Thursday, June 04, 2026

 

Rising seas could ‘drown’ mangroves and release carbon




University of Exeter
Mangroves at Cispata Bay 

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Mangroves – like this one at Cispata Bay – are efficient carbon sinks, but they may drown and lose their ability to store carbon under sea-level rise. 

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Credit: Luisa Gomez Vargaz





Mangroves could store less carbon – and even begin releasing it – as sea levels rise, new research suggests.

Mangroves are made up of salt-tolerant plants that grow in coastal areas. They cover less than 1% of Earth’s surface but store about 15% of all ocean carbon, most of it in their soils. This ability to store carbon makes them important in efforts to limit climate change.

Previous research has suggested rising seas could increase carbon storage in mangroves, but the new study challenges this.

The research team, led by the University of Exeter with partners in Colombia and the United States, developed a new model to assess how sea-level rise will affect carbon storage across entire mangrove forests.

The findings show that, while carbon storage might increase in localised spots as sea levels rise, storage at the scale of whole forests is likely to decline over the next 100 years.

“Mangrove forests are efficient carbon sinks and are therefore crucial for slowing climate change,” said Dr Arya Iwantoro, who carried out the research at the University of Exeter and is now based at the University of Plymouth.

“Research about carbon storage in mangroves is usually based on field observations, and such studies have found that carbon storage can increase as sea levels rise.

“But this may not reveal the wider picture of what is happening across the forest as a whole.

“To investigate this, we developed a new model that links water flow and sediment transport, mangrove growth and dieback, and carbon storage while keeping track of changes in the composition of muddy beds where mangroves grow.

“In effect, we created three models in one to assess the way these complex ecosystems may respond to rising seas.”

The results suggest that sea-level rise will initially trigger more carbon accumulation in some locations, but will reduce carbon storage in the forest as a whole.

“Mangrove plants are highly specialised, and they require a certain duration of flooding with each tide,” said Luisa Fernanda Gómez Vargas, also from the University of Exeter.

“If this period is exceeded, a location will no longer be suitable – the plants will ‘drown’ and mangroves will die back.

“Mortality and erosion of carbon-rich soils can turn mangroves from a carbon sink (storing carbon) into a source (releasing it).”

The study assessed the impact of different sea-level rise scenarios from the Intergovernmental Panel on Climate Change (IPCC), and found that greater sea-level rise leads to stronger negative impacts on mangrove carbon storage.

Dr Barend van Maanen, who leads the mangrove and carbon project at Exeter, said: “Mangroves face an uncertain future due to climate change and other human impacts on rivers and coasts.

“As well as being vital carbon stores, mangroves protect coasts from storms, provide livelihoods to coastal communities and habitats for a wide range of species.

“Our findings emphasise that understanding the coastal landscape as a whole is crucial when predicting how mangroves might respond to climate change, and how we can protect them.”

The study was funded by the Natural Environment Research Council.

The paper, published in the journal Earth’s Future, is entitled: “The importance of scale in the future of mangrove blue carbon under sea-level rise.”


Channels are a typical feature of mangrove landscapes, but they can expand and erode carbon-rich soils as sea levels rise. Cispata Bay mangrove

Credit

Luisa Gomez Vargaz


Air pollution may be harming your brain’s ‘encyclopedia’


Particulate air pollution and domain-specific cognition among Black adults

Fine air pollution (PM2.5) is linked to lower semantic memory — the type of memory used for facts, words and general knowledge




University of California - Davis Health





(SACRAMENTO, Calif.) — A new study by researchers at UC Davis Health and Kaiser Permanente found that higher exposure to very small air pollution particles (PM2.5) over a 17-year span was associated with lower semantic memory. Semantic memory acts like the brain’s “encyclopedia” for things like facts, words and long-term general knowledge.

“Semantic memory is essential for communication, comprehension and navigating everyday life,” said senior author Kathryn Conlon, an associate professor in the UC Davis Department of Public Health Sciences. “Our findings suggest that long-term exposure to air pollution doesn’t just affect physical health — it may also shape how the brain ages, particularly in ways that matter for independence and quality of life.”

Two other measures of cognitive function — executive function and verbal episodic memory — did not show an impact related to the pollution.

The findings were published in Alzheimer’s & Dementia: Behavior & Socioeconomics of Aging.

Reducing air pollution may reduce dementia burden

The data for the research comes from the Kaiser Permanente Study of Healthy Aging in African Americans (STAR). Launched in 2017, the ongoing study aims to identify factors that impact healthy brain aging among Black adults.

Black adults in the United States experience 1.5 to 2 times higher rates of Alzheimer's disease and other dementias compared with non-Hispanic White adults.

In the new study, the researchers focused on particulate matter (PM), a mixture of solid particles and liquid droplets found in the air. Particles less than 2.5 micrometers in diameter (about 1/30th of a human hair) are referred to as PM2.5, or fine particulates.

Previous research has linked PM2.5 to cardiovascular disease and mortality; however, a growing area of study is focused on the role of fine particulate exposure in the progression of Alzheimer's disease.

Methods and findings

The researchers analyzed data from 740 adults, aged 53 to 94, who were participants in the STAR study. Individual-level long-term average PM2.5 exposures were computed by averaging daily estimates of PM2.5 levels at the participants’ residential addresses.

Cognitive performance was assessed for semantic memory, verbal episodic memory and executive function. They evaluated associations with 5-, 10-, and 17-year average PM2.5 exposure.

The researchers found:

  • People who were exposed to higher levels of PM2.5 pollution over many years scored noticeably lower on semantic memory tests than those exposed to lower levels of pollution.
  • The association with PM2.5 pollution persisted even after accounting for other factors such as age, education, income and marital status.
  • The effect of long-term PM2.5 exposure on semantic memory was greater than what researchers would expect from 10 years of normal aging.

Lowering air pollution could lower Alzheimer’s burden

Long-term exposure to air pollution has been shown to cause greater harm to under-resourced communities. In addition, studies led by the U.S. Environmental Protection Agency (EPA) have found that people who are Black, Latino or Asian are more likely to live in areas with higher levels of particulate air pollution.

“Understanding environmental contributors to cognitive decline is critical for addressing disparities in dementia risk,” said Rachel Whitmer, co-author of the study and the co-director of the Alzheimer’s Disease Research Center at UC Davis Health. “Air pollution is a modifiable exposure. That makes it a powerful target for prevention — both at the individual level and through public policy.”

How individuals can reduce exposure to air pollution

While air pollution is largely a community-level issue, there are many ways individuals can reduce their exposure to air pollution:

  • Check daily air quality forecasts on AirNow. The EPA website lets you enter your ZIP code to find out about air quality, which accounts for fine particulates, in your area.
  • Limit outdoor activity when pollution levels are high, especially during wildfire smoke events.
  • Use high-efficiency (HEPA) air filters indoors.
  • Keep windows closed on poor air quality days.
  • Avoid exercising near busy roads or heavily trafficked areas.
  • Use recirculated air settings in vehicles during heavy traffic or smoky situations.

Resources

 

McMaster researchers discover a new antibiotic — and a new way to kill drug-resistant bacteria




McMaster University





Researchers at McMaster University have discovered a new antibiotic that kills some of the world’s most dangerous and drug-resistant bacteria — and does so by targeting a previously unknown vulnerability, opening the door to an entirely new class of treatments.

The new compound, called manikomycin, was identified by a team led by McMaster Professor Gerry Wright and has shown early effectiveness against priority pathogens including Salmonella, E. coli, and Klebsiella.

Unlike any antibiotic currently used in clinics, it works by blocking the exit site of the ribosome, the protein-producing machinery found inside every bacterial cell.

The discovery, published on June 3 in Nature, marks the fourth new antibiotic candidate from Wright’s lab in just over a year, underscoring a promising new approach to drug discovery at a time when antibiotic resistance is a growing global threat.

“Not a single antibiotic prescribed in clinics today does what manikomycin does,” says Wright, a member of the Michael G. DeGroote Institute of Infectious Disease Research. “Not azithromycin, not tetracycline — none of them. So, we’ve not only found a brand-new drug candidate, but we’ve also established a brand-new target in bacteria that could potentially be exploited with other new drugs.”

It’s the latter part of the discovery that has researchers most excited. Wright notes that because most antibiotics used today target the same handful of vulnerabilities on the ribosome, bacteria have evolved broad defense strategies against such attacks; however, drugs that attack a different part of the ribosome — the exit site — leave them defenceless.

“Even newly discovered drugs that attack those same old targets may quickly face resistance,” says Wright, a professor in McMaster’s Department of Biochemistry and Biomedical Sciences. “But, over the history of medicine, we’ve put absolutely no selective pressure on this particular target, so bacteria have no existing resistance mechanisms for manikomycin.”

Wright likens the ribosome to a factory assembly line. Finished components, he says, must be moved off of the line before the next piece can advance. Manikomycin blocks the exit lane, causing the entire assembly process to jam and eventually grind to a halt. And, without the ability to produce proteins, bacteria cannot survive.

The discovery of manikomycin builds on work that began more than 75 years ago, when scientists first discovered that the soil bacterium Streptomyces rimosus produced oxytetracycline, a powerful new drug that would help usher medicine into the antibiotic age.

While the breakthrough was one of several like discoveries made in the mid-1900s, S. rimosus and related bacteria have long since been abandoned as a potential source of new antibiotics.

“There is an overwhelming perception in science that these bacteria have been mined completely dry — that we’ve found all there is to find,” Wright says. “Our lab has found that this is not at all the case.”

Wright’s group, working with collaborators at the University of Illinois Chicago and the University of Hamburg in Germany, used an advanced laboratory technique called fractionation to uncover the new antibiotic. By filtering out oxytetracycline and other abundant compounds from the chemical mixtures produced by S. rimosus, the researchers were able to isolate scarcer molecules that had gone unnoticed over the years.

Manpreet Kaur, a postdoctoral fellow in Wright’s lab and first author on the new study, says that finding a viable new drug candidate this way signals new opportunities for antibiotic discovery. 

“There is likely so much still to be discovered through fractionation,” says Kaur. “Revisiting the extracts of even-well studied bacteria like Streptomyces may lead to similar discoveries in the future.”

Wright’s team is now advancing manikomycin toward clinical development. They have already shown that the new antibiotic is not toxic to human cells, and that it works well in a lab-controlled model of infection — both key milestones on the early development pathway.

They are now working on optimizing the drug’s “residency time” — or how long it stays active in the body — and have produced 60 different derivatives with plans to push the best one forward.

“We’re excited about this molecule’s potential,” Wright says. “There’s a clear path forward, and we may even be able to expand its spectrum so that it eventually affects even more bacteria, too.”

This research was supported by funding from the Canadian Institutes of Health Research.


How honeybees really crown their queens


Royal cribs and ladies-in-waiting: new details about the creation of bee royalty


University of California - Riverside

Royal crib 

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Hatching queen surrounded by royal guards. 

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Credit: More than Honey/Markus Imhoof





For generations, scientists believed a queen honeybee was made almost entirely by diet: feed an ordinary larva enough royal jelly and a ruler emerges. But new research suggests queens are created through a more elaborate process.

Young worker bees construct specialized nursery chambers complete with custom wax, warmer temperatures, and devoted attendants that help determine whether a larva becomes royalty.

Published today in the journal Nature, the study found that wax chambers where future queens develop, called queen cells or “royal cribs,” are not simply protective shelters, but carefully engineered environments essential to producing healthy queens. Researchers identified a previously unrecognized class of young worker bees dubbed “queen cell builders” that appear uniquely adapted for the task.

“The old idea was relatively simple: take an egg, move it into a queen cell, feed it royal jelly, and you get a queen,” said Boris Baer, entomologist and director of the Center for Integrative Bee Research (CIBER) at the University of California, Riverside, whose laboratory contributed to the work. “What we found is that there’s an entire machinery behind this process. It’s much more sophisticated than we imagined.”

Honeybee queens and workers begin life the same way: as nearly identical eggs. Yet queens grow larger, mature faster, and live dramatically longer than worker bees. They are also the colony’s sole egg layer, responsible for producing the next generation of bees.

Scientists have long credited royal jelly, a milky, nutrient-rich substance worker bees feed to young larvae, as the primary force behind that transformation.

The new study suggests food is only part of the story.

Using thermal imaging, behavioral tracking, materials science, and chemical testing, the researchers found that queen cells differ sharply from the familiar hexagonal chambers used to rear worker bees.

The peanut-shaped queen cells are built from wax with distinct physical and chemical properties, making them less dense, more pliable, and better able to maintain warmth and moisture for developing larvae. The wax also differed in its fatty acids and chemical signals, creating what researchers describe as a specialized developmental environment.

To test whether the nursery itself mattered, the researchers raised developing queens in cells made either from queen wax or ordinary worker wax. Larvae raised in worker wax were more likely to die and grew into smaller queens, even when fed the same diet, suggesting that the surrounding environment plays a critical role in development.

The study also revealed the workers behind the process. Queen cell builders, typically younger than other hive workers, maintain elevated body temperatures and altered physiology while tending future queens. The extra warmth appears to speed development: queen bees mature in about 16 days, compared with roughly 21 days for worker bees, an advantage when a colony urgently needs a new ruler.

Rather than simply recycling wax, the bees actively gather, modify, and enrich materials for royal chambers. They also activate different biological processes tied to wax production, essentially changing how their bodies function while tending future queens.

Researchers even tracked how the bees repurposed material from elsewhere in the hive. By adding trace amounts of graphite to ordinary honeycomb, the team showed that darkened wax eventually appeared in queen cells, evidence that workers were selectively gathering and transforming material for royal use.

The process, Baer said, resembles something closer to a royal court than a simple insect nursery. It is clear that bees execute a tightly coordinated effort devoted to producing the colony’s next ruler.

“You can think of it as something like Buckingham Palace,” he said. “There is a dedicated group of bees focused entirely on raising the queen, and if they don’t get it right, the colony cannot reproduce.”

The researchers found the same pattern in both Asian and European honeybee species, suggesting the strategy may be deeply rooted in honeybee evolution.

This work brought together researchers with expertise ranging from behavior and physiology to materials science, chemistry, and genomics. It was led by two former UCR postdoctoral researchers, Yu Fang and Yahya Al Naggar. “In its collaborative nature, this project reflects the broader CIBER philosophy of bringing different disciplines together to tackle complex biological questions,” Baer said.

Beyond honeybees, the findings may change how scientists think about development more broadly, including the ways surroundings, social groups, and built environments shape biology.

For decades, queen bees seemed to offer one of biology’s simpler stories: special food makes a special insect. The new findings suggest that a queen emerges not from diet alone, but from an entire society working together to shape her future.

“This work highlights how much sophistication exists inside insect societies,” Baer said. “Honeybee colonies are not simply collections of individuals. They function as integrated biological systems capable of engineering their own environments.”


Queen cell 

A queen cell with the royal guard attendants. 

Credit

Fang Yu/UCR

 

It may not just be what’s in ultra-processed foods, but how they’re made



New observational study suggests processing itself could partly explain links to diabetes, heart disease, and early death




Tufts University

Ultra-processed foods in a grocery store 

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"Addressing structural and policy-related barriers to accessing fresh and minimally processed foods remains critical for promoting dietary changes that improve the health and life span for all Americans,” said Dariush Mozaffarian, cardiologist and director of the Food is Medicine Institute at the Friedman School of Nutrition Science and Policy at Tufts University.

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Credit: Imani Khayaam for Tufts University





Concerns about the health effects of ultra-processed foods are growing, as studies increasingly link them to conditions such as heart disease, diabetes, and even early death. But scientists are still debating what’s driving those risks: the nutritional quality of these foods—which are often high in saturated fat, sodium, and added sugars—or the industrial processing and additives used to make them. 

A new study from researchers at the Food is Medicine Institute at the Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy at Tufts University, published in American Journal of Public Health, suggests the processing itself may play an independent role. The researchers found that people who ate more ultra-processed foods had worse health outcomes, even after accounting for the overall nutritional quality of the foods. 

“The findings suggest ultra-processed-food factors beyond nutrients—such as changes to foods’ cellular structure, loss of beneficial chemical compounds, additives, and chemicals from packaging—may create health risks not addressed by traditional nutrition metrics or policies,” said the study’s senior author, Dariush Mozaffarian, cardiologist and director of the Food is Medicine Institute. 

For the observational study, the researchers analyzed data from 10 consecutive cycles of the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018, linked to National Death Index through 2018. Study participants had completed one or two 24-hour dietary recalls. 

Using a standard classification system, the team grouped foods based on how they were made—from minimally processed food-based ingredients like fruits and vegetables to ultra-processed products made with industrial ingredients and additives not typically used in cooking. The researchers also rated the nutritional quality of foods using a system that scores foods based on their overall healthfulness. Each participant received an overall diet-quality score based on the foods they reported eating. The team then examined how ultra-processed food consumption was linked to current health measures—such as weight, blood sugar, and cholesterol—as well as long-term risk of death.  

For every 10% increase in calories from ultra-processed foods, the researchers found worse health markers. People who ate more of these foods tended to have higher body weight, worse blood sugar control, higher blood pressure, and less favorable cholesterol levels. They were also more likely to have conditions such as diabetes, metabolic syndrome, and cancer and had a slightly higher risk of dying during the study period. 

These links remained even after researchers accounted for reported foods’ nutrient quality and the amounts of saturated fat, added sugar, or sodium present in the ultra-processed foods. The patterns were largely the same across different subgroups of people. 

“Ultra-processed foods make up a substantial portion of the American diet, accounting for more than 50% of adults’ and about 60% of children’s caloric intake,” said Juna Hatta-Langedyk, first author and an undergraduate biology student at Tufts. “Understanding how these foods affect health is a critical public health priority, given the large proportion of the population affected.” 

“Addressing structural and policy-related barriers to accessing fresh and minimally processed foods remains critical for promoting dietary changes that improve the health and life span for all Americans,” said Mozaffarian. “Our findings can help inform many current policy efforts, such as a national definition of ultra-processed foods, and multiple states’ endeavors to propose and pass laws addressing ultra-processed foods, including warning labels, bans on certain additives, and limits in school meals.”  

Lu Wang, Bingbing Fan, and Peilin Shi from the Friedman School of Nutrition Science and Policy are also co-authors on this study. Research reported in this article was supported by the National Institutes of Health’s National Heart, Lung, and Blood Institute under award number R01HL115189, as well as by an American Diabetes Association’s Pathway to Stop Diabetes award and the Laidlaw Foundation’s Laidlaw Scholars Leadership & Research Programme. Complete information on methodology, limitations, and conflicts of interest is available in the published paper. 

The content is solely the responsibility of the authors and does not necessarily represent the official views of the funders.