It's been a hot and muggy week with smoke from fires in the north clouding the atmosphere. Some nights in the last few days have been quite cool however. July often is the beginning of a late summer drought, but not this year, so far. Still plenty of rain and no need for garden watering. Rabbits and squirrels abound in plenty. It seems the robins are feeding a second brood of the year. Mosquitos, are plentiful enough
my favorite day lily
bee balm, it took me years to find this colour
another daylily
the small bed around the street number sign is coming along.
peachy, lol
One of the few plants I bought, this one from Holland years ago.
Astilbe
St. John's wort, at Rachelle's used in herbal remedies.
Dead cells after self-destructing, with the small green circles showing the F-ApoEVs left behind.
(La Trobe University)
The cell churn that goes on inside our bodies is vast, with hundreds of billions of cells dying off and being replaced every day. Keeping that constant biological overhaul running smoothly is crucial in maintaining good health.
Researchers have now identified a new 'footprint of death' that cells leave behind as they die to guide the immune system in its waste-removal role.
It seems this process can also be hijacked by viruses to spread themselves further.
The discoveries, published in a recent study in Nature Communications led by a team from La Trobe University in Australia, have implications for understanding how programmed cell death and renewal keep us healthy.
Illustration showing how the 'footprints of death' (smaller pink blobs) are left behind by dying cells.
(Rutter et al., Nat. Commun., 2026)
Further down the line, it may also be possible to develop drug treatments that make use of these death footprints – and prevent them from being infiltrated by viruses.
"Billions of cells are programmed to die each day as a part of normal turnover and disease progression, and until now, it was believed that the cell fragmentation process during cell death was random and fairly simple," says biochemist Ivan Poon, from the La Trobe Institute for Molecular Science (LIMS).
"Our findings demonstrate the complexity of this process and highlight how each step in the process is actually critical to help the dying cell break down efficiently and to be cleared away by the immune system."
A process called apoptosis is often used to schedule cell death in the body, taking out cells that are no longer needed, damaged, or potentially harmful. It was this process that the new study took a closer look at.
Using 3D timelapse imagery to analyze different types of cells as they died, the researchers identified the proteins left behind by apoptosis, and the way the immune system subsequently interacted with them.
https://www.youtube.com/watch?v=Ft-2LCqmdQY
As expected, the death debris included extracellular vesicles (EVs), small pockets of proteins, DNA, and RNA that cells shed to signal to each other.
In this case, the researchers spotted a previously unknown type of EV, which they're naming F-ApoEVs: footprint of death-derived, apoptosis-triggered EVs.
These F-ApoEVs act a little like a trail of breadcrumbs that the immune system can follow to clean up cells that have perished.
"We know that the body clears away dead cell fragments to prevent them lingering and causing inflammation and autoimmune diseases such as Systemic Lupus Erythematosis, and we saw F-ApoEVs are readily cleared from the site of cell death," says lead researcher Stephanie Rutter, a biochemist from LIMS.
"What we didn't expect was how viruses can also take advantage of this process and cause infection by hiding in F-ApoEVs."
When the researchers infected dying cells with influenza, the virus hid some of its particles inside the F-ApoEVs. As the immune system cleans up after the cell, these pathogen fragments get spread to neighboring, healthy cells.
It's a new way for viruses to spread that we haven't seen before.
These mechanisms still need testing and analyzing outside of a lab, but potential treatments could improve F-ApoEVs function to better protect against autoimmune diseases and to stop viral spread.
"This study has revealed that dying cells can continue to communicate from the grave and may impact immune function," says cell biologist Georgia Atkin-Smith, from the Walter and Eliza Hall Institute of Medical Research in Australia.
Fundamentally, these processes are all about communication: cells talking to each other and all staying on the same page in terms of biological maintenance.
There's now another element to that communication that can both support and potentially damage health. Future research could help scientists get more clarity on exactly how F-ApoEVs work and how they might be manipulated.
"Understanding this basic biological process could open new avenues of research to develop new treatments that harness these steps and help the immune system better fight disease," says Poon.
Empty Manila clam shells blanketing the intertidal zone in Boston Harbor’s Spectacle Island.
Credit: Aly Putnam
A research team found reproducing populations of Manila clams in Cape Cod and Boston Harbor.
A stretch of Atlantic shoreline that had remained free of Manila clams now appears to support reproducing populations of the invasive shellfish.
Biologists led by the University of Massachusetts Amherst, MIT Sea Grant at the Massachusetts Institute of Technology and the Center for Coastal Studies confirmed that Ruditapes philippinarum has established itself along the northwestern Atlantic coast. Published in Biological Invasions, the findings capture a rarely documented stage of biological invasion, when a species is first becoming established and beginning to spread through a new region.
Manila clams are native to waters extending from Russia’s Sakhalin Islands through Japan and southern China. Since at least the early 20th century, however, people have introduced them both intentionally and accidentally to the Pacific coast of North America and to Europe, allowing the species to spread across much of the Northern Hemisphere.
The clams are widely valued as food and support an industry worth about $7 billion annually. At the same time, dense populations can compete with native shellfish, hybridize with related species, and alter surrounding ecological communities.
Co-author Bastidas in Squantum, Massachusetts, holding a native quahog clam. Mussels and Manila clams are visible in the tray.
Credit: Carolina Bastidas
Their arrival may also bring some benefits. Manila clams can provide abundant food for seabirds, crabs, raccoons, and other animals that prey on shellfish.
“Given that Manila clams are everywhere else in the northern hemisphere, it was only a matter of time before they showed up here, and we’ve been keeping an eye out for them,” says marine scientist Aly Putnam, who is a postdoctoral researcher at UMass Amherst and lecturer at Smith College, as well as the paper’s lead author.
A text message starts the search
The Northeastern U.S. had represented the last major gap in the Manila clam’s Northern Hemisphere range. Evidence that the species had reached this coastline emerged from something remarkably ordinary: a text message.
During the summer of 2025, Putnam was leading a small workshop on intertidal biodiversity at Spectacle Island in Boston Harbor when El Fernekees Hartshorn sent her a photograph of an unfamiliar clam. Fernekees Hartshorn, a recent University of Rhode Island graduate who had worked with Putnam on regional Rapid Assessment Surveys for marine invasive species, suggested that the shellfish might be a Manila clam. Fernekees Hartshorn is also a co-author of the paper.
Aly Putnam holding a baby Manila clam, much smaller than a thumbnail. Newly born clams are evidence that the species has established itself.
Credit: Aly Putnam
Carolina Bastidas, a research scientist with MIT Sea Grant and Putnam’s co-investigator, was also participating in the Spectacle Island trip. The two began searching the shoreline for Manila clam shells and soon found them in large numbers.
At the same time, another group led by Owen Nichols of the Center for Coastal Studies had been following separate reports. Beginning in 2023, local clammers had described finding “weird clams” around Provincetown at the northern end of Cape Cod and at other locations across the Cape.
The Boston Harbor and Cape Cod investigations might have continued independently if James T. Carlton had not connected them. Carlton, an emeritus professor of marine sciences at Williams College and a leading authority on invasive marine species, learned about the shells found on Spectacle Island and urged Putnam and Bastidas to determine whether they represented an established population rather than discarded food or bait.
“Find me living clams,” he told the group—especially baby clams and clams that showed evidence of having reproduced.
Co-author Owen Nichols (l), from the Center for Coastal Studies, conducting field research along with Jess Mateik (center) and fisherman Dave Seitler, one of the first to report “weird clams” in Cape Cod.
Credit: Owen Nichols
Young clams confirm a new population
Putnam and Bastidas soon found the evidence Carlton requested. After spending hours digging at Squantum in Quincy and Calf Pasture Park in Boston, the researchers used sieve-based sampling to recover dozens of small living clams. The juvenile specimens showed that Manila clams had recently reproduced and that young clams were joining the population.
Nichols’s group then investigated the unusual clams reported around Cape Cod. They found female Manila clams that also showed evidence of reproduction, strengthening the case that the species was established at multiple locations rather than appearing only as isolated individuals.
Co-author El Fernekees Hartshorn with a baby Manila Clam. Their text message to Putnam launched this investigation.
Credit: El Fernekees Hartshorn
“When I learned about what each group was working on,” Carlton says, “I realized that this was a golden opportunity to not only combine forces but also to catch a detailed snapshot of the moment a new invasive species establishes itself.”
“As a marine biologist, I have worked with invasive species and with Rapid Assessment Surveys from the Northeast Aquatic Nuisance Species (NEANS) Panel for 11 years now,” says Bastidas. “Collaboration is invaluable for these sorts of efforts, and the fact we had already a network of people looking into Manila clams, means that we could catch them at the moment they established themselves.”
The ecological consequences remain uncertain
Researchers do not yet know how Manila clams reached the northwestern Atlantic or what their establishment could mean for coastal waters in the Northeastern U.S. Their presence could affect commercial shellfishing, native species and broader ecological relationships, but the direction and scale of those effects remain unclear.
Putnam (l) and Bastidas (r) conducting a winter sample.
Credit: Aly Putnam
Bastidas says, “We do need more research to understand the Manila clam’s potential effects on the shellfishing industry and ecological communities. On the positive side, because Manila clams can become a source of food for other animals, they can relieve pressure on native species—for example, the predatory pressure of green crabs on softshell clams. So, there could also be positive impacts.”
“Discoveries like this remind us how much there is still a lot to learn about our coastal ecosystems,” said Putnam. “Finding the species is only the beginning. Now we are working to understand its distribution, if these populations are expanding and how these clams interact with other species in New England coastal systems. This research will help us determine whether this newcomer becomes a minor addition to the ecosystem or a more influential player in the years ahead.”
Human Chest Cavity illustration: Right lung, left lung, heart.
Credit: American Heart Association
A gum disease bacterium may contribute to aortic valve calcification through inflammation, according to preliminary human tissue and mouse research.
A bacterium best known for damaging gums may also be involved in the hardening of the heart’s aortic valve. Preliminary research presented at the American Heart Association’s Basic Cardiovascular Sciences Scientific Sessions 2026 points to a possible biological connection between chronic periodontal disease and a serious heart valve disorder.
The condition, called calcific aortic valve stenosis (CAVS), develops when calcium accumulates in the aortic valve, causing it to thicken and narrow. Because this valve controls blood leaving the heart, the narrowing can restrict circulation throughout the body.
CAVS may cause no noticeable problems at first. As it advances, however, patients can develop fatigue, chest pain, shortness of breath, fainting, heart failure, and premature death. Severe cases are generally treated by replacing the damaged valve because no medication has been proven to stop or slow the disease.
The researchers identified a possible pathway through which long-term gum infection could contribute to valve calcification.
4 chambers of the heart: right atrium, right ventricle, left atrium, left ventricle.
Credit: American Heart Association
“There are currently no medications proven to prevent or slow the progression of CAVS. We hope our findings demonstrating the link between periodontal disease and CAVS will stimulate further research into new preventive and therapeutic approaches for this condition,” said co-lead author of the study, Chenyang Li, M.D., a Ph.D. candidate in the department of cardiology at the State Key Laboratory of Cardiovascular Disease of Fuwai Hospital’s National Center for Cardiovascular Diseases, the Chinese Academy of Medical Sciences and Peking Union Medical College all in Beijing.
A gum bacterium emerges as a suspect
The investigation centered on Porphyromonas gingivalis (P. gingivalis), a bacterium that plays an unusually influential role in gum inflammation and the breakdown of tissue supporting the teeth.
Chenyang Li, M.D., a Ph.D. candidate in the department of cardiology at the State Key Laboratory of Cardiovascular Disease of Fuwai Hospital’s National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College in Beijing.
Credit: Chenyang Li
Previous research has also connected P. gingivalis with inflammation beyond the mouth and with cardiovascular problems, including plaque buildup inside arteries and coronary artery disease. That history made it a plausible candidate for examining the possible link between periodontal disease and damaged heart valves.
Diseased valves contained more bacteria
The researchers first turned to human tissue for evidence. They measured bacterial levels in heart valves removed during replacement surgery, comparing samples from patients with CAVS with samples from people who had other valve disorders.
The goal was to determine whether particular microbes appeared more often in calcified valves. P. gingivalis was not the most common bacterium detected, but its presence differed sharply between valves affected by CAVS and those without the condition.
“We were surprised by how much P. gingivalis was present in the calcified aortic valves,” Li said. “Although it was not one of the most abundant bacteria overall, it showed one of the largest differences between valves with CAVS and valves without CAVS. This unexpected finding led us to investigate its potential role in the development of CAVS.”
The human tissue findings could show an association, but they could not establish whether the bacterium contributed to calcification. To explore that question more directly, the researchers moved to experiments in mice.
Inflammation drove calcification in mice
The researchers exposed mice to either live P. gingivalis or bacteria that had been inactivated by heat. They then examined whether the microbe accumulated in the aortic valve, increased calcium deposits, and produced signs resembling aortic stenosis.
Some animals received antibiotics to test whether reducing the bacteria would change the outcome. In another group, the researchers genetically removed or disabled the inflammatory pathway involving interleukin-1 beta (IL-1β).
Interleukin-1 beta is a signaling protein produced mainly by immune cells. It helps trigger inflammation, the body’s response to infection or injury, but excessive or persistent activity can also damage tissues.
Repeated exposure to live P. gingivalis caused the bacterium to build up in the aortic valves of the mice. The animals also developed more valve calcification and stronger signs of aortic stenosis. Preventive antibiotic treatment reduced those effects.
Inside mouse valve cells, P. gingivalis activated interleukin 1 beta (IL-1b), providing a possible explanation for how infection could encourage calcium buildup.
The researchers then removed IL-1b genetically. Even when P. gingivalis remained present, the mice developed substantially less valve calcification and fewer symptoms, suggesting that the inflammatory pathway played an important role in the damage.
The human link still needs testing
The results do not yet show that P. gingivalis causes CAVS in people. The human tissue analysis identified an association, while the experiments demonstrating a possible mechanism were performed in mice.
“The key message is simple: take good care of your oral health,” Li said. ”Good oral hygiene and treatment of periodontal disease are important for overall health and may also have benefits for cardiovascular health. While it is still too early to recommend specific treatments for preventing CAVS, our findings suggest that periodontal health could be an important piece of the puzzle.”
“This study adds to the growing evidence that oral health and heart health are closely connected,” said Eduardo Sanchez, M.D., M.P.H., FAHA, chief medical officer for prevention for the American Heart Association. “For many people, regular visits to the dentist are their only connection to the healthcare system. That makes dental professionals important partners in spotting health conditions, including periodontal disease early — which can lead to quicker healthcare referrals and results, better health and lives saved.”
Because the findings have not been confirmed in people, they remain preliminary. The researchers have begun a clinical study to investigate whether gum disease and P. gingivalis are linked to CAVS in human patients.
The dome of the Pantheon in Rome is one of the most famous examples of ancient Roman engineering.
(Livioandronico2013/ Wikimedia Commons, CC BY-SA 4.0)
The arrow of time flies one way, and with it comes decay.
We build our structures to last as long as possible, but even the toughest materials eventually crack, weaken, and crumble.
Ancient Roman concrete did things a little differently.
Scientists have long known that the concrete built during the Roman Empire seems to grow stronger over time.
Previous research suggested this extraordinary durability was largely due to a reaction between volcanic ash, called pozzolan, and quicklime, which produced exceptionally resilient minerals within the concrete.
Now, scientists have discovered that there's another part of the story: the slow yet steady reactions of carbon dioxide from the air.
"While the pozzolanic reaction is of fundamental importance," says engineer Paulo Monteiro of UC Berkeley, "our findings suggest that carbonation over a long period of time also enhances the durability of concrete and can help it seal cracks as it ages."
The team's discovery, detailed in Science Advances, gives us a new appreciation of even the more mundane Roman structures that were nevertheless imbued with engineering prowess.
https://www.youtube.com/watch?v=l1cofsNRGcE&t=42s
One of the wondrous things about Roman engineering is how many structures remain in excellent condition where so many contemporaneous buildings have fallen to rubble.
The Pantheon in Rome is the most famous example – a 2,000-year-old temple capped with an enormous dome of unreinforced concrete, the largest structure of its kind in the world.
But to discover the secrets of Roman concrete, Monteiro, his co-lead Xiaohong Zhu of Beijing University of Technology, and their colleagues turned to an unlikely, much less glamorous source.
In the 2nd century CE, the emperor Hadrian had a villa at Tivoli in Italy, much of which is still – you guessed it – standing.
From there, the researchers extracted a small piece of concrete from a communal toilet that once supported imperial bottoms.
Hadrian's villa, also known as Villa Adriana, in Tivoli, Italy.
(Anna Eden 86/Wikimedia Commons, CC BY-SA 4.0)
Using a suite of high-resolution imaging techniques, the researchers examined their sample down to the nanoscale.
As expected, they found evidence of the pozzolanic reaction, in which volcanic ash and lime react to form exceptionally durable minerals within the concrete.
But they found something else, as well.
Over centuries, carbon dioxide from the atmosphere had reacted with leftover lime in the concrete to produce calcite – the same mineral that can be found in limestone.
This was no mere by-product of the aging process, the researchers found.
The calcite appears to have made the concrete stronger. It crystallized within tiny pores and cracks, making the concrete denser and gradually sealing weaknesses that would otherwise have spread over time.
The concrete sample the researchers studied (left) and a cross-section (right).
(Zhu et al., Sci. Adv., 2026)
Earlier studies had identified calcite in Roman concrete, but had not studied it in three dimensions or mapped its architecture.
The work, the researchers say, suggests that calcite may have played an overlooked role in Roman concrete's incredible longevity – not replacing the known contribution from the pozzolanic reaction, but working alongside it.
Scientists had already been working on reproducing Roman concrete.
Carbonation happens naturally in lime-based concrete whether you know it's there or not, but understanding the role it plays could give researchers another tool as they try to engineer concrete that lasts longer while producing less carbon.
Latrines were a common feature at Roman settlements, ranging from double-seaters like this one in modern-day Algeria to lavish lavatories for dozens of people.
"Understanding how calcium carbonate crystallization dynamics bind concrete together and contribute to its long-term durability could provide new insights into the long-term mineralogical evolution and natural carbonation of lime-based binders," Monteiro says.
Ancient Roman structures from the grand Pantheon to Hadrian's humble toilet give us mind-blowing examples of concrete that has remained structurally sound for millennia.
That doesn't mean we can simply build as the Romans did.
Modern buildings place far greater demands on their materials, and reinforced concrete faces a challenge Roman engineers never had to contend with: the corrosion of the steel rebar embedded inside it.
What the new findings can do is help researchers as they try to design longer-lasting, more sustainable concrete for the future.
"This study shows how exploring ancient engineering techniques can lead to important revelations," Monteiro says.
"We hope that by unlocking Roman secrets for enhancing concrete durability, we can someday attain sustainable modern infrastructure development."
The Andean leaf-eared mouse has the same kind of muscle tissue as a marathon runner, one of multiple complex adaptations that allow it to survive in an extremely cold, inhospitable environment.
Credit: Marcial Quiroga-Carmona
A leaf-eared mouse living more than 6,700 meters (22,000 feet) above sea level in the Andes has shattered assumptions about where mammals can survive.
Near the summit of an Andean volcano, where the air contains barely half as much oxygen as it does at sea level, scientists found something that should not have been there: a living mouse.
The Andean leaf-eared mouse, Phyllotis vaccarum, has been documented above 6,700 meters (22,000 feet), higher than any other mammal known to live. At these elevations, freezing winds sweep across a landscape with almost no vegetation, liquid water, or obvious source of food.
Its presence has overturned a long-standing assumption about the upper limit of mammalian life. Scientists once believed mammals could survive only up to about 5,500 meters (18,000 feet), roughly the elevation of the world’s highest permanent human settlements.
“It was completely unexpected. People did not think mammals could survive at these altitudes, but they’re there,” says Graham Scott, a professor in the Department of Biology who co-authored the study.
How High-Altitude Mice Survive
Now, an international research team has uncovered how these small rodents endure an environment often compared to the surface of Mars. The answer is not one extraordinary trait. The mice have evolved an entire collection of physiological and genetic changes that work together.
Scott and fellow McMaster University biologist Grant McClelland joined researchers studying mice collected along the western Andes in Chile. The species has an unusually broad range, with populations living from sea level to mountain summits more than 6,700 meters (22,000 feet) high. This natural gradient allowed the team to compare extreme highland mice with members of the same species from lower elevations, as well as with a closely related lowland species.
In controlled experiments, the researchers recreated conditions equivalent to elevations approaching 7,000 meters (23,000 feet). The highland mice maintained their ability to generate heat far more effectively than the lowland animals, even when exposed to both severe cold and oxygen scarcity.
“Evolution is a complex process,” says McClelland, a co-author of the study and a professor in the Department of Biology. “When animals encounter really challenging environments, there are a lot of different things they need to cope with, not just the obvious ones.”
Built Like Endurance Athletes
The mice are especially good at keeping their bodies warm while continuing to use oxygen efficiently. That combination is crucial because producing heat requires energy, yet the thin mountain air limits the oxygen available to release that energy.
Their muscles also operate more like those of endurance athletes than short-distance sprinters.
“They’re more like a marathon runner than a sprinter,” explains Scott. “Their muscle cells are packed with mitochondria that allow them to sustain heat-producing activity for longer periods.”
Fat Fuels Life in the Cold
Mitochondria convert nutrients into usable energy. Having more of them allows the mice to maintain heat production for longer periods without quickly exhausting their muscles.
The animals also burn more fat. Fat provides a concentrated source of energy for shivering muscles and specialized tissues that produce heat without movement, helping the mice remain warm through prolonged exposure to freezing conditions.
Yet cold and oxygen were only part of the puzzle.
An Unexpected Diet at the Summit
At such extreme elevations, finding enough food may be just as difficult as breathing. The barren volcanic slopes support little plant life, forcing the mice to eat whatever becomes available. Their diet can include lichens growing on rocks, along with seeds or insects carried upward by the wind.
Genetic evidence suggests that highland populations have adapted to process these unusual foods. Researchers identified changes in genes involved in metabolism and in the removal of potentially toxic plant chemicals. The result suggests that reaching the highest summits required the mice to evolve not only a better respiratory and heating system, but also a digestive system capable of handling an unpredictable diet.
“We were initially focused on the most obvious environmental challenges, things like low oxygen and cold, but there were important factors we didn’t expect, including how these animals deal with what they’re eating,” says Scott.
Evolution Rebuilds the Whole Body
The study, published in Science, shows that extreme survival rarely depends on a single biological breakthrough. Instead, natural selection reshaped the animals’ muscles, metabolism, heat production, fuel use, and ability to tolerate unfamiliar foods.
That complexity may help explain how the species occupies an elevational range extending from the Pacific coast to some of the highest volcanic summits in the Andes.
“Sometimes our assumptions about the most extreme environments animals can live in can be questioned,” says McClelland. “Evolution has a lot of room to experiment.”
Lessons for a Changing Climate
The findings may also offer a lesson for species confronting rapid environmental change. Temperature is only one part of the challenge. Shifting climates can alter oxygen availability, food supplies, water, predators, and competition at the same time.
“We tend to focus on temperatures as the big challenge,” says Scott. “But animals are dealing with many pressures at once, and evolution may push them in ways we don’t always anticipate.”
RNAscope image of small intestinal crypts showing expression of intestinal stem cell markers Lgr5 (white) and Olfm4 (yellow), Clu+ revival stem cells (red), and ChgA+ enteroendocrine cells (green). Nuclei are counterstained with DAPI (blue).
Credit: The University of Texas MD Anderson Cancer Center
A gut bacterium appears essential to the intestinal repair benefits linked to fasting before radiation.
During radiation treatment for abdominal cancer, the therapy aimed at a tumor can also injure the delicate lining of the small intestine. That damage can lead to severe digestive problems and may restrict how much radiation a patient can safely receive.
The bacterium, Akkermansia muciniphila, or AKK, appears to work with metabolic changes caused by short-term fasting to place intestinal cells into a state that supports regeneration after radiation injury. The findings, published in Proceedings of the National Academy of Sciences, could eventually help researchers develop ways to protect healthy tissue during cancer treatment, although the work has not yet been tested in patients.
Helen Piwnica-Worms, Ph.D., professor of Experimental Radiation Oncology, and Kunal Rai, Ph.D., professor of Genomic Medicine, co-led the research.
“Fasting helps prepare intestinal cells to respond more quickly and effectively after injury, almost like training the cells with an emergency preparedness plan,” Piwnica-Worms said. “This study helps explain how that plan is organized and identifies a key bacterium involved in coordinating the response.”
Helen Piwnica-Worms, Ph.D.
Credit: The University of Texas MD Anderson Cancer Center
Intestinal damage can limit radiation treatment
Radiation therapy is frequently used against abdominal cancers, including pancreatic, colorectal, and gynecologic cancers. The difficulty is that the small intestine contains rapidly renewing cells that are especially vulnerable to radiation.
When the intestinal lining is injured, patients can experience nausea, diarrhea, and infection. Severe damage can lead to life-threatening complications, which may restrict the amount of radiation doctors can safely deliver.
Earlier preclinical research from the Piwnica-Worms Laboratory showed that fasting before treatment improved intestinal recovery after radiation. That result raised a more difficult question: what changed inside the intestine during fasting, and how did those changes prepare the tissue to repair itself?
Fasting recruits a key gut bacterium
The researchers found that fasting for 24 hours increased the abundance of AKK in the small intestine. That shift mattered because AKK produces propionate, a small molecule created when microbes process nutrients.
Propionate worked alongside other metabolic changes caused by fasting to modify histones inside intestinal cells. Histones are proteins that package DNA, much like spools organizing long threads. Small chemical tags added to these proteins can loosen or tighten access to particular genes without changing the underlying genetic code.
In this case, the tags helped expose genes connected with tissue regeneration. A group of intestinal cells that accumulated during fasting appeared to carry these repair programs in a more accessible state, leaving them prepared to respond once injury occurred.
After radiation exposure, those cells multiplied and helped rebuild the intestinal lining. The sequence offered the researchers a possible explanation for how fasting before treatment could influence recovery afterward.
Repair requires both fasting and AKK
To determine whether AKK was simply present during the response or actually necessary for it, the researchers selectively removed the bacterium. The protective benefit associated with fasting then disappeared.
Kunal Rai, Ph.D.
Credit: The University of Texas MD Anderson Cancer Center
Restoring AKK by itself was not enough. The regenerative response returned only when the bacterium was reintroduced together with fasting, indicating that the microbial and metabolic changes worked as a combined system.
The results suggest that fasting alters intestinal cells before radiation arrives rather than merely helping them recover afterward. By changing gut microbes, metabolism, and access to regeneration genes, the process may allow repair to begin more rapidly once tissue is damaged.
This connection between diet, microbes, and gene activity could help researchers understand how healthy tissues organize their response to injury. It may also point toward ways to reduce treatment-related harm while preserving the cancer-fighting effects of radiation.
Future studies will need to determine whether the pathway operates similarly in patients receiving abdominal radiation. Researchers also want to investigate whether it could protect other rapidly dividing tissues, including bone marrow, from damage caused by cancer treatment.
New therapies may avoid fasting
Fasting can be physically difficult or medically inappropriate for people undergoing cancer therapy. For that reason, the researchers are interested in reproducing its protective effects without requiring patients to stop eating.
Possible approaches could include treatments based on AKK, propionate, or other metabolites involved in the repair pathway. Dietary interventions might offer another way to influence the same biological response.
“Fasting is not always practical for cancer patients, and this work supports several other potential ways to enhance recovery after treatment,” Rai said. “Whether through dietary interventions, targeted microbes or their metabolites, the goal is to help repair healthy tissue more effectively while patients receive the cancer therapies they need.”
A photo of the baby T. rex puppet used in The Lost World: Jurassic Park.
(Michael Irving/ScienceAlert)
Jurassic Park was wrong. Again.
In the second movie, hunters find an infant Tyrannosaurus rex and use it to lure the adults into a trap.
But in reality, that baby would have been much smaller, about the size of a cat. And it probably wouldn't have been alone – the nest may have been absolutely crawling with dozens of them.
It likely wouldn't have been very useful as bait either: Its parents probably would have considered losing a baby or two as just part of the process, and wouldn't have cared enough to push a research trailer off a cliff.
So why are we updating our understanding of T. rex's childhood?
In a "vanishingly rare" discovery, paleontologists have found and closely examined fossils of tyrannosaur hatchlings. The remarkable findings are published in the journal Biology – and the implications go way beyond everyone's favorite dinosaur.
"Going through museum collections, my colleagues and I have discovered the first remains of hatchling tyrannosaurs," announced Nick Longrich, paleontologist and evolutionary biologist at the University of Bath in the UK.
A size comparison between Tyrannosaurus rex hatchlings and a modern cat.
(Longrich et al., Biology, 2026)
When people think of dinosaurs, they tend to think of giants with long necks craning into the treetops, huge horned herbivores duking it out, and of course, the biggest land carnivores the planet has ever known.
But we know far less about the smaller species of reptiles, mammals, and other dinosaurs that were running around underfoot. That's because not only did their remains fossilize less frequently than the behemoth's, but modern scientists also tend to favor the big, attention-grabbing bones.
"Paleontologists overlook these little remains, which are almost always isolated bones, in favor of larger and more complete skulls and skeletons," Longrich told ScienceAlert.
"There's just a bias in what people study. Partly the small isolated stuff is hard to study, and partly people just assume it's not that important, so it ends up stuck in a museum and neglected."
Longrich and his team set out to investigate these fragmented fossils gathering dust in storeroom drawers, expecting to find adult specimens of small dinosaurs. Instead, ironically, the work led the team back to the big guys.
One of the small bones appeared to be a third metatarsal – the middle foot bone – of a theropod dinosaur. But on closer inspection, it didn't look like it came from a fully grown animal.
"The surface of the bone was incredibly porous," Longrich says in a video on his YouTube channel.
"And this is the result of all these little microscopic blood vessels creating this dense network of blood vessels. And these nourish the bone as it grows. So they're providing blood to the bone cells as they deposit bone tissue and remodel the bone. And this is typical of an immature dinosaur."
The tiny metatarsal that started it all.
(Longrich et al., Biology, 2026)
When the bone was compared to others of its era, the researchers realized only one species fit the characteristics they were seeing.
"This is the foot bone of a very, very tiny T. rex. This is the smallest T. rex that we've ever seen," said Longrich.
After that find, the team began to look more closely at other small fossils of bones and teeth, and realized that many could also be attributed to tyrannosaur hatchlings.
"I was most surprised by how closely the hatchling Tyrannosaurus fossils resembled those of big adults," Eric Snively, paleontologist at Oklahoma State University in the US, told ScienceAlert.
"The foot bone had all the traits of a huge adult Tyrannosaurus; it was just narrower compared to its length. The teeth were chunky and worn, so the babies were biting into bone just like a 10-ton adult sundering bones of a big Triceratops."
Importantly, these bones were distinct from Nanotyrannus, a pygmy tyrannosaur species that can be mistaken for a juvenile T. rex. Other bone features excluded the possibility that these tiny tyrannosaurs were just embryos.
In the end, the researchers paint a very different picture of T. rex hatchlings, of which we know almost nothing. They estimate the main specimen to have been about 75 centimeters (30 inches) long and to have weighed around 2.5 kilograms (5.5 pounds).
Scaling back, it could have been as light as 1.7 kilograms when it first hatched. That's much smaller than previous estimates, which suggested tyrannosaurs could have been up to a meter long when they hatched.
From this new size estimate, the team was able to calculate roughly how big an egg these hatchlings emerged from. These were surprisingly small too, given the sheer size of the monster laying them.
That suggests tyrannosaurs laid many eggs: the researchers estimated 20 to 30 per clutch. And that has some fascinating implications for their reproductive strategy.
No complete or certain Tyrannosaurus rex egg has ever been found.
The goal of reproduction is obviously to make more of yourself, and in a general sense, organisms use one of two broad strategies to get there.
They either have lots of offspring, quickly and often, so that it doesn't really matter if some (or most) of them don't live very long – there are plenty of backups. Organisms that use this method, such as rodents, are known as r-strategists.
The other method is to have fewer babies, but invest heavily in making sure they survive. These are the K-strategists, and that group includes whales and, of course, us.
It's a trade-off, for sure: Do you leave dozens of your offspring on a beach to fend for themselves from birth? Or will you still be bringing snacks to their room after two decades? Both strategies seem to work for different species.
Because larger animals and modern dinosaurs (ie, birds) tend to be K-strategists, it was long thought that tyrannosaurs would raise their young with care.
But the new discovery that tyrannosaur young were small and numerous suggests they had more r-strategist tendencies than we thought.
That's not to say T. rex parents were completely (tiny) hands-off, though. They seem to mark a kind of transitional phase that was happening throughout the animal kingdom during the time of the dinosaurs.
"It shows tyrannosaurs are transitional between reptiles like crocodilians and turtles on the one hand, and modern birds on the other," said Longrich.
"Avian-mammal intensive parental investment and care seems to evolve gradually in the Mesozoic. At the same time tyrannosaurs are evolving larger and fewer young (relative to reptiles), we see mammals and plesiosaurs and even insects making similar shifts. Parental investment strategies change a lot in the Jurassic and Cretaceous."
Ancient Egyptian princesses actually knew how to use the weapons they were buried with, according to a new study published in Frontiers in Environmental Archaeology.
Any doubts around the women's prowess with the weapons – which include daggers, bows, and maces – have been quashed by a new analysis of the princesses' long-lost mummified remains.
At the apex of the 1890s Egyptomania craze, French archeologist Jacques de Morgan discovered the 4,000-year-old bodies within the Dahshur pyramid complex.
In 1895, scientific investigations were carried out on the two most high-ranking royals in the burial complex, King Hor and Princess Noub-Hotep.
19th-century handwriting is visible on the bones, and the papers they were wrapped with.
(Hashesh et al., Front. Environ. Archaeol., 2026)
In 1915, the Dahshur bodies were brought to the Egyptian Museum in Tahrir, where they were left in a wooden box and forgotten for over a century.
Then, in 2020, Zeinab Hashesh, an archaeologist at Beni-Suef University in Egypt, rediscovered the remains: King Hor and Princess Noub-Hotep, Princess Itaweret, Princess Khenmet, Princess Ita, and another female skeleton whose identity remains unknown.
"Early curators at the Egyptian museum gave the whole box only one number and described it as 'human remains'. That's it," Hashesh told ScienceAlert.
The women's skulls are still nowhere to be seen.
The skulls of Noub-Hotep (B) and the other princesses are missing.
Only the king's (A) skull remains paired with his body.
(Hashesh et al., Front. Environ. Archaeol., 2026)
"In 1906, the crania (skulls) were separated from the bodies and sent to the Cairo School of Medicine for examination," Hashesh adds.
"They were eventually lost, which made a complete assessment of the individuals impossible for later researchers."
Now, Hashesh and her colleagues have re-examined the bodies, analyzing bone features along with X-rays to better understand the lives of these ancient people.
The dagger found buried alongside Princess Ita.
(DCHNwam/Flickr)
"Finding and analyzing these skeletons after they had spent 130 years in a box was a profoundly moving experience. As scientists, we felt a sense of responsibility to finally give a 'voice' to these individuals who were central to the Middle Kingdom royal court," Hashesh said.
"There was a mix of scientific excitement and a sense of historical justice in proving that these women were more than just the silent, decorative figures they had been assumed to be."
Turns out, these long-lost women were actually kind of formidable.
"These were not just symbolic gifts but tools they actively used." - Zeinab Hashesh
They were buried with a powerful arsenal of weapons, traditionally associated with males – something that really confused French egyptologists back in 1894 – and which archaeologists have continued to dismiss as "purely symbolic or 'votive' tokens for the afterlife," Hashesh said.
There's plenty of evidence the princesses knew how to use them, based on the state of the muscle attachments on their bones, and the signs of injuries these women sustained in life.
(A) Dagger of Princess Ita, courtesy of the Egyptian Museum;
(B) Arrows of Princess Noub-Hotep, courtesy of Eman Shawky.
(Hashesh et al., Front. Environ. Archaeol., 2026)
The princesses' bones developed to sustain heavy muscle use that corresponds directly to the weapons that were found buried with them in their tombs.
For instance, Princess Noub-Hotep and the king both have the kind of robust muscle attachments you see in skilled archers.
"We found pronounced development in the upper limbs of these individuals, which correlates to repetitive, high-intensity actions like pulling a bowstring or stabilizing a weapon, proving these activities were habitual throughout their lives," Hashesh says.
"This directly explains the presence of bows, arrows, and maces in the women's tombs; these were not just symbolic gifts but tools they actively used."
The other princesses bear similar signs of a life of weapon-wielding, for activities like archery and hunting.
"Princess Ita was a young woman aged between 28 and 34 with strong upper-body muscle attachments, suggesting she habitually used weapons like maces or daggers," says Hashesh.
"Princess Khenmet was a woman in her late 30s or 40s who showed signs of thinning bones, but had very robust ligament attachments.
"Princess Itaweret was a young woman aged between 20 and 34 who survived broken ribs and foot fractures; her skeleton shows she was a skilled archer."
The princesses' bodies show many signs of active, rigorous lifestyles, and wear-and-tear specific to the weapons they were buried with.
(Hashesh et al., Front. Environ. Archaeol., 2026)
This was not a sedentary royal family: they kept up their physical activity throughout their lives.
Hashesh explained that their training may be linked to ancient Egyptian beliefs about the afterlife: that with proper training, it was possible for the spiritual body to survive beyond death.
"These women held the title mesu-nisut ('King's Children'), and their presence was integral to the ritual regeneration of the divine king," Hashesh told ScienceAlert.
"Far from leading sedentary lives of luxury, they were well-conditioned athletes and skilled practitioners of archery and martial arts hunting."
"In the elite sphere of Dahshur, these princesses were viewed as active ritual agents. They were not imitating men; rather, their royal blood and their role in the 'machine for surviving death' required them to be disciplined, powerful actors capable of wielding skilled force," she said.
It's an incredible example of just how much we can learn from what is left behind – and that some of the most exciting discoveries might be hiding in the basement, waiting to be seen with fresh eyes.
