, rarely leaving the nest during their extended lifespans while generations of regular workers tend to their every whim.

And throughout all this, the tapeworm larvae are just biding their time. Eventually, a woodpecker may come knocking, and while the healthy ants scatter, the infected ones sit there helpless, providing an easy snack.

A worker ant of the species Temnothorax nylanderi. 

(Herman/Wikimedia Commons/CC BY SA 2.0)



Finally, the tapeworm larvae can reach their ultimate goal: the bird's gut. There, they develop into adult tapeworms, breed, and lay eggs – which are then pooped out by the woodpecker to begin the whole cycle over again.

But biologically, how does the tapeworm manage to pull off such extreme manipulation from inside the ant?

To find out, a team of biologists from Johannes Gutenberg University of Mainz (JGU) in Germany and Zhejiang University in China has now investigated the gene expression in infected and uninfected ants, as well as queens.

The researchers examined the ants' brains and fat bodies – a type of tissue in the insects that helps with metabolic and immune function.

Perhaps unsurprisingly, the team found that gene expression in the fat bodies of queens had a lot more in common with infected workers than uninfected ones.

"Our genetic analyses show that the infection does not simply make the ants sick, but alters their physiology in a highly targeted way," says Susanne Foitzik, lead author of the study and a behavioral ecologist at JGU.

"At the molecular level, infected workers showed a profile that was partially queen-like."

These changes were linked to metabolism, the immune system, stress, and aging, which helps explain their longer lives and why other ants give them the royal treatment.

Close-up of the head of a Temnothorax nylanderi. 

(April Nobile/AntWeb/CC BY 4.0)



Intriguingly, the similarities between queens and infected workers disappeared when the researchers looked at their brains. Infected ants seemed to have suppressed signaling molecules and receptors, which could explain why they seem to entirely lose the work ethic these industrious insects are known for.

Strangely though, the researchers found that the signaling molecules in the brains of infected ants don't really resemble those produced by the parasite.

This could shut down one hypothesis: that the tapeworms use their own peptides to hack into their host's brain.

"The data rather suggest that the parasite influences the ant indirectly by intervening in the host's own regulatory networks, which control metabolism, the immune system, aging, and behavior, among other processes," says Giulia Blasi, first author of the study and a biologist at JGU.

This tapeworm is far from the only parasite that preys on ants in a way worthy of a horror movie.

The cordyceps fungus hacks the nervous system of its victims and turns them into 'zombies', before forcing them to climb a plant and lock their mandibles onto the underside of a leaf.

A stalk then grows from their head, which bursts open, spreading spores to unsuspecting ants on the forest floor below.

Given the choice, we think most ants would probably pick the tapeworm.

The Life of Earth

https://chuckincardinal.blogspot.com/

Common Food Additive Linked To Gut Inflammation

By M. Fernanda Ziegler, São Paulo Research Foundation, July 23, 2026

https://scitechdaily.com/common-food-additive-linked-to-gut-inflammation/

Rats that consumed the thickener over an extended period developed structural and inflammatory changes in the colon, along with reduced intestinal barrier integrity. 

Credit: Shutterstock



A widely used food thickener may have more complex effects on the gut than previously recognized.

Xanthan gum helps give ice cream, yogurt, sauces, cakes, and gluten-free pasta their familiar texture. Valued for its thickening, stabilizing, and gelling properties, it is among the food industry’s most widely used additives. It also helps make liquids safer to swallow for people with dysphagia, a condition that causes difficulty swallowing.

Research from the Federal University of São Paulo (UNIFESP) in Brazil, however, raises questions about the effects of prolonged consumption. Rats that received xanthan gum for ten weeks developed colon inflammation, changes in their gut microbiota, and reduced intestinal barrier integrity. The study was supported by FAPESP.

“This isn’t about demonizing xanthan gum. Rather, it’s about emphasizing the need to invest in translational studies involving humans. It’s possible that occasional use in small amounts as an additive doesn’t harm health. The concern is with daily use as an ingredient and the cumulative effect of the thickener,” explains Alessandra Rischiteli, the nutritionist and speech-language pathologist who conducted the study. The findings were published in PLOS One.

Daily exposure raises broader concerns

Scientific and clinical interest in xanthan gum has increased partly because children and older adults with dysphagia may consume it every day, Rischiteli notes. The additive is also common in ultra-processed foods, protein shakes, and supplements. “Here, once again, the guidelines set forth in the Dietary Guidelines for the Brazilian Population – which recommend avoiding ultra-processed foods and foods high in additives – are relevant,” she says.

Xanthan gum is produced through biotechnology by fermenting material with the bacterium Xanthomonas campestris. “It’s a plant pathogen that, in nature, infects a variety of plants and can be observed when cabbage or kale, for example, begin to spoil,” she says.

Some people with dysphagia rely on thickeners to consume enough food and liquids, especially when they cannot tolerate natural options such as cornstarch. For these patients, Rischiteli says the goal should be to reduce possible harm rather than simply remove a necessary product. “Based on the results of the study, the recommendation is to monitor gut health and adopt strategies to protect the gut, such as using probiotics,” she states.

Infant cases gain a possible explanation

The results may help clarify earlier reports connecting xanthan gum with necrotizing enterocolitis in premature infants in the United States. This serious disease causes intestinal inflammation that can lead to tissue death.

In 2012, 22 newborns developed the condition after receiving formula thickened with xanthan gum, and at least three died. The U.S. Food and Drug Administration (FDA) subsequently prohibited its use in premature infants and advises against using it in infants more generally.

“Until then, the link between xanthan gum and the disease in infants was merely a clinical hypothesis or an empirical observation. This study on rats proved causality – that is, that xanthan gum does cause inflammation,” says Claudia Oller, a professor at UNIFESP who coordinated the study.

The intestinal barrier begins to weaken

The researchers also examined the biological pathway through which the inflammatory response developed in the colon. “Xanthan gum is reactive and opens the intestinal barrier, altering a protein [Claudin-2] that’s responsible for regulating permeability between intestinal cells, which triggers an inflammatory cascade,” Rischiteli explains.

According to the researchers, this process supports the mechanism previously proposed by American physicians to explain what may occur in the immature intestines of premature infants.

Rats fed the additive developed an inflammatory state marked by greater numbers of lymphocytes, immune defense cells, within the intestinal wall. The response was strongest among animals receiving medium and high doses of xanthan gum.

Microscopic tissue examinations found higher inflammation scores, while biochemical testing identified significant disruption of the intestinal barrier.

“This protein [Claudin-2] showed higher expression in the animals’ intestinal epithelium, indicating a loss of intestinal barrier integrity,” Rischiteli explains.

The rats also had elevated levels of the pro-inflammatory cytokines IL-1β and TNF-α, providing further evidence of an inflammatory response. “TNF-alpha, in particular, is associated with the death of cells lining the intestine [epithelium] and the development of inflammatory diseases,” she says.

Gut bacteria shift toward dysbiosis

Long-term xanthan gum consumption did not significantly reduce the overall diversity of the rats’ gut microbiota. It did, however, change the balance among microbial groups.

One shift involved an increase in bacteria belonging to the phylum Elusimicrobiota, which has been associated with inflammatory conditions.

“This change indicates a state of dysbiosis, even without major alterations in the dominant bacterial groups,” she states.

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Common Diet Advice About Water and Spicy Food May Be Completely Wrong

By L. Reiley, Cornell U. July 23, 2026

https://scitechdaily.com/common-diet-advice-about-water-and-spicy-food-may-be-completely-wrong/

New research suggests that everyday mealtime habits may influence how much people eat in unexpected ways Credit: Shutterstock

Water and spice influenced eating in opposite and unexpected ways during controlled meal experiments.

A glass of water beside a meal is often treated as an easy way to eat less. The usual explanation is that the water stretches the stomach and creates a sense of fullness before too much food is consumed.

A Cornell analysis, however, found no evidence that this happened during the meals researchers observed.

Participants actually consumed about 39 additional grams of food, or roughly 49 more calories, for every extra 100 grams of water they drank. Those who alternated more often between eating and drinking also consumed more food, with each additional switch associated with another 4.4 grams eaten.

One possible explanation involves sensory-specific satiety, the gradual decline in a food’s appeal as a person continues eating it. Taking sips of water between bites may refresh the sensory contrast of the meal, allowing the food to remain enjoyable for longer and postponing the point when eating stops.
Water may prolong eating, not fullness

“There’s been this widespread advice that if we drink water, it fills us up,” said Paige Cunningham, assistant professor in the Division of Nutritional Sciences in the College of Human Ecology. “But water is emptied quickly from the stomach so it likely doesn’t fill us up for long. Instead, water may increase how much we eat, providing lubrication which can speed up eating, and preventing a dry mouth which can prolong enjoyment of the food.”

Credit: Laila Milevski/Cornell University



Cunningham served as corresponding author of the analysis, published in July in Appetite and completed with longtime collaborator John Hayes of Penn State’s Department of Food Science. A separate but related experiment examined how the heat of salsa affected the amount people ate and produced another unexpected result.

“Both studies show how mealtime behaviors and food properties can significantly influence how much we eat, without us even realizing. We found that just drinking more water was associated with greater consumption, while adding a bit more spice to a snack slowed eating and decreased how much participants ate,” said Cunningham.

Faster drinking complicates the pattern

For the water analysis, researchers combined data from two earlier laboratory experiments involving 86 adults. Participants received either beef chili or chicken tikka masala with water and were allowed to eat as much as they wanted while cameras recorded every bite and sip.

One finding did not fit the researchers’ expectations. People who consumed their water more quickly ate less food rather than more. The researchers do not yet have a firm explanation, noting that the pattern might involve how long water remains in the mouth or simply reflect the total duration of the meal.

“This was a secondary analysis looking at associations,” Cunningham said. “We are following up on this right now so we can make those causal inferences.”

Spicier salsa slowed eating and intake

A separate experiment, published in April in Food Quality and Preference, involved 49 adults who ate tortilla chips with either mild or spicy salsa once a week for two weeks. The amount of cayenne in the salsa was the only difference between the two conditions.

When the salsa was spicier, participants consumed 28% less of the snack overall. The reduction included both the salsa and the unchanged tortilla chips.

Credit: Laila Milevski/Cornell University



Participants also ate the spicy snack about 30% more slowly than the mild version. The researchers suspect the heat reduced intake by slowing the pace of eating. Participants drank similar amounts of water under both conditions, making increased drinking an unlikely explanation for the result.

“We were interested in whether making the salsa spicy would result in people eating the same amount of chips,” Cunningham said. “And they didn’t. The takeaway is that adding spice to one part of the snack can significantly influence how much people eat overall.”

The results challenge familiar diet advice

Together, the studies complicate two familiar ideas about eating. Water consumed with meals is commonly promoted as a straightforward way to reduce intake, while spicy foods may be viewed cautiously by people trying to control how much they eat. In these laboratory settings, the opposite patterns appeared: drinking more water was associated with greater food consumption, while additional spice was associated with eating less.

“These strategies might help consumers achieve their goals to reduce energy intake,” Cunningham said.

Both studies also have clear limitations. Researchers tested only beef chili, chicken tikka masala, and one combination of tortilla chips and salsa, all under controlled laboratory conditions. They caution that different foods or everyday eating environments may not produce the same results.

“We are looking to future experiments that explore what other factors or properties of foods we can leverage to influence behaviors,” Cunningham said.

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https://chuckincardinal.blogspot.com/

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

By Purdue U., July 20, 2026

https://scitechdaily.com/new-metal-alloy-is-up-to-10-times-stronger-than-structural-steel/

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

https://www.sciencealert.com/orcas-keep-punching-giant-sunfish-to-smithereens-and-scientists-are-mesmerized

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.

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

22 July 2026, By M. Starr

https://www.sciencealert.com/ultimate-limit-of-the-human-lifespan-may-be-identified-study-suggests

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

https://www.sciencealert.com/moss-behaves-a-little-like-a-really-slow-brain-scientist-discovers

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.

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