Record-Shattering 20,000 Mph Winds Detected on Wild Alien Planet Winds circling a gas giant more than 500 light years from Earth have been detected flowing at supersonic speeds approaching 33,000 kilometers (20,000 miles) per hour, making them the fastest air currents on any known planet by a wide margin. Researchers from Europe cleaned and analyzed the spectrum of light reflected from the planet WASP-127b, uncovering two contrasting peaks in water and carbon dioxide signals suggestive of supersonic flows disturbing the planet's cloud tops.
Part of the atmosphere of this planet is moving towards us at a high velocity while another part is moving away from us at the same speed. This signal shows us that there is a very fast, supersonic, jet wind around the planet's equator.
Fast is an understatement. At an incredible 7.5 to 7.9 kilometers per second, they outstrip any hurricane or jetstream known to science. Here on Earth, the fastest puff of wind on record was a blustery 407 kilometers (253 miles) per hour, measured on Australia's Barrow Island in 1996. Neptune has the highest wind speeds in our Solar System, but even its 1,770 kilometer-per-hour high-altitude currents feel more like a mild breeze by comparison.
It's also believed to be tidally locked, rotating in step with every 4.2-Earth-day lap around its star, so one side is perpetually baked to temperatures exceeding 1,000 degrees Celsius (1832 degrees Fahrenheit), and the other never turns from the cold night sky.
Scientists uncover how cancer cells hijack T-cells, making it harder for the body to fight back
Researchers have discovered a surprising way cancer evades the immune system. It essentially hacks the immune cells, transferring its own faulty mitochondrial DNA (mtDNA) into the T-cells meant to attack it.
This sneaky move weakens the immune cells, making them less effective at stopping the tumor. The findings could help explain why some cancer treatments, like immunotherapy, are effective for some patients but not others.
In the study, "Immune evasion through mitochondrial transfer in the tumour microenvironment," published in Nature, the multi-group collaboration looked at how cancer cells interact with tumor-infiltrating lymphocytes, a type of T-cell that typically fights tumors. The research is also featured in a News and Views piece.
Clinical specimens from melanoma and non-small-cell lung cancer patients were analyzed for mtDNA mutations. Mitochondrial transfer was studied using mitochondrial-specific fluorescent reporters and multiple in vitro and in vivo models. Tumor-infiltrating lymphocyte functions, metabolic profiles, and responses to immune checkpoint inhibitors were evaluated.
Melanoma and lung sample analysis showed that mitochondria, the energy-making engines of cells, could jump from cancer cells into T-cells. These transferred mitochondria carried functional errors in their DNA that interfered with the T-cells' energy production and function processes.
Mitochondria are essential for powering cells, including T-cells, which depend heavily on energy production to fight cancer. But when cancer cells pass on their defective mitochondria, they lose their ability to function properly, throttling the energy of the T-cells and causing them to become exhausted.
Transfer was observed in two main ways: tunneling nanotubes and extracellular vesicles. The nanotubes extend out and tunnel into the T-cell, creating tiny passages between cells that deliver mitochondria directly. Extracellular vesicles form as bubbles released by the cancer cells, encapsulating mtDNA and other molecules.
Once inside the T-cells, the damaged mitochondria replace the healthy ones through a mechanism that would normally operate in reverse, where healthy mitochondria would migrate to replace damaged ones. The study found that cancer cells protect their transferred mitochondria by attaching molecules that prevent the T-cells from breaking them down.
Immune checkpoint inhibitors have revolutionized cancer treatment. But not everyone responds well to these drugs. This study found that patients whose tumors had more mitochondrial mutations were less likely to benefit from checkpoint inhibitors, likely because the mitochondrial hack already compromised their T-cells.
Researchers blocked extracellular vesicle release from cancer cells using a compound called GW4869, which inhibits the production of small extracellular vesicle-like exosomes. Applying this inhibitor in their models showed a significant reduction in mitochondrial transfer from cancer cells to T-cells. This intervention helped prevent the T-cells from taking up damaged mitochondria, reducing their dysfunction.
As a result, T-cells showed improved energy production, reduced markers of exhaustion, and a better ability to perform their immune functions. The blocking strategy restored the effectiveness of immune checkpoint inhibitors, particularly in tumors with high levels of mitochondrial transfer. These findings suggest that targeting extracellular vesicles could be a promising strategy to counteract cancer's immune-evasion tactic. Typically, science works in small, iterative steps toward discovery, with each new element of knowledge putting a piece of the larger puzzle into place. This discovery helps explain why some treatments are ineffective and discovers the mechanism behind their ineffectiveness. Remarkably, it also found a potential solution, representing a significant leap for future research to build from.
Hideki Ikeda et al, Immune evasion through mitochondrial transfer in the tumour microenvironment,Nature(2025).DOI: 10.1038/s41586-024-08439-0
Jonathan R. Brestoff, Mitochondrial swap from cancer to immune cells thwarts anti-tumour defences,Nature(2025).DOI: 10.1038/d41586-025-00077-4
Research reveals how specific types of liver immune cells are required to deal with injury
Our livers contain many different types of immune cells. New research now reveals that a specific activation state of one of these cell types is required for tissue repair following injury. This suggests these cells may be useful as new therapeutic targets for various liver conditions. The work appears in the journal Immunity.
Macrophages are specialized immune cells located in every tissue of the body, where they play crucial roles in maintaining tissue homeostasis, responding to injury, and facilitating tissue repair. In the healthy liver, most macrophages are classified as Kupffer cells (KCs). However, upon liver injury, as seen, for example, in obesity, another subset of macrophages called lipid-associated macrophages (LAMs) is recruited.
This work shows that the LAM phenotype is critical for liver repair. Moreover, this research revealed that the KCs are not static post-injury, as previously thought, and instead adapt to the new microenvironment also taking on a LAM-like phenotype, allowing them to also participate in the repair.
Federico F. De Ponti et al, Spatially restricted and ontogenically distinct hepatic macrophages are required for tissue repair, Immunity (2025). DOI: 10.1016/j.immuni.2025.01.002
Astronauts' eyes weaken during long space missions, raising concerns for Mars travel
The low levels of gravity (microgravity) in space cause significant changes in astronauts' eyes and vision after six to 12 months aboard the International Space Station (ISS), according to a study published in the IEEE Open Journal of Engineering in Medicine and Biology.
Researchers found that at least 70% of astronauts on the ISS have been affected by spaceflight-associated neuro-ocular syndrome, or SANS.
They analyzed data collected by the Canadian team at NASA on 13 astronauts who spent between 157 and 186 days on the ISS.
The subjects had an average age of 48 and came from the U.S., European, Japanese and Canadian space agencies; 31% were women; eight were on their first mission.
The researchers compared three ocular parameters before and after the astronauts' space missions: ocular rigidity, intraocular pressure, and ocular pulse amplitude. They measured ocular rigidity using optical coherence tomography with a customized video module to improve the quality of images of the choroid. The other two parameters, intraocular pressure and ocular pulse amplitude, were measured using tonometry.
The study found significant changes in the biomechanical properties of the astronauts' eyes: a 33% decrease in ocular rigidity, an 11% decrease in intraocular pressure, and a 25% reduction in ocular pulse amplitude.
These changes were accompanied by symptoms including reduced eye size, altered focal field and, in some cases, optic nerve edema and retinal folds.
The researchers also found that five astronauts had a choroidal thickness greater than 400 micrometers, which was not correlated with age, gender or previous space experience.
Weightlessness alters the distribution of blood in the body, increasing blood flow to the head and slowing venous circulation in the eye. This is probably what causes the expansion of the choroid, the vascular layer that nourishes the retina. According to the researchers, the expansion of the choroid during weightlessness could stretch the collagen in the sclera, the white outer layer of the eye, causing long-lasting changes in the eye's mechanical properties.
They also think that blood pulsations under microgravity can create a water-hammer effect in which sudden changes in blood-flow-pressure cause a mechanical shock to the eye, leading to significant tissue remodeling. According to the researchers, these ocular changes are generally not cause for concern when the space mission lasts six to 12 months. Although 80% of the astronauts they studied developed at least one symptom, their eyes returned to normal once back on Earth.
In most cases, wearing corrective eyeglasses was sufficient to correct the symptoms developed aboard the ISS.
However, the research community and international space agencies are cautious about the consequences of longer missions, such as a flight to Mars. The eye-health effects of prolonged exposure to microgravity remain unknown, and no preventive or palliative measures now exist.
Marissé Masís Solano et al, Ocular Biomechanical Responses to Long-Duration Spaceflight, IEEE Open Journal of Engineering in Medicine and Biology (2024). DOI: 10.1109/OJEMB.2024.3453049
Scientists trace deadly cell-to-cell message chain that spreads in sepsis
Dying cells prick their neighbours with a lethal message. This may worsen sepsis, researchers report in the Jan. 23 issue of Cell. Their findings could lead to a new understanding of this dangerous illness.
Sepsis is one of the most frequent causes of death worldwide, according to the World Health Organization (WHO), killing 11 million people each year. It's characterized by runaway inflammation, usually sparked by an infection. It can lead to shock, multiple organ failure, and death if treatment is not rapid enough or effective.
But recent research has shown that it isn't actually the infection that causes the spiraling inflammation: it's the cells caught up in it. Even if those cells aren't infected, they act as if they are, and die. As they die, they send out messages to other cells. Those messages somehow cause the recipient cells to die.
If scientists understood what caused this deadly message chain, they might be able to stop it. And that could help heal sepsis.
The deadly message mystery may now be solved. It appears that the "messages" are a byproduct of the cells trying to stay alive.
The process starts with cells that really are infected. To prevent the infection from spreading, those cells destroy themselves by sending a protein called gasdermin-D to their surface. Several gasdermin-D proteins will link together to create a round poreon the cell, like a hole punched in a balloon. The cell's contents leak out, the cell collapses, and dies.
But the collapse isn't inevitable. Sometimes cells can act quickly and eject the section of their surface membrane with the gasdermin-D pore. The cell then zips the membrane closed and survives. The ejected membrane forms a little bubble, called a vesicle , that just happens to carry the deadly gasdermin-D pore. The vesicle floats around, and when it encounters a cell nearby, that deadly gasdermin-D pore punches into the healthy nearby cell's membrane and causes that cell to spill and die.
When a dying cell releases these vesicles, they can transplant these pores to a neighboring cell's surface, which leads to the neighboring cell's death.
In other words, the deadly messages are a side effect of cells just trying to save themselves. A group of dying cells can release enough gasdermin-D vesicles to kill a considerable number of nearby cells. That spreading message of death fuels the spiraling inflammation of sepsis.
Researchers are now looking for a way to tamp down the deadly gasdermin-D vesicles. If successful, it could lead to a treatment for inflammatory diseases like sepsis.
Skylar S. Wright et al, Transplantation of gasdermin pores by extracellular vesicles propagates pyroptosis to bystander cells, Cell (2024). DOI: 10.1016/j.cell.2024.11.018
Sleep is a more physiologically ‘active’ state. Hibernation, in contrast, requires animals (like this hedgehog, above) to substantially reduce all activities to conserve energy.
Hibernating animals reduce their breathing rate, lower their body temperature and decrease their metabolic rate to around five per cent of their usual levels. There’s simply not enough brain activity while an animal is hibernating to enable dreaming.
There is one exception, however: the fat-tailed lemur. As the only primate to hibernate, scientists have observed them having periods of rapid eye movement (REM) sleep.
New water purification technology helps turn seawater into drinking water without using tons of chemicals
Water desalination plants could replace expensive chemicals with new carbon cloth electrodes that remove boron from seawater, an important step of turning seawater into safe drinking water.
A study describing the new technology has been published in Nature Water.
Boron is a natural component of seawater that becomes a toxic contaminant in drinking water when it sneaks through conventional filters for removing salts. Seawater's boron levels are around twice as high as the World Health Organization's most lenient limits for safe drinking water, and five to 12 times higher than the tolerance of many agricultural plants.
Most reverse osmosis membranes don't remove very much boron, so desalination plants typically have to do some post treatment to get rid of the boron, which can be expensive. So researchers developed a new technology that's fairly scalable and can remove boron in an energy-efficient way compared to some of the conventional technologies.
In seawater, boron exists as electrically neutral boric acid, so it passes through reverse osmosis membranes that typically remove salt by repelling electrically charged atoms and molecules called ions. To get around this problem, desalination plants normally add a base to their treated water, which causes boric acid to become negatively charged. Another stage of reverse osmosis removes the newly charged boron, and the base is neutralized afterward by adding acid. Those extra treatment steps can be costly.
The new device now developed reduces the chemical and energy demands of seawater desalination, significantly enhancing environmental sustainability and cutting costs by up to 15 percent, or around 20 cents per cubic meter of treated water.
The new electrodes remove boron by trapping it inside pores studded with oxygen-containing structures. These structures specifically bind with boron while letting other ions in seawater pass through, maximizing the amount of boron they can capture.
But the boron-catching structures still need the boron to have a negative charge. Instead of adding a base, the charge is created by splitting water between two electrodes, creating positive hydrogen ions and negative hydroxide ions. The hydroxide attaches to boron, giving it a negative charge that makes it stick to the capture sites inside the pores in the positive electrode. Capturing boron with the electrodes also enables treatment plants to avoid spending more energy on another stage of reverse osmosis. Afterward, the hydrogen and hydroxide ions recombine to yield neutral, boron-free water.
Weiyi Pan et al, A highly selective and energy efficient approach to boron removal overcomes the Achilles heel of seawater desalination, Nature Water (2025). DOI: 10.1038/s44221-024-00362-y
AI-based pregnancy analysis discovers previously unknown warning signs for stillbirth and newborn complications
A new AI-based analysis of almost 10,000 pregnancies has discovered previously unidentified combinations of risk factors linked to serious negative pregnancy outcomes, including stillbirth.
The study also found that there may be up to a tenfold difference in risk for infants who are currently treated identically under clinical guidelines.
The researchers started with an existing dataset of 9,558 pregnancies, which included information on social and physical characteristics ranging from pregnant people's level of social support to their blood pressure, medical history, and fetal weight, as well as the outcome of each pregnancy. By using AI to look for patterns in the data, they identified new combinations of maternal and fetal characteristics that were linked to unhealthy pregnancy outcomes such as stillbirth.
Usually, female fetuses are at slightly lower risk for complications than male fetuses—a small but well-established effect. But the research team found that if a pregnant person has pre-existing diabetes, female fetuses are at higher risk than males.
This previously undetected pattern shows that the AI model can help researchers learn new things about pregnancy health.
The researchers were especially interested in developing better risk estimates for fetuses in the bottom 10% for weight, but not the bottom 3%. These babies are small enough to be concerning, but large enough that they are usually perfectly healthy. Figuring out the best course of action in these cases is challenging: Will a pregnancy need intensive monitoring and potentially early delivery, or can the pregnancy proceed largely as normal? Current clinical guidelines advise intensive medical monitoring for all such pregnancies, which can represent a significant emotional and financial burden.
But the researchers found that within this fetal weight class, the risk of an unhealthy pregnancy outcome varied widely, from no riskier than an average pregnancy to nearly ten times the average risk. The risk was based on a combination of factors such as fetal sex, presence or absence of pre-existing diabetes, and presence or absence of a fetal anomaly such as a heart defect.
For humans or AI models, estimating pregnancy risks involves taking a very large number of variables into account, from maternal health to ultrasound data. Experienced clinicians can weigh all these variables to make individualized care decisions, but even the best doctors probably wouldn't be able to quantify exactly how they arrived at their final decision. Human factors like bias, mood, or sleep deprivation almost inevitably creep into the mix and can subtly skew judgment calls away from ideal care.
To help address this problem, the researchers used a type of model called "explainable AI," which provides the user with the estimated risk for a given set of pregnancy factors and also includes information on which variables contributed to that risk estimation, and how much.
Essentially, explainable AI approximates the flexibility of expert clinical judgment while avoiding its pitfalls. The researchers' model is also especially well-suited to judging risk for rare pregnancy scenarios, accurately estimating outcomes for people with unique combinations of risk factors. This kind of tool could ultimately help personalize care by guiding informed decisions for people whose situations are one-of-a-kind. AI models can essentially estimate a risk that is specific to a given person's context and they can do it transparently and reproducibly, which is what human brains can't do.
AI-based analysis of fetal growth restriction in a prospective obstetric cohort quantifies compound risks for perinatal morbidity and mortality and identifies previously unrecognized high risk clinical scenarios, BMC Pregnancy and Childbirth (2025). DOI: 10.1186/s12884-024-07095-6
How tackling sepsis can save millions of lives—and prevent future pandemic deaths
Sepsis is an underestimated killer. Nearly a quarter of patients treated for sepsis in hospital will die, but because so many different illnesses can predispose patients to experiencing it, it's overlooked as a direct cause of death. Yet approximately 20% of deaths worldwide are caused by sepsis, and currently we have no treatments that tackle it directly.
Now researchers writing in Frontiers in Scienceexplain how systems immunology can help us understand and treat sepsis—and how this could cut the death toll of future pandemics, no matter what disease causes them.
One of the reasons it's so hard to understand and treat sepsis is that it is multifaceted. Sepsis arises when the immune system fails to control an infection and malfunctions, causing multi-organ failure. Many different infections can cause sepsis, and its symptoms and progression vary between patients and over time in the same patient. Its early symptoms are similar to those of many other illnesses, which makes it difficult to diagnose quickly and initiate timely treatment, contributing to high mortality.
Systems immunology offers a potential solution to this diagnosis problem by using mathematical and computational modeling to study the immune system in the context of all the body's other systems. It does this by using different types of clustering analysis to identify patterns in large volumes of omics data, ranging from transcriptomic data (what genes show altered expression) to proteomic and metabolomic data—data that tell us about the body's reaction to its physical circumstances, in this case sepsis, in incredibly fine-grained detail.
These patterns help us work out the patterns and basis for the immune dysregulation that drives sepsis, come up with new hypotheses that we can research and use to develop new treatments, and identify diagnostic markers that we can use to catch sepsis early.
For instance, using these clustering analyses, scientists have identified changes to gene expressionthat act as early warnings for sepsis. They've also been able to identify five different subtypes of sepsis which are caused by different kinds of immune dysregulation and have different prognoses. In the future, we could build on these advances to diagnose different subtypes of sepsis earlier and treat them with the right drugs when we do.
However, systems immunology analysis is not yet in widespread use, because it is expensive and demands significant volumes of data—so we don't yet know how these diagnostics could translate into clinical results. The researchers call urgently for targeted funding and greater data availability.
"In sepsis we lack the depth of information required to enable more effective systems immunology and machine learning approaches.
Successfully treating sepsis would be a multipurpose life-saver, preventing mortality regardless of the illness that triggered it. Viral sepsis is a major cause of deaths triggered by severe COVID-19, while many deaths in historical pandemics like the 1919 influenza pandemic and the bubonic plague are thought to have resulted from sepsis.
If we can tackle sepsis, we might be able to protect ourselves against the worst consequences and the highest death tolls in future pandemics, no matter what kind of infection causes them. Since immune dysregulation linked to sepsis can linger, causing symptoms similar to post-viral syndromes like long COVID-19, learning to treat this could also benefit some chronic illness patients.
But to make this happen, the researchers caution, more funding and larger studies will be needed. The omics methods that underlie systems immunology are relatively expensive on a per patient basis. It will require a concerted drive from stakeholders to generate the data needed for further insights. We need to invest in larger omics studies of patients, develop new animal and organoid models that reflect sepsis heterogeneity, and invest in early diagnostics for sepsis and treatments that correct or supplement defective immunity in sepsis patients.
Deciphering sepsis: transforming diagnosis and treatment through systems immunology, Frontiers in Science (2025). DOI: 10.3389/fsci.2024.1469417
New research published in the journal Science uncovers how scratching aggravates inflammation and swelling in a mouse model of a type of eczema called allergic contact dermatitis.
Scratching is often pleasurable, which suggests that, in order to have evolved, this behaviour must provide some kind of benefit. This new study helps resolve this paradox by providing evidence that scratching also provides defense against bacterial skin infections.
Allergic contact dermatitis is an allergic reaction to allergens or skin irritants—including poison ivy and certain metals such as nickel—leading to an itchy, swollen rash. Succumbing to the often-irresistible urge to scratch triggers further inflammation that worsens symptoms and slows healing.
To figure out what drives this vicious cycle, researchers used itch-inducing allergens to induce eczema-like symptoms on the ears of normal mice and those that don't get itchy because they lack an itch-sensing neuron.
When normal mice were allowed to scratch, their ears became swollen and filled with inflammatory immune cells called neutrophils. In contrast, inflammation and swelling were much milder in normal mice that couldn't scratch because they wore tiny Elizabethan collars, similar to a cone that a dog might sport after a visit to the vet, and in animals that lacked the itch-sensing neuron. This experiment confirmed that scratching further aggravates the skin.
Next, the researchers showed that scratching causes pain-sensing neurons to release a compound called substance P. In turn, substance P activates mast cells, which are key coordinators of inflammation that drive itchiness and inflammation via recruitment of neutrophils.
In contact dermatitis, mast cells are directly activated by allergens, which drives minor inflammation and itchiness.
In response to scratching, the release of substance P activates mast cells through a second pathway, so the reason that scratching triggers more inflammation in the skin is because mast cells have been synergistically activated through two pathways.
Mast cells are culprits in a range of inflammatory skin conditions and allergic reactions, but they're also important for protecting against bacteria and other pathogens. As such, the researchers wondered if scratching-induced activation of mast cells could affect the skin microbiome. The researchers showed that scratching reduced the amount of Staphylococcus aureus, the most common bacteria involved in skin infections, on the skin. The finding that scratching improves defense against Staphylococcus aureus suggests that it could be beneficial in some contexts. But the damage that scratching does to the skin probably outweighs this benefit when itching is chronic.
Your fridge still uses tech from the 50s, but scientists have an update
Researchers report on Jan. 30 in the journal Joule that a more efficient and environmentally friendly form of refrigeration might be on the horizon. The new technology is based on thermogalvanic cells that produce a cooling effect by way of a reversible electrochemical reaction.
Thermogalvanic refrigeration is cheaper and more environmentally friendly than other cooling methods because it requires a far lower energy input, and its scalability means that it could be used for various applications—from wearable cooling devices to industrial-grade scenarios.
Thermogalvanic cells use the heat produced by reversible electrochemical reactions to create electrical power. In theory, reversing this process—applying an external electrical current to drive electrochemical reactions—enables cooling power to be generated.
Previous studies have shown that thermogalvanic cells have a limited potential to produce cooling power, but this new work was able to dramatically increase this potential by optimizing the chemicals used in the technology.
By tweaking the solutes and solvents used in the electrolyte solution, the researchers were able to improve the hydrogalvanic cell's cooling power. They used a hydrated iron salt containing perchlorate, which helped the iron ions dissolve and dissociate more freely compared to other previously tested iron-containing salts such as ferricyanide. By dissolving the iron salts in a solvent containing nitriles rather than pure water, the researchers were able to improve the hydrogalvanic cell's cooling power by 70%.
The optimized system was able to cool the surrounding electrolyte by 1.42 K, which is a big improvement compared to the 0.1 K cooling capacity reported by previously published thermogalvanic systems.
Looking ahead, the team plans to continue optimizing their system's design and is also investigating potential commercial applications.
Complex engineering of human cell lines reveals genome's unexpected resilience to structural changes
The most complex engineering of human cell lines ever has been achieved by scientists, revealing that our genomes are more resilient to significant structural changes than was previously thought.
Researchers used CRISPR prime editing to create multiple versions of human genomes in cell lines, each with different structural changes. Using genome sequencing, they were able to analyze the genetic effects of these structural variations on cell survival .
The research, published in Science, shows that as long as essential genes remain intact, our genomes can tolerate significant structural changes, including large deletions of the genetic code. The work opens the door to studying and predicting the role of structural variation in disease.
Structural variation is a change in the structure of an organism's genome, such as deletions, duplications and inversions of the genetic sequence. These structural changes to the genome can be significant, sometimes affecting hundreds to many thousands of nucleotides—the basic building blocks of DNA and RNA.
Structural variants are associated with developmental diseases and cancer. However, our ability to study the effects of structural variation in the genomes of mammals, and the role they play in disease, has been difficult due to the inability to engineer these genetic changes.
To overcome this challenge, researchers set out to develop new approaches for creating and studying structural variation.
In a new study, the team used a combination of CRISPR prime editing and human cell lines—groups of human cells in a dish—to generate thousands of structural variants in human genomes within a single experiment.
To do this, researchers used prime editing to insert a recognition sequence into the genomes of the human cell lines to target with recombinase—an enzyme that enabled the team to 'shuffle' the genome.
By inserting these recombinase handles into repetitive sequences, which are hundreds and thousands of identical sequences in the genome, with a single prime editor they were able to integrate up to almost 1,700 recombinase recognition sites into each cell line.
This resulted in more than 100 random large-scale genetic structural changes per cell. This is the first time that it's been possible to 'shuffle' a mammalian genome, especially at this scale.
The team then studied the impacts of the structural variation on the human cell lines. Using genomic sequencing, the team was able to take 'snapshots' of the human cells and their 'shuffled' genomes over the course of a few weeks, watching which cells survived and which died.
As expected, they found that when structural variation deleted essential genes, this was heavily selected against and the cells died. However, they found that groups of cells with large-scale deletions in the genomes that avoided essential genes survived.
The team also conducted RNA sequencing of the human cell lines, which measures gene activity, known as gene expression. This revealed that large-scale deletions of the genetic code, especially in non-coding regions, did not seem to impact the gene expression of the rest of the cell.
The researchers suggest that human genomes are extremely tolerant of structural variation, including variants that change the position of hundreds of genes, as long as essential genes are not deleted.
In another study related to this another research team used a different approach, adding recombinase sites to transposons—mobile genetic elements—that randomly integrated in the genomes of human cell lines and mouse embryonic stem cells.
Using their method, they demonstrated that the effects of the induced structural variants can be read out using single-cell RNA sequencing. This advance paves the way for large screens of structural variant impact, potentially improving the classification of structural variants found in human genomes as benign or clinically significant.
Both studies came to similar conclusions that human genomes are surprisingly tolerant to some substantial structural changes, although the full extent of this tolerance remains to be explored in future studies enabled by these technologies.
Hidden within our bones, marrow sustains life by producing billions of blood cells daily, from oxygen-carrying red cells to immune-boosting white cells. This vital function is often disrupted in cancer patients undergoing chemotherapy or radiation, which can damage the marrow and lead to dangerously low white cell counts, leaving patients vulnerable to infection.
Now researchers have developed a platform that emulates human marrow's native environment. This breakthrough addresses a critical need in medical science, as animal studies often fail to fully replicate the complexities of human marrow.
The team's new device is a small plastic chip whose specially designed chambers are filled with human blood stem cells and the surrounding support cells with which they interact in a hydrogel to mimic the intricate process of bone marrow development in the human embryo. This biologically inspired platform makes it possible to build living human marrow tissue that can generate functional human blood cells and release them into culture media flowing in engineered capillary blood vessels.
The bone marrow-on-a-chip allows researchers to simulate and study common side effects of medical treatments, such as radiotherapy and chemotherapy for cancer patients. When connected to another device, it can even model how the bone marrow communicates with other organs, like the lungs, to protect them from infections and other potentially life-threatening conditions.
Described in a new paper published in Cell Stem Cell, the bone marrow model and the demonstration of its large-scale production and automation could advance fields as diverse as drug development by enabling automated, high-throughput preclinical screening of marrow toxicity of anticancer drugs) and space travel (by allowing researchers to study the effects of prolonged radiation exposure and microgravity on the immune system of astronauts).
Andrei Georgescu et al, Self-organization of the hematopoietic vascular niche and emergent innate immunity on a chip, Cell Stem Cell (2024). DOI: 10.1016/j.stem.2024.11.003
Future antibiotics face early bacterial resistance challenges, studies show
Researchers have made a concerning discovery about the future of antibiotics. Two recent studies, published just days apart in Nature Microbiology and Science Translational Medicine found that resistance can develop against new antibiotics even before they are widely used, compromising their effectiveness from the start. The studies focused on five critical bacterial species that cause major hospital infections and examined 18 new antibiotics, some already on the market and others still in development.
New antibiotics are often marketed as resistance-free, but this claim relies on limited data.
This new work highlights a major issue: antibiotic development tends to prioritize broad-spectrum activity - that is the number of bacterial species a drug targets- over long-term sustainability. While many new antibiotics indeed offer a broader spectrum, this doesn't guarantee they will remain effective in the long run in clinical use.
The studies found that resistance developed rapidly against nearly all the tested antibiotics, defying earlier expectations. For example, teixobactin, once hailed as a revolutionary drug, was believed to be less prone to resistance. However, the research revealed that bacteria can adapt to it with this adaptation resulting in cross-resistance to other critical antibiotics.
Alarmingly, the team also found that resistance mutations may already exist in bacterial populations, likely due to the overuse of older antibiotics and the shared resistance mechanisms between those and new drugs. These pre-existing mutations could render even the newest drugs ineffective shortly after they are introduced into clinical use.
Rethinking antibiotic development: The studies call for a fundamental shift in how antibiotics are developed. Drug companies must incorporate resistance studies early in the development process to anticipate and mitigate risks before antibiotics are released. Integrating resistance prediction and genetic surveillance into drug design could reduce the chances of failure.
Some new antibiotics show more promise than others, as resistance develops more slowly or only in specific bacterial species. Understanding why these drugs perform better is the next crucial step.
The studies emphasize the importance of prioritizing antibiotics with novel modes of action to bypass existing resistance. In cases where only certain bacterial species are prone to resistance, narrow-spectrum therapy could provide an effective alternative. Finally, the studies stress the urgency of responsible antibiotic use to slow down the evolution of resistance and ensure the prolonged efficacy of new treatments in the future.
Lejla Daruka et al, ESKAPE pathogens rapidly develop resistance against antibiotics in development in vitro,Nature Microbiology(2025).DOI: 10.1038/s41564-024-01891-8
Ana Martins et al, Antibiotic candidates for Gram-positive bacterial infections induce multidrug resistance,Science Translational Medicine(2025).DOI: 10.1126/scitranslmed.adl2103
Bats' genetic adaptations: How they tolerate coronaviruses without becoming ill
New research has shown that bats can tolerate coronaviruses and other viruses without becoming ill, thanks to special adaptations of their immune system.
The study, published in Nature, shows that bats have more genetic adaptations in immune genes than other mammals. The ISG15 gene in particular plays a key role: in some bats, it can reduce the production of SARS-CoV-2 by up to 90%.
The results could help to develop new medical approaches to combat viral diseases.
Bats have unique characteristics. As the only mammals that can actively fly, they play an important role in the ecosystem: They pollinate plants, spread seeds and contribute to the balance of the insect population through their feeding habits. Their exceptional orientation using ultrasonic echolocation shows how perfectly they are adapted to their nocturnal lifestyle.
Bats are of great interest to medical advancement, as their immune systems and unique viral tolerances can provide valuable insights for the development of new therapies. They are also known to carry numerous viruses, including those that are transmissible to humans—such as coronaviruses. However, bats do not show any symptoms of disease when infected with such viruses.
The new research team has sequenced high-quality genomes of 10 new bat species, as part of the international Bat1K project, including species known to carry coronaviruses and other viruses. Such adaptations can be detected as traces of positive selection and can indicate functional changes.
The result of the extensive analysis shows that bats exhibit such adaptations in immune genes much more frequently than other mammals.
The research also showed that the common ancestor of all bats had an unexpectedly high number of immune genes with selection signatures. This suggests that the evolution of the immune system could be closely linked to the evolution of the ability to fly.
Ariadna E. Morales et al, Bat genomes illuminate adaptations to viral tolerance and disease resistance, Nature (2025). DOI: 10.1038/s41586-024-08471-0
India doubled its tiger population in a decade and credits conservation efforts
India doubled its tiger population in a little over a decade by protecting the big cats from poaching and habitat loss, ensuring they have enough prey, reducing human-wildlife conflict, and increasing communities' living standards near tiger areas, a study published this week found.
The number of tigers grew from an estimated 1,706 tigers in 2010 to around 3,682 in 2022, according to estimates by the National Tiger Conservation Authority, making India home to roughly 75% of the global tiger population. The study found that some local communities near tiger habitats have also benefited from the increase in tigers because of the foot traffic and revenues brought in by ecotourism.
The study in the journal Science says India's success "offers important lessons for tiger-range countries" that conservation efforts can benefit both biodiversity and nearby communities.
Wildlife conservationists and ecologists welcomed the study but said that tigers and other wildlife in India would benefit if source data were made available to a larger group of scientists. The study was based on data collected by Indian government-supported institutions.
Also there are several species, including the great Indian bustard and caracal which are all on the edge. "And there is really not enough focus on that."
Yadvendradev V. Jhala et al, Tiger recovery amid people and poverty, Science (2025). DOI: 10.1126/science.adk4827
Amniotic fluid's protective properties: Study uncovers its role in blood clotting
Researchers have made new discoveries about amniotic fluid, a substance historically not well understood in medical research due to the difficulty in obtaining it during pregnancy, especially across gestation.
Amniotic fluid is the vital fluid that surrounds and protects a fetus during pregnancy. In addition to providing much-needed cushion and protection for the fetus, it also aids in development of vital organs—especially the lungs, digestive tract and skin—and stabilizes the temperature inside the womb.
The new study,publishedin the journalResearch and Practice in Thrombosis and Haemostasis, found that the addition of amniotic fluid to plasma—the liquid portion of blood—improves the blood's ability to thicken and clot, which is a critical and likely a protective function throughout pregnancy and during delivery for both the birthing parent and the baby.
Researchers analyzed the properties of amniotic fluid obtained by amniocentesis, a prenatal test that involves sampling a small amount of amniotic fluid to examine the health of the pregnancy, from both human and non-human primates at gestational-age matched timepoints. The findings showed that amniotic fluid increases blood clotting through key fatty acids and proteins that change each trimester and help regulate coagulation.
Chih Jen Yang et al, Characterization of the procoagulant phenotype of amniotic fluid across gestation in rhesus macaques and humans, Research and Practice in Thrombosis and Haemostasis (2025). DOI: 10.1016/j.rpth.2024.102676
Asteroid find upends story of life’s origin Fragments collected from the asteroid Bennu contain the building blocks for life — all five nucleobases that form DNA and RNA and 14 of the 20 amino acids needed to make known proteins. But there’s a twist: on Earth, amino acids in living organisms tend to have a ‘left-handed’ structure. Those on Bennu, however, contain nearly equal amounts of these structures and their ‘right-handed’, mirror-image forms. This calls into question a hypothesis favoured by many scientists that asteroids similar to this one might have seeded life on Earth.
Ear muscle we thought humans didn't use—except for wiggling our ears—activates during focused listening
If you can wiggle your ears, you can use muscles that helped our distant ancestors listen closely. These auricular muscles helped change the shape of the pinna, or the shell of the ear, funneling sound to the eardrums.
There are three large muscles which connect the auricle to the skull and scalp and are important for ear wiggling. These muscles, particularly the superior auricular muscle, exhibit increased activity during effortful listening tasks. This suggests that these muscles are engaged not merely as a reflex but potentially as part of an attentional effort mechanism, especially in challenging auditory environments.
It's difficult to test how hard someone is listening without self-reported measures. But electromyography, which measures electrical activity in a muscle, can help identify activity in the auricular muscles linked to listening closely.
Similar research has already shown that the largest muscles, posterior and superior auricular muscles, react during attentive listening. Because they pull the ears up and back, they are considered likely to have been involved in moving the pinna to capture sounds.
The exact reason these became vestigial is difficult to tell, as our ancestors lost this ability about 25 million years ago. One possible explanation could be that the evolutionary pressure to move the ears ceased because we became much more proficient with our visual and vocal systems.
Scientists now found that the two auricular muscles reacted differently to the different conditions. The posterior auricular muscles reacted to changes in direction, while the superior auricular muscles reacted to the difficulty level of the task.
Electromyographic Correlates of Effortful Listening in the Vestigial Auriculomotor System, Frontiers in Neuroscience (2025). DOI: 10.3389/fnins.2024.1462507
Gut microbes may mediate the link between drinking sugary beverages and diabetes risk
It is well known that consuming sugary drinks increases the risk of diabetes, but the mechanism behind this relationship is unclear. Now, in a paper appearing in Cell Metabolism, researchers show that metabolites produced by gut microbes might play a role.
In a long-term cohort of US Hispanic/Latino adults, the researchers identified differences in the gut microbiota and blood metabolites of individuals with a high intake of sugar-sweetened beverages. The altered metabolite profile seen in sugary beverage drinkers was associated with a higher risk of developing diabetes in the subsequent 10 years. Since some of these metabolites are produced by gut microbes, this suggests that the microbiome might mediate the association between sugary beverages and diabetes.
This study suggests a potential mechanism to explain why sugar-sweetened beverages are bad for your metabolism.
Previous studies in Europe and China have shown that sugar-sweetened beverages alter gut microbiome composition, but this is the first study to investigate whether this microbial change impacts host metabolism and diabetes risk.
The researchers found that high sugary beverage intake—defined as two or more sugary beverages per day—was associated with changes in the abundance of nine species of bacteria. Four of these species are known to produce short-chain fatty acids—molecules that are produced when bacteria digest fiber and that are known to positively impact glucose metabolism. In general, bacterial species that were positively associated with sugary beverage intake correlated with worse metabolic traits. Interestingly, these bacteria were not associated with sugar ingested from non-beverage sources.
The researchers also found associations between sugary beverage consumption and 56 serum metabolites, including several metabolites that are produced by gut microbiota or are derivatives of gut-microbiota-produced metabolites.
These sugar-associated metabolites were associated with worse metabolic traits, including higher levels of fasting blood glucose and insulin, higher BMIs and waist-to-hip ratios, and lower levels of high-density lipoprotein cholesterol ("good" cholesterol). Notably, individuals with higher levels of these metabolites had a higher likelihood of developing diabetes in the 10 years following their initial visit.
They found that several microbiota-related metabolites are associated with the risk of diabetes. In other words, these metabolites may predict future diabetes.
These results have to be validated in other populations too for a final conclusion.
BioSonics spectroscopy can 'listen' to the sounds made by individual viruses
A team of chemists and microbiologists has found that an all-optical method can be used to detect natural vibrational frequencies made by individual viruses as a way to identify them. In their study published in Proceedings of the National Academy of Sciences, the group found a way to bounce light off viruses and detect the resulting patterns of vibrations, which could be easily identified.
Light can be used to identify nanoparticle-scale objects. Prior research has shown that firing beams of light at such objects can cause them to vibrate slightly. The vibration patterns that emerge are unique for different targets. Thus, the technique can be used to identify nanoscale objects even among other similarly scaled objects.
The researchers wondered if the same technique could be used with biological agents like viruses and bacteria, so they conducted experiments that involved firing extremely tiny amounts of light at both kinds of microorganisms at such a small scale that they were able to watch the impact of single photons.
Eventually, they shifted their focus to viruses only and found that with the appropriate parameter settings, they could detect the vibrations emitted by the virus using a technique that they call BioSonics spectroscopy. The sound was not just too faint to hear with the human ear, but too high, at a frequency 1 million times higher than humans can hear.
After testing multiple viruses, the research team found that each of them vibrated in their own unique ways, distinct from one another and from all the other molecules they tested. That meant that BioSonics could be used as a sensor of sorts, enabling devices that could, for example, scan a room, detect viruses in the air and identify them.
They also note that the technologycould reveal individual virus activity, opening the door to better understanding them. It could be used, for example, to watch as individual viruses assemble themselves, a phenomenon that is still not well understood.
Yaqing Zhang et al, Nanoscopic acoustic vibrational dynamics of a single virus captured by ultrafast spectroscopy, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2420428122
Myth busting: Purpose-bred dogs are not better at biting or scenting than those not bred for that purpose
Since their domestication millennia ago, dogs have been man's best friend, and aside from friendship, centuries of selective breeding have tailored them for tasks like herding, hunting and guarding—or so we thought.
Now, the results of a new study challenge the prevailing belief that some breeds are inherently superior at specific tasks, based on their skull morphology.
The study published in Science Advances on January 29, used advanced 3D reconstruction techniques to analyze 117 skulls from 40 domestic dog breeds and 18 wild canid species.
The researchers found substantial overlap in skull shapes across breeds and functional categories, but no clear evidence that breeds selected for bite work or scent work have developed distinct morphological traits that enhance these abilities. This suggests that humans have been breeding dogs primarily for preferred visible traits, and that other factors like individual personality affect dogs' performance of tasks.
In the past 200 years, humans have created hundreds of dog breeds that look really different and are pretty specialized at some tasks like herding, protecting, and detecting odors. We have assumed that these dogs look different because they are 'structurally' specialized at these tasks, but this new study shows that, at least for their skulls, they 'are not' specialized for tasks that involve the skull, such as biting tasks and scent work.
The study examined dog breeds commonly used for tasks like bite work and scent work, such as those in law enforcement and military programs, where dogs are trained for patrol and detection. Researchers used advanced methods, including 3D skull analysis, to compare breeds across various functional groups.
The results showed that domesticated dog breeds exhibit exceptional diversity in their skull shapes, but have high overlap among the parts of the skulls that correspond with functional tasks.
This indicates that specific breeds are not as morphologically specialized for such tasks as previously thought. For instance, bite-force measurements did not show any significant differences between breeds purpose-bred for bite work and those not.
There are many news stories about dogs attacking people badly and often there are specific breeds that are targets of this reporting (such as pit bulls). Some people claim that these dogs will bite harder than other dogs of the same size, or they have special features like 'locking jaws' that make them especially dangerous to people. This study shows that this is simply not true; dogs bred to bite things aren't structurally different than dogs that have been bred to do other things. Similarly, breeds selected for scent work did not demonstrate significantly enhanced olfactory morphology compared to other breeds. The lone group that showed distinct skull morphology was brachycephalic breeds (e.g., bulldogs), which are characterized by their shortened snouts, but this feature is not tied to functional specialization. Instead, human aesthetic preferences have played a larger role in shaping dog morphology. Humans have done so much breeding work to alter the visual appearance of these animals that the researchers honestly expected to see really marked groupings of some kind but they really didn't see much of that. However, researchers found that domesticated dog breeds' morphologies differed greatly from wild canids, such as wolves and foxes, which tend to have skull shapes that align more closely with their natural functional needs. Wolves and foxes tend to possess elongated snouts relative to their cranial length, which is a typical feature of species that rely on keen senses like smell.
Undomesticated animals, particularly wolves, show skull morphologies that reflect evolutionary adaptations for hunting and scent work, which contrasts with the lack of strong morphological specialization in domesticated breeds.
Interestingly, foxes' skull shapes overlap significantly with some domestic dogs, particularly terrier breeds, which were historically bred for pest control, suggesting functional similarities in skull structure for small prey pursuit.
While these results run counter to the popular notion that purpose-bred dogs are better at biting or scenting than those not bred for that purpose, they suggest that observable behavior traits are associated with performance, rather than morphological traits. Recent research suggests that many breed-associated behaviors are partially heritable. This has important implications for how dogs are bred and selected for specific tasks in areas such as law enforcement and search and rescue—behavioral traits and individual trainability may be more important determinants of performance.
Nicholas Hebdon et al, Dog skull shape challenges assumptions of performance specialization from selective breeding, Science Advances (2025). DOI: 10.1126/sciadv.adq9590
Study uncovers new link between infections and heart failure
People hospitalized for infections—almost any infections—are at substantially increased risk years later for heart failure, according to a collaborative research.
The study of more than 14,000 people over two decades doesn't establish cause and effect, but advocates said this week that it establishes a strong enough correlation that people should take heed and try to reduce their infection risks.
Heart failure, which affects millions around the world, is a weakening of the heart that prevents it from pumping sufficient blood and oxygen. Researchers were surprised to find that hospitalizations resulting from common skin and urinary tract infections increased heart failure risks, alongside respiratory infections such as influenza and blood infections such as sepsis.
That suggests that the body's response to infection is a big part of the heart failure risk, say the researchers.
There's some notion that really severe infections sort of turn on the immune system in a way where it just doesn't quite turn off, and it stays revved up, possibly for many years.
Other possibilities include that serious infections cause genetic or biological changes that lay dormant after hospitalization but emerge later in life to cause heart failure.
Other studies have found hospitalizations increase risks of health problems later in life, so it's possible infections are driving people to as-yet unknown risks from those hospital visits, they stress.
Even without cause and effect being established, they say the results should encourage people to prevent infections through vaccines and good hygiene. People who have already been hospitalized because of infections can talk with their doctors about ways to reduce cardiac risks.
They had already discovered in 2023 that infection-related hospitalizations increased the risk for dementia later in life.
Over the course of three decades, about one in four people in the surveillance program suffered episodes of heart failure. The risk was more than twice as likely among patients who at some point had been hospitalized for infections, according to the latest study, published in the Journal of the American Heart Association.
Risks were highest following bloodstream and respiratory infections, but were also significant for skin and urinary tract infections. Digestive infections were only weakly correlated with heart failure later in life.
Risks were highest following bloodstream and respiratory infections, but were also significant for skin and urinary tract infections. Digestive infections were only weakly correlated with heart failure later in life.
Heart failure can lead to cardiac arrest or damage the kidney and liver. Treatments range from medications to increase blood flow to surgeries to implant pacemakers or remove obstructions in blood vessels.
Establishing a precise cause-and-effect relationship between infections and heart failure will be difficult, because researchers can't deny preventive care to patients just to see if it increases their risks.
Rebecca L. Molinsky et al, Infection‐Related Hospitalization and Incident Heart Failure: The Atherosclerosis Risk in Communities Study, Journal of the American Heart Association (2025). DOI: 10.1161/JAHA.123.033877
Why 'cough CPR' is not the lifesaver it's made out to be
Misinformation has circulated for years on social media about how coughing forcefully can treat a heart attack. Health experts are quick to debunk that myth and warn that "cough CPR" is ineffective.
Anytime anyone is having chest pain or other symptoms of a heart attack, get to a hospital. Calling an emergency ambulance service is the safest way to get to a hospital for chest pain.
The term itself is a misnomer because CPR is for someone in cardiac arrest, meaning the heart has stopped beating. At that point, coughing would not be possible, nor would it be considered CPR.
It physiologically does not make sense. Coughing just would not work to restart a heart that's not beating, say the experts.
Heart attack and cardiac arrest are medical emergencies requiring immediate medical treatment, though it is important to note they are two different conditions. A heart attack is a circulation problem and occurs when blood flow to the heart is blocked. Cardiac arrest is an electrical problem and occurs when the heart suddenly stops beating. A heart attack is a common cause for cardiac arrest.
Someone who goes into cardiac arrest will become unresponsive and stop breathing or gasp for air. Cardiac arrest can lead to death if not treated within minutes.
Confusion about cough CPR might be traced to a temporary measure that may be used for a sudden arrhythmia, or abnormal heartbeat, in medical settings in which patients are constantly monitored, such as a cardiac catheterization lab.
During a sudden arrhythmia, a doctor or nurse may coach a patient to cough vigorously to maintain enough blood flow to the brain to remain conscious for a few seconds until the arrhythmia is treated. But this technique is not effective in all patients and should not delay definitive treatment, according to the American Heart Association.
The misconception about cough CPR and heart attack may be tied to an idea that coughing can change the pressure in the chest, and, in turn, affect the heart.
People believe that it is changing, somehow, the heart's squeeze. But (coughing) has not been shown to do that. If somebody has lost a pulse, we very much know that you have to do CPR.
A literature review to prepare for that update did not yield any research about cough CPR.
It's certainly not something that is recommended in those guidelines because there is no evidence to support it.
If you're around someone who has gone into cardiac arrest, call emergency services helpline and start hands-only CPR. This means placing the heel of one hand in the center of the chest at the nipple line. Place the other hand on top and interlock the fingers. Start pushing hard at a rate between 100 and 120 beats per minute.
Get an automated external defibrillator, or AED, if one is close by or send someone to find an AED. People should use an AED as soon as it's available. Even untrained people can use the device by following its voice instructions. Because a heart attack can lead to a cardiac arrest, experts say it's critical to call emergency services immediately when symptoms start. These can include chest pain, jaw pain, shortness of breath, sweating and nausea.
Then sit and rest until the ambulance arrives. "Avoid exertion." An aspirin may help for those not allergic to it. Someone with a prescription for nitroglycerin for chest pain should take the medication.
But one thing people don't need to do is cough. Source: American Heart Association
How microbes help detoxify the atmosphere: Study provides atomic-level insights
Researchers have discovered crucial new information about how microbes consume huge amounts of carbon monoxide (CO) and help reduce levels of this deadly gas.
Over two billion metric tons of carbon monoxide are released into the atmosphere globally each year. Microbes consume about 250 million tons of this, reducing CO to safer levels.
The study, published in Nature Chemical Biology, reveals at an atomic level how microbes consume CO present in the atmosphere. They use a special enzyme, called the CO dehydrogenase, to extract energy from this universally present but highly toxic gas.
The study showed for the first time how this enzyme extracted atmospheric CO and powered cells.
This enzyme is used by trillions of microbes in our soils and waters. These microbes consume CO for their own survival, but in the process inadvertently help us. This 's a fantastic example of microbial 'ingenuity': how life has evolved ways to turn something toxic into something useful.
These microbes help clean our atmosphere. This counteracts air pollution, which kills many millions of people each year, and also reduces global warming given CO is indirectly a greenhouse gas.
While this discovery is unlikely to be directly used to combat or monitor CO emissions, it deepens our understanding of how the atmosphere is regulated and how it might respond to future changes.
Microbes 're a big reason why our air 's breathable. They make half the oxygen we breathe and detoxify various pollutants like CO. It's crucial we better understand and appreciate how they support our own survival, say the researchers.
Kropp, A., et al. Quinone extraction drives atmospheric carbon monoxide oxidation in bacteria, Nature Chemical Biology (2025). DOI: 10.1038/s41589-025-01836-0
Stress during pregnancy could leave traces in placenta that affect baby's development, study suggests
Maternal stress could leave epigenetic imprints on genes in the placenta associated with cortisol—a necessary hormone for fetal development—and this would affect the baby's development from very early stages, according to a paper published in the journal European Neuropsychopharmacology.
The study suggests that a mother's emotional well-being during pregnancy is not only important for her, but could also influence the future health of her baby.
The placenta is an essential organ during pregnancy, as it not only provides oxygen and nutrients to the fetus, but also responds to factors such as maternal stress and helps the fetus adapt to its environment. However, the mechanisms by which the placenta adjusts to these stressors and how it influences fetal development remain largely unexplored.
The research team observed that maternal stress may leave epigenetic marks on certain placental genes. Specifically, these marks do not modify the genetic structure, but they do alter its function. The study identified epigenetic changes in genes related to the regulation of cortisol, an essential hormone in the body's response to stress.
The pilot studyinvolved 45 healthy, first-time pregnant women. During pregnancy, their cortisol levelsand depressive symptomswere measured and, after delivery, placentas were analyzed. At seven weeks, the neurodevelopment of the babies was assessed using a specialized test (Brazelton's NBAS).
The research team used an advanced sequencing technique that allows them to look at epigenetic changes in large areas of DNA and thus gain a very detailed view of the placental response to maternal stress. This method identified changes in key genes involved in cortisol regulation, such as HSD11B2, NR3C1 and FKBP5.
The results suggest that maternal stress—especially in early pregnancy—can cause alterations in these genes, which could affect fetal development and the future health of the baby.
This study reinforces the importance of taking care of the mental health of mothers from the beginning of pregnancy, since stress could leave a biological imprint on the baby's development through epigenetic mechanisms that we are just beginning to understand.
While these findings need to be replicated in larger studies, this breakthrough underscores the importance of psychological care and emotional support during pregnancy, not only for the mother's well-being, but also for the long-term health of the baby.
Agueda Castro-Quintas et al, Placental epigenetic signatures of maternal distress in glucocorticoid-related genes and newborn outcomes: A study of Spanish primiparous women, European Neuropsychopharmacology (2024). DOI: 10.1016/j.euroneuro.2024.10.001
Giant Radio Galaxy Could Hold 30 Milky Ways, Astronomers Say
Giant radio galaxies are cosmic megastructures that can span millions of light-years, making them some of the largest-known structures in the Universe.
Yet space is big, and despite their size, giant radio galaxies can be hard to find. Discovering one is a big deal, especially if it's as colossal – and peculiar – as one recently found by astronomers using South Africa's MeerKAT telescope.
The newly discovered galaxy measures over 3 million light-years from end to end, including the huge jets of hot plasma it's blasting into intergalactic space, the astronomers report in a new study.
That means it's more than 30 times the size of our own Milky Way galaxy.
It's also enigmatic, the researchers say, with unusual qualities that defy simple explanation. They decided to name it after this troublesome nature, choosing a word from two Bantu languages indigenous to Southern Africa.
Scientists nicknamed this giant galaxy 'Inkathazo,' meaning 'trouble' in isiZulu and isiXhosa because it has been a bit troublesome to understand the physics behind what's going on here.
Radio galaxies already feature mind-bending physics, with supermassive black holesaccreting matter at the galactic core and sending out vast plasma jets that glow at radio frequencies. Those larger than roughly 2 million light-years may be classified as giant radio galaxies, or GRGs.
Yet even by radio-galaxy standards, Inkathazo is puzzling.
It doesn't have the same characteristics as many other giant radio galaxies. For example, the plasma jets have an unusual shape: Rather than extending straight across from end to end, one of the jets is bent.
And while Inkathazo's size would be impressive anywhere, it's especially surprising given the galaxy's location. Inkathazo is nestled amid a cluster of other galaxies, researchers report, where conditions should discourage the growth of such gargantuan jets.
Mouse Created With Two Fathers And No Mother Survives to Adulthood
A mouse with no biological mother has survived to adulthood in China – a major scientific achievement that's been years in the making.
The feat was pulled off by a team of researchers in China using precise stem cell engineering.
This isn't the first time that scientists have created a mouse with two male parents. In 2023, researchers in Japan manageda similar feat using a different technique.
Before that, attempts to generate eggs from male stem cellsproved unsuccessful. The motherless offspring, born through a female surrogate, are typically nonviable and show severe developmental defects.
Not so for the 'bi-paternal' mice recently created in China. These adult mammals are not capable of reproducing themselves, but they are healthier than their predecessors, without fatal feeding or respiratory difficulties.
That said, roughly half of their siblings failed to make it to adulthood, and nearly 90 percent of the viable embryos did not make it to birth, which means the success rate for the process can still be improved upon.
There's still a long way to go before the same sort of technique could be achieved in our own species, but the authors of the study say their work helps scientists better understand human congenital disorders caused by similar genetic issues.
The scientist heroes that starved to protect their science
In his bookThe Forbidden Garden of Leningrad, author Simon Parkin tellsthe story of the city’s Plant Institute — the world’s first proper seed bank — during the 1941-1944Nazisiege. “The institute’s staff members sacrificed themselves, one by one, to protect a collection for which the whole raison d’être was to one day save humanity from starvation,” writes reviewer Simon Ings. Despite unthinkable privation, Vadim Stepanovich Lekhnovich, the curator of the tuber collection, later said that “it wasn’t difficult not to eat the collection. It was impossible to eat this, your life’s work, the work of the lives of your colleagues.”
Astronomers Discover Exoplanets Falling Apart in Space
Astronomers have found two planets around two separate stars that are succumbing to their stars' intense heat. Both are disintegrating before our telescopic eyes, leaving trails of debris similar to a comet's. Both are ultra-short-period planets (USPs) that orbit their stars rapidly.
These planets are a rare sub-class of USPs that are not massive enough to hold onto their material. Astronomers know of only three other disintegrating planets.
USPs are known for their extremely rapid orbits, some completing an orbit in only a few hours. Since they're extremely close to their stars, they're subjected to intense heat, stellar radiation, and gravity.
Many USPs are tidally locked to their star, turning the star-facing side into an inferno. USPs seldom exceed two Earth radii, and astronomers think that about 1 in 200 Sun-like stars has one. They were only discovered recently and are pushing the boundaries of our understanding of planetary systems.
Man on carnivore diet develops yellowish nodules on his hands, feet and elbows
A trio of cardiologists, two at Tampa General Hospital and the third at the University of Texas' MD Anderson Cancer Center, have reported an incident of an adult man developing yellowish nodules on his hands, feet and elbows after adopting a carnivore diet.
In their paperpublishedin the journalJAMA Cardiology, Konstantinos Marmagkiolis, Jaime Caballero, and Cezar Iliescu, describe the symptoms of a patient who had come to Tampa General seeking aid after experiencing yellowish nodules appearing on various parts of his body, and their diagnosis.
The patient, a man in his 40s, told the doctors that the nodules had appeared three weeks prior to his hospital visit. After questioning, they determined that the patient had adopted the so-called carnivore diet approximately eight months prior to the appearance of the nodules.
The carnivore diet is a fad diet based on eating large amounts of animal fats and very little of anything else. The patient in this case reported eating nearly 10 pounds of butter, cheese and other fatty foods every day since embarking on the diet—even going so far as to add fat to the hamburgers he consumed daily.
Blood tests showed the patient's cholesterol was approximately four times normal levels. The doctors diagnosed the patient with xanthelasma, a condition in which yellowish deposits of cholesterol build up in various parts of the body—in this case, on the palms, the soles of his feet and his elbows. His case had progressed to the point that some of the cholesterol was pushing through cracks in the skin.
The doctors advised the man to cut back on his fat intake. But they also noted that doing so would not get rid of the nodules—they required surgical excision or burning them with liquid nitrogen. They also reminded the patient that such high levels of cholesterol could lead to a host of other conditions such as cardiovascular disease, a greatly increased risk of stroke, and eventually, liver problems.
Konstantinos Marmagkiolis et al, Yellowish Nodules on a Man Consuming a Carnivore Diet, JAMA Cardiology (2025). DOI: 10.1001/jamacardio.2024.5209
Yellowish nodules on the palms of a man in his 40s. Painless yellowish nodules were observed on the patient's palms (A) and elbows. B, Magnified view of the palmar lesions. These lesions are consistent with xanthelasma, likely resulting from severe hypercholesterolemia associated with a high-fat carnivore diet. Total cholesterol levels exceeded 1000 mg/dL. Credit:JAMA Cardiology(2025). DOI: 10.1001/jamacardio.2024.5209
Large magma bodies found beneath dormant volcanoes
New research challenges the long-standing belief that active volcanoes have large magma bodies that are expelled during eruptions and then dissipate over time as the volcanoes become dormant.
Researchers used seismic waves to identify magma chambers beneath the surface of six volcanoes of various sizes and dormancy within the Cascade Range, which includes half of the U.S. volcanoes designated by the U.S. Geological Survey as "very high threat." The team found that all of the volcanoes, including dormant ones, have persistent and large magma bodies.
The results are surprising given that some of these volcanoes, such as the Crater Lake volcano in Oregon, have not been active in millennia.
Regardless of eruption frequency, we see large magma bodies beneath many volcanoes, the researchers said. It appears that these magma bodies exist beneath volcanoes over their whole lifetime, not just during an active state.
The fact that more volcanoes have sustained magma bodies is an important consideration for how researchers may monitor and predict future volcanic activity.
Guanning Pang et al, Long-lived partial melt beneath Cascade Range volcanoes, Nature Geoscience (2025). DOI: 10.1038/s41561-024-01630-y
An overlooked nuclear force helps keep matter stable, study reveals
Researchers have revealed how a special type of force within an atom's nucleus, known as the three-nucleon force, impacts nuclear stability. The study, published in Physics Letters B, provides insight into why certain nuclei are more stable than others and may help explain astrophysical processes, such as the formation of heavy elements within stars.
All matter is made of atoms, the building blocks of the universe. Most of an atom's mass is packed into its tiny nucleus, which contains protons and neutrons (known collectively as nucleons). Understanding how these nucleons interact to keep the nucleus stable and in a low energy state has been a central question in nuclear physics for over a century.
The most powerful nuclear force is the two-nucleonforce, which attracts two nucleons at long range to pull them together and repels at short range to stop the nucleons from getting too close.
Scientists have formed a good understanding of the two-nucleon force and how it impacts nuclear stability. On the other hand, three-nucleon force, which is when three nucleons interact with each other simultaneously, is much more complicated and poorly understood.
The researchers describe nuclear forces by likening them to a game of catch. With the two-nucleon force, two players, or nucleons, interact by throwing a ball to each other. The ball, a subatomic particle called a meson, can vary in heaviness, with the lightest meson, known as a pion, responsible for the long-range attraction between nucleons.
With the three-nucleon force, there are three players, or nucleons, and balls, or mesons, are passed between them. At the same time as throwing and catching the balls, the players, or nucleons, also spin and move in an orbit within the nucleus.
Although the three-nucleon force has historically been considered to be of little significance when compared to the two-nucleon force, a growing number of recent studies have highlighted its importance. Now, this new study clarifies the mechanism of how the three-nucleon force enhances nuclear stability, and demonstrates that as the nucleus grows, the force gains in strength.
The researchers used advanced nuclear theory and supercomputer simulations to study the exchange of pions between three nucleons. They found that when two pions are exchanged between three nucleons, the nucleons are constrained in how they move and spin, with only four combinations possible. Their calculations revealed that one of these combinations, known as the "rank-1 component," plays a crucial role in promoting nuclear stability.
Increased stability occurs, the researchers explain, due to enhancing a process known as spin-orbit splitting. When nucleons spin and orbit in the same direction, the alignment of these nucleons leads to a reduction in energy. But when nucleons spin and orbit in opposing directions, these nucleons exist in a higher energy state. This means that nucleons "split" into different energy shells, providing the nucleus with a stable structure.
The supercomputer simulations showed that while the three-nucleon force increases the energy state of the nucleons with an aligned spin and orbit, it causes the nucleons with opposing spins and orbits to gain even more energy. This results in a larger energy gap between the shells, making the nuclei even more stable .
Importantly, this effect becomes more pronounced in heavier nuclei that contain more nucleons. In the heaviest element examined—carbon-12, which has 12 nucleons—the three-nucleon force caused the energy gap to widen by a factor of 2.5.
This effect is so large that it has almost equal weighting to the impact of the two-nucleon force. The three-nucleon force could play a key role in understanding how heavy elements form from the fusion of lighter elements in stars. As this force grows stronger in heavier nuclei, it increases their stability by creating larger energy gaps between nuclear shells.
This stability makes it more challenging for the nucleus to capture additional neutrons, which are essential for forming heavier elements. In cases where the nucleus already contains a "magic number" of protons or neutrons that completely fills its shells, the nucleus becomes exceptionally stable, which can further hinder the fusion process. Finally, the researchers discovered another surprising effect of the three-nucleon force on nucleon spins. With only the two-nucleon force, the spin states of both nucleons can be measured individually. However, the three-nucleon force creates quantum entanglement, where two of the three nucleons have spins that exist in both states at once until measured.
Tokuro Fukui et al, Uncovering the mechanism of chiral three-nucleon force in driving spin-orbit splitting, Physics Letters B (2024). DOI: 10.1016/j.physletb.2024.138839
Ocean-surface warming has more than quadrupled since the late-1980s, research shows
The rate of ocean warming has more than quadrupled over the past four decades, a new study has shown. Ocean temperatures were rising at about 0.06 degrees Celsius per decade in the late 1980s, but are now increasing at 0.27 degrees Celsius per decade.
Published 28 January 2025 in Environmental Research Letters, the study helps explain why 2023 and early 2024 saw unprecedented ocean temperatures.
This accelerating ocean warming is driven by the Earth's growing energy imbalance—whereby more energy from the sun is being absorbed in the Earth's system than is escaping back to space. This imbalance has roughly doubled since 2010, in part due to increasing greenhouse gas concentrations, and because the Earth is now reflecting less sunlight to space than before.
Global ocean temperatures hit record highs for 450 days straight in 2023 and early 2024. Some of this warmth came from El Niño, a natural warming event in the Pacific.
When scientists compared it to a similar El Niño in 2015–16, they found that the rest of the record warmth is explained by the sea surface warming up faster in the past 10 years than in earlier decades; 44% of the record warmth was attributable to the oceans absorbing heat at an accelerating rate.
Quantifying the acceleration of multidecadal global sea surface warming driven by Earth's energy imbalance, Environmental Research Letters (2025). DOI: 10.1088/1748-9326/adaa8a
Microplastics found in the brains of mice within hours of consumption
A team of environmental biologists has found that it takes microplastics consumed by mice just a few hours to make their way to their brains.
In their paper published in the journal Science Advances, the group describes experiments they conducted with lab mice consuming water tainted with different sized microplastics, and what they learned by doing so.
Prior research has shown that microplastics have made their way into the environment to such an extent that they have made their way into the bodies of nearly everyone on Earth (*). It is still not known what harm consumption of such materials causes, but most in the medical field believe they are likely causing damage that is blamed on other sources. Still, many in the field suggest that there is enough evidence of possible health problems associated with microplastics that action should be taken globally to address their impact.
In this new effort, the research team sought to learn more about the medical impact of a mammal consuming different sizes of microplastics. The experiments consisted of feeding test mice water with different sized bits of fluorescent plastic in it, from micro to nano. They then tracked the progress of the plastic bits to see where they wound up in the bodies of the mice.
Knowing that the plastic would make its way from the digestive tract into the bloodstream, the researchers used two-photon microscopy to capture imagery of it inside blood vessels. Also, suspecting that the tiniest bits would make it into their brains, the team installed tiny windows in their skulls, allowing them to track the movement of the plastic in their brains.
In studying the imagery they created, the researchers were able to watch as the plastics made their way around the mice's bodies, eventually reaching their brains. They also noted that the plastic bits tended to get backed up, like cars in a traffic jam at different points. In taking a closer look at some of the backups in the brain, the researchers found that the plastic bits had been captured by immune cells, which led to even more backups.
Wondering if the plastic in their brains was causing any impairment, the researchers tested several of the mice and found that many of them experienced memory loss, reductions in motor skills and lower endurance.
Haipeng Huang et al, Microplastics in the bloodstream can induce cerebral thrombosis by causing cell obstruction and lead to neurobehavioral abnormalities, Science Advances (2025). DOI: 10.1126/sciadv.adr8243
Star formation in the early universe was a vigorous process that created gigantic stars. Called Population III stars, these giants were massive, extremely luminous stars that lived short lives, many of which ended when they exploded as primordial supernovae.
But even these early stars faced growth limitations.
Stellar feedback plays a role in modern star formation. As young starsgrow, they emit powerful radiation that can disperse nearby gas they need to keep growing. This is called protostellar radiative feedback, and it takes place in addition to the restrictive effect their magnetic fields have on their growth.
However, new research shows that the growth of Pop III stars was limited by their magnetic fields.
The research is titled "Magnetic fields limit the mass of Population III stars even before the onset of protostellar radiation feedback"
The paper is published on the arXiv preprint server.
Piyush Sharda et al, Magnetic fields limit the mass of Population III stars even before the onset of protostellar radiation feedback, arXiv (2025). DOI: 10.48550/arxiv.2501.12734
Scientists create 'molecular trap' to remove pollutants from water
Scientists have developed a new material that could help reduce water pollution caused by harmful chemicals, such as from leftover medicines and hygiene products, that end up in rivers and lakes.
Water pollution is one of the growing challenges of modern life. Many everyday items, from medications to cosmetics, leave behind residues that don't fully break down after use. These pollutants often find their way into water systems, where they disrupt ecosystems and cause harm to plants, animals and humans.
The research, published in the journal Cell Reports Physical Science, describes a new method using a molecular structure called a metal-organic cage (MOC). These tiny cages act like traps designed to catch and hold harmful molecules commonly found in our water supplies.
The cages are made up of metal ions connected by organic molecules forming a hollow pyramid-like structure. These hollow spaces at the center of these structures are where the MOCs trap specific molecules, like pollutants or gases.
The new structure incorporates chemical groups called sulfonates to make it compatible with water, allowing it to function in real-world water systems, like rivers or wastewater.
It uses a natural effect called hydrophobic binding, where contaminant molecules preferentially "stick" to the inside of the cage rather than staying in the water. This allows the material to selectively capture and hold pollutants, even in challenging water environments.
Jack D. Wright et al, Encapsulation of Hydrophobic Pollutants within a Large Water-Soluble [Fe4L6]4- Cage, Cell Reports Physical Science (2025). DOI: 10.1016/j.xcrp.2025.102404
Catching the culprits: DNA 'fingerprints' of drug-makers can be linked to capsules and packaging
DNA profiling technologies are rapidly advancing, creating the potential to identify individuals involved in making, packing and transporting illegal capsules by analyzing the exterior of the illicit drugs and the plastic bag in which they are carried.
Experiments carried out by Flinders University forensic science experts have found that DNA accumulates in different areas, depending on an individual's involvement in the process, which could aid identification of people involved in the drug-making and trade.
The work ispublishedin the journalForensic Science International: Genetics.
The study also found DNA from the surface of capsules can be transferred to the inner surface of ziplock bags (ZLBs) commonly used in transportation.
This small-scale study indicates that capsule packers deposit less DNA than capsule makers who spend more time handling drug casing, and those that make the capsules can leave enough DNA for a complete profile with as little as 30 seconds of contact.
Furthermore, the DNA yield on these commonly used plastic bags is higher when handled by several people compared with little-to-no contact.
"Generating informative DNA profiles from the inside surface of the ziplock bag could be more useful than the outer side, as could be testing of other 'protected' areas of the bag such as the zip or inner edge of the seal.
Illicit substances frequently distributed in secure ziplock bags can be seized by police and tested by forensic investigators.
Strong DNA profiles 're generated for the individual who made the capsules and for the individual responsible for packing the ziplock bag.
Madison Nolan et al, Illicit drug distribution: Evaluation of DNA transfer between ziplock bags and capsules, Forensic Science International: Genetics (2024). DOI: 10.1016/j.fsigen.2024.103182
Octopuses have some of the oldest known sex chromosomes, study finds
The octopus just revealed another one of its secrets: what determines its sex.
Researchers have identified a sex chromosome in the California two-spot octopus. This chromosome has likely been around for 480 million years, since before octopuses split apart from the nautilus on the evolutionary tree. That makes it one of the oldest known animal sex chromosomes.
The finding also is evidence that octopuses and other cephalopods, a class of sea animals that includes squid and nautiluses, do use chromosomes to determine their sex, answering a longstanding mystery.
In humans and most mammals, sex is determined largely by chromosomes. But "there's a tremendous amount of diversity" in how animals determine their sex.
In turtles, for instance, sex is determined by the temperature at which the eggs are incubated. Some fish have a gene that determines sex, but not a whole chromosome. Even in humans, the X/Y sex chromosome system isn't as clear-cut as it might look on paper; gene mutations or inheriting extra sex chromosomes can lead to development that doesn't neatly fit in a male/female binary.
When researchers recently sequenced the DNA of a female California two-spot octopus, they found something unexpected: a chromosome with only half the amount of genetic material. It looked different from all the others, and it hadn't been found in male octopuses whose DNA was previously sequenced.
This particular chromosome had half the amount of sequencing data, which indicated there was only one copy.
To confirm, the researchers sorted through other octopus genomic data previously collected by other researchers.
They found another example of the half-sized chromosome in another species of octopus. They also found it in squid, which diverged evolutionarily from octopuses somewhere between 248 and 455 million years ago. And after more digging, they also found evidence for the chromosome in the nautilus, a mollusk that split apart from the octopus approximately 480 million years ago.
The fact that these species share this unique chromosome suggests that it's been around in some form for a very long time.
This indicates that their common ancestor had this similar sex determination system.
That's somewhat unusual for sex chromosomes. Because they directly impact reproductive capabilities, they're subject to a lot of selective pressure and so tend to undergo rapid evolutionary change. But cephalopods seem to have found what works and have stuck with it.
Other ancient sex chromosomes have been discovered in plant groups like mosses and liverworts, which were some of the first plants to evolve. And insect sex chromosomes might be 450 million years old, but they've also changed a lot over time.
Dr. Krishna Kumari Challa
Record-Shattering 20,000 Mph Winds Detected on Wild Alien Planet
Winds circling a gas giant more than 500 light years from Earth have been detected flowing at supersonic speeds approaching 33,000 kilometers (20,000 miles) per hour, making them the fastest air currents on any known planet by a wide margin.
Researchers from Europe cleaned and analyzed the spectrum of light reflected from the planet WASP-127b, uncovering two contrasting peaks in water and carbon dioxide signals suggestive of supersonic flows disturbing the planet's cloud tops.
Part of the atmosphere of this planet is moving towards us at a high velocity while another part is moving away from us at the same speed.
This signal shows us that there is a very fast, supersonic, jet wind around the planet's equator.
Fast is an understatement. At an incredible 7.5 to 7.9 kilometers per second, they outstrip any hurricane or jetstream known to science.
Here on Earth, the fastest puff of wind on record was a blustery 407 kilometers (253 miles) per hour, measured on Australia's Barrow Island in 1996. Neptune has the highest wind speeds in our Solar System, but even its 1,770 kilometer-per-hour high-altitude currents feel more like a mild breeze by comparison.
It's also believed to be tidally locked, rotating in step with every 4.2-Earth-day lap around its star, so one side is perpetually baked to temperatures exceeding 1,000 degrees Celsius (1832 degrees Fahrenheit), and the other never turns from the cold night sky.
https://www.aanda.org/articles/aa/full_html/2025/01/aa50438-24/aa50...
Jan 24
Dr. Krishna Kumari Challa
Scientists uncover how cancer cells hijack T-cells, making it harder for the body to fight back
Researchers have discovered a surprising way cancer evades the immune system. It essentially hacks the immune cells, transferring its own faulty mitochondrial DNA (mtDNA) into the T-cells meant to attack it.
This sneaky move weakens the immune cells, making them less effective at stopping the tumor. The findings could help explain why some cancer treatments, like immunotherapy, are effective for some patients but not others.
In the study, "Immune evasion through mitochondrial transfer in the tumour microenvironment," published in Nature, the multi-group collaboration looked at how cancer cells interact with tumor-infiltrating lymphocytes, a type of T-cell that typically fights tumors. The research is also featured in a News and Views piece.
Clinical specimens from melanoma and non-small-cell lung cancer patients were analyzed for mtDNA mutations. Mitochondrial transfer was studied using mitochondrial-specific fluorescent reporters and multiple in vitro and in vivo models. Tumor-infiltrating lymphocyte functions, metabolic profiles, and responses to immune checkpoint inhibitors were evaluated.
Melanoma and lung sample analysis showed that mitochondria, the energy-making engines of cells, could jump from cancer cells into T-cells. These transferred mitochondria carried functional errors in their DNA that interfered with the T-cells' energy production and function processes.
Mitochondria are essential for powering cells, including T-cells, which depend heavily on energy production to fight cancer. But when cancer cells pass on their defective mitochondria, they lose their ability to function properly, throttling the energy of the T-cells and causing them to become exhausted.
Transfer was observed in two main ways: tunneling nanotubes and extracellular vesicles. The nanotubes extend out and tunnel into the T-cell, creating tiny passages between cells that deliver mitochondria directly. Extracellular vesicles form as bubbles released by the cancer cells, encapsulating mtDNA and other molecules.
Once inside the T-cells, the damaged mitochondria replace the healthy ones through a mechanism that would normally operate in reverse, where healthy mitochondria would migrate to replace damaged ones. The study found that cancer cells protect their transferred mitochondria by attaching molecules that prevent the T-cells from breaking them down.
Part 1
Jan 25
Dr. Krishna Kumari Challa
Immune checkpoint inhibitors have revolutionized cancer treatment. But not everyone responds well to these drugs. This study found that patients whose tumors had more mitochondrial mutations were less likely to benefit from checkpoint inhibitors, likely because the mitochondrial hack already compromised their T-cells.
Researchers blocked extracellular vesicle release from cancer cells using a compound called GW4869, which inhibits the production of small extracellular vesicle-like exosomes. Applying this inhibitor in their models showed a significant reduction in mitochondrial transfer from cancer cells to T-cells. This intervention helped prevent the T-cells from taking up damaged mitochondria, reducing their dysfunction.
As a result, T-cells showed improved energy production, reduced markers of exhaustion, and a better ability to perform their immune functions. The blocking strategy restored the effectiveness of immune checkpoint inhibitors, particularly in tumors with high levels of mitochondrial transfer. These findings suggest that targeting extracellular vesicles could be a promising strategy to counteract cancer's immune-evasion tactic.
Typically, science works in small, iterative steps toward discovery, with each new element of knowledge putting a piece of the larger puzzle into place. This discovery helps explain why some treatments are ineffective and discovers the mechanism behind their ineffectiveness. Remarkably, it also found a potential solution, representing a significant leap for future research to build from.
Hideki Ikeda et al, Immune evasion through mitochondrial transfer in the tumour microenvironment, Nature (2025). DOI: 10.1038/s41586-024-08439-0
Jonathan R. Brestoff, Mitochondrial swap from cancer to immune cells thwarts anti-tumour defences, Nature (2025). DOI: 10.1038/d41586-025-00077-4
Part 2
Jan 25
Dr. Krishna Kumari Challa
Research reveals how specific types of liver immune cells are required to deal with injury
Our livers contain many different types of immune cells. New research now reveals that a specific activation state of one of these cell types is required for tissue repair following injury. This suggests these cells may be useful as new therapeutic targets for various liver conditions. The work appears in the journal Immunity.
Macrophages are specialized immune cells located in every tissue of the body, where they play crucial roles in maintaining tissue homeostasis, responding to injury, and facilitating tissue repair. In the healthy liver, most macrophages are classified as Kupffer cells (KCs). However, upon liver injury, as seen, for example, in obesity, another subset of macrophages called lipid-associated macrophages (LAMs) is recruited.
This work shows that the LAM phenotype is critical for liver repair. Moreover, this research revealed that the KCs are not static post-injury, as previously thought, and instead adapt to the new microenvironment also taking on a LAM-like phenotype, allowing them to also participate in the repair.
Federico F. De Ponti et al, Spatially restricted and ontogenically distinct hepatic macrophages are required for tissue repair, Immunity (2025). DOI: 10.1016/j.immuni.2025.01.002
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Jan 25
Dr. Krishna Kumari Challa
Astronauts' eyes weaken during long space missions, raising concerns for Mars travel
The low levels of gravity (microgravity) in space cause significant changes in astronauts' eyes and vision after six to 12 months aboard the International Space Station (ISS), according to a study published in the IEEE Open Journal of Engineering in Medicine and Biology.
Researchers found that at least 70% of astronauts on the ISS have been affected by spaceflight-associated neuro-ocular syndrome, or SANS.
They analyzed data collected by the Canadian team at NASA on 13 astronauts who spent between 157 and 186 days on the ISS.
The subjects had an average age of 48 and came from the U.S., European, Japanese and Canadian space agencies; 31% were women; eight were on their first mission.
The researchers compared three ocular parameters before and after the astronauts' space missions: ocular rigidity, intraocular pressure, and ocular pulse amplitude.
They measured ocular rigidity using optical coherence tomography with a customized video module to improve the quality of images of the choroid. The other two parameters, intraocular pressure and ocular pulse amplitude, were measured using tonometry.
The study found significant changes in the biomechanical properties of the astronauts' eyes: a 33% decrease in ocular rigidity, an 11% decrease in intraocular pressure, and a 25% reduction in ocular pulse amplitude.
These changes were accompanied by symptoms including reduced eye size, altered focal field and, in some cases, optic nerve edema and retinal folds.
Part 1
Jan 25
Dr. Krishna Kumari Challa
The researchers also found that five astronauts had a choroidal thickness greater than 400 micrometers, which was not correlated with age, gender or previous space experience.
Weightlessness alters the distribution of blood in the body, increasing blood flow to the head and slowing venous circulation in the eye. This is probably what causes the expansion of the choroid, the vascular layer that nourishes the retina.
According to the researchers, the expansion of the choroid during weightlessness could stretch the collagen in the sclera, the white outer layer of the eye, causing long-lasting changes in the eye's mechanical properties.
They also think that blood pulsations under microgravity can create a water-hammer effect in which sudden changes in blood-flow-pressure cause a mechanical shock to the eye, leading to significant tissue remodeling.
According to the researchers, these ocular changes are generally not cause for concern when the space mission lasts six to 12 months. Although 80% of the astronauts they studied developed at least one symptom, their eyes returned to normal once back on Earth.
In most cases, wearing corrective eyeglasses was sufficient to correct the symptoms developed aboard the ISS.
However, the research community and international space agencies are cautious about the consequences of longer missions, such as a flight to Mars. The eye-health effects of prolonged exposure to microgravity remain unknown, and no preventive or palliative measures now exist.
Marissé Masís Solano et al, Ocular Biomechanical Responses to Long-Duration Spaceflight, IEEE Open Journal of Engineering in Medicine and Biology (2024). DOI: 10.1109/OJEMB.2024.3453049
Part 2
Jan 25
Dr. Krishna Kumari Challa
Scientists trace deadly cell-to-cell message chain that spreads in sepsis
Dying cells prick their neighbours with a lethal message. This may worsen sepsis, researchers report in the Jan. 23 issue of Cell. Their findings could lead to a new understanding of this dangerous illness.
Sepsis is one of the most frequent causes of death worldwide, according to the World Health Organization (WHO), killing 11 million people each year. It's characterized by runaway inflammation, usually sparked by an infection. It can lead to shock, multiple organ failure, and death if treatment is not rapid enough or effective.
But recent research has shown that it isn't actually the infection that causes the spiraling inflammation: it's the cells caught up in it. Even if those cells aren't infected, they act as if they are, and die. As they die, they send out messages to other cells. Those messages somehow cause the recipient cells to die.
If scientists understood what caused this deadly message chain, they might be able to stop it. And that could help heal sepsis.
The deadly message mystery may now be solved. It appears that the "messages" are a byproduct of the cells trying to stay alive.
The process starts with cells that really are infected. To prevent the infection from spreading, those cells destroy themselves by sending a protein called gasdermin-D to their surface. Several gasdermin-D proteins will link together to create a round pore on the cell, like a hole punched in a balloon. The cell's contents leak out, the cell collapses, and dies.
But the collapse isn't inevitable. Sometimes cells can act quickly and eject the section of their surface membrane with the gasdermin-D pore. The cell then zips the membrane closed and survives. The ejected membrane forms a little bubble, called a vesicle , that just happens to carry the deadly gasdermin-D pore. The vesicle floats around, and when it encounters a cell nearby, that deadly gasdermin-D pore punches into the healthy nearby cell's membrane and causes that cell to spill and die.
When a dying cell releases these vesicles, they can transplant these pores to a neighboring cell's surface, which leads to the neighboring cell's death.
In other words, the deadly messages are a side effect of cells just trying to save themselves. A group of dying cells can release enough gasdermin-D vesicles to kill a considerable number of nearby cells. That spreading message of death fuels the spiraling inflammation of sepsis.
Researchers are now looking for a way to tamp down the deadly gasdermin-D vesicles. If successful, it could lead to a treatment for inflammatory diseases like sepsis.
Skylar S. Wright et al, Transplantation of gasdermin pores by extracellular vesicles propagates pyroptosis to bystander cells, Cell (2024). DOI: 10.1016/j.cell.2024.11.018
Jan 25
Dr. Krishna Kumari Challa
Why hibernating animals don't dream
Because hibernation isn’t the same as sleep.
Sleep is a more physiologically ‘active’ state. Hibernation, in contrast, requires animals (like this hedgehog, above) to substantially reduce all activities to conserve energy.Hibernating animals reduce their breathing rate, lower their body temperature and decrease their metabolic rate to around five per cent of their usual levels. There’s simply not enough brain activity while an animal is hibernating to enable dreaming.
There is one exception, however: the fat-tailed lemur. As the only primate to hibernate, scientists have observed them having periods of rapid eye movement (REM) sleep.
Jan 26
Dr. Krishna Kumari Challa
New water purification technology helps turn seawater into drinking water without using tons of chemicals
Water desalination plants could replace expensive chemicals with new carbon cloth electrodes that remove boron from seawater, an important step of turning seawater into safe drinking water.
A study describing the new technology has been published in Nature Water.
Boron is a natural component of seawater that becomes a toxic contaminant in drinking water when it sneaks through conventional filters for removing salts. Seawater's boron levels are around twice as high as the World Health Organization's most lenient limits for safe drinking water, and five to 12 times higher than the tolerance of many agricultural plants.
Most reverse osmosis membranes don't remove very much boron, so desalination plants typically have to do some post treatment to get rid of the boron, which can be expensive. So researchers developed a new technology that's fairly scalable and can remove boron in an energy-efficient way compared to some of the conventional technologies.
In seawater, boron exists as electrically neutral boric acid, so it passes through reverse osmosis membranes that typically remove salt by repelling electrically charged atoms and molecules called ions. To get around this problem, desalination plants normally add a base to their treated water, which causes boric acid to become negatively charged. Another stage of reverse osmosis removes the newly charged boron, and the base is neutralized afterward by adding acid. Those extra treatment steps can be costly.
The new device now developed reduces the chemical and energy demands of seawater desalination, significantly enhancing environmental sustainability and cutting costs by up to 15 percent, or around 20 cents per cubic meter of treated water.
The new electrodes remove boron by trapping it inside pores studded with oxygen-containing structures. These structures specifically bind with boron while letting other ions in seawater pass through, maximizing the amount of boron they can capture.
But the boron-catching structures still need the boron to have a negative charge. Instead of adding a base, the charge is created by splitting water between two electrodes, creating positive hydrogen ions and negative hydroxide ions. The hydroxide attaches to boron, giving it a negative charge that makes it stick to the capture sites inside the pores in the positive electrode. Capturing boron with the electrodes also enables treatment plants to avoid spending more energy on another stage of reverse osmosis. Afterward, the hydrogen and hydroxide ions recombine to yield neutral, boron-free water.
Weiyi Pan et al, A highly selective and energy efficient approach to boron removal overcomes the Achilles heel of seawater desalination, Nature Water (2025). DOI: 10.1038/s44221-024-00362-y
Jan 27
Dr. Krishna Kumari Challa
AI-based pregnancy analysis discovers previously unknown warning signs for stillbirth and newborn complications
A new AI-based analysis of almost 10,000 pregnancies has discovered previously unidentified combinations of risk factors linked to serious negative pregnancy outcomes, including stillbirth.
The study also found that there may be up to a tenfold difference in risk for infants who are currently treated identically under clinical guidelines.
The researchers started with an existing dataset of 9,558 pregnancies, which included information on social and physical characteristics ranging from pregnant people's level of social support to their blood pressure, medical history, and fetal weight, as well as the outcome of each pregnancy. By using AI to look for patterns in the data, they identified new combinations of maternal and fetal characteristics that were linked to unhealthy pregnancy outcomes such as stillbirth.
Usually, female fetuses are at slightly lower risk for complications than male fetuses—a small but well-established effect. But the research team found that if a pregnant person has pre-existing diabetes, female fetuses are at higher risk than males.
This previously undetected pattern shows that the AI model can help researchers learn new things about pregnancy health.
The researchers were especially interested in developing better risk estimates for fetuses in the bottom 10% for weight, but not the bottom 3%. These babies are small enough to be concerning, but large enough that they are usually perfectly healthy. Figuring out the best course of action in these cases is challenging: Will a pregnancy need intensive monitoring and potentially early delivery, or can the pregnancy proceed largely as normal? Current clinical guidelines advise intensive medical monitoring for all such pregnancies, which can represent a significant emotional and financial burden.
But the researchers found that within this fetal weight class, the risk of an unhealthy pregnancy outcome varied widely, from no riskier than an average pregnancy to nearly ten times the average risk. The risk was based on a combination of factors such as fetal sex, presence or absence of pre-existing diabetes, and presence or absence of a fetal anomaly such as a heart defect.
For humans or AI models, estimating pregnancy risks involves taking a very large number of variables into account, from maternal health to ultrasound data. Experienced clinicians can weigh all these variables to make individualized care decisions, but even the best doctors probably wouldn't be able to quantify exactly how they arrived at their final decision. Human factors like bias, mood, or sleep deprivation almost inevitably creep into the mix and can subtly skew judgment calls away from ideal care.
To help address this problem, the researchers used a type of model called "explainable AI," which provides the user with the estimated risk for a given set of pregnancy factors and also includes information on which variables contributed to that risk estimation, and how much.
Part 1
Jan 31
Dr. Krishna Kumari Challa
Essentially, explainable AI approximates the flexibility of expert clinical judgment while avoiding its pitfalls. The researchers' model is also especially well-suited to judging risk for rare pregnancy scenarios, accurately estimating outcomes for people with unique combinations of risk factors. This kind of tool could ultimately help personalize care by guiding informed decisions for people whose situations are one-of-a-kind.
AI models can essentially estimate a risk that is specific to a given person's context and they can do it transparently and reproducibly, which is what human brains can't do.
AI-based analysis of fetal growth restriction in a prospective obstetric cohort quantifies compound risks for perinatal morbidity and mortality and identifies previously unrecognized high risk clinical scenarios, BMC Pregnancy and Childbirth (2025). DOI: 10.1186/s12884-024-07095-6
Part 2
Jan 31
Dr. Krishna Kumari Challa
How tackling sepsis can save millions of lives—and prevent future pandemic deaths
Sepsis is an underestimated killer. Nearly a quarter of patients treated for sepsis in hospital will die, but because so many different illnesses can predispose patients to experiencing it, it's overlooked as a direct cause of death. Yet approximately 20% of deaths worldwide are caused by sepsis, and currently we have no treatments that tackle it directly.
Now researchers writing in Frontiers in Science explain how systems immunology can help us understand and treat sepsis—and how this could cut the death toll of future pandemics, no matter what disease causes them.
One of the reasons it's so hard to understand and treat sepsis is that it is multifaceted. Sepsis arises when the immune system fails to control an infection and malfunctions, causing multi-organ failure. Many different infections can cause sepsis, and its symptoms and progression vary between patients and over time in the same patient. Its early symptoms are similar to those of many other illnesses, which makes it difficult to diagnose quickly and initiate timely treatment, contributing to high mortality.
Systems immunology offers a potential solution to this diagnosis problem by using mathematical and computational modeling to study the immune system in the context of all the body's other systems. It does this by using different types of clustering analysis to identify patterns in large volumes of omics data, ranging from transcriptomic data (what genes show altered expression) to proteomic and metabolomic data—data that tell us about the body's reaction to its physical circumstances, in this case sepsis, in incredibly fine-grained detail.
These patterns help us work out the patterns and basis for the immune dysregulation that drives sepsis, come up with new hypotheses that we can research and use to develop new treatments, and identify diagnostic markers that we can use to catch sepsis early.
For instance, using these clustering analyses, scientists have identified changes to gene expression that act as early warnings for sepsis. They've also been able to identify five different subtypes of sepsis which are caused by different kinds of immune dysregulation and have different prognoses. In the future, we could build on these advances to diagnose different subtypes of sepsis earlier and treat them with the right drugs when we do.
However, systems immunology analysis is not yet in widespread use, because it is expensive and demands significant volumes of data—so we don't yet know how these diagnostics could translate into clinical results. The researchers call urgently for targeted funding and greater data availability.
"In sepsis we lack the depth of information required to enable more effective systems immunology and machine learning approaches.
Part 1
Jan 31
Dr. Krishna Kumari Challa
Successfully treating sepsis would be a multipurpose life-saver, preventing mortality regardless of the illness that triggered it. Viral sepsis is a major cause of deaths triggered by severe COVID-19, while many deaths in historical pandemics like the 1919 influenza pandemic and the bubonic plague are thought to have resulted from sepsis.
If we can tackle sepsis, we might be able to protect ourselves against the worst consequences and the highest death tolls in future pandemics, no matter what kind of infection causes them. Since immune dysregulation linked to sepsis can linger, causing symptoms similar to post-viral syndromes like long COVID-19, learning to treat this could also benefit some chronic illness patients.
But to make this happen, the researchers caution, more funding and larger studies will be needed.
The omics methods that underlie systems immunology are relatively expensive on a per patient basis. It will require a concerted drive from stakeholders to generate the data needed for further insights. We need to invest in larger omics studies of patients, develop new animal and organoid models that reflect sepsis heterogeneity, and invest in early diagnostics for sepsis and treatments that correct or supplement defective immunity in sepsis patients.
Deciphering sepsis: transforming diagnosis and treatment through systems immunology, Frontiers in Science (2025). DOI: 10.3389/fsci.2024.1469417
Part 2
Jan 31
Dr. Krishna Kumari Challa
Why you shouldn't scratch an itchy rash
New research published in the journal Science uncovers how scratching aggravates inflammation and swelling in a mouse model of a type of eczema called allergic contact dermatitis.
Scratching is often pleasurable, which suggests that, in order to have evolved, this behaviour must provide some kind of benefit. This new study helps resolve this paradox by providing evidence that scratching also provides defense against bacterial skin infections.
Allergic contact dermatitis is an allergic reaction to allergens or skin irritants—including poison ivy and certain metals such as nickel—leading to an itchy, swollen rash. Succumbing to the often-irresistible urge to scratch triggers further inflammation that worsens symptoms and slows healing.
To figure out what drives this vicious cycle, researchers used itch-inducing allergens to induce eczema-like symptoms on the ears of normal mice and those that don't get itchy because they lack an itch-sensing neuron.
When normal mice were allowed to scratch, their ears became swollen and filled with inflammatory immune cells called neutrophils. In contrast, inflammation and swelling were much milder in normal mice that couldn't scratch because they wore tiny Elizabethan collars, similar to a cone that a dog might sport after a visit to the vet, and in animals that lacked the itch-sensing neuron. This experiment confirmed that scratching further aggravates the skin.
Next, the researchers showed that scratching causes pain-sensing neurons to release a compound called substance P. In turn, substance P activates mast cells, which are key coordinators of inflammation that drive itchiness and inflammation via recruitment of neutrophils.
In contact dermatitis, mast cells are directly activated by allergens, which drives minor inflammation and itchiness.
In response to scratching, the release of substance P activates mast cells through a second pathway, so the reason that scratching triggers more inflammation in the skin is because mast cells have been synergistically activated through two pathways.
Part 1
Jan 31
Dr. Krishna Kumari Challa
Mast cells are culprits in a range of inflammatory skin conditions and allergic reactions, but they're also important for protecting against bacteria and other pathogens. As such, the researchers wondered if scratching-induced activation of mast cells could affect the skin microbiome.
The researchers showed that scratching reduced the amount of Staphylococcus aureus, the most common bacteria involved in skin infections, on the skin.
The finding that scratching improves defense against Staphylococcus aureus suggests that it could be beneficial in some contexts. But the damage that scratching does to the skin probably outweighs this benefit when itching is chronic.
Andrew W. Liu et al, Scratching promotes allergic inflammation and host defense via neurogenic mast cell activation, Science (2025). DOI: 10.1126/science.adn9390. www.science.org/doi/10.1126/science.adn9390
Part 2
Jan 31
Dr. Krishna Kumari Challa
Your fridge still uses tech from the 50s, but scientists have an update
Researchers report on Jan. 30 in the journal Joule that a more efficient and environmentally friendly form of refrigeration might be on the horizon. The new technology is based on thermogalvanic cells that produce a cooling effect by way of a reversible electrochemical reaction.
Thermogalvanic refrigeration is cheaper and more environmentally friendly than other cooling methods because it requires a far lower energy input, and its scalability means that it could be used for various applications—from wearable cooling devices to industrial-grade scenarios.
Thermogalvanic cells use the heat produced by reversible electrochemical reactions to create electrical power. In theory, reversing this process—applying an external electrical current to drive electrochemical reactions—enables cooling power to be generated.
Previous studies have shown that thermogalvanic cells have a limited potential to produce cooling power, but this new work was able to dramatically increase this potential by optimizing the chemicals used in the technology.
By tweaking the solutes and solvents used in the electrolyte solution, the researchers were able to improve the hydrogalvanic cell's cooling power. They used a hydrated iron salt containing perchlorate, which helped the iron ions dissolve and dissociate more freely compared to other previously tested iron-containing salts such as ferricyanide.
By dissolving the iron salts in a solvent containing nitriles rather than pure water, the researchers were able to improve the hydrogalvanic cell's cooling power by 70%.
The optimized system was able to cool the surrounding electrolyte by 1.42 K, which is a big improvement compared to the 0.1 K cooling capacity reported by previously published thermogalvanic systems.
Looking ahead, the team plans to continue optimizing their system's design and is also investigating potential commercial applications.
Solvation entropy engineering of thermogalvanic electrolytes for efficient electrochemical refrigeration, Joule (2025). DOI: 10.1016/j.joule.2025.101822. www.cell.com/joule/fulltext/S2542-4351(25)00003-0
Jan 31
Dr. Krishna Kumari Challa
Complex engineering of human cell lines reveals genome's unexpected resilience to structural changes
The most complex engineering of human cell lines ever has been achieved by scientists, revealing that our genomes are more resilient to significant structural changes than was previously thought.
Researchers used CRISPR prime editing to create multiple versions of human genomes in cell lines, each with different structural changes. Using genome sequencing, they were able to analyze the genetic effects of these structural variations on cell survival .
The research, published in Science, shows that as long as essential genes remain intact, our genomes can tolerate significant structural changes, including large deletions of the genetic code. The work opens the door to studying and predicting the role of structural variation in disease.
Structural variation is a change in the structure of an organism's genome, such as deletions, duplications and inversions of the genetic sequence. These structural changes to the genome can be significant, sometimes affecting hundreds to many thousands of nucleotides—the basic building blocks of DNA and RNA.
Structural variants are associated with developmental diseases and cancer. However, our ability to study the effects of structural variation in the genomes of mammals, and the role they play in disease, has been difficult due to the inability to engineer these genetic changes.
To overcome this challenge, researchers set out to develop new approaches for creating and studying structural variation.
In a new study, the team used a combination of CRISPR prime editing and human cell lines—groups of human cells in a dish—to generate thousands of structural variants in human genomes within a single experiment.
To do this, researchers used prime editing to insert a recognition sequence into the genomes of the human cell lines to target with recombinase—an enzyme that enabled the team to 'shuffle' the genome.
By inserting these recombinase handles into repetitive sequences, which are hundreds and thousands of identical sequences in the genome, with a single prime editor they were able to integrate up to almost 1,700 recombinase recognition sites into each cell line.
This resulted in more than 100 random large-scale genetic structural changes per cell. This is the first time that it's been possible to 'shuffle' a mammalian genome, especially at this scale.
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Jan 31
Dr. Krishna Kumari Challa
The team then studied the impacts of the structural variation on the human cell lines. Using genomic sequencing, the team was able to take 'snapshots' of the human cells and their 'shuffled' genomes over the course of a few weeks, watching which cells survived and which died.
As expected, they found that when structural variation deleted essential genes, this was heavily selected against and the cells died. However, they found that groups of cells with large-scale deletions in the genomes that avoided essential genes survived.
The team also conducted RNA sequencing of the human cell lines, which measures gene activity, known as gene expression. This revealed that large-scale deletions of the genetic code, especially in non-coding regions, did not seem to impact the gene expression of the rest of the cell.
The researchers suggest that human genomes are extremely tolerant of structural variation, including variants that change the position of hundreds of genes, as long as essential genes are not deleted.
In another study related to this another research team used a different approach, adding recombinase sites to transposons—mobile genetic elements—that randomly integrated in the genomes of human cell lines and mouse embryonic stem cells.
Using their method, they demonstrated that the effects of the induced structural variants can be read out using single-cell RNA sequencing. This advance paves the way for large screens of structural variant impact, potentially improving the classification of structural variants found in human genomes as benign or clinically significant.
Both studies came to similar conclusions that human genomes are surprisingly tolerant to some substantial structural changes, although the full extent of this tolerance remains to be explored in future studies enabled by these technologies.
Jonas Koeppel et al, Randomizing the human genome by engineering recombination between repeat elements, Science (2025). DOI: 10.1126/science.ado3979. www.science.org/doi/10.1126/science.ado3979
Science (2025). DOI: 10.1126.science.ado5978
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Jan 31
Dr. Krishna Kumari Challa
Scientists replicate bone marrow
Hidden within our bones, marrow sustains life by producing billions of blood cells daily, from oxygen-carrying red cells to immune-boosting white cells. This vital function is often disrupted in cancer patients undergoing chemotherapy or radiation, which can damage the marrow and lead to dangerously low white cell counts, leaving patients vulnerable to infection.
Now researchers have developed a platform that emulates human marrow's native environment. This breakthrough addresses a critical need in medical science, as animal studies often fail to fully replicate the complexities of human marrow.
The team's new device is a small plastic chip whose specially designed chambers are filled with human blood stem cells and the surrounding support cells with which they interact in a hydrogel to mimic the intricate process of bone marrow development in the human embryo. This biologically inspired platform makes it possible to build living human marrow tissue that can generate functional human blood cells and release them into culture media flowing in engineered capillary blood vessels.
The bone marrow-on-a-chip allows researchers to simulate and study common side effects of medical treatments, such as radiotherapy and chemotherapy for cancer patients. When connected to another device, it can even model how the bone marrow communicates with other organs, like the lungs, to protect them from infections and other potentially life-threatening conditions.
Described in a new paper published in Cell Stem Cell, the bone marrow model and the demonstration of its large-scale production and automation could advance fields as diverse as drug development by enabling automated, high-throughput preclinical screening of marrow toxicity of anticancer drugs) and space travel (by allowing researchers to study the effects of prolonged radiation exposure and microgravity on the immune system of astronauts).
Andrei Georgescu et al, Self-organization of the hematopoietic vascular niche and emergent innate immunity on a chip, Cell Stem Cell (2024). DOI: 10.1016/j.stem.2024.11.003
Jan 31
Dr. Krishna Kumari Challa
Future antibiotics face early bacterial resistance challenges, studies show
Researchers have made a concerning discovery about the future of antibiotics. Two recent studies, published just days apart in Nature Microbiology and Science Translational Medicine found that resistance can develop against new antibiotics even before they are widely used, compromising their effectiveness from the start. The studies focused on five critical bacterial species that cause major hospital infections and examined 18 new antibiotics, some already on the market and others still in development.
New antibiotics are often marketed as resistance-free, but this claim relies on limited data.
This new work highlights a major issue: antibiotic development tends to prioritize broad-spectrum activity - that is the number of bacterial species a drug targets- over long-term sustainability. While many new antibiotics indeed offer a broader spectrum, this doesn't guarantee they will remain effective in the long run in clinical use.
The studies found that resistance developed rapidly against nearly all the tested antibiotics, defying earlier expectations. For example, teixobactin, once hailed as a revolutionary drug, was believed to be less prone to resistance. However, the research revealed that bacteria can adapt to it with this adaptation resulting in cross-resistance to other critical antibiotics.
Alarmingly, the team also found that resistance mutations may already exist in bacterial populations, likely due to the overuse of older antibiotics and the shared resistance mechanisms between those and new drugs. These pre-existing mutations could render even the newest drugs ineffective shortly after they are introduced into clinical use.
Rethinking antibiotic development: The studies call for a fundamental shift in how antibiotics are developed. Drug companies must incorporate resistance studies early in the development process to anticipate and mitigate risks before antibiotics are released. Integrating resistance prediction and genetic surveillance into drug design could reduce the chances of failure.
Some new antibiotics show more promise than others, as resistance develops more slowly or only in specific bacterial species. Understanding why these drugs perform better is the next crucial step.
The studies emphasize the importance of prioritizing antibiotics with novel modes of action to bypass existing resistance. In cases where only certain bacterial species are prone to resistance, narrow-spectrum therapy could provide an effective alternative. Finally, the studies stress the urgency of responsible antibiotic use to slow down the evolution of resistance and ensure the prolonged efficacy of new treatments in the future.
Lejla Daruka et al, ESKAPE pathogens rapidly develop resistance against antibiotics in development in vitro, Nature Microbiology (2025). DOI: 10.1038/s41564-024-01891-8
Ana Martins et al, Antibiotic candidates for Gram-positive bacterial infections induce multidrug resistance, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adl2103
Jan 31
Dr. Krishna Kumari Challa
Bats' genetic adaptations: How they tolerate coronaviruses without becoming ill
New research has shown that bats can tolerate coronaviruses and other viruses without becoming ill, thanks to special adaptations of their immune system.
The study, published in Nature, shows that bats have more genetic adaptations in immune genes than other mammals. The ISG15 gene in particular plays a key role: in some bats, it can reduce the production of SARS-CoV-2 by up to 90%.
The results could help to develop new medical approaches to combat viral diseases.
Bats have unique characteristics. As the only mammals that can actively fly, they play an important role in the ecosystem: They pollinate plants, spread seeds and contribute to the balance of the insect population through their feeding habits. Their exceptional orientation using ultrasonic echolocation shows how perfectly they are adapted to their nocturnal lifestyle.
Bats are of great interest to medical advancement, as their immune systems and unique viral tolerances can provide valuable insights for the development of new therapies. They are also known to carry numerous viruses, including those that are transmissible to humans—such as coronaviruses. However, bats do not show any symptoms of disease when infected with such viruses.
The new research team has sequenced high-quality genomes of 10 new bat species, as part of the international Bat1K project, including species known to carry coronaviruses and other viruses. Such adaptations can be detected as traces of positive selection and can indicate functional changes.
The result of the extensive analysis shows that bats exhibit such adaptations in immune genes much more frequently than other mammals.
The research also showed that the common ancestor of all bats had an unexpectedly high number of immune genes with selection signatures. This suggests that the evolution of the immune system could be closely linked to the evolution of the ability to fly.
Ariadna E. Morales et al, Bat genomes illuminate adaptations to viral tolerance and disease resistance, Nature (2025). DOI: 10.1038/s41586-024-08471-0
Jan 31
Dr. Krishna Kumari Challa
India doubled its tiger population in a decade and credits conservation efforts
India doubled its tiger population in a little over a decade by protecting the big cats from poaching and habitat loss, ensuring they have enough prey, reducing human-wildlife conflict, and increasing communities' living standards near tiger areas, a study published this week found.
The number of tigers grew from an estimated 1,706 tigers in 2010 to around 3,682 in 2022, according to estimates by the National Tiger Conservation Authority, making India home to roughly 75% of the global tiger population. The study found that some local communities near tiger habitats have also benefited from the increase in tigers because of the foot traffic and revenues brought in by ecotourism.
The study in the journal Science says India's success "offers important lessons for tiger-range countries" that conservation efforts can benefit both biodiversity and nearby communities.
Wildlife conservationists and ecologists welcomed the study but said that tigers and other wildlife in India would benefit if source data were made available to a larger group of scientists. The study was based on data collected by Indian government-supported institutions.
Also there are several species, including the great Indian bustard and caracal which are all on the edge. "And there is really not enough focus on that."
Yadvendradev V. Jhala et al, Tiger recovery amid people and poverty, Science (2025). DOI: 10.1126/science.adk4827
Jan 31
Dr. Krishna Kumari Challa
Amniotic fluid's protective properties: Study uncovers its role in blood clotting
Researchers have made new discoveries about amniotic fluid, a substance historically not well understood in medical research due to the difficulty in obtaining it during pregnancy, especially across gestation.
Amniotic fluid is the vital fluid that surrounds and protects a fetus during pregnancy. In addition to providing much-needed cushion and protection for the fetus, it also aids in development of vital organs—especially the lungs, digestive tract and skin—and stabilizes the temperature inside the womb.
The new study, published in the journal Research and Practice in Thrombosis and Haemostasis, found that the addition of amniotic fluid to plasma—the liquid portion of blood—improves the blood's ability to thicken and clot, which is a critical and likely a protective function throughout pregnancy and during delivery for both the birthing parent and the baby.
Researchers analyzed the properties of amniotic fluid obtained by amniocentesis, a prenatal test that involves sampling a small amount of amniotic fluid to examine the health of the pregnancy, from both human and non-human primates at gestational-age matched timepoints. The findings showed that amniotic fluid increases blood clotting through key fatty acids and proteins that change each trimester and help regulate coagulation.
Chih Jen Yang et al, Characterization of the procoagulant phenotype of amniotic fluid across gestation in rhesus macaques and humans, Research and Practice in Thrombosis and Haemostasis (2025). DOI: 10.1016/j.rpth.2024.102676
Jan 31
Dr. Krishna Kumari Challa
Asteroid find upends story of life’s origin
Fragments collected from the asteroid Bennu contain the building blocks for life — all five nucleobases that form DNA and RNA and 14 of the 20 amino acids needed to make known proteins. But there’s a twist: on Earth, amino acids in living organisms tend to have a ‘left-handed’ structure. Those on Bennu, however, contain nearly equal amounts of these structures and their ‘right-handed’, mirror-image forms. This calls into question a hypothesis favoured by many scientists that asteroids similar to this one might have seeded life on Earth.
https://www.nature.com/articles/s41550-024-02472-9?utm_source=Live+...
https://www.nature.com/articles/d41586-025-00264-3?utm_source=Live+...
Jan 31
Dr. Krishna Kumari Challa
Ear muscle we thought humans didn't use—except for wiggling our ears—activates during focused listening
If you can wiggle your ears, you can use muscles that helped our distant ancestors listen closely. These auricular muscles helped change the shape of the pinna, or the shell of the ear, funneling sound to the eardrums.
There are three large muscles which connect the auricle to the skull and scalp and are important for ear wiggling. These muscles, particularly the superior auricular muscle, exhibit increased activity during effortful listening tasks. This suggests that these muscles are engaged not merely as a reflex but potentially as part of an attentional effort mechanism, especially in challenging auditory environments.
It's difficult to test how hard someone is listening without self-reported measures. But electromyography, which measures electrical activity in a muscle, can help identify activity in the auricular muscles linked to listening closely.
Similar research has already shown that the largest muscles, posterior and superior auricular muscles, react during attentive listening. Because they pull the ears up and back, they are considered likely to have been involved in moving the pinna to capture sounds.
The exact reason these became vestigial is difficult to tell, as our ancestors lost this ability about 25 million years ago. One possible explanation could be that the evolutionary pressure to move the ears ceased because we became much more proficient with our visual and vocal systems.
Scientists now found that the two auricular muscles reacted differently to the different conditions. The posterior auricular muscles reacted to changes in direction, while the superior auricular muscles reacted to the difficulty level of the task.
Electromyographic Correlates of Effortful Listening in the Vestigial Auriculomotor System, Frontiers in Neuroscience (2025). DOI: 10.3389/fnins.2024.1462507
Feb 1
Dr. Krishna Kumari Challa
Gut microbes may mediate the link between drinking sugary beverages and diabetes risk
It is well known that consuming sugary drinks increases the risk of diabetes, but the mechanism behind this relationship is unclear. Now, in a paper appearing in Cell Metabolism, researchers show that metabolites produced by gut microbes might play a role.
In a long-term cohort of US Hispanic/Latino adults, the researchers identified differences in the gut microbiota and blood metabolites of individuals with a high intake of sugar-sweetened beverages. The altered metabolite profile seen in sugary beverage drinkers was associated with a higher risk of developing diabetes in the subsequent 10 years. Since some of these metabolites are produced by gut microbes, this suggests that the microbiome might mediate the association between sugary beverages and diabetes.
This study suggests a potential mechanism to explain why sugar-sweetened beverages are bad for your metabolism.
Previous studies in Europe and China have shown that sugar-sweetened beverages alter gut microbiome composition, but this is the first study to investigate whether this microbial change impacts host metabolism and diabetes risk.
The researchers found that high sugary beverage intake—defined as two or more sugary beverages per day—was associated with changes in the abundance of nine species of bacteria. Four of these species are known to produce short-chain fatty acids—molecules that are produced when bacteria digest fiber and that are known to positively impact glucose metabolism. In general, bacterial species that were positively associated with sugary beverage intake correlated with worse metabolic traits. Interestingly, these bacteria were not associated with sugar ingested from non-beverage sources.
The researchers also found associations between sugary beverage consumption and 56 serum metabolites, including several metabolites that are produced by gut microbiota or are derivatives of gut-microbiota-produced metabolites.
These sugar-associated metabolites were associated with worse metabolic traits, including higher levels of fasting blood glucose and insulin, higher BMIs and waist-to-hip ratios, and lower levels of high-density lipoprotein cholesterol ("good" cholesterol). Notably, individuals with higher levels of these metabolites had a higher likelihood of developing diabetes in the 10 years following their initial visit.
They found that several microbiota-related metabolites are associated with the risk of diabetes. In other words, these metabolites may predict future diabetes.
These results have to be validated in other populations too for a final conclusion.
Sugar-sweetened beverage intake, gut microbiota, circulating metabolites, and diabetes risk in Hispanic Community Health Study/Study of Latinos, Cell Metabolism (2025). DOI: 10.1016/j.cmet.2024.12.004. www.cell.com/cell-metabolism/f … 1550-4131(24)00486-8
Feb 1
Dr. Krishna Kumari Challa
BioSonics spectroscopy can 'listen' to the sounds made by individual viruses
A team of chemists and microbiologists has found that an all-optical method can be used to detect natural vibrational frequencies made by individual viruses as a way to identify them. In their study published in Proceedings of the National Academy of Sciences, the group found a way to bounce light off viruses and detect the resulting patterns of vibrations, which could be easily identified.
Light can be used to identify nanoparticle-scale objects. Prior research has shown that firing beams of light at such objects can cause them to vibrate slightly. The vibration patterns that emerge are unique for different targets. Thus, the technique can be used to identify nanoscale objects even among other similarly scaled objects.
The researchers wondered if the same technique could be used with biological agents like viruses and bacteria, so they conducted experiments that involved firing extremely tiny amounts of light at both kinds of microorganisms at such a small scale that they were able to watch the impact of single photons.
Eventually, they shifted their focus to viruses only and found that with the appropriate parameter settings, they could detect the vibrations emitted by the virus using a technique that they call BioSonics spectroscopy. The sound was not just too faint to hear with the human ear, but too high, at a frequency 1 million times higher than humans can hear.
After testing multiple viruses, the research team found that each of them vibrated in their own unique ways, distinct from one another and from all the other molecules they tested. That meant that BioSonics could be used as a sensor of sorts, enabling devices that could, for example, scan a room, detect viruses in the air and identify them.
They also note that the technology could reveal individual virus activity, opening the door to better understanding them. It could be used, for example, to watch as individual viruses assemble themselves, a phenomenon that is still not well understood.
Yaqing Zhang et al, Nanoscopic acoustic vibrational dynamics of a single virus captured by ultrafast spectroscopy, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2420428122
Feb 1
Dr. Krishna Kumari Challa
Myth busting: Purpose-bred dogs are not better at biting or scenting than those not bred for that purpose
Since their domestication millennia ago, dogs have been man's best friend, and aside from friendship, centuries of selective breeding have tailored them for tasks like herding, hunting and guarding—or so we thought.
Now, the results of a new study challenge the prevailing belief that some breeds are inherently superior at specific tasks, based on their skull morphology.
The study published in Science Advances on January 29, used advanced 3D reconstruction techniques to analyze 117 skulls from 40 domestic dog breeds and 18 wild canid species.
The researchers found substantial overlap in skull shapes across breeds and functional categories, but no clear evidence that breeds selected for bite work or scent work have developed distinct morphological traits that enhance these abilities. This suggests that humans have been breeding dogs primarily for preferred visible traits, and that other factors like individual personality affect dogs' performance of tasks.
In the past 200 years, humans have created hundreds of dog breeds that look really different and are pretty specialized at some tasks like herding, protecting, and detecting odors. We have assumed that these dogs look different because they are 'structurally' specialized at these tasks, but this new study shows that, at least for their skulls, they 'are not' specialized for tasks that involve the skull, such as biting tasks and scent work.
The study examined dog breeds commonly used for tasks like bite work and scent work, such as those in law enforcement and military programs, where dogs are trained for patrol and detection. Researchers used advanced methods, including 3D skull analysis, to compare breeds across various functional groups.
The results showed that domesticated dog breeds exhibit exceptional diversity in their skull shapes, but have high overlap among the parts of the skulls that correspond with functional tasks.
This indicates that specific breeds are not as morphologically specialized for such tasks as previously thought. For instance, bite-force measurements did not show any significant differences between breeds purpose-bred for bite work and those not.
Part 1
Feb 1
Dr. Krishna Kumari Challa
There are many news stories about dogs attacking people badly and often there are specific breeds that are targets of this reporting (such as pit bulls). Some people claim that these dogs will bite harder than other dogs of the same size, or they have special features like 'locking jaws' that make them especially dangerous to people. This study shows that this is simply not true; dogs bred to bite things aren't structurally different than dogs that have been bred to do other things.
Similarly, breeds selected for scent work did not demonstrate significantly enhanced olfactory morphology compared to other breeds. The lone group that showed distinct skull morphology was brachycephalic breeds (e.g., bulldogs), which are characterized by their shortened snouts, but this feature is not tied to functional specialization. Instead, human aesthetic preferences have played a larger role in shaping dog morphology.
Humans have done so much breeding work to alter the visual appearance of these animals that the researchers honestly expected to see really marked groupings of some kind but they really didn't see much of that.
However, researchers found that domesticated dog breeds' morphologies differed greatly from wild canids, such as wolves and foxes, which tend to have skull shapes that align more closely with their natural functional needs. Wolves and foxes tend to possess elongated snouts relative to their cranial length, which is a typical feature of species that rely on keen senses like smell.
Undomesticated animals, particularly wolves, show skull morphologies that reflect evolutionary adaptations for hunting and scent work, which contrasts with the lack of strong morphological specialization in domesticated breeds.
Interestingly, foxes' skull shapes overlap significantly with some domestic dogs, particularly terrier breeds, which were historically bred for pest control, suggesting functional similarities in skull structure for small prey pursuit.
While these results run counter to the popular notion that purpose-bred dogs are better at biting or scenting than those not bred for that purpose, they suggest that observable behavior traits are associated with performance, rather than morphological traits.
Recent research suggests that many breed-associated behaviors are partially heritable. This has important implications for how dogs are bred and selected for specific tasks in areas such as law enforcement and search and rescue—behavioral traits and individual trainability may be more important determinants of performance.
Nicholas Hebdon et al, Dog skull shape challenges assumptions of performance specialization from selective breeding, Science Advances (2025). DOI: 10.1126/sciadv.adq9590
Part 2
Feb 1
Dr. Krishna Kumari Challa
Study uncovers new link between infections and heart failure
People hospitalized for infections—almost any infections—are at substantially increased risk years later for heart failure, according to a collaborative research.
The study of more than 14,000 people over two decades doesn't establish cause and effect, but advocates said this week that it establishes a strong enough correlation that people should take heed and try to reduce their infection risks.
Heart failure, which affects millions around the world, is a weakening of the heart that prevents it from pumping sufficient blood and oxygen. Researchers were surprised to find that hospitalizations resulting from common skin and urinary tract infections increased heart failure risks, alongside respiratory infections such as influenza and blood infections such as sepsis.
That suggests that the body's response to infection is a big part of the heart failure risk, say the researchers.
There's some notion that really severe infections sort of turn on the immune system in a way where it just doesn't quite turn off, and it stays revved up, possibly for many years.
Other possibilities include that serious infections cause genetic or biological changes that lay dormant after hospitalization but emerge later in life to cause heart failure.
Other studies have found hospitalizations increase risks of health problems later in life, so it's possible infections are driving people to as-yet unknown risks from those hospital visits, they stress.
Even without cause and effect being established, they say the results should encourage people to prevent infections through vaccines and good hygiene. People who have already been hospitalized because of infections can talk with their doctors about ways to reduce cardiac risks.
They had already discovered in 2023 that infection-related hospitalizations increased the risk for dementia later in life.
Part 1
Feb 1
Dr. Krishna Kumari Challa
Over the course of three decades, about one in four people in the surveillance program suffered episodes of heart failure. The risk was more than twice as likely among patients who at some point had been hospitalized for infections, according to the latest study, published in the Journal of the American Heart Association.
Risks were highest following bloodstream and respiratory infections, but were also significant for skin and urinary tract infections. Digestive infections were only weakly correlated with heart failure later in life.
Risks were highest following bloodstream and respiratory infections, but were also significant for skin and urinary tract infections. Digestive infections were only weakly correlated with heart failure later in life.
Heart failure can lead to cardiac arrest or damage the kidney and liver. Treatments range from medications to increase blood flow to surgeries to implant pacemakers or remove obstructions in blood vessels.
Establishing a precise cause-and-effect relationship between infections and heart failure will be difficult, because researchers can't deny preventive care to patients just to see if it increases their risks.
Rebecca L. Molinsky et al, Infection‐Related Hospitalization and Incident Heart Failure: The Atherosclerosis Risk in Communities Study, Journal of the American Heart Association (2025). DOI: 10.1161/JAHA.123.033877
Part 2
Feb 1
Dr. Krishna Kumari Challa
Why 'cough CPR' is not the lifesaver it's made out to be
Misinformation has circulated for years on social media about how coughing forcefully can treat a heart attack. Health experts are quick to debunk that myth and warn that "cough CPR" is ineffective.
Anytime anyone is having chest pain or other symptoms of a heart attack, get to a hospital. Calling an emergency ambulance service is the safest way to get to a hospital for chest pain.
The term itself is a misnomer because CPR is for someone in cardiac arrest, meaning the heart has stopped beating. At that point, coughing would not be possible, nor would it be considered CPR.
It physiologically does not make sense. Coughing just would not work to restart a heart that's not beating, say the experts.
Heart attack and cardiac arrest are medical emergencies requiring immediate medical treatment, though it is important to note they are two different conditions. A heart attack is a circulation problem and occurs when blood flow to the heart is blocked. Cardiac arrest is an electrical problem and occurs when the heart suddenly stops beating. A heart attack is a common cause for cardiac arrest.
Someone who goes into cardiac arrest will become unresponsive and stop breathing or gasp for air. Cardiac arrest can lead to death if not treated within minutes.
Confusion about cough CPR might be traced to a temporary measure that may be used for a sudden arrhythmia, or abnormal heartbeat, in medical settings in which patients are constantly monitored, such as a cardiac catheterization lab.
During a sudden arrhythmia, a doctor or nurse may coach a patient to cough vigorously to maintain enough blood flow to the brain to remain conscious for a few seconds until the arrhythmia is treated. But this technique is not effective in all patients and should not delay definitive treatment, according to the American Heart Association.
The misconception about cough CPR and heart attack may be tied to an idea that coughing can change the pressure in the chest, and, in turn, affect the heart.
People believe that it is changing, somehow, the heart's squeeze. But (coughing) has not been shown to do that. If somebody has lost a pulse, we very much know that you have to do CPR.
A literature review to prepare for that update did not yield any research about cough CPR.
It's certainly not something that is recommended in those guidelines because there is no evidence to support it.
Part 1
Feb 1
Dr. Krishna Kumari Challa
If you're around someone who has gone into cardiac arrest, call emergency services helpline and start hands-only CPR. This means placing the heel of one hand in the center of the chest at the nipple line. Place the other hand on top and interlock the fingers. Start pushing hard at a rate between 100 and 120 beats per minute.
Get an automated external defibrillator, or AED, if one is close by or send someone to find an AED. People should use an AED as soon as it's available. Even untrained people can use the device by following its voice instructions.
Because a heart attack can lead to a cardiac arrest, experts say it's critical to call emergency services immediately when symptoms start. These can include chest pain, jaw pain, shortness of breath, sweating and nausea.
Then sit and rest until the ambulance arrives. "Avoid exertion." An aspirin may help for those not allergic to it.
Someone with a prescription for nitroglycerin for chest pain should take the medication.
But one thing people don't need to do is cough.
Source: American Heart Association
Feb 1
Dr. Krishna Kumari Challa
How microbes help detoxify the atmosphere: Study provides atomic-level insights
Researchers have discovered crucial new information about how microbes consume huge amounts of carbon monoxide (CO) and help reduce levels of this deadly gas.
Over two billion metric tons of carbon monoxide are released into the atmosphere globally each year. Microbes consume about 250 million tons of this, reducing CO to safer levels.
The study, published in Nature Chemical Biology, reveals at an atomic level how microbes consume CO present in the atmosphere. They use a special enzyme, called the CO dehydrogenase, to extract energy from this universally present but highly toxic gas.
The study showed for the first time how this enzyme extracted atmospheric CO and powered cells.
This enzyme is used by trillions of microbes in our soils and waters. These microbes consume CO for their own survival, but in the process inadvertently help us. This 's a fantastic example of microbial 'ingenuity': how life has evolved ways to turn something toxic into something useful.
These microbes help clean our atmosphere. This counteracts air pollution, which kills many millions of people each year, and also reduces global warming given CO is indirectly a greenhouse gas.
While this discovery is unlikely to be directly used to combat or monitor CO emissions, it deepens our understanding of how the atmosphere is regulated and how it might respond to future changes.
Microbes 're a big reason why our air 's breathable. They make half the oxygen we breathe and detoxify various pollutants like CO. It's crucial we better understand and appreciate how they support our own survival, say the researchers.
Kropp, A., et al. Quinone extraction drives atmospheric carbon monoxide oxidation in bacteria, Nature Chemical Biology (2025). DOI: 10.1038/s41589-025-01836-0
Feb 2
Dr. Krishna Kumari Challa
Stress during pregnancy could leave traces in placenta that affect baby's development, study suggests
Maternal stress could leave epigenetic imprints on genes in the placenta associated with cortisol—a necessary hormone for fetal development—and this would affect the baby's development from very early stages, according to a paper published in the journal European Neuropsychopharmacology.
The study suggests that a mother's emotional well-being during pregnancy is not only important for her, but could also influence the future health of her baby.
The placenta is an essential organ during pregnancy, as it not only provides oxygen and nutrients to the fetus, but also responds to factors such as maternal stress and helps the fetus adapt to its environment. However, the mechanisms by which the placenta adjusts to these stressors and how it influences fetal development remain largely unexplored.
The research team observed that maternal stress may leave epigenetic marks on certain placental genes. Specifically, these marks do not modify the genetic structure, but they do alter its function. The study identified epigenetic changes in genes related to the regulation of cortisol, an essential hormone in the body's response to stress.
The pilot study involved 45 healthy, first-time pregnant women. During pregnancy, their cortisol levels and depressive symptoms were measured and, after delivery, placentas were analyzed. At seven weeks, the neurodevelopment of the babies was assessed using a specialized test (Brazelton's NBAS).
The research team used an advanced sequencing technique that allows them to look at epigenetic changes in large areas of DNA and thus gain a very detailed view of the placental response to maternal stress. This method identified changes in key genes involved in cortisol regulation, such as HSD11B2, NR3C1 and FKBP5.
The results suggest that maternal stress—especially in early pregnancy—can cause alterations in these genes, which could affect fetal development and the future health of the baby.
This study reinforces the importance of taking care of the mental health of mothers from the beginning of pregnancy, since stress could leave a biological imprint on the baby's development through epigenetic mechanisms that we are just beginning to understand.
While these findings need to be replicated in larger studies, this breakthrough underscores the importance of psychological care and emotional support during pregnancy, not only for the mother's well-being, but also for the long-term health of the baby.
Agueda Castro-Quintas et al, Placental epigenetic signatures of maternal distress in glucocorticoid-related genes and newborn outcomes: A study of Spanish primiparous women, European Neuropsychopharmacology (2024). DOI: 10.1016/j.euroneuro.2024.10.001
Feb 2
Dr. Krishna Kumari Challa
Giant Radio Galaxy Could Hold 30 Milky Ways, Astronomers Say
Giant radio galaxies are cosmic megastructures that can span millions of light-years, making them some of the largest-known structures in the Universe.
Yet space is big, and despite their size, giant radio galaxies can be hard to find. Discovering one is a big deal, especially if it's as colossal – and peculiar – as one recently found by astronomers using South Africa's MeerKAT telescope.
The newly discovered galaxy measures over 3 million light-years from end to end, including the huge jets of hot plasma it's blasting into intergalactic space, the astronomers report in a new study.
That means it's more than 30 times the size of our own Milky Way galaxy.
It's also enigmatic, the researchers say, with unusual qualities that defy simple explanation. They decided to name it after this troublesome nature, choosing a word from two Bantu languages indigenous to Southern Africa.
Scientists nicknamed this giant galaxy 'Inkathazo,' meaning 'trouble' in isiZulu and isiXhosa because it has been a bit troublesome to understand the physics behind what's going on here.
Radio galaxies already feature mind-bending physics, with supermassive black holes accreting matter at the galactic core and sending out vast plasma jets that glow at radio frequencies. Those larger than roughly 2 million light-years may be classified as giant radio galaxies, or GRGs.
Yet even by radio-galaxy standards, Inkathazo is puzzling.
It doesn't have the same characteristics as many other giant radio galaxies. For example, the plasma jets have an unusual shape: Rather than extending straight across from end to end, one of the jets is bent.
And while Inkathazo's size would be impressive anywhere, it's especially surprising given the galaxy's location. Inkathazo is nestled amid a cluster of other galaxies, researchers report, where conditions should discourage the growth of such gargantuan jets.
https://academic.oup.com/mnras/article/537/1/272/7958396?login=false
Feb 2
Dr. Krishna Kumari Challa
Mouse Created With Two Fathers And No Mother Survives to Adulthood
A mouse with no biological mother has survived to adulthood in China – a major scientific achievement that's been years in the making.
The feat was pulled off by a team of researchers in China using precise stem cell engineering.
This isn't the first time that scientists have created a mouse with two male parents. In 2023, researchers in Japan managed a similar feat using a different technique.
Before that, attempts to generate eggs from male stem cells proved unsuccessful. The motherless offspring, born through a female surrogate, are typically nonviable and show severe developmental defects.
Not so for the 'bi-paternal' mice recently created in China. These adult mammals are not capable of reproducing themselves, but they are healthier than their predecessors, without fatal feeding or respiratory difficulties.
That said, roughly half of their siblings failed to make it to adulthood, and nearly 90 percent of the viable embryos did not make it to birth, which means the success rate for the process can still be improved upon.
There's still a long way to go before the same sort of technique could be achieved in our own species, but the authors of the study say their work helps scientists better understand human congenital disorders caused by similar genetic issues.
https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(25)00005-0
Feb 2
Dr. Krishna Kumari Challa
The scientist heroes that starved to protect their science
In his book The Forbidden Garden of Leningrad, author Simon Parkin tells the story of the city’s Plant Institute — the world’s first proper seed bank — during the 1941-1944 Nazi siege. “The institute’s staff members sacrificed themselves, one by one, to protect a collection for which the whole raison d’être was to one day save humanity from starvation,” writes reviewer Simon Ings. Despite unthinkable privation, Vadim Stepanovich Lekhnovich, the curator of the tuber collection, later said that “it wasn’t difficult not to eat the collection. It was impossible to eat this, your life’s work, the work of the lives of your colleagues.”
https://www.nature.com/articles/d41586-025-00055-w?utm_source=Live+...
Feb 2
Dr. Krishna Kumari Challa
Astronomers Discover Exoplanets Falling Apart in Space
Astronomers have found two planets around two separate stars that are succumbing to their stars' intense heat. Both are disintegrating before our telescopic eyes, leaving trails of debris similar to a comet's. Both are ultra-short-period planets (USPs) that orbit their stars rapidly.
These planets are a rare sub-class of USPs that are not massive enough to hold onto their material. Astronomers know of only three other disintegrating planets.
USPs are known for their extremely rapid orbits, some completing an orbit in only a few hours. Since they're extremely close to their stars, they're subjected to intense heat, stellar radiation, and gravity.
Many USPs are tidally locked to their star, turning the star-facing side into an inferno. USPs seldom exceed two Earth radii, and astronomers think that about 1 in 200 Sun-like stars has one. They were only discovered recently and are pushing the boundaries of our understanding of planetary systems.
The new observations are in two new papers available at the pre-press site arxiv.org. One is "A Disintegrating Rocky Planet with Prominent Comet-like Tails Aroun..."
The second paper is "A Disintegrating Rocky World Shrouded in Dust and Gas: Mid-IR Obser..."
Feb 2
Dr. Krishna Kumari Challa
Man on carnivore diet develops yellowish nodules on his hands, feet and elbows
A trio of cardiologists, two at Tampa General Hospital and the third at the University of Texas' MD Anderson Cancer Center, have reported an incident of an adult man developing yellowish nodules on his hands, feet and elbows after adopting a carnivore diet.
In their paper published in the journal JAMA Cardiology, Konstantinos Marmagkiolis, Jaime Caballero, and Cezar Iliescu, describe the symptoms of a patient who had come to Tampa General seeking aid after experiencing yellowish nodules appearing on various parts of his body, and their diagnosis.
The patient, a man in his 40s, told the doctors that the nodules had appeared three weeks prior to his hospital visit. After questioning, they determined that the patient had adopted the so-called carnivore diet approximately eight months prior to the appearance of the nodules.
The carnivore diet is a fad diet based on eating large amounts of animal fats and very little of anything else. The patient in this case reported eating nearly 10 pounds of butter, cheese and other fatty foods every day since embarking on the diet—even going so far as to add fat to the hamburgers he consumed daily.
Blood tests showed the patient's cholesterol was approximately four times normal levels. The doctors diagnosed the patient with xanthelasma, a condition in which yellowish deposits of cholesterol build up in various parts of the body—in this case, on the palms, the soles of his feet and his elbows. His case had progressed to the point that some of the cholesterol was pushing through cracks in the skin.
The doctors advised the man to cut back on his fat intake. But they also noted that doing so would not get rid of the nodules—they required surgical excision or burning them with liquid nitrogen. They also reminded the patient that such high levels of cholesterol could lead to a host of other conditions such as cardiovascular disease, a greatly increased risk of stroke, and eventually, liver problems.
Konstantinos Marmagkiolis et al, Yellowish Nodules on a Man Consuming a Carnivore Diet, JAMA Cardiology (2025). DOI: 10.1001/jamacardio.2024.5209
Part 1
Feb 3
Dr. Krishna Kumari Challa
Feb 3
Dr. Krishna Kumari Challa
Large magma bodies found beneath dormant volcanoes
New research challenges the long-standing belief that active volcanoes have large magma bodies that are expelled during eruptions and then dissipate over time as the volcanoes become dormant.
Researchers used seismic waves to identify magma chambers beneath the surface of six volcanoes of various sizes and dormancy within the Cascade Range, which includes half of the U.S. volcanoes designated by the U.S. Geological Survey as "very high threat." The team found that all of the volcanoes, including dormant ones, have persistent and large magma bodies.
The study was published in Nature Geoscience .
The results are surprising given that some of these volcanoes, such as the Crater Lake volcano in Oregon, have not been active in millennia.
Regardless of eruption frequency, we see large magma bodies beneath many volcanoes, the researchers said. It appears that these magma bodies exist beneath volcanoes over their whole lifetime, not just during an active state.
The fact that more volcanoes have sustained magma bodies is an important consideration for how researchers may monitor and predict future volcanic activity.
Guanning Pang et al, Long-lived partial melt beneath Cascade Range volcanoes, Nature Geoscience (2025). DOI: 10.1038/s41561-024-01630-y
Feb 3
Dr. Krishna Kumari Challa
An overlooked nuclear force helps keep matter stable, study reveals
Researchers have revealed how a special type of force within an atom's nucleus, known as the three-nucleon force, impacts nuclear stability. The study, published in Physics Letters B, provides insight into why certain nuclei are more stable than others and may help explain astrophysical processes, such as the formation of heavy elements within stars.
All matter is made of atoms, the building blocks of the universe. Most of an atom's mass is packed into its tiny nucleus, which contains protons and neutrons (known collectively as nucleons). Understanding how these nucleons interact to keep the nucleus stable and in a low energy state has been a central question in nuclear physics for over a century.
The most powerful nuclear force is the two-nucleon force, which attracts two nucleons at long range to pull them together and repels at short range to stop the nucleons from getting too close.
Scientists have formed a good understanding of the two-nucleon force and how it impacts nuclear stability. On the other hand, three-nucleon force, which is when three nucleons interact with each other simultaneously, is much more complicated and poorly understood.
The researchers describe nuclear forces by likening them to a game of catch. With the two-nucleon force, two players, or nucleons, interact by throwing a ball to each other. The ball, a subatomic particle called a meson, can vary in heaviness, with the lightest meson, known as a pion, responsible for the long-range attraction between nucleons.
With the three-nucleon force, there are three players, or nucleons, and balls, or mesons, are passed between them. At the same time as throwing and catching the balls, the players, or nucleons, also spin and move in an orbit within the nucleus.
Although the three-nucleon force has historically been considered to be of little significance when compared to the two-nucleon force, a growing number of recent studies have highlighted its importance. Now, this new study clarifies the mechanism of how the three-nucleon force enhances nuclear stability, and demonstrates that as the nucleus grows, the force gains in strength.
The researchers used advanced nuclear theory and supercomputer simulations to study the exchange of pions between three nucleons. They found that when two pions are exchanged between three nucleons, the nucleons are constrained in how they move and spin, with only four combinations possible. Their calculations revealed that one of these combinations, known as the "rank-1 component," plays a crucial role in promoting nuclear stability.
Increased stability occurs, the researchers explain, due to enhancing a process known as spin-orbit splitting. When nucleons spin and orbit in the same direction, the alignment of these nucleons leads to a reduction in energy. But when nucleons spin and orbit in opposing directions, these nucleons exist in a higher energy state. This means that nucleons "split" into different energy shells, providing the nucleus with a stable structure.
The supercomputer simulations showed that while the three-nucleon force increases the energy state of the nucleons with an aligned spin and orbit, it causes the nucleons with opposing spins and orbits to gain even more energy. This results in a larger energy gap between the shells, making the nuclei even more stable .
Part 1
Feb 3
Dr. Krishna Kumari Challa
Importantly, this effect becomes more pronounced in heavier nuclei that contain more nucleons. In the heaviest element examined—carbon-12, which has 12 nucleons—the three-nucleon force caused the energy gap to widen by a factor of 2.5.
This effect is so large that it has almost equal weighting to the impact of the two-nucleon force.
The three-nucleon force could play a key role in understanding how heavy elements form from the fusion of lighter elements in stars. As this force grows stronger in heavier nuclei, it increases their stability by creating larger energy gaps between nuclear shells.
This stability makes it more challenging for the nucleus to capture additional neutrons, which are essential for forming heavier elements. In cases where the nucleus already contains a "magic number" of protons or neutrons that completely fills its shells, the nucleus becomes exceptionally stable, which can further hinder the fusion process.
Finally, the researchers discovered another surprising effect of the three-nucleon force on nucleon spins. With only the two-nucleon force, the spin states of both nucleons can be measured individually. However, the three-nucleon force creates quantum entanglement, where two of the three nucleons have spins that exist in both states at once until measured.
Tokuro Fukui et al, Uncovering the mechanism of chiral three-nucleon force in driving spin-orbit splitting, Physics Letters B (2024). DOI: 10.1016/j.physletb.2024.138839
Part 2
Feb 3
Dr. Krishna Kumari Challa
Ocean-surface warming has more than quadrupled since the late-1980s, research shows
The rate of ocean warming has more than quadrupled over the past four decades, a new study has shown. Ocean temperatures were rising at about 0.06 degrees Celsius per decade in the late 1980s, but are now increasing at 0.27 degrees Celsius per decade.
Published 28 January 2025 in Environmental Research Letters, the study helps explain why 2023 and early 2024 saw unprecedented ocean temperatures.
This accelerating ocean warming is driven by the Earth's growing energy imbalance—whereby more energy from the sun is being absorbed in the Earth's system than is escaping back to space. This imbalance has roughly doubled since 2010, in part due to increasing greenhouse gas concentrations, and because the Earth is now reflecting less sunlight to space than before.
Global ocean temperatures hit record highs for 450 days straight in 2023 and early 2024. Some of this warmth came from El Niño, a natural warming event in the Pacific.
When scientists compared it to a similar El Niño in 2015–16, they found that the rest of the record warmth is explained by the sea surface warming up faster in the past 10 years than in earlier decades; 44% of the record warmth was attributable to the oceans absorbing heat at an accelerating rate.
Quantifying the acceleration of multidecadal global sea surface warming driven by Earth's energy imbalance, Environmental Research Letters (2025). DOI: 10.1088/1748-9326/adaa8a
Feb 3
Dr. Krishna Kumari Challa
Microplastics found in the brains of mice within hours of consumption
A team of environmental biologists has found that it takes microplastics consumed by mice just a few hours to make their way to their brains.
In their paper published in the journal Science Advances, the group describes experiments they conducted with lab mice consuming water tainted with different sized microplastics, and what they learned by doing so.
Prior research has shown that microplastics have made their way into the environment to such an extent that they have made their way into the bodies of nearly everyone on Earth (*). It is still not known what harm consumption of such materials causes, but most in the medical field believe they are likely causing damage that is blamed on other sources. Still, many in the field suggest that there is enough evidence of possible health problems associated with microplastics that action should be taken globally to address their impact.
In this new effort, the research team sought to learn more about the medical impact of a mammal consuming different sizes of microplastics. The experiments consisted of feeding test mice water with different sized bits of fluorescent plastic in it, from micro to nano. They then tracked the progress of the plastic bits to see where they wound up in the bodies of the mice.
Knowing that the plastic would make its way from the digestive tract into the bloodstream, the researchers used two-photon microscopy to capture imagery of it inside blood vessels. Also, suspecting that the tiniest bits would make it into their brains, the team installed tiny windows in their skulls, allowing them to track the movement of the plastic in their brains.
In studying the imagery they created, the researchers were able to watch as the plastics made their way around the mice's bodies, eventually reaching their brains. They also noted that the plastic bits tended to get backed up, like cars in a traffic jam at different points. In taking a closer look at some of the backups in the brain, the researchers found that the plastic bits had been captured by immune cells, which led to even more backups.
Wondering if the plastic in their brains was causing any impairment, the researchers tested several of the mice and found that many of them experienced memory loss, reductions in motor skills and lower endurance.
* Richard C. Thompson, Twenty years of microplastics pollution research—what have we learned?, Science (2024). DOI: 10.1126/science.adl2746. www.science.org/doi/10.1126/science.adl2746
Haipeng Huang et al, Microplastics in the bloodstream can induce cerebral thrombosis by causing cell obstruction and lead to neurobehavioral abnormalities, Science Advances (2025). DOI: 10.1126/sciadv.adr8243
Feb 3
Dr. Krishna Kumari Challa
Why the first stars couldn't grow forever
Star formation in the early universe was a vigorous process that created gigantic stars. Called Population III stars, these giants were massive, extremely luminous stars that lived short lives, many of which ended when they exploded as primordial supernovae.
But even these early stars faced growth limitations.
Stellar feedback plays a role in modern star formation. As young stars grow, they emit powerful radiation that can disperse nearby gas they need to keep growing. This is called protostellar radiative feedback, and it takes place in addition to the restrictive effect their magnetic fields have on their growth.
However, new research shows that the growth of Pop III stars was limited by their magnetic fields.
The research is titled "Magnetic fields limit the mass of Population III stars even before the onset of protostellar radiation feedback"
The paper is published on the arXiv preprint server.
Piyush Sharda et al, Magnetic fields limit the mass of Population III stars even before the onset of protostellar radiation feedback, arXiv (2025). DOI: 10.48550/arxiv.2501.12734
Feb 3
Dr. Krishna Kumari Challa
Scientists create 'molecular trap' to remove pollutants from water
Scientists have developed a new material that could help reduce water pollution caused by harmful chemicals, such as from leftover medicines and hygiene products, that end up in rivers and lakes.
Water pollution is one of the growing challenges of modern life. Many everyday items, from medications to cosmetics, leave behind residues that don't fully break down after use. These pollutants often find their way into water systems, where they disrupt ecosystems and cause harm to plants, animals and humans.
The research, published in the journal Cell Reports Physical Science, describes a new method using a molecular structure called a metal-organic cage (MOC). These tiny cages act like traps designed to catch and hold harmful molecules commonly found in our water supplies.
The cages are made up of metal ions connected by organic molecules forming a hollow pyramid-like structure. These hollow spaces at the center of these structures are where the MOCs trap specific molecules, like pollutants or gases.
The new structure incorporates chemical groups called sulfonates to make it compatible with water, allowing it to function in real-world water systems, like rivers or wastewater.
It uses a natural effect called hydrophobic binding, where contaminant molecules preferentially "stick" to the inside of the cage rather than staying in the water. This allows the material to selectively capture and hold pollutants, even in challenging water environments.
Jack D. Wright et al, Encapsulation of Hydrophobic Pollutants within a Large Water-Soluble [Fe4L6]4- Cage, Cell Reports Physical Science (2025). DOI: 10.1016/j.xcrp.2025.102404
Feb 3
Dr. Krishna Kumari Challa
Catching the culprits: DNA 'fingerprints' of drug-makers can be linked to capsules and packaging
DNA profiling technologies are rapidly advancing, creating the potential to identify individuals involved in making, packing and transporting illegal capsules by analyzing the exterior of the illicit drugs and the plastic bag in which they are carried.
Experiments carried out by Flinders University forensic science experts have found that DNA accumulates in different areas, depending on an individual's involvement in the process, which could aid identification of people involved in the drug-making and trade.
The work is published in the journal Forensic Science International: Genetics.
The study also found DNA from the surface of capsules can be transferred to the inner surface of ziplock bags (ZLBs) commonly used in transportation.
This small-scale study indicates that capsule packers deposit less DNA than capsule makers who spend more time handling drug casing, and those that make the capsules can leave enough DNA for a complete profile with as little as 30 seconds of contact.
Furthermore, the DNA yield on these commonly used plastic bags is higher when handled by several people compared with little-to-no contact.
"Generating informative DNA profiles from the inside surface of the ziplock bag could be more useful than the outer side, as could be testing of other 'protected' areas of the bag such as the zip or inner edge of the seal.
Illicit substances frequently distributed in secure ziplock bags can be seized by police and tested by forensic investigators.
Strong DNA profiles 're generated for the individual who made the capsules and for the individual responsible for packing the ziplock bag.
Madison Nolan et al, Illicit drug distribution: Evaluation of DNA transfer between ziplock bags and capsules, Forensic Science International: Genetics (2024). DOI: 10.1016/j.fsigen.2024.103182
Feb 3
Dr. Krishna Kumari Challa
Octopuses have some of the oldest known sex chromosomes, study finds
The octopus just revealed another one of its secrets: what determines its sex.
Researchers have identified a sex chromosome in the California two-spot octopus. This chromosome has likely been around for 480 million years, since before octopuses split apart from the nautilus on the evolutionary tree. That makes it one of the oldest known animal sex chromosomes.
The finding also is evidence that octopuses and other cephalopods, a class of sea animals that includes squid and nautiluses, do use chromosomes to determine their sex, answering a longstanding mystery.
The researchers described the findings Feb. 3 in the journal Current Biology.
In humans and most mammals, sex is determined largely by chromosomes. But "there's a tremendous amount of diversity" in how animals determine their sex.
In turtles, for instance, sex is determined by the temperature at which the eggs are incubated. Some fish have a gene that determines sex, but not a whole chromosome. Even in humans, the X/Y sex chromosome system isn't as clear-cut as it might look on paper; gene mutations or inheriting extra sex chromosomes can lead to development that doesn't neatly fit in a male/female binary.
When researchers recently sequenced the DNA of a female California two-spot octopus, they found something unexpected: a chromosome with only half the amount of genetic material. It looked different from all the others, and it hadn't been found in male octopuses whose DNA was previously sequenced.
This particular chromosome had half the amount of sequencing data, which indicated there was only one copy.
To confirm, the researchers sorted through other octopus genomic data previously collected by other researchers.
They found another example of the half-sized chromosome in another species of octopus. They also found it in squid, which diverged evolutionarily from octopuses somewhere between 248 and 455 million years ago. And after more digging, they also found evidence for the chromosome in the nautilus, a mollusk that split apart from the octopus approximately 480 million years ago.
The fact that these species share this unique chromosome suggests that it's been around in some form for a very long time.
This indicates that their common ancestor had this similar sex determination system.
That's somewhat unusual for sex chromosomes. Because they directly impact reproductive capabilities, they're subject to a lot of selective pressure and so tend to undergo rapid evolutionary change. But cephalopods seem to have found what works and have stuck with it.
Other ancient sex chromosomes have been discovered in plant groups like mosses and liverworts, which were some of the first plants to evolve. And insect sex chromosomes might be 450 million years old, but they've also changed a lot over time.
Cephalopod Sex Determination and its Ancient Evolutionary Origin, Current Biology (2025). DOI: 10.1016/j.cub.2025.01.005. www.cell.com/current-biology/f … 0960-9822(25)00005-3
Feb 4