How HPV reprograms immune cells to help cancer grow

The most common cancer-causing strain of human papillomavirus (HPV), HPV16, undermines the body's defenses by reprogramming immune cells surrounding the tumor, according to new research.

In mice, blocking this process boosted the ability of experimental treatments for HPV to eliminate cancer cells. The results were published in the Journal for ImmunoTherapy of Cancer.

HPV16 causes more than half of cervical cancer cases and roughly 90% of HPV-linked throat cancers. It can be neutralized with the preventive vaccine Gardasil-9, but only if vaccination occurs prior to HPV exposure.

Researchers are now working to develop "therapeutic vaccines," which can be taken after HPV exposure—for instance, following an abnormal pap smear or cancer diagnosis—to trigger an immune response against infected cells by T-cells, a type of "fighter" cell that helps defend the body from disease. But these vaccines, now in clinical trials, have limited effectiveness—and the new study helps explain why.

The research focuses on a signalling protein in the immune system with inflammatory properties called Interleukin-23 or IL-23. While IL-23 was previously implicated in cervical and throat cancers, its exact role was unclear.

In a series of tests in mice and cell cultures,  researchers found that two HPV proteins, E6 and E7, prompt nearby cells to release IL-23, which in turn prevents the body's T-cells from attacking the tumor.

In order to eliminate the cancer, T-cells need to proliferate and destroy infected cells. But IL-23 stops them from working effectively, so the tumor keeps growing.

HPV16 E6 and E7 expressing cancer cells suppress the anti-tumor immune response by upregulating KLF2 mediated IL-23 expression in macrophages, Journal for ImmunoTherapy of Cancer (2025). DOI: 10.1136/jitc-2025-011915

Restricted blood flow speeds tumor growth by aging the immune system, study finds

Cutting off blood flow can prematurely age the bone marrow, weakening the immune system's ability to fight cancer, according to a new study .

Published online in JACC-CardioOncology, the study showed that peripheral ischemia–restricted blood flow in the arteries in the legs–caused breast tumors in mice to grow at double the rate seen in mice without restricted flow. These findings build on a 2020 study by the same team that found ischemia during a heart attack to have the same effect.

Ischemia occurs when fatty deposits, such as cholesterol, accumulate in artery walls, leading to inflammation and clotting that restrict the flow of oxygen-rich blood. When this happens in the legs, it causes peripheral artery disease, which affects millions of people, and can increase the risk of heart attack or stroke.

This new study  shows that impaired blood flow drives cancer growth regardless of where it happens in the body.

This link between peripheral artery disease and breast cancer growth underscores the critical importance of addressing metabolic and vascular risk factors as part of a comprehensive cancer treatment strategy.

Importantly, the research team found that restricted blood flow triggers a shift toward immune cell populations that cannot efficiently fight infections and cancer, mirroring changes seen with aging.

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To examine the mechanisms behind the link between cardiovascular disease and cancer growth, the study authors developed a mouse model with breast tumors and induced temporary ischemia in one hind limb. The team then compared cancer growth in mice with and without impaired blood flow.

Their findings build on the nature of the immune system, which evolved to attack invading bacteria and viruses, and, under normal conditions, to detect and eliminate cancer cells. These protective functions rely on stem cell reserves in the bone marrow, which can be activated as needed to produce key white blood cell populations throughout life.

Normally, the immune system responds to injury or infection by ramping up inflammation to eliminate threats, then scaling back to avoid harm to healthy tissue. This balance is maintained by a mix of immune cells that either activate or suppress inflammation.

The researchers found that reduced blood flow disrupts this equilibrium. It reprograms stem cells in the bone marrow to favor the production of "myeloid" immune cells (monocytes, macrophages, neutrophils) that dampen immune responses, while reducing output of lymphocytes like T cells that help to mount strong anti-tumor responses.

The local environment within tumors showed a similar shift, accumulating more immune-suppressive cells– including Ly6Chi monocytes, M2-like F4/80+ MHCIIlo macrophages, and regulatory T cells—that shield cancer from immune attack.

Further experiments showed that these immune changes were long-lasting. Ischemia not only altered the expression of hundreds of genes, shifting immune cells into a more cancer-tolerant state, but also reorganized the structure of chromatin–the protein scaffolding that controls access to DNA–making it harder for immune cells to activate genes involved in fighting cancer.
results reveal a direct mechanism by which ischemia drives cancer growth, reprogramming stem cells in ways that resemble aging and promote immune tolerance.
These findings open the door to new strategies in cancer prevention and treatment, like earlier cancer screening for patients with peripheral artery disease and using inflammation-modulating therapies to counter these effects."

Moving forward, the research team hopes to help design clinical studies that evaluate whether existing inflammation-targeted therapies can counter post-ischemic changes driving tumor growth.

Ischemic Injury Drives Nascent Tumor Growth via Accelerated Hematopoietic Aging, JACC CardioOncology (2025). DOI: 10.1016/j.jaccao.2025.05.016

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Hight-salt diet sparks brain inflammation that could explain stubborn high blood pressure

A new study finds that a high-salt diet triggers brain inflammation that drives up blood pressure. 

The research suggests the brain may be a missing link in certain forms of high blood pressure—or hypertension—traditionally attributed to the kidneys.

This is new evidence that high blood pressure can originate in the brain, opening the door for developing treatments that act on the brain.

Hypertension affects two-thirds of people over 60 and contributes to 10 million deaths worldwide each year. Often symptomless, the condition increases the risk of heart disease, stroke and other serious health problems.

About one-third of patients don't respond to standard medications, which primarily target the blood vessels and kidneys based on the long-standing view that hypertension begins there.

The study, published in the journal Neuron, suggests the brain may also be a key driver of the condition, particularly in treatment-resistant cases.

How salt disrupts the brain

To mimic human eating patterns, rats were given water containing 2% salt, comparable to a daily diet high in fast food and items like bacon, instant noodles and processed cheese.

The high-salt diet activated immune cells in a specific brain region, causing inflammation and a surge in the hormone vasopressin, which raises blood pressure. Researchers tracked these changes using cutting-edge brain imaging and lab techniques that only recently became available.

The brain's role in hypertension has largely been overlooked, in part because it's harder to study.

The researchers used rats instead of the more commonly studied mice because rats regulate salt and water more like humans. That makes the findings more likely to apply to people.

Next, the scientists plan to study whether similar processes are involved in other forms of hypertension.

Ning Gu et al, Microglia regulate neuronal activity via structural remodeling of astrocytes, Neuron (2025). DOI: 10.1016/j.neuron.2025.07.024

Imagination won't take you everywhere—study reveals limitations of the mind's eye

Our imagination might not be as powerful as we think when it comes to holding visual images, according to a first-of-its-kind study by psychologists.

 The research found that people can remember more items when they've seen them, compared to when they must imagine them.

While short-term visual memory can hold three to four items at once, our imagination can manage only two items before becoming less accurate.

Across a series of five experiments, more than 150 participants were asked to either remember or imagine the locations of objects on a grid.

Researchers examined how accurately participants could detect changes in specific locations under various conditions, including timing, cueing, display type, and object complexity. They then compared the number of items participants could correctly remember after viewing them with the number they could accurately imagine and recall without having seen them.

Findings showed that even when given more time or simpler images, people still imagined fewer items than they could remember visually.

The study, "The relation between the capacities of imagination and visual memory in the short-term," published in the Journal of Experimental Psychology: Human Perception and Performance, offers the first direct comparison of how much information people can hold in visual imagination versus visual memory.

Imagination and memory use similar parts of the brain, but this is the first time scientists have measured exactly how they differ when it comes to capacity. These findings demonstrate that actually seeing something, even a brief glimpse, gives our brain extra sensory support that bolsters our memory. In fact, researchers estimate that 17–35% of visual memory capacity depends on sensory input. When we imagine something from scratch, we don't have that input from our eyes, so it's harder to hold detailed images.

We use imagination constantly in everyday life, as imagery is seen as essential for navigating and predicting our environment and is involved in decision-making and emotion regulation, but the study reveals that our capacity to visualize is surprisingly limited, and this might affect how we make decisions, remember plans, or follow instructions when we rely on mental imagery alone.

Christopher Atkin et al, The relation between the capacities of imagination and visual memory in the short term., Journal of Experimental Psychology: Human Perception and Performance (2025). DOI: 10.1037/xhp0001364

“Logic will get you from A to B.  Imagination will take you everywhere.” –Albert Einstein

Epigenetic noise: Unappreciated process helps cells change identity

All cells in the body contain the same DNA, but different cell types express different genes; skin cells express genes for the skin, liver cells express liver genes, and so on. This coordination is crucial to help cells differentiate into their assigned roles, but a new study by researchers shows how cells can randomly "shake up" regions of the genome to express genes normally reserved for other cell types.

The study, "Thymic epithelial cells amplify epigenetic noise to promote immune tolerance," published in Nature, suggests that randomness or variability in the way DNA is packaged can create a kind of "epigenetic noise," enabling cells to take on the identity of different cell types. This flexibility plays an important role in tissue repair and the immune system but can also be exploited for the development of tumors.

The researchers worked with an incredibly resourceful group of cells called medullary thymic epithelial cells (mTECs). These cells are found in the thymus, a small, specialized organ of the immune system located just above the heart. They are one of the few cell types in the body that can express a wide variety of genes and alter their identity to mirror cell types from other tissues.

mTECs play an important role in training the immune system to prevent autoimmunity. They present proteins that are normally expressed only in specialized tissues and organs to T cells developing in the thymus. Then, the T cells that react too strongly to molecules from the body's own cells are purged so they don't later trigger an autoimmune response.

The capability to express almost any gene and alter their identities makes mTECs a great candidate for studying how cells can change their fates.

Each individual cell does not express the entire genome. Instead, they express only a unique subset of the tissue-specific genes at any given snapshot. There's a great deal of heterogeneity, so the researchers thought that it was really important to look cell-by-cell to uncover the mechanisms that allow the activation of each subset of tissue-specific genes.

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Since such heterogeneity is important, they used a series of single cell sequencing techniques to study gene expression and chromatin structure in individual mTECs, instead of using traditional bulk sequencing tools that average the results over thousands of cells.

Chromatin is the complex of DNA and proteins in the nucleus that packages long stretches of DNA into more compact structures. When chromatin is more loosely packed, or open, genes are more poised to be activated than if it's tightly coiled.

When the researchers analyzed the data, they did not find links between peak levels of chromatin accessibility and the expression of tissue-specific genes. Instead, they saw a lot of accessibility "noise" that gave cells the potential to activate genes solely expressed in other specialized tissues. This "ectopic expression" in turn helped train T cells to discriminate between self and non-self.

Chromatin is usually tightly regulated to sequester regions that encode other cell fates and focus accessibility for regions pertinent for the established cell identity.
In this work context, the researchers found the genomic regions that should be tightly packed were more labile or 'jiggly," allowing more opportunities for factors to access and activate genes specific to different cell types."
The team then tried to understand how this "chromatin noise" is amplified in cells. They found that the activity of the tumor suppressor protein p53, known as "the guardian of the genome," is repressed by mTECs prior to their genome becoming noisy. p53 is usually activated when DNA is damaged and can trigger cell death or stop tumor cell growth.

So, it made sense to the researchers that it would be implicated in a process where epithelial cells promiscuously express genes dedicated to other tissues and organs.
When the researchers genetically engineered p53 activity to be enhanced in mTECs, their chromatin became more stable, epigenetic noise was turned down, and the cells could no longer activate tissue-specific genes. This ultimately resulted in the escape of self-reactive T cells from the thymus to cause multi-organ autoimmune disease.
This suggests that thymic epithelial cells adopt deviant states that should normally trigger p53 activation and cell death.But because p53 is downregulated, the cells survive and facilitate this ectopic gene expression to promote the self/non-self discrimination.
It's a fascinating idea to think that cells are programmed to loosen their grip on genes to give them more freedom to get creative and solve problems like preventing T cells from attacking their own tissues.
The researchers extended their studies and found that epigenetic noise also allows lung cancer to sample more of the genome once p53 is deleted. This activates programs specific to other tissues to develop into more aggressive, malignant states. They hope to continue studying whether other cancer types exploit similar mechanisms for tumorigenesis.
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The team also wants to see if epigenetic noise is amplified for wound healing and tissue repair, and whether or not it can be leveraged to reprogram cells to alternate phenotypes for various clinical contexts, including cancer immunotherapy and treating autoimmunity.

It makes sense that to empower an immune system that uses a random process to recognize virtually any entity in the universe, thymic epithelial cells amplify random noise in the genome to ensure the immune system is focused on pathogens and cancers and not its own tissues. It's fighting fire with fire
Sometimes the random background noise can be just as important as the signal.

Thymic epithelial cells amplify epigenetic noise to promote immune tolerance, Nature (2025). DOI: 10.1038/s41586-025-09424-x

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Mitochondria defend cells against infections by competing with pathogens for nutrients

Chronic infections impact a substantial portion of the global population, presenting ongoing challenges to health care systems and compromising patient well-being.

In a new study, researchers have discovered a surprising ally in the fight against infection: the cell's own mitochondria. Best known for providing energy to cells, mitochondria also play a defensive role by competing with pathogens for vital nutrients.

The paper is published in the journal Science.

During infection, mitochondria enter a metabolic tug-of-war with intracellular parasites, like Toxoplasma gondii, battling for access to folate, thereby inhibiting pathogen growth.

This discovery highlights a unique defensive strategy employed by host cells and opens up new possibilities for developing therapies against folate-dependent pathogens, such as Toxoplasma and Plasmodium, which cause toxoplasmosis and malaria respectively.

During infection with the human parasite Toxoplasma gondii, researchers observed the activation of the integrated stress response, which rewires mitochondrial metabolism.

This response enhanced mitochondrial activity, leading to increased demand for folate, a critical nutrient for nucleotide synthesis. Consequently, mitochondria limit the parasite's access to folate, curtailing its growth and proliferation. Mice unable to activate this stress response showed faster parasite growth, confirming the pathway's protective role in vivo.

 Tânia Catarina Medeiros et al, Mitochondria protect against an intracellular pathogen by restricting access to folate, Science (2025). DOI: 10.1126/science.adr6326

Saharan bacteria shield themselves with biofilms to survive dust storm journeys

How do living bacteria survive on the surface of dust particles carried by desert storms from the Sahara and Egypt to Israel?

Researchers  discovered that these bacteria can form microscopic biofilms over dust particles. These protective structures shield the bacteria from desiccation, extreme radiation, and severe nutrient scarcity during their atmospheric journey.

The research, published in Communications Earth and Environment, contributes to the growing field of atmospheric microbiology. This discipline explores the survival and activity of microorganisms while in the atmosphere, sometimes over thousands of kilometers, and their impact on global cycles, ecosystems, and human health. These processes significantly impact disease patterns, atmospheric CO₂ levels, plant diseases, and even antibiotic resistance dispersal.

In this study, the researchers successfully isolated and cultured bacteria brought in by dust storms under atmospheric conditions, focusing on beneficial Bacillus strains known for their positive applications in agriculture, construction, and medical probiotics.

The team thinks that natural selection during dust storms favors more innovative bacterial strains—a phenomenon that could potentially enhance their practical applications. This study also expands the traditional soil microbiome concept to include airborne microbial communities, broadening the known repertoire of survival strategies among these remarkable organisms.

Naama Lang-Yona et al, Bacillus biofilm formation and niche adaptation shape long-distance transported dust microbial community, Communications Earth & Environment (2025). DOI: 10.1038/s43247-025-02534-4

Brain scans reveal action-based organization in people born without hands

Conventional wisdom among neuroscientists suggests that the brain's motor functions are organized around the body, meaning certain brain areas control the hand; others the foot. An emerging alternative theory is that parts of the brain may be organized by the types of action, like reaching or using tools, no matter which body part is used to complete the task.

Researchers  recently set out to understand these theories, because knowing how the brain is organized around function versus body part has profound implications for rehabilitation and a person's return to function following a brain injury.

The findings are published in the Proceedings of the National Academy of Sciences. The work is titled "Action-type mapping principles extend beyond evolutionarily-conserved actions, even in people born without hands."

If motor control is partly based on actions rather than body parts, it's possible the brain can use this flexibility to compensate for the loss of specific limbs.

To gain a deeper understanding of the emerging theory, neuroscientists conducted a novel study with volunteers who were born without hands, and instead use their feet for everyday tasks with and without tools.

Using fMRI brain scans, the researchers showed that in these individuals, brain areas typically involved in hand tool use are still active—even though the individuals were using their feet, not their hands. This finding is consistent with the same action preference for control participants, who perform the action with either their hands or feet.

They  found that some regions in the brain care about the type of action a person is doing and not whether this action was performed with the hand or with the foot.

It appears this organization can arise without typical motor experience, providing evidence for action-type as a core driving factor in motor organization and development.

Interestingly, this was not true for all brain areas.

The primary motor cortex, which is tightly mapped to the body, did not reorganize for foot-based tool use, even in people who have been using tools with their feet their whole lives. This suggests that some brain areas demonstrate more plasticity than others.

Still, the study reveals a kind of brain organization that goes beyond the body—one that is abstract and action-centered, and that develops even without typical experience.

 Florencia Martinez-Addiego et al, Action-type mapping principles extend beyond evolutionarily conserved actions, even in people born without hands, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2503188122

Cancer-associated nerve injury can lead to chronic inflammation and immunotherapy resistance

Cancer cells can break down the protective covers around nerves, causing nerve injury that triggers chronic inflammation, leading to immune exhaustion and eventual resistance to immunotherapy, according to new research .

Tumors can sometimes infiltrate the space around nerves and nervous system fibers that are in close proximity, a process known as perineural invasion, which leads to poor prognosis and treatment escalation in various cancer types. 

The study, published today in Nature, underscores the importance of investigating interactions between cancer and the nervous system—a field known as cancer neuroscience. The results suggest that targeting the signaling pathways involved can reverse this inflammation and improve treatment responses.

These findings uncover novel mechanisms by which the immune system and nerves within the tumor microenvironment interact, revealing actionable targets that could transform the way we approach resistance to immunotherapy in patients with cancer.

 Baruch, E.N. et al, Cancer-induced nerve injury promotes resistance to anti-PD-1 therapy, Nature (2025). DOI: 10.1038/s41586-025-09370-8 www.nature.com/articles/s41586-025-09370-8

What happens in the brain when it learns something new

Memories of significant learning experiences—like the first time a driver gets a speeding ticket—are sharp, compared to the recollection of everyday events—like what someone ate for dinner two weeks ago. That's because the human brain is primed to learn from helpful associations.

Researchers have identified specific neural connections that are especially sensitive to this process of learning about causality. The discovery, while seemingly intuitive, could have widespread implications for understanding how humans learn and inform new ways to address learning challenges.

What's happening inside the brain when experiencing something for the first time—and how it decides if it's meaningful—is the subject of new research which focuses on how memory and learning shape the brain. The study is published in the journal Cell Reports.

 Researchers looked at how the connection between two different types of neurons—cells that transmit information to different parts of the brain—changes in response to new learning experiences. They found that the strength of the connection only changed if an experience was meaningful. These neurons are located in the sensory cortex, a part of the brain that other animals—like cows and dogs—have as well. That means that this finding could have a wider significance and help researchers understand how a broad range of animals learn.

Researchers found this change in the brain if something was useful to learn. If there was nothing to learn, there was no change.

This means that somehow the brain can distinguish whether there is a useful association to make, or there is nothing to learn.

The research shows that the brain is primed to learn new important things and that our brains are very sensitive to things that make sense.

 Eunsol Park et al, Somatostatin neurons detect stimulus-reward contingencies to reduce neocortical inhibition during learning, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.115606

Breast tumors tunnel into fat cells to fuel up

Scientists caught cancer cells in the act of breaking into fat cells and releasing their fat. The energy heist seems to be critical for the growth of deadly breast cancer. The study appears in Nature Communications.

When triple-negative breast cancer grows, the fat cells around it seem to shrink. Researchers have discovered that the cells of these tumors, which are among the deadliest types of breast cancer, build molecular tunnels, called gap junctions, into nearby fat cells. The tumor cells then send instructions that trigger the fat cells to release stores of energy that could feed the cancer.

Blocking the gap junctions stopped tumors from growing.

The findings have immediate clinical implications. Although no one is yet testing drugs that block gap junctions for breast cancer, there are ongoing clinical trials using these drugs for brain cancer.

Nature Communications (2025). DOI: 10.1038/s41467-025-62486-3

What happened before the Big Bang? Computational method may provide answers

We're often told it is "unscientific" or "meaningless" to ask what happened before the Big Bang. But a new paper by astrophysicists and cosmologists published in Living Reviews in Relativity, proposes a way forward: using complex computer simulations to numerically (rather than exactly) solve Einstein's equations for gravity in extreme situations.

The team argues that numerical relativity should be applied increasingly in cosmology to probe some of the universe's biggest questions–including what happened before the Big Bang, whether we live in a multiverse, if our universe has collided with a neighboring cosmos, or whether our universe cycled through a series of bangs and crunches.

Einstein's equations of general relativity describe gravity and the motion of cosmic objects. But wind the clock back far enough and you'll typically encounter a singularity—a state of infinite density and temperature—where the laws of physics collapse.

Cosmologists simply cannot solve Einstein's equations in such extreme environments—their normal simplifying assumptions no longer hold. And the same impasse applies to objects involving singularities or extreme gravity, such as black holes.

One issue might be what cosmologists take for granted. They normally assume that the universe is "isotropic" and "homogeneous"—looking the same in every direction to every observer. This is a very good approximation for the universe we see around us, and one that makes it possible to easily solve Einstein's equations in most cosmic scenarios. But is this a good approximation for the universe during the Big Bang?

Numerical relativity allows you to explore those questions. 

Numerical relativity was first suggested in the 1960s and 1970s to try to work out what kinds of gravitational waves (ripples in the fabric of spacetime) would be emitted if black holes collided and merged. This is an extreme scenario for which it is impossible to solve Einstein's equations with paper and pen alone—sophisticated computer code and numerical approximations are required.

Its development received renewed focus when the LIGO experiment was proposed in the 80s, although the problem was only solved in this way in 2005, raising hopes that the method could also be successfully applied to other puzzles.

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One longstanding puzzle that researchers are particularly excited about is cosmic inflation, a period of extremely rapid expansion in the early universe. Inflation was initially proposed to explain why the universe looks the way it does today, stretching out an initially small patch, so that the universe looks similar across a vast expanse.
If you don't have inflation, a lot of things fall apart. But while inflation helps explain the state of the universe today, nobody has been able to explain how or why the baby universe had this sudden short-lived growth spurt.

The trouble is, to probe this using Einstein's equations, cosmologists have to assume that the universe was homogeneous and isotropic in the first place—something which inflation was meant to explain. If you instead assume it started out in another state, then you don't have the symmetry to write down your equations easily.
But numerical relativity could help us get around this problem—allowing radically different starting conditions. It isn't a simple puzzle to solve, though, as there's an infinite number of ways spacetime could have been before inflation. Researchers are therefore hoping to use numerical relativity to test the predictions coming from more fundamental theories that generate inflation, such as string theory.
There are other exciting prospects, too. Physicists could use numerical relativity to try to work out what kind of gravitational waves could be generated by hypothetical objects called cosmic strings—long, thin "scars" in spacetime–potentially helping to confirm their existence. They might also be able to predict signatures, or "bruises," on the sky from our universe colliding with neighboring universes (if they even exist), which could help us verify the multiverse theory.
Excitingly, numerical relativity could also help reveal whether there was a universe before the Big Bang. Perhaps the cosmos is cyclic and goes through "bounces" from old universes into new ones—experiencing repeated rebirths, big bangs and big crunches. That's a very hard problem to solve analytically.

"Bouncing universes are an excellent example, because they reach strong gravity where you can't rely on your symmetries. Several groups are already working on them—it used to be that nobody was."
Numerical relativity simulations are so complex that they require supercomputers to run. As the technology of these machines improves, we might expect significant improvement in our understanding of the universe.
Cosmologists who are interested in solving some of the questions they cannot solve, can use numerical relativity, the researchers say.

Josu C. Aurrekoetxea et al, Cosmology using numerical relativity, Living Reviews in Relativity (2025). DOI: 10.1007/s41114-025-00058-z

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Novel cement lets buildings cool themselves

When temperatures get too hot to handle, most of us crank up the air conditioning to keep cool. It does the job, but it's expensive and uses a significant amount of energy. But now an innovation by scientists could help us cut our reliance on AC. They've developed a new type of cement that allows buildings to stay cool on their own. Their research is published in the journal Science Advances.

Typically, cement absorbs infrared radiation from the sun and stores it as heat, which increases the temperature inside a building. To address this, a research team modified the building material's formula. They created a cement that reflects light and emits heat instead of absorbing it, using tiny reflective crystals of a mineral called ettringite on its surface.

The scientists developed the material from the ground up, starting with its basic chemical recipe. They ground tiny pellets made from minerals like limestone and gypsum into a fine dust and mixed it with water. The mixture was then poured into a silicon mold covered in holes that created depressions in the cement's surface where the ettringite crystals could grow. The result was a supercool cement that acts like a mirror and a radiator, bouncing away sunlight and emitting heat.

Once the cement was created, it was put to the test on a rooftop at Purdue University. Under a strong midday sun, the cement's surface was 5.4 degrees Celsius cooler than the surrounding air. The material also underwent rigorous mechanical, environmental, and optical durability testing.

Additionally, the team used machine learning to analyze its potential environmental benefits, which revealed that it could potentially lead to a net-negative carbon footprint over a 70-year period.

This breakthrough holds the potential to turn the heavy cement industry into a negative-carbon emission system, where supercool cement could play a key role in driving an energy-efficient, carbon-free future for the construction industry.

Buildings currently account for about 40% of global energy use and 36% of carbon emissions. If the supercool cement is successfully scaled up for commercial use, its benefits could be significant. As well as helping to cool the planet, it could dramatically cut energy bills by reducing our reliance on air conditioning. And by keeping buildings and the surrounding air cooler, this novel cement could also create a more pleasant and healthier urban environment.

Guo Lu et al, Scalable metasurface-enhanced supercool cement, Science Advances (2025). DOI: 10.1126/sciadv.adv2820

New research shows the brain's map of the body remains unchanged after amputation

The brain holds a "map" of the body that remains unchanged even after a limb has been amputated, contrary to the prevailing view that it rearranges itself to compensate for the loss, according to new research.

The findings, published in Nature Neuroscience, have implications for the treatment of "phantom limb" pain, but also suggest that controlling robotic replacement limbs via neural interfaces may be more straightforward than previously thought.

Studies have previously shown that within an area of the brain known as the somatosensory cortex there exists a map of the body, with different regions corresponding to different body parts.

These maps are responsible for processing sensory information, such as touch, temperature and pain, as well as body position. For example, if you touch something hot with your hand, this will activate a particular region of the brain; if you stub your toe, a different region activates.

For decades now, the commonly-accepted view among neuroscientists has been that following amputation of a limb, neighboring regions rearrange and essentially take over the area previously assigned to the now missing limb. This has relied on evidence from studies carried out after amputation, without comparing activity in the brain maps beforehand.

But this has presented a conundrum. Most amputees report phantom sensations, a feeling that the limb is still in place—this can also lead to sensations such as itching or pain in the missing limb. Also, brain imaging studies where amputees have been asked to 'move' their missing fingers have shown brain patterns resembling those of able-bodied individuals.

To investigate this contradiction, researchers followed three individuals due to undergo amputation of one of their hands.

This is the first time a study has looked at the hand and face maps of individuals both before and after amputation. 

Prior to amputation, all three individuals were able to move all five digits of their hands. While lying in a functional magnetic resonance imaging (fMRI) scanner—which measures activity in the brain—the participants were asked to move their individual fingers and to purse their lips. The researchers used the brain scans to construct maps of the hand and lips for each individual. In these maps, the lips sit near to the hand.

The participants repeated the activity three months and again six months after amputation, this time asked to purse their lips and to imagine moving individual fingers. One participant was scanned again 18 months after amputation and a second participant five years after amputation.

The researchers examined the signals from the pre-amputation finger maps and compared them against the maps post-amputation. Analysis of the 'before' and 'after' images revealed a remarkable consistency: even with their hand now missing, the corresponding brain region activated in an almost identical manner.

Bearing in mind that the somatosensory cortex is responsible for interpreting what's going on within the body, it seems astonishing that it doesn't seem to know that the hand is no longer there!

As previous studies had suggested that the body map reorganizes such that neighboring regions take over, the researchers looked at the region corresponding to the lips to see if it had moved or spread. They found that it remained unchanged and had not taken over the region representing the missing hand.

Part 1

To complement their findings, the researchers compared their case studies with 26 participants who had their upper limbs amputated, on average, 23.5 years beforehand. These individuals showed similar brain representations of the hand and lips to those in their three case studies, suggesting long-term evidence for the stability of hand and lip representations despite amputation.

Schone, HR et al. Stable Cortical Body Maps Before and After Arm Amputation, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02037-7

Part 2

Rising temperatures linked to declining moods around the world

Rising global temperatures affect human activity in many ways. Now, a new study illuminates an important dimension of the problem: very hot days are associated with more negative moods, as shown by a large-scale look at social media postings.

Overall, the study examined 1.2 billion social media posts from 157 countries over the span of a year. The research finds that when the temperature rises above 95 degrees Fahrenheit, or 35 degrees Celsius, expressed sentiments become about 25% more negative in lower-income countries and about 8% more negative in better-off countries. Extreme heat affects people emotionally, not just physically.

This study reveals that rising temperatures don't just threaten physical health or economic productivity—they also affect how people feel, every day, all over the world. 

This work opens up a new frontier in understanding how climate stress is shaping human well-being at a planetary scale.

Unequal Impacts of Rising Temperatures on Global Human Sentiment, One Earth (2025). DOI: 10.1016/j.oneear.2025.101422. www.cell.com/one-earth/fulltex … 2590-3322(25)00248-9

Even I have noticed this around my home. Birds are singing in the night!

Birds in light-polluted areas stay up late into the night

Birds that are active during the day sing later into the night in places with significant light pollution, according to new research.

Researchers analyzed data gathered from around the world, comparing more than 180 million bird vocalizations in a single year with global satellite imagery.

They were shocked by their findings: Under the brightest night skies, a bird's day is extended by nearly an hour. But birds staying up an hour past their normal bedtimes was an average. Actual times varied by species.

What is driving this response bybirds? We had the idea that maybe it was a species' photoreceptor sensitivity—their eyesight. And this turned out to be a key factor. Species with large eyes relative to their body size had a disproportionately stronger response to artificial light at night. They were more sensitive to light at night than species with small eyes.

Birds might have more time to forage for food and to mate, but an hour less sleep could be detrimental to their health.

Brent S. Pease et al, Light pollution prolongs avian activity, Science (2025). DOI: 10.1126/science.adv9472. www.science.org/doi/10.1126/science.adv9472

Viruses hidden within fungi could be secret drivers of deadly lung infections

Researchers have discovered that a virus living inside the fungus Aspergillus fumigatus significantly boosts the fungus's ability to survive stress and cause severe infections in mammals. Removing the virus made the fungus weaker and less virulent, while antiviral treatments improved survival outcomes. This finding reveals a hidden factor driving the deadliness of fungal infections and opens the door to potential new treatments that target the virus rather than the fungus itself.

The research reveals that a virus residing within the Aspergillus fumigatus fungus gives it a powerful survival advantage—making it tougher, more resilient, and ultimately, more dangerous to human health.

Aspergillus fumigatus is already notorious in medical circles. Responsible for the majority of invasive fungal infections in humans, it's especially lethal for people with weakened immune systems. Despite decades of research, mortality rates from infections remain alarmingly high—approaching 50%.

A double-stranded RNA virus, quietly riding along inside the fungus, appears to act like a hidden booster pack for the pathogen. When this virus is present, the fungus becomes far more adept at surviving environmental stress, including the heat and oxidative conditions inside the lungs of mammals.

To test the impact of the virus, the researchers removed it from fungal strains and compared their behavior to their virus-infected counterparts. The difference was striking. The virus-free fungi lost their ability to reproduce effectively, showed weaker defenses like reduced melanin production, and became significantly less dangerous when introduced into mammalian lungs.

The findings suggest that these so-called "mycoviruses" may play a quiet but critical role in the development and progression of fungal diseases in humans—a role that has largely gone unnoticed in the field of medical mycology.

Perhaps most promising of all: when antiviral treatments were used to suppress the virus during infection, survival outcomes improved in the mammalian model. This hints at a whole new treatment avenue—not just targeting the fungus itself, but the virus helping it thrive.

This discovery opens the door to rethinking how fungal infections are treated. By targeting the virus within the fungus, researchers may one day weaken the pathogen enough for the immune system—or existing antifungal drugs—to fight back more effectively.

In a world where fungal pathogens are becoming more drug-resistant and harder to treat, the study provides a rare glimmer of hope: Perhaps we've been overlooking a key player all along.

Marina Campos Rocha et al, Aspergillus fumigatus dsRNA virus promotes fungal fitness and pathogenicity in the mammalian host, Nature Microbiology (2025). DOI: 10.1038/s41564-025-02096-3

How climate change increases air turbulence

For many fliers, air turbulence can be an unnerving experience—and in a world warming under the effects of climate change, it is only set to worsen, according to a growing body of scientific evidence.

Beyond making people uneasy, turbulence is also the leading cause of in-flight weather accidents, according to official data.

The numbers remain relatively small: there were 207 reported injuries on US commercial flights between 2009 and 2024. But high-profile incidents have thrust the issue into the spotlight.

These include an Air Europa flight last year, in which 40 passengers were hurt, and a Singapore Airlines flight where one elderly passenger died and dozens were injured.

Typically injuries occur due to un- belting of passengers or cabin crew rather than structural damage. Modern aircraft withstand turbulence, so the main risk is occupant injury, not loss of the plane.

Still, planes must be inspected after "severe" encounters with turbulence—about 1.5 times the normal force of Earth's gravity. Turbulence also increases fuel consumption when pilots must leave optimal altitudes, alter routes or change speeds.

There are three main types of turbulence: convective, mountain wave and clear-air turbulence (CAT), according to experts.

Researchers find a clear, positive trend—an increase in turbulence frequency over many regions, including the North Atlantic, North America, East Asia, the Middle East and North Africa,with increases ranging from 60% to 155%.
Further analysis attributed the rising turbulence in certain regions to increased greenhouse gas emissions.
A 2023 paper led by Isabel Smith at the University of Reading found that for every degree Celsius of near-surface warming, winters would see an increase of about nine percent in moderate CAT in the North Atlantic, and summers a rise of 14%.

Winter has historically been the roughest season for turbulence, but warming is now amplifying CAT in summer and autumn, closing the gap.

Jet stream disruption is not the only concern: climate change is also fueling stronger storms.

Climate change may also increase the frequency and severity of thunderstorms under future scenarios, and turbulence encounters near thunderstorms are a major component of turbulence accidents.
In terms of mitigation strategies, researchers are working on two studies: optimizing flight routes to avoid turbulence hotspots and improving forecasting accuracy.

Some airlines are moving towards strategies involving passengers wearing seatbelts more often, such as ending cabin service earlier.

Promising technologies are also being tested, including onboard LIDAR, which beams lasers into the atmosphere to detect subtle shifts in air density and wind speed.

Ultimately, cutting greenhouse gas emissions will be essential, say the researchers.
Ironically, aviation is responsible for about 3.5% of human-caused warming.
Source: News agencies

Part 2
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Breast cancer drug side effects: Study reveals how tamoxifen raises risk of secondary tumors in uterus

An international research team has identified a previously unknown mechanism by which the breast cancer drug tamoxifen can increase the risk of secondary tumors in the uterus.

The study shows that tamoxifen directly activates a key cellular signaling pathway (known as PI3K) a central driver in the development of sporadic uterine cancers, thereby challenging previously accepted models of therapy-related cancer development.

Since its introduction in the 1970s, tamoxifen has significantly improved survival rates for millions of patients with estrogen receptor–positive breast cancer. However, alongside its life-saving benefits, tamoxifen has also been linked—though rarely—to an elevated risk of uterine cancer. Until now, the precise molecular cause of this effect has remained unclear.

The new findings, published in Nature Genetics, reveal the mechanism: in tamoxifen-associated uterine carcinomas, mutations in the cancer-related gene PIK3CA—which are very common in spontaneously arising uterine tumors and lead to the activation of the PI3K signaling pathway—occur significantly less frequently. Instead, tamoxifen itself takes on the role of a signal activator of the PI3K pathway, making such mutations unnecessary.

Kirsten Kübler et al, Tamoxifen induces PI3K activation in uterine cancer, Nature Genetics (2025). DOI: 10.1038/s41588-025-02308-w

Rethinking phototherapy: Why skin color matters for infant jaundice treatment

Jaundice is one of the most common medical issues in newborns, affecting nearly 80% of full-term infants in their first days of life. The condition occurs when excess bilirubin, a yellow pigment formed as red blood cells break down, builds up in the body. While mildcases usually resolve on their own, dangerously high bilirubin levels can cause brain damage or even death. The standard treatment, phototherapy, uses blue light to break bilirubin down into forms the body can excrete.

A theoretical study recently published in Biophotonics Discovery used computer modeling to examine how skin color and other skin properties might influence how much therapeutic light reaches target tissues.

Researchers employed advanced computer simulations to model light penetration in newborn skin. The simulations incorporated factors such as skin pigmentation, hemoglobin levels, bilirubin concentration, skin thickness, and treatment light wavelength.  

Since specific data on skin color variations in newborns have not yet been reported, the researchers based their pigmentation parameters on established measurements from adult skin data. The modeling predicted that skin pigmentation would have the largest effect on light penetration.

Compared with light-skinned infants, the simulations suggested dark-skinned infants might receive up to 5.7 times less effective light dose under identical settings. This theoretical difference translated into predicted bilirubin reductions of about 40.8% for light-skinned newborns after 24 hours of phototherapy, versus 25.6% for dark-skinned newborns. The model also predicted that epidermal thickness and bilirubin levels would influence treatment effectiveness, though to a lesser degree.

The simulations further suggested that optimal treatment wavelength might vary by skin color. While light-skinned infants were predicted to respond best at around 460 nanometers (nm), dark-skinned infants showed better theoretical responses at slightly longer wavelengths, around 470 nm. The researchers propose that a compromise wavelength near 465 nm could provide more consistent results across skin tones.

Current phototherapy guidelines use a standardized approach without adjustments for skin tone. While phototherapy generally demonstrates effectiveness across populations, the authors note their theoretical findings suggest it might be less efficient in darker-skinned infants, potentially affecting treatment duration and outcomes.

Highlighting the importance of obtaining more fundamental insight into newborn skin pigmentation, they also emphasize the critical need for clinical studies to validate these computational predictions and determine whether actual bilirubin reduction varies by skin color in real patients.

 Alida Johanna Dam-Vervloet et al, Effect of skin color and other skin properties on the delivered light dose in phototherapy for neonatal hyperbilirubinemia, Biophotonics Discovery (2025). DOI: 10.1117/1.BIOS.2.3.032508

Hidden body fat linked to faster heart aging

Excessive amounts of visceral fat—the hidden fat surrounding organs—is linked with faster aging of the heart, a new study has found.

Aging is the biggest risk factor for heart disease, but why some people age faster than others isn't fully understood. The scientists leading the research say that visceral body fat could play an important role in accelerating aging of the heart and blood vessels. This type of fat is known to be harmful to health and this study now links it to faster heart aging.

In the study, published in the European Heart Journal, the scientists analyzed data from 21,241 participants in the UK Biobank, which includes whole-body imaging to map the amount of fat and where it is located in the body.

The UK Biobank data also includes detailed imaging of the heart and blood vessels. Artificial intelligence was used to analyze these images to capture signs of organ aging—such as tissues becoming stiff and inflamed. An individual was given a "heart age" which can be compared to their actual age at the time of the scan.

The researchers found that faster heart aging was linked to having more visceral adipose tissue. Visceral adipose tissue is fat found deep inside the abdomen around organs such as the stomach, intestines, and liver. This type of fat cannot be seen from the outside, and some people can have large amounts of visceral fat despite having a healthy weight.

The researchers found signs on blood tests that visceral fat is linked to increased inflammation in the body—which is a potential cause of premature aging.

They also found differences between the sexes. Male-type fat distribution (fat around the belly, often called 'apple' shaped) was particularly predictive of early aging in men.

In contrast, a genetic predisposition to female-type fat (fat on the hips and thighs, often called "pear" shaped) was protective against heart aging in women.

The researchers also found a link between higher estrogen levels in premenopausal women and a slowing of heart aging, which they suggest could indicate a role for hormones in protecting against heart aging.

Declan P O'Regan et al, Sex-specific body fat distribution predicts cardiovascular ageing, European Heart Journal (2025). DOI: 10.1093/eurheartj/ehaf553

Croatian Freediver Shatters Record For Longest-Held Breath
This year, on June 14, Croatian freediver Vitomir Maričić set a world record when he held his breath for 29 minutes and 3 seconds.

That’s longer than a bottlenose dolphin, and 5 minutes longer than the previous Guinness World Record holder.
Nearly half an hour without air is mind boggling. That's roughly twice as long as a bottlenose dolphin is thought to hold its breath.
With each breath, a seal can replace 90 percent of the air in its lungs – but our species can only replace 20 percent. To keep up, we need more breaths to fill our lungs with fresh air.

To get as much oxygen into his body as it could possibly carry, Maričić inhaled pure oxygen for 10 minutes before the attempt.
This increased the oxygen dissolved in his blood plasma, which is a crucial reservoir for the body's tissues.

On an Instagram reel, Maričić explains that he started his record-breaking attempt with nearly five times more oxygen in his body than usual. Without that, he never could have lasted so long.

https://www.sciencealert.com/croatian-freediver-shatters-record-for...

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Scientists Have Just Created The Most Synthetic Life Form Ever

Scientists have created a bacteria with a genetic code more streamlined – and more meddled with – than any other life on Earth. This bacteria, a synthetic Escherichia coli called Syn57, has been engineered to build its body using just 57 of the 64 'codons' that have served all known organisms for billions of years. The recipe for life is written in a language that uses 64 different codons, each composed of a triplet of nucleotides. It's the long sentences of 'three-letter' codons that make up our DNA and RNA. They provide our cells with the essential instructions to translate ordinary matter into the building blocks of life, amino acids, which are threaded in sequence to form proteins. When a cell is building proteins, it 'reads' the codon sequence, written using those 64 nucleotide triplets, to know which amino acids to add next, and when to stop.By engineering the entire genome from scratch, the researchers set out to eliminate four of the six codons associated with the amino acid serine, two of the four alanine codons, and one 'stop' codon. Where these redundant codons appeared in the bacteria's genome, the researchers substituted them with synonymous codons that give the same instructions. This required more than 101,000 changes to the genetic code. These were planned out on the computer first, in 100-kilobyte fragments, and then came the arduous work of assembling the gene. To make sure they weren't inserting fundamentally harmful changes into the microbes, the team tested small fragments of the synthetic genome in living bacteria bit by bit, eventually stitching it all together to form the final, entirely synthetic strain.

https://www.science.org/doi/10.1126/science.ady4368

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Scientists discover rare freshened water beneath the seafloor

How did freshened water end up beneath the New England Shelf miles offshore?

Researchers are attempting to answer the question by studying samples collected from three sites off the coast of Nantucket. Sampling of this offshore freshened groundwater to the extent that they can make comprehensive geochemical assessments of its history, including its age, is unprecedented in scientific ocean drilling.

The salinity levels of sediments below the seafloor are typically close to those in the overlying ocean, yet offshore New England, the subseafloor contains an unusually large reservoir of freshened water.

The sheer freshness of the water, which was close to drinking water limits, was a surprise.

The cores will be archived and made accessible for further scientific research for the scientific community after a one-year moratorium period. All expedition data will be open access and resulting outcomes will be published.

https://www.uri.edu/news/2025/05/gso-professor-joins-expedition-to-...

Earliest evidence discovered of interbreeding between Homo sapiens and Neanderthals

An international study by researchers provides the first scientific evidence that Neanderthals and Homo sapiens had biological and social relations, and even interbred for the first time, in the Land of Israel.

The research team found a combination of Neanderthal and Homo sapiens traits in the skeleton of a five-year-old child discovered about 90 years ago in the Skhul Cave on Mount Carmel. The fossil, estimated to be about 140,000 years old, is the earliest human fossil in the world to display morphological features of both of these human groups, which until recently were considered two separate species.

Genetic studies over the past decade have shown that these two groups exchanged genes.

Even today, 40,000 years after the last Neanderthals disappeared, part of our genome—2% to 6%—is of Neanderthal origin. But these gene exchanges took place much later, between 60,000 to 40,000 years ago.

In the new study, the researchers were dealing with a human fossil that is 140,000 years old. They  show that the child's skull, which in its overall shape resembles that of Homo sapiens—especially in the curvature of the skull vault—has an intracranial blood supply system, a lower jaw, and an inner ear structure typical of Neanderthals.

For years, Neanderthals were thought to be a group that evolved in Europe, migrating to the Land of Israel only about 70,000 years ago, following the advance of European glaciers.

Part 1

This human type, which the researchers called "Nesher Ramla Homo" (after the archaeological site near the Nesher Ramla factory where it was found), encountered Homo sapiens groups that began leaving Africa about 200,000 years ago, and according to the current study's findings, interbred with them.

The child from the Skhul Cave is the earliest fossil evidence in the world of the social and biological ties forged between these two populations over thousands of years. The local Neanderthals eventually disappeared when they were absorbed into the Homo sapiens population, much like the later European Neanderthals.

The researchers reached these conclusions after conducting a series of advanced tests on the fossil.
The fossil they studied is the earliest known physical evidence of mating between Neanderthals and Homo sapiens.
The current study reveals that at least some of the fossils from the Skhul Cave are the result of continuous genetic infiltration from the local—and older—Neanderthal population into the Homo sapiens population.

Bastien Bouvier et al, A new analysis of the neurocranium and mandible of the Skhūl I child: Taxonomic conclusions and cultural implications, L'Anthropologie (2025). DOI: 10.1016/j.anthro.2025.103385

Part 2

Cells from the spleen found to play a surprising role after heart attack

After a person survives a heart attack, the heart has a brief window of time in which it can heal if the right circumstances exist. But most of the time, scar tissue forms in the areas that lacked oxygen during the heart attack. This scar tissue impairs heart function, which can worsen into heart failure, reducing quality of life and increasing the risk of early death.

A new study has identified a surprising role for the spleen—a small organ near the ribs that filters blood and fights infections—in helping the heart heal after a heart attack.

The research, published in Circulation, demonstrated in mice that specific immune cells called marginal metallophilic macrophages, which originate in the spleen, travel from the spleen to the heart and support a healing response after a heart attack.

Using mouse models, single-cell RNA sequencing and other advanced techniques, the researchers established that these specialized macrophages from the spleen help clear damaging immune cells, suppress inflammation and activate genes that help repair the injured cardiac tissue following a heart attack.

To assess whether the same thing occurs in humans, the researchers measured levels of marginal metallophilic macrophages in blood samples collected from people upon their hospital admission due to a heart attack. The researchers compared these levels with those of cardiac patients who had coronary artery disease but had not recently had a heart attack. The researchers  found that levels of the specialized macrophages were higher in patients who had just had a heart attack.

The researchers also demonstrated that they could boost the numbers of these specialized immune cells in mice with an experimental drug, and that doing so improved the healing and anti-inflammatory effects. This medical intervention is not yet in clinical trials, but it suggests a possible future cardiac immunotherapy targeting the spleen to prevent heart failure in patients who survive a heart attack.

 Mohamed Ameen Ismahil et al, Splenic CD169⁺Tim4⁺ Marginal Metallophilic Macrophages Are Essential for Wound Healing After Myocardial Infarction, Circulation (2025). DOI: 10.1161/CIRCULATIONAHA.124.071772

Kidney fibrosis linked to molecule made by gut bacteria

A molecule made by bacteria in the gut can hitch a ride to the kidneys, where it sets off a chain reaction of inflammation, scarring and fibrosis—a serious complication of diabetes and a leading cause of kidney failure—according to a new study from researchers .

After finding high levels of corisin—a small peptide produced by Staphylococcus bacteria in the gut—in the blood of patients with diabetic kidney fibrosis, the researchers used computer simulations and tissue and mouse experiments to track how corisin affects the kidneys, how it gets there from the gut, and a possible method of countering it with antibody treatment.

These  new findings suggest corisin is indeed a hidden culprit behind progressive kidney damage in diabetes, and that blocking it could offer a new way to protect kidney health in patients.

Taro Yasuma et al, Microbiota-derived corisin accelerates kidney fibrosis by promoting cellular aging, Nature Communications (2025). DOI: 10.1038/s41467-025-61847-2

Positive emotional bias could be an early sign of cognitive decline in aging populations

As people age, they display a bias in recognizing emotions as positive—to the point of improperly labeling neutral or negative emotions as positive.

Some researchers theorize this bias is an adaptive mechanism to support mental and emotional wellness, but new evidence suggests it may be a sign of cognitive decline.

In a JNeurosci paper, researchers advance understanding of what this positive emotional bias that elders exhibit signifies about their brains' health.

A large pool of participants (665) viewed faces in an emotion recognition task. Age-related positivity bias correlated with poorer cognitive performance in two assessments, but not necessarily emotional decline as measured by examining nonclinical depressive symptoms.

The researchers also observed structural changes in brain areas associated with emotional processing and changes in how these areas communicate to another brain region involved in social decisions. Thus, positivity bias from aging impacts the brain in observable ways that could be leveraged clinically to detect early rising signs of age-related neurodegeneration and cognitive decline.

Researchers are now  exploring how these findings relate to older adults with early cognitive decline, particularly those showing signs of apathy, which is often another early sign of dementia.

 Age-Related Positivity Bias in Emotion Recognition is Linked to Lower Cognitive Performance and Altered Amygdala–Orbitofrontal Connectivity, JNeurosci (2025). DOI: 10.1523/JNEUROSCI.0386-25.2025

Exercise intensity could be impacting your gut

While exercise is great for both your mental and physical health, new research from Edith Cowan University (ECU) has found that exercise intensity could result in changes to the internal gut biome.

Researchers undertook research into the impact of high and low training loads on athletes, in the hope of assisting athletes to improve their overall health, well-being and performance by better understanding the gut microbiome.

It appears that athletes have a different gut microbiota when compared with the general population. This includes greater total short chain fatty acid concentrations, alpha diversity, an increased abundance of some bacteria and a lower abundance of others.

 while the differing microbiome between athletes and the public could likely be due to the differences in their dietary intake , fitness markers, which include oxygen uptake, have also been correlated.

Published in the Journal of the International Society of Sports Nutrition, this research uncovered that training load had an influence on gut health markers in athletes, with differences detected in short-chain fatty acid concentrations and the abundance of specific bacteria.

 One of the potential reasons for the change in the gut could be the higher levels of blood lactate which results from higher intensity training. The lactate produced in muscle is transported to the gut to be metabolized, which could potentially result in increased bacteria in the gut.

The changes found in the gut biome when comparing high training loads to low training loads, were also related to diet.

Another observation made during the research was the significant slowing of gut transit times in athletes during low training loads. That slowing of transit time during the low training load appears to also be impacting the gut microbiome for an athlete.

The gut may play a role in lactate metabolism and regulating pH levels, both of which could impact performance and overall athlete health, say the researchers. 

B. Charlesson et al, Training load influences gut microbiome of highly trained rowing athletes, Journal of the International Society of Sports Nutrition (2025). DOI: 10.1080/15502783.2025.2507952

Why Were Dinosaurs So Big?

Metabolic adaptations, air sac-filled bones, and evolutionary pressure likely contributed to dinosaurs’ gigantism.

Scientists have found evidence that the long-necked and long-tailed sauropods had a comparatively slower metabolism relative to today’s large mammals, which indicates that they likely didn’t have to eat as much. (1)

And when sauropods did eat, they likely swallowed most of their food whole: Sauropods’ teeth had very little wear, unlike those of other herbivorous species, such as the duck-billed dinosaurs, and even mammals. (2,3)They could ‘vacuum up’ a lot of food without having to spend a lot of time chewing.

Some sauropod bones were also filled with air sacs, which could make even larger body sizes mechanically feasible.  (4)This adaptive anatomical feature is found in many birds, dinosaurs’ closest living relatives, and it helps reduce their body weight and promote flight.

Sources: 

1. Baumgart SL, et al. The living dinosaur: accomplishments and challenges of reconstructi.... Biol Lett. 2025;21(5):20250126.

2. Whitlock JA. Inferences of diplodocoid (Sauropoda: Dinosauria) feeding behavior .... PLoS One. 2011;6(4):e18304.

3. Fiorillo AR. Dental micro wear patterns of the sauropod dinosaurs camarasaurus a.... Hist Biol. 1998;13(1):1-16.

4. Wedel MJ. Evidence for bird-like air sacs in saurischian dinosaurs. J Exp Zool A Ecol Genet Physiol. 2009;311(8):611-628.

5. https://www.the-scientist.com/why-were-dinosaurs-so-big-73254?utm_c...

Cells 'vomit' waste to promote healing, but it comes with a trade-off

When injured, cells have well-regulated responses to promote healing. These include a long-studied self-destruction process that cleans up dead and damaged cells as well as a more recently identified phenomenon that helps older cells revert to what appears to be a younger state to help grow back healthy tissue.

Now, a new study in mice  reveals a previously unknown cellular purging process that may help injured cells revert to a stem cell-like state more rapidly. The investigators have dubbed this newly discovered response cathartocytosis, taking from Greek root words that mean cellular cleansing.

Published in the journal Cell Reports, the study used a mouse model of stomach injury to provide new insights into how cells heal—or fail to heal—in response to damage, such as from an infection or inflammatory disease.

After an injury, the cell's job is to repair that injury. But the cell's mature cellular machinery for doing its normal job gets in the way. So, this cellular cleanse is a quick way of getting rid of that machinery so it can rapidly become a small, primitive cell capable of proliferating and repairing the injury. Researchers identified this process in the GI tract, but they suspect it is relevant in other tissues as well.

The researchers identified cathartocytosis within an important regenerative injury response called paligenosis. 

In paligenosis, injured cells shift away from their normal roles and undergo a reprogramming process to an immature state, behaving like rapidly dividing stem cells, as happens during development. Originally, the researchers assumed the decluttering of cellular machinery in preparation for this reprogramming happens entirely inside cellular compartments called lysosomes, where waste is digested in a slow and contained process. From the start, though, the researchers noticed debris outside the cells. They initially dismissed this as unimportant, but the more external waste they saw in their early studies, the more they began to suspect that something deliberate was going on. They utilized a model of mouse stomach injury that triggered the reprogramming of mature cells to a stem cell state all at once, making it obvious that the "vomiting" response—now happening in all the stomach cells simultaneously—was a feature of paligenosis, not a bug.

In other words, the vomiting process was not just an accidental spill here and there, but a newly identified, standard way cells behaved in response to injury.

Although they discovered cathartocytosis happening during paligenosis, the researchers said cells could potentially use cathartocytosis to jettison waste in other, more worrisome situations, like giving mature cells that ability to start to act like cancer cells.

While the newly discovered cathartocytosis process may help injured cells proceed through paligenosis and regenerate healthy tissue more rapidly, the trade-off comes in the form of additional waste products that could fuel inflammatory states, making chronic injuries harder to resolve and correlating with an increased risk of cancer development.

 Jeffrey W. Brown et al, Cathartocytosis: Jettisoning of cellular material during reprogramming of differentiated cells, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.116070

Glow-in-the-dark succulents that recharge with sunlight could pave way to plant-based lighting systems

From mushrooms that cast a soft green glow to plankton that glimmers sparkling blue, glowing plants are nothing new to nature. Now, scientists are bringing that light to houseplants.

Reporting in the journal Matter, researchers crafted glow-in-the-dark succulents that recharge in sunlight. Injected with light-emitting compounds, the plants can shine in various colors and rival a small night light at their brightest. The simple, low-cost method may help lay the foundation for sustainable, plant-based lighting systems.

Researchers used afterglow phosphor particles—materials similar to those found in glow-in-the-dark toys. These compounds absorb light and release it slowly over time.

For the particles to travel through leaf tissues, the researchers had to get the size just right: around 7 micrometers, roughly the width of a red blood cell.

Smaller, nano-sized particles move easily within the plant but are dimmer. Larger particles glowed brighter but couldn't travel far inside the plant.

The team then injected the particles into several plant species, including succulents and non-succulents like golden pothos and bok choy. But only the succulents produced a strong glow, thanks to the narrow, uniform, and evenly distributed channels within the leaf that helped to disperse the particles more effectively. After a couple of minutes of exposure to sunlight or indoor LED light, the modified plants glowed for up to two hours.

The particles diffused in just seconds, and the entire succulent leaf glowed.

By using different types of phosphors, the researchers created plants that shine in various colors, including green, red, and blue. They even built a glowing plant wall with 56 succulents, bright enough to illuminate nearby objects and read texts.

Each plant takes about 10 minutes to prepare.

The glowing succulents' light fades over time, and the team is still studying the long-term safety of the materials for the plants.

Sunlight-powered multicolor and uniform luminescence in material-engineered living plants, Matter (2025). DOI: 10.1016/j.matt.2025.102370

How pigments affect the weight of bird feathers

Birds are some of the most striking creatures on Earth, coming in a rainbow of colors that serve several important functions, such as attracting a mate and communicating with other birds. These vibrant hues are produced by pigments, primarily melanin, but a major unknown until now was how much these pigments weigh. Since wings need to be as light as possible for flight, understanding pigmentation weight may tell us something about the trade-off between the evolutionary benefits of colored feathers and the physical cost of carrying that weight.

In a new study published in the journal Biology Letters, scientists  have investigated how much melanin adds to the weight of feathers and the difference in weight between the two main chemical forms of melanin—eumelanin (responsible for brown and black colors) and pheomelanin (responsible for reds and lighter colors).

The researchers analyzed the feathers from 109 bird specimens across 19 different species, including the common kingfisher (Alcedo atthis), the golden eagle (Aquila chrysaetos) and the Eurasian bullfinch (Pyrrhula pyrrhula). They examined feathers with mixed colors and those with single, pure colors, and used a chemical process involving sodium hydroxide or caustic soda, as it is more commonly known, to extract the pigments. Once extracted, they were weighed and compared to the original weight of the feathers.

According to the scientists, melanin pigments account for about 22% of a feather's total weight, and in the most pigmented feathers, this weight is no more than 25%. Additionally, the two types of pigments don't weigh the same. Eumelanin, which makes feathers black or brown, was significantly heavier than pheomelanin, which produces lighter colors.

The paper suggests that a bird has to expend more energy to carry the weight of certain feather colors, which could explain why birds have evolved such a wide variety of hues, as the scientists write in their paper. 

The researchers suggested that birds in cold climates, like snowy owls, didn't just evolve white feathers for camouflage. The lack of a heavy pigment would allow them to grow thicker, more insulating feathers without adding too much weight. Therefore, they can stay warm and still be able to fly. Additionally, migratory birds may have evolved lighter feathers to reduce the energy cost of flying long distances.

Ismael Galván et al, Pigment contribution to feather mass depends on melanin form and is restricted to approximately 25%, Biology Letters (2025). DOI: 10.1098/rsbl.2025.0299

 Microbes in soil may affect hormones tied to love, mental health and social bonds

Experts are exploring evidence that microbes in the soil and the environments around us can affect human microbiota and the "gut-brain axis," potentially shaping emotional states and relationship dynamics—including aspects of romantic love.

They outline the idea in a review article in mSystems proposing how the human gut microbiome might influence hormonal pathways involved in emotions commonly associated with love.

This is not claiming microbes 'cause' love or hatred. The aim is to map plausible biological routes, grounded in microbiology and endocrinology, that researchers can now evaluate with rigorous human studies.

The mini-review, "Does a microbial-endocrine interplay shape love-associated emotions in humans? A hypothesis," synthesizes evidence that microbes can modulate hormones and key neurotransmitters such as dopamine, serotonin and oxytocin.

The researchers are exploring how the evolutionary underpinnings of microbial-endocrine interactions could provide important insights into how microbes influence emotions beyond love, including hate and aggression.

If these pathways are confirmed, the findings could open avenues for microbiome-informed strategies to support mental health and relational well-being. For now, it provides a roadmap for careful, hypothesis-driven science.

Jake M. Robinson et al, Does a microbial-endocrine interplay shape love-associated emotions in humans? A hypothesis, mSystems (2025). DOI: 10.1128/msystems.00415-25

Xin Sun et al, Unforeseen high continental-scale soil microbiome homogenization in urban greenspaces, Nature Cities (2025). DOI: 10.1038/s44284-025-00294-y

Inflammation may explain why women with no standard modifiable risk factors have heart attacks and strokes

Several people ask me this question: Why do people who lead very healthy lives get heart attacks and strokes?

Yes why?

Cardiologists have long known that up to half of all heart attacks and strokes occur among apparently healthy individuals who do not smoke and do not have high blood pressure, high cholesterol, or diabetes, the "standard modifiable risk factors" which doctors often call "SMuRFs."

How to identify risk among the "SMuRF-Less" has been an elusive goal in preventive cardiology, particularly in women who are often under-diagnosed and under-treated.

A new study now has found hsCRP—a marker of inflammation—can help identify women who are at risk but are missed by current screening algorithms.

Results were presented at a late-breaking clinical science session at the European Society of Cardiology Congress (ESC) and simultaneously published in The European Heart Journal.

Women who suffer from heart attacks and strokes yet have no standard modifiable risk factors are not identified by the risk equations doctors use in daily practice.

Yet the new data clearly shows that apparently healthy women who are inflamed are at substantial lifetime risk. Medical professionals should be identifying these women in their 40s, at a time when they can initiate preventive care, not wait for the disease to establish itself in their 70s when it is often too late to make a real difference.

As part of the study, researchers studied 12,530 initially healthy women with no standard modifiable risk factors who had the inflammatory biomarker hsCRP measured at study entry and who were then followed over 30 years.

Despite the lack of traditional risks, women who were inflamed as defined by hsCRP levels > 3 mg/L had a 77% increased lifetime risk of coronary heart disease, a 39% increased lifetime risk of stroke, and a 52% increased lifetime risk of any major cardiovascular event.

Additionally, researchers released a new analysis of randomized trial data showing that "SMuRF-Less but Inflamed" patients can reduce their risk of heart attack and stroke by 38% using statin therapy.

While those with inflammation should aggressively initiate lifestyle and behavioral preventive efforts, statin therapy could also play an important role in helping reduce risk among these individuals, say the researchers.

 Paul Ridker et al, C-Reactive Protein and Cardiovascular Risk Among Women with No Standard Modifiable Risk Factors: Evaluating The "SMuRF-Less but Inflamed", (2025). DOI: 10.1093/eurheartj/ehaf658

Placebo pain relief works differently across the human body

Researchers have used placebo pain relief to uncover a map-like system in the brainstem that controls pain differently depending on where it's felt in the body. The findings may pave the way for safer, more targeted treatments for chronic pain that don't rely on opioids.

Like a highway, the brainstem connects the brain to the spinal cord and manages all signals going to and from the brain. It produces and releases nearly all the neurochemicals needed for thinking, survival and sensing.

Published in Science, the study used 7-Tesla functional magnetic resonance imaging (fMRI)—one of the most powerful brain scanners available—to pinpoint how two key brainstem regions manage pain through placebo effects. 

Researchers exposed 93 healthy participants to heat pain on different body parts and applied a placebo pain-relief cream while secretly lowering the temperature, conditioning them to believe the cream was alleviating their pain.

The temperature used was individually adjusted to be moderately painful as perceived by each participant. Researchers used a self-report scale, where 0 was no pain and 100 was the worst pain imaginable, and sought a temperature between 40 and 50 for each participant.

Later, the same pain stimulus was applied to the placebo-treated area as well as a separate untreated area for comparison. Up to 61% of participants still reported less pain in the area where the placebo cream was originally applied, typical of a true placebo response.

They  found that upper parts of the brainstem were more active when relieving facial pain, while lower regions were engaged for arm or leg pain.

Two key brainstem regions are involved in this process: the periaqueductal gray (PAG) and the rostral ventromedial medulla (RVM). These areas showed distinct patterns of activity depending on where pain relief was directed, with the upper parts of the PAG and RVM more active for facial pain, while lower parts were more active for arm or leg pain.

The brain has a built-in system to control pain in specific areas. It's not just turning pain off everywhere; but working in a highly coordinated, anatomically precise system.

Understanding which brainstem areas are linked to different parts of the body may open new avenues for developing non-invasive therapies that reduce pain without widespread side effects.

The study also challenges long-held assumptions about how placebo pain relief works. Instead of relying on the brain's opioid system, experts say a different part of the brainstem—the lateral PAG—is not only responsible but works without using opioids and could instead be linked to cannabinoid activity.

Opioid-based pain relief typically activates central areas of the brain and can affect the whole body, whereas the cannabinoid circuit that they identified now appears to operate in more targeted regions of the brainstem.

Knowing exactly where pain relief is happening in the brain means we can target that area or assess whether a drug is working in the right place.

Lewis S. Crawford et al, Somatotopic organization of brainstem analgesic circuitry, Science (2025). DOI: 10.1126/science.adu8846

The AI breakthrough that uses almost no power to create images

From creating art and writing code to drafting emails and designing new drugs, generative AI tools are becoming increasingly indispensable for both business and personal use. As demand increases, they will require even more computing power, memory and, therefore, energy. That's got scientists looking for ways to reduce their energy consumption.

In a paper published in the journal Nature, researchers describe the development of an AI image generator that consumes almost no power.

AI image generators use a process called diffusion to generate images from text. First, they are trained on a large dataset of images and repeatedly add a statistical noise, a kind of digital static, until the image has disappeared.

Then, when you give AI a prompt such as "create an image of a house," it starts with a screen full of static and then reverses the process, gradually removing the noise until the image appears. If you want to perform large-scale tasks, such as creating hundreds of millions of images, this process is slow and energy intensive.

Shiqi Chen et al, Optical generative models, Nature (2025). DOI: 10.1038/s41586-025-09446-5

Daniel Brunner, Machine-learning model generates images using light, Nature (2025). DOI: 10.1038/d41586-025-02523-9

AI tool targets RNA structures to unravel secrets of the dark genome

We mapped the human genome decades ago, but most of it is still a black box. Now,  scientists have developed a tool to peer inside and what they find could reshape how we think about disease.

Your genome is the genetic map of you, and we understand almost none of it.
Our handle on the bits of the genome that tell the body how to do things ("make eyes blue," "build heart tissue," "give this person sickle cell anemia") is OK, but there are vast areas of the genome that don't appear to do anything.
Scientists long assumed this was just "junk" DNA, leftovers from the billions of years it took us to evolve from primordial soup into the complex life we know today. But it turns out we just didn't know what to look for, nor how to look for it.
Now, new tools developed by researchers are helping us understand just how important the dark genome really is.

Understanding that, scientists hope, will offer new avenues for drug discovery, and transform how we think about disease and even life itself.

Your genome is broken up into protein-coding genes (around 2%), and the rest.

Proteins are the little machines that do the actual work of running an organism;protein-coding genes are the instructions for those proteins.

The other 98% doesn't build proteins, it doesn't follow the same rules, and it's much harder to understand. It contains "long non-coding RNAs," the stuff that was long dismissed as junk.

Scientists are  trying to decode the logic circuitry of the human genome—the hidden rules that tell our DNA how to build and run a human being.

Part 1

It's a tough job, but a crucial one because studies show that the roots of many diseases, including heart disease, cancer, and some psychiatric disorders, lie outside the well-understood, protein-coding regions of the genome.

Non-protein coding genes have key regulatory roles, turning certain genes on and off or altering their shape.

Do any of that at the wrong time, and things start to break down.

Scientists think that these RNAs act like software, orchestrating the protein 'hardware' into a functioning symphony.
Not junk at all.
You might have heard that you share 60% of your DNA with a banana.

It's not strictly speaking true, unfortunately, but there is a germ of truth there.

Humans and bananas (and everything else) all evolved from the same soup of bacteria and single-celled organisms about four billion years ago, and some of our DNA has been conserved over that time because it performs fundamental functions in our cells.

Studies have shown that about 10% of the human genome shows obvious conservation, but the rest is harder to pin down.

Scientists suspect that the remaining approximately 90% of the genome harbors many conserved RNA structures that are invisible to traditional approaches—hidden regulatory elements camouflaged in the genome.
Which is where the the newly developed AI—a tool called ECSFinder—comes in. It has been detailed in a paper in the journal Nucleic Acids Research.
Scientists trained the program on known RNA structures to detect secrets hidden in the genome. The program outperformed other available tools and is now ready to be unleashed on the entire genome.

They expect to uncover hundreds of thousands of new RNA structures, adding a new dimension to our understanding of the genome.

The holy grail of medicine right now is personalized therapy, treatments designed specifically for your individual illness.

One day, it's hoped, clinicians will be able to take a sample of your cancer's DNA, map its genome, then design ultra-specific drugs around its weaknesses, all within a few weeks.

And if the secrets of all gene-driven illnesses are hidden somewhere in the dark genome, learning how to read it is imperative.

Because RNA structures can be targeted by drugs, they present an exciting new frontier for therapies.

 Vanda Gaonac'h-Lovejoy et al, ECSFinder: optimized prediction of evolutionarily conserved RNA secondary structures from genome sequences, Nucleic Acids Research (2025). DOI: 10.1093/nar/gkaf780

Part 2

Scientists move toward developing vaccine against pathogenic Staphylococcus aureus

Antibiotics are the old medicine cabinet standby for treating infections caused by multidrug-resistant Staphylococcus aureus, but as antimicrobial resistance continues to mount globally, scientists say there's a need for new strategies.

While vaccines are a potential answer, achieving an effective way to immunize against multidrug-resistant S. aureus has led scientists down dozens of blind alleys. Ten candidate vaccines that looked promising in preclinical animal studies in recent years failed miserably in human clinical trials.

Now, scientists are investigating a way to sidestep the myriad problems that plagued vaccine investigators in the past by choosing not to target a whole antigen. Instead, they say, it's time to home in on a critical "surface loop" as a vaccine target. The infinitesimal loop is located on the S. aureus antigen known as MntC.

The loop is an ideal target, scientists  say, because it has been shown to be essential for aiding survival in S. aureus by mitigating oxidative stress. By triggering vaccine-induced antibodies that zero in on that site, survival is impossible. As a vaccine target, the surface loop is known as an epitope.

Writing in Science Translational Medicine, researchers at institutions from throughout China report on the creation of a first-of-its-kind vaccine that has been tested in animal models based on a target pinpointed in samples from human clinical trials. The evolving strategy overcomes past obstacles and confers protection against drug-resistant S. aureus with a vaccine.

Xiaokai Zhang et al, An epitope vaccine derived by analyzing clinical trial samples safeguards hosts with prior exposure to S. aureus against reinfection, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adr7464

Cancer can smuggle mitochondria in neighboring cells and put them to work

Cancer cells provide healthy neighboring cells with additional mitochondria to put them to work. This has been demonstrated by researchers  in a new study. In this way, cancer is exploiting a mechanism that frequently serves to repair damaged cells.

Tumors have developed many strategies and tricks to gain advantages in the body. Researchers have now discovered another surprising trick that certain tumors resort to in ensuring their survival and growth.

In a study published in the journal Nature Cancer, biologists show that skin cancer cells are able to transfer their mitochondria to healthy connective tissue cells (fibroblasts) in their immediate vicinity. Mitochondria are the cell compartments that provide energy in the form of the molecule ATP.

The cancer cells use tiny tubes made of cell membrane material to transfer the mitochondria and connect the two cells—much like in a pneumatic tube system.

The mitochondrial transfer reprograms the fibroblasts functionally into tumor-associated fibroblasts, which mainly support cancer cells: tumor-associated fibroblasts usually multiply faster than normal fibroblasts and produce more ATP, while also secreting higher amounts of growth factors and cytokines. And all this benefits the tumor cells: they also multiply faster, making the tumor more aggressive.

The hijacked fibroblasts also alter the cell environment—the so-called extracellular matrix—by increasing the production of certain matrix components in such a way that cancer cells thrive. The extracellular matrix is vital for the mechanical stability of tissues and influences growth, wound healing and intercellular communication.

Finally, the researchers also clarified the molecular mechanism behind the mitochondrial transfer. Some proteins were already known to assist in transporting mitochondria. The researchers investigated which of these proteins were present in large numbers in cancer cells that transfer mitochondria and came across the protein MIRO2. This protein is produced in very high quantities in cancer cells that transfer their mitochondria.

The researchers detected MIRO2 not only in cell cultures, but also in samples of human tissue—especially in tumor cells at the edges of tumors that grow invasively into the tissue and occur in close proximity to fibroblasts.

The new findings offer starting points for arresting tumor growth. When the researchers blocked the formation of MIRO2, the mitochondrial transfer was inhibited, and the fibroblasts did not develop into tumor-promoting fibroblasts.

The MIRO2 blockade worked in the test tube and in mouse models. Whether it also works in human tissue remains to be seen, say the researchers.

Michael Cangkrama et al, MIRO2-mediated mitochondrial transfer from cancer cells induces cancer-associated fibroblast differentiation, Nature Cancer (2025). DOI: 10.1038/s43018-025-01038-6

Metformin changes blood metal levels in humans, offering further insight into its mechanism of action

The widely used diabetes drug metformin changes blood metal levels in humans. A new study is an important step in understanding the drug's many actions and designing better ones in the future.

Metformin is the most widely prescribed diabetes drug in the world. Apart from lowering blood sugar levels, it is also known to have a broad range of beneficial side effects such as against tumors, inflammation and atherosclerosis. However, although it has been used for more than 60 years now, its mechanism of action is still not clear, hampering the development of even better drugs against these conditions.

It is known that diabetes patients experience changes in the blood levels of metals such as copper, iron and zinc.

In addition, chemical studies found that metformin has the ability to bind certain metals, such as copper, and recent studies showed that it is this binding ability that might be responsible for some of the drug's beneficial effects. 

In the journal BMJ Open Diabetes Research & Care, researchers have published the first clinical evidence of altered blood metal levels in patients taking metformin. They showed that drug-taking patients have significantly lower copper and iron levels and heightened zinc levels.

Furthermore, since decreases in copper and iron concentrations and an increase in zinc concentration are all considered to be associated with improved glucose tolerance and prevention of complications, these changes may indeed be related to metformin's action.

 Association of metformin treatment with changes in metal dynamics in individuals with type 2 diabetes, BMJ Open Diabetes Research & Care (2025). DOI: 10.1136/bmjdrc-2025-005255