Scientists develop remarkable method to battle emerging threat to world's oceans: 'Stick to just about any surface'
North Carolina State University researchers in a news release detailed their breakthrough, which uses environmentally safe materials that work even in wet, salty conditions. In fact, they thrive — thanks to the amazing design of the self-dispersing microcleaners.
The idea behind the new technology — "Can we make the cleaning materials in the form of soft particles that self-disperse in water, capture microplastics as they sink, and then return to the surface with the captured microplastic contaminants?" — was a moon shot. Those were the words of chemical and biomolecular engineering professor and corresponding author Orlin Velev.
The team stuck the landing.
Its paper was published in Advanced Functional Materials in March. The research shows how ingenuity can reverse the harm done to the planet by microplastics, a scourge of both human health and the environment. The tiny plastic fragments, less than 5 millimeters in size, come from larger plastics, which do not break down but just continually degrade. Microplastics have been found everywhere on Earth and linked to Alzheimer's disease, fertility problems, and cancer.
The process features eugenol, a plant-based oil that works as a dispersant when these soft dendritic colloids hit the water. The polymer-based colloids — in the form of small pellets — can "stick to just about any surface," per the release, hosted by Phys.org.
"The cleansing particles in this research are made from chitosan, a biodegradable polymer originating from chitin, which comes from processed shellfish waste," Velev said.
Magnesium makes the pellets bubble and rise to the surface after they've rounded up microplastics. A gelatin coating delays the magnesium's reaction with water, so the colloids have time to collect the targets. They rise in "a dense, scummy mixture," doctoral candidate and first author Haeleen Hong said.
The particles' method of movement may be even neater — and they can "swim" for 30 minutes.
Eugenol "makes the pellets move in the water by the so-called 'camphor boat effect,' decreasing the surface tension on one side of the pellet and driving it forward. This allows our microcleaners to spread out across a larger area, capturing microplastics as they move and descend," Hong said.
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And the process could even be circular, with the skimmed scum being used to make more chitosan and then more microcleaners. The paper shows proof of concept, and more research is necessary to ensure it can be scaled up.
Until then, you can avoid microplastics by ditching single-use water bottles, filtering your drinking water, cooking and heating food in nonplastic products, and storing hot food in safe containers. There are other simple steps to take to use less plastic, too.
Join our free newsletter for weekly updates on the latest innovations improving our lives and shaping our future, and don't miss this cool list of easy ways to help yourself while helping the planet.
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Newsweek
a day ago
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Hidden Human 'Superpowers' Could Help Fight Diabetes
Based on facts, either observed and verified firsthand by the reporter, or reported and verified from knowledgeable sources. Newsweek AI is in beta. Translations may contain inaccuracies—please refer to the original content. Hidden human 'superpowers' could one day help develop new treatments to reverse diabetes and neurodegeneration. This the conclusion of research from University of Utah that suggests hibernating animals' superpowers could lie dormant within our own DNA and could potentially be unlocked to improve our health. "We were fascinated by one big mystery: how do hibernating mammals completely rewire their metabolism—and then reverse it—without damaging their brains or bodies?" Chris Gregg, paper author and U of U Health neurobiology professor, told Newsweek. "They gain huge amounts of fat, become insulin resistant, shut down metabolism and body temperature for weeks or months... and then bounce back without the chronic diseases that plague humans under similar conditions. "That led us to a key idea: maybe the answers aren't in protein-coding genes, which are mostly shared across mammals, but in the noncoding regulatory elements—the parts of the genome that act like switches and dimmers for gene activity." The dangerous health changes hibernating animals can recover from are similar to those seen in type 2 diabetes, Alzheimer's disease, and stroke. It appears humans have the genetic framework to do this, too, if we can figure out how to bypass some of our metabolic switches. A medical doctor using advanced DNA technology, looking at computer screens. A medical doctor using advanced DNA technology, looking at computer screens. AndreyPopov/Getty Images The researchers discovered that a gene cluster called the 'fat mass and obesity (FTO) locus' plays an important role in hibernators' abilities—and humans have these genes too. "What's striking about this region is that it is the strongest genetic risk factor for human obesity," Gregg said in a statement. But hibernators have been observed to be able to use genes in the FTO locus in new ways to their advantage. The team identified hibernator-specific DNA regions near the FTO locus that regulate the activity of neighboring genes, turning them up or down. The research team speculate that this process, including those in or near the FTO locus, allows hibernators to gain weight before settling in for winter. During hibernation, they slowly use these fat reserves for energy. The hibernator-specific regulatory regions outside of the FTO locus seem particularly crucial for tweaking metabolism. When the researchers mutated the hibernator-specific regions in mice, they saw changes in their weight and metabolism. Some mutations sped up or slowed down weight gain under specific dietary conditions, while others affected the ability to recover body temperature after a hibernation-like state or tuned overall metabolic rate up or down, according to the study. Instead of being genes themselves, the hibernator-specific DNA regions the researchers identified were in fact DNA sequences that contact nearby genes and turn their expression up or down, "fine-tuning" them. A hedgehog hibernating in a natural woodland habitat. A hedgehog hibernating in a natural woodland habitat. Callingcurlew23/Getty images "Our research reveals that hidden 'superpowers' from hibernating mammals may be linked to specific genetic elements that exist in human DNA—in the form of conserved, noncoding regulatory elements that control metabolism, brain health and resilience to stress," Gregg explained. "By comparing the genomes of hibernators and non-hibernators, we identified thousands of DNA elements that hibernators have lost or rewired—especially those regulating how the brain responds to fasting and recovery after fasting. When we deleted some of these elements in mice, they changed body weight, energy use, thermoregulation, and even age-related memory behaviors. 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He explained that if we can understand how to reactivate or mimic these genetic programs, it could lead to new treatments for type 2 diabetes and obesity "by improving metabolic flexibility", Alzheimer's and other neurodegenerative diseases "via the activation of neuroprotective and regenerative gene programs" and stroke and injury recovery "by tapping into natural repair and neuroprotection". It could also potentially help with healthy aging and longevity. A medical device with a hand pointing to a blood sugar meter for diabetes. A medical device with a hand pointing to a blood sugar meter for diabetes. MarcelaTo narrow down the regions involved, the researchers used multiple independent whole-genome technologies to ask which regions might be relevant for hibernation, before looking for overlap between the results from each technique. For example, they looked for sequences of DNA that most mammals share but had recently changed rapidly in hibernators. They also found the genes that act as central coordinators or "hubs" of these fasting-induced changes to gene activity. They discovered that many of the DNA regions that had recently changed also appeared to interact with these central hubs. Hence, the researchers expect that the evolution of hibernation requires specific changes to the controls of the hub genes—helping to narrow down further the DNA elements that are worth further investigation. Crucially, most of the hibernator-associated changes in the genome appeared to "break" the function of specific pieces of DNA, rather than make new functions. This suggests hibernators may have lost constraints that would otherwise prevent extreme flexibility in the ability to control metabolism. "In essence, we're learning to unlock a dormant resilience code in the human genome, using lessons from species that have mastered the art of survival under extreme conditions. It is a big idea that needs much more work to be tested," said Gregg. He said their next areas of focus include testing their "genomic brakes" hypothesis further and exploring the hibernation hub genes and potentially developing them as novel drug targets that enable them to develop medicines that promote metabolic health and neuroprotection. They are also studying hibernation mechanisms in cancer cell evolution and treatment resistance. Do you have a tip on a health story that Newsweek should be covering? Do you have a question about diabetes? Let us know via health@ Reference Ferris, E., Gonzalez Murcia, J. D., Rodriguez, A. C., Steinwand, S., Stacher Hörndli, C., Traenkner, D., Maldonado-Catala, P. J., & Gregg, C. (2025). Genomic convergence in hibernating mammals elucidates the genetics of metabolic regulation in the hypothalamus. Science, 381(6663), 494–500. Steinwand, S., Stacher Hörndli, C., Ferris, E., Emery, J., Gonzalez Murcia, J. D., Rodriguez, A. C., Spotswood, R. J., Chaix, A., Thomas, A., Davey, C., & Gregg, C. (2025). Conserved noncoding cis elements associated with hibernation modulate metabolic and behavioral adaptations in mice. Science, 381(6663), 501–507.
Yahoo
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Scientists Find 2 Existing Drugs Can Reverse Alzheimer's Brain Damage in Mice
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