There is less room to store carbon dioxide, driver of climate change, than previously thought, finds a new study

The world has far fewer places to securely store carbon dioxide deep underground than previously thought, steeply lowering its potential to help stem global warming, according to a new study that challenges long-held industry claims about the practice.

The study, published last week in the journal Nature, found that global carbon storage capacity was 10 times less than previous estimates after ruling out geological formations where the gas could leak, trigger earthquakes or contaminate groundwater, or had other limitations. That means carbon capture and storage would only have the potential to reduce human-caused warming by 0.7 degrees Celsius (1.26 Fahrenheit)—far less than previous estimates of around 5-6 degrees Celsius (9-10.8 degrees Fahrenheit), researchers said.

Carbon storage is often portrayed as a way out of the climate crisis. These new findings make clear that it is a limited tool and reaffirms the extreme importance of reducing emissions as fast and as soon as possible.

 Matthew J. Gidden et al, A prudent planetary limit for geologic carbon storage, Nature (2025). DOI: 10.1038/s41586-025-09423-y

Smart patch runs tests using sweat instead of blood

It is possible now to precisely assess the body's health status using only sweat instead of blood tests. 

A research team has now developed a smart patch that can precisely observe internal changes through sweat when simply attached to the body. This is expected to greatly contribute to the advancement of chronic disease management and personalized health care technologies. 

The researchers developed a wearable sensor that can simultaneously and in real-time analyze multiple metabolites in sweat. 

The research team developed a thin and flexible wearable sweat patch that can be directly attached to the skin. This patch incorporates both microchannels for collecting sweat and an ultrafine nanoplasmonic structure that analyzes sweat components using light. Thanks to this, multiple sweat metabolites can be simultaneously analyzed without the need for separate staining or labels, with just one patch application.

A nanoplasmonic structure is an optical sensor structure where nanoscale metallic patterns interact with light, designed to sensitively detect the presence or changes in concentration of molecules in sweat.

The patch was created by combining nanophotonics technology, which manipulates light at the nanometer scale (one-hundred-thousandth the thickness of a human hair) to read molecular properties, with microfluidics technology, which precisely controls sweat in channels thinner than a hair.

In other words, within a single sweat patch, microfluidic technology enables sweat to be collected sequentially over time, allowing for the measurement of changes in various metabolites without any labeling process. Inside the patch are six to 17 chambers (storage spaces), and sweat secreted during exercise flows along the microfluidic structures and fills each chamber in order.

The research team applied the patch to actual human subjects and succeeded in continuously tracking the changing components of sweat over time during exercise.

In this study, they demonstrated for the first time that three metabolites—uric acid, lactic acid, and tyrosine—can be quantitatively analyzed simultaneously, as well as how they change depending on exercise and diet.

In particular, by using artificial intelligence analysis methods, they were able to accurately distinguish signals of desired substances even within the complex components of sweat.

In the future,  this technology can be expanded to diverse fields such as chronic disease management, drug response tracking, environmental exposure monitoring, and the discovery of next-generation biomarkers for metabolic diseases.

Jaehun Jeon et al, All-flexible chronoepifluidic nanoplasmonic patch for label-free metabolite profiling in sweat, Nature Communications (2025). DOI: 10.1038/s41467-025-63510-2

Microbiome instability linked to poor growth in kids

Malnutrition is a leading cause of death in children under age 5, and nearly 150 million children globally under this age have stunted growth from lack of nutrition. Although an inadequate diet is a major contributor, researchers  found over a decade ago that dysfunctional communities of gut microbes play an important role in triggering malnutrition.

They  have discovered that toddlers in Malawi—among the places hardest hit by malnutrition—who had a fluctuating gut microbiome showed poorer growth than kids with a more stable microbiome. All of the children were at high risk for stunting and acute malnutrition.

The findings, published in Cell, establish a pediatric microbial genome library—a public health database containing complete genetic profiles of 986 microbes from fecal samples of eight Malawian children collected over nearly a year that can be used for future studies to help predict, prevent and treat malnutrition.

Culture-independent meta-pangenomics enabled by long-read metagenomics reveals associations with pediatric undernutrition, Cell (2025). DOI: 10.1016/j.cell.2025.08.020. www.cell.com/cell/fulltext/S0092-8674(25)00975-4

Discovery reveals how chromosome ends can be protected

Researchers have uncovered a previously unknown mechanism that safeguards the chromosome ends from being mistakenly repaired by the cell. While DNA repair is vital for survival, attempts to repair the chromosome ends—called telomeres—can have catastrophic outcomes for cells.

The research, published in Nature, increases the understanding of how cancer and certain rare diseases develop.

Cells constantly monitor their DNA. A DNA helix that ends abruptly is a signal that DNA has been severely damaged—at least in most cases. The most severe DNA damage a cell can suffer is when a DNA helix breaks up in two pieces. 

Normally, the cells would try to promptly repair all damage to DNA. The dilemma is that our chromosomes have ends that look just like broken DNA. If cells were to "repair" them, looking for another loose end to join them with, this would lead to the fusion between two or more chromosomes, making the cell susceptible to transform into a cancer cell.

Therefore, the chromosome ends—called telomeres—must be protected from the cell's DNA repair machinery.

The cells have to constantly repair DNA damage to avoid mutations, cell death, and cancer, while at the same time, they must not repair the chromosome ends by mistake, since that would result in the same catastrophic outcome. What's the difference between damaged DNA and the natural chromosome end? This problem has been known for almost a century, but some aspects are still not completely resolved.

Although the telomeres are not to be repaired as if they were broken DNA, several DNA repair proteins can be found at the chromosome ends. 

The research team has previously shown that a key repair protein, DNA Protein Kinase (called DNA-PK) helps in processing telomeres and in protecting them from degradation. But how DNA-PK at the same time is prevented from trying to repair these blunt DNA ends remained a mystery until now.

The researchers have now shown that two other proteins, called RAP1 and TRF2, have an important role to play in regulating DNA-PK.

They show genetically, biochemically and structurally how the protein RAP1, brought to telomeres by TRF2, ensure by  direct interaction that DNA-PK doesn't 'repair' the telomeres.

Part1

The role of telomeres in processes such as cancer development and aging, and what happens when they do not work properly, has long interested scientists. Diseases caused by disturbances in telomere maintenance are rare, but very serious, and include premature aging, blood cell deficiency called aplastic anemia and fibrosis in the lungs.

In about half of cases, the disease is explained by a known mutation that affects telomere stability, but in many cases, there is currently no known medical explanation for why the individual is sick.
Their research is also relevant to cancer research. On one hand, inappropriate "repair" of telomeres can trigger catastrophic events leading to the accumulation of mutations and cancer.

On the other hand, cancer cells are often less efficient at repairing damage to DNA compared to normal cells. This weakness is exploited in cancer treatments and many therapies kill tumor cells by causing DNA damage or inhibiting repair, or both.

In other words, knowledge of how cells regulate DNA repair and protect telomeres has a bearing on both prevention and treatment of cancer.

Increased understanding of which proteins play key roles in these cellular processes can, in the long term, contribute to more precise and targeted treatment strategies.

Patrik Eickhoff et al, Chromosome end protection by RAP1-mediated inhibition of DNA-PK, Nature (2025). DOI: 10.1038/s41586-025-08896-1

Part 2

Fathers' drinking plays role in fetal alcohol spectrum disorder, study shows

It's a well-known fact that fetal alcohol spectrum disorder (FASD) in children is caused by mothers who drink during pregnancy. But it turns out that the father's drinking habits could also affect a child's growth and development.

A team of international researchers found that a father's alcohol use may have a small but direct negative impact on a child's development by the age of seven. A father's drinking contributes to the harm caused by alcohol use during pregnancy.

The findings of their study were published recently in the journal Alcohol: Clinical & Experimental Research.

The researchers analyzed data from five studies on the prevalence and characteristics of FASD among Grade 1 learners in the Western Cape to explore whether a father's drinking affects children diagnosed with FASD. The children's biological mothers or legal guardians completed a questionnaire on the risk factors for FASD.

According to the researchers, there is a growing recognition that factors beyond pregnant women's drinking habits can affect their children's development. They add that increased attention is currently paid to the role of fathers, not only as a contributing factor to women's drinking habits, but also as an independent contributing factor to the growth and development of children.

The findings show that children whose fathers drank alcohol were more likely to be shorter, have smaller heads, and score lower on verbal IQ tests. It was also clear from the study that the highest risk to the child's development exists when both parents use alcohol during pregnancy. It also appeared that 'binge drinking' by the father, but especially by both parents, has the most detrimental effect on the child's development. 

Data analysis showed that between 66% and 77% of fathers of children on the FAS spectrum drank during their partner's pregnancy with the child in question. These fathers drank an average of 12 drinks per drinking day. The number of drinks that fathers drank per drinking day was significantly correlated with smaller head circumference in their children. Head circumference is used as a measure of brain development."

The researchers add that fathers who drank an average of five or more drinks per drinking day had shorter children with smaller head circumferences. These children also performed worse on measures in verbal intelligence tests.

"In general, it was found that the more fathers drank, the worse their children performed. However, it should also be noted that all these effects were observed in children whose mothers consumed alcohol during pregnancy."

They note that a father's drinking alone didn't increase the chances of a child being diagnosed with FASD. However, when the mother drank during pregnancy and the father was also a heavy drinker, the child was more likely to have the most serious symptoms of FASD.
"When looking at both parents' drinking patterns, the father's alcohol use alone didn't show a clear link to the child's physical or brain development problems. While both parents' drinking was considered, the main effects on a child's development and physical features were linked to the mother's alcohol use.
Part 1

"Even after accounting for alcohol use by mothers during pregnancy, the father's drinking was still linked to lower child height, smaller head size and reduced verbal IQ. This suggests that paternal alcohol use may have its own, though limited, impact on a child's growth and development.

"Data analyses of children where both parents consumed alcohol during pregnancy had significantly negative effects on growth, head circumference, verbal intelligence and general birth defect scores than in children where neither parent consumed alcohol."

The researchers say that, while it is not yet clear whether the impact of a father's drinking on a child's growth and development stems from impaired sperm quality or other epigenetic influences (changes in how genes work that don't involve altering the DNA code itself), the father's role in the development of FASD cannot be overlooked.

Philip A. May et al, Does paternal alcohol consumption affect the severity of traits of fetal alcohol spectrum disorders?, Alcohol, Clinical and Experimental Research (2025). DOI: 10.1111/acer.70105

Part 2

Why some influenza viruses are more dangerous than others

Serious infections with influenza A viruses are characterized by an excessive immune response, known as cytokine storm. It was previously unclear why some virus strains trigger these storms, while others do not. Researchers investigated 11 different influenza A virus strains and their effect on different human immune cells.

The results, published in Emerging Microbes & Infections, show that highly pathogenic avian influenza viruses infect specific kinds of immune cells and thus stimulate the production of type I interferon. This could explain why these viruses are particularly dangerous.

The new research results show that not only the immune cells that have always been the focus of attention regarding type I interferon production, but also other immune system cells could be decisive in whether an influenza infection triggers an excessive immune system response. This knowledge is important in order to be able to better assess the risk of dangerous virus variants.

Influenza viruses are some of the most significant respiratory disease pathogens worldwide. While most infections are relatively mild, certain virus strains can cause severe pneumonia, leading to acute respiratory failure. Highly pathogenic influenza viruses are particularly dangerous. They often spread from birds to humans and are associated with significantly higher mortality rates.

The immune system plays a crucial role in this danger: some virus strains cause the body to release an excessive amount of messenger substances known as cytokines. If a cytokine storm occurs, the immune response will end up damaging the body's tissue more than the virus itself.

But why do some influenza viruses trigger such excessive reactions, while others only cause infections with mild progression?

The researchers  tested how the flu viruses infect different immune cells and stimulate the release of messenger substances.

The aim of their research is to decipher the mechanisms behind mild and severe disease progression and to develop long-term approaches for better protection and treatment options.

Part 1

The investigations showed that a certain type of immune cell, so-called plasmacytoid dendritic cells, produce large amounts of the important antiviral messenger interferon-α (IFN-α) upon infection with influenza—regardless of the virus strain. This means that these immune cells generally respond strongly to influenza viruses without the need for the virus to productively infect them.

If this is the case, why do not all viruses cause the same severity of the disease? The research team found that other immune cells, namely myeloid dendritic cells and different types of macrophages, are infected with highly pathogenic influenza viruses and produce large amounts of IFN-α. Viral replication in these immune cells appears to be an important factor in the production of type I interferon and the development of an excessive immune response (cytokine storm).
These results provide an explanation of why some influenza viruses could be so much more dangerous than others: it might be their ability to replicate in certain immune cells and thereby trigger an extremely strong immune reaction that leads to severe inflammation and harm to health. This knowledge can help to develop targeted therapies and better identify risk groups.

Marc A. Niles et al, Influenza A virus induced interferon-alpha production by myeloid dendritic cells and macrophages requires productive infection, Emerging Microbes & Infections (2025). DOI: 10.1080/22221751.2025.2556718

Part 2

Giant DNA discovered in people's mouths could impact oral health, immunity and even cancer risk

Researchers have made a surprising discovery hiding in people's mouths: Inocles, giant DNA elements that had previously escaped detection. These appear to play a central role in helping bacteria adapt to the constantly changing environment of the mouth.

The findings, published in the journal Nature Communications, provide fresh insight into how oral bacteria colonize and persist in humans, with potential implications for health, disease and microbiome research.

They discovered Inocles, an example of extrachromosomal DNA—chunks of DNA that exist in cells, in this case bacteria, but outside their main DNA. It's like finding a book with extra footnotes stapled to it, and  scientists are just starting to read them to find out what they do.

Detecting Inocles was not easy, as conventional sequencing methods fragment genetic data, making it impossible to reconstruct large elements.

To overcome this, the team applied advanced long-read sequencing techniques, which can capture much longer stretches of DNA.

Inocle genomes, turned out to be hosted by the bacteria Streptococcus salivarius.

The average genome size of Inocle is 350 kilobase pairs, a measure of length for genetic sequences, so it is one of the largest extrachromosomal genetic elements in the human microbiome. Plasmids, other forms of extrachromosomal DNA, are at most a few tens of kilobase pairs.

This long length endows Inocles with genes for various functions, including resistance to oxidative stress, DNA damage repair and cell wall-related genes, possibly involved in adapting to extracellular stress response.

What's remarkable is that, given the range of the human population the saliva samples represent, researchers think 74% of all human beings may possess Inocles. And even though the oral microbiome has long been studied, Inocles remained hidden all this time because of technological limitations.

Now that we know they exist, we can begin to explore how they shape the relationship between humans, their resident microbes and our oral health. And there's even some hints that Inocles might serve as markers for serious diseases like cancer, say the researchers.

 Yuya Kiguchi et al, Giant extrachromosomal element "Inocle" potentially expands the adaptive capacity of the human oral microbiome, Nature Communications (2025). DOI: 10.1038/s41467-025-62406-5

Scientists find quasi-moon orbiting the Earth for the last 60 years

Everyone who has ever lived on Earth has been well-aware of the moon, but it turns out Earth also has some frequent temporary companions. These "quasi-moons" are small asteroids that enter into a kind of resonance with Earth's orbit, although they aren't technically orbiting Earth. In August, this small group of asteroids, called Arjunas, offered another companion to add to the list.

Astronomers at the Pan-STARRS observatory in Hawaii discovered the new quasi-moon, referred to as "2025 PN7," on August 2, 2025. Their research was recently published in Research Notes of the AAS. Using JPL's Horizons system and Python tools, they analyzed the orbital data and compared it to other Arjunas and quasi-satellites.

The team found that 2025 PN7 had been in a quasi-orbit for about 60 years already and would likely be nearby for another 60 or so years before departing. Compared to other quasi-moons, this period is relatively short. The quasi-moon Kamo'oalewa has an expected near-Earth orbit of around 381 years, while the total time for 2025 PN7 is 128 years.

Scientists have been aware of these quasi-satellites since 1991, when they first discovered 1991 VG—which some thought was an interstellar probe at the time.

Over three decades later, it is now widely accepted that such objects are natural and constitute a secondary asteroid belt that occupies the region in which the Earth–moon system orbits around the sun, defining the Arjuna dynamical class. The Arjunas with the most Earth-like orbits can experience temporary captures as mini-moons of our planet.

However, mini-moons are distinct from quasi-moons, like 2025 PN7, as mini-moons do temporarily  orbit Earth and quasi-moons only appear to do so. Currently, there are six other known quasi-moons: 164207 Cardea (2004 GU9), 469219 Kamo'oalewa (2016 HO3), 277810 (2006 FV35), 2013 LX28, 2014 OL339 and 2023 FW13.

Carlos de la Fuente Marcos et al, Meet Arjuna 2025 PN7, the Newest Quasi-satellite of Earth, Research Notes of the AAS (2025). DOI: 10.3847/2515-5172/ae028f

Hawking and Kerr black hole theories confirmed by gravitational wave

Scientists have confirmed two long-standing theories relating to black holes—thanks to the detection of the most clearly recorded gravitational wave signal to date.

Ten years after detecting the first gravitational wave, the LIGO-Virgo-KAGRA Collaboration has (10 Sep) announced the detection of GW250114—a ripple in spacetime which offers unprecedented insights into the nature of black holes and the fundamental laws of physics.

The study confirms Professor Stephen Hawking's 1971 prediction that when black holes collide, the total event horizon area of the resulting black hole is bigger than the sum of individual black holes—it cannot shrink.

Research also confirmed the Kerr nature of black holes—a set of equations developed in 1963 by New Zealand mathematician Roy Kerr elegantly explaining what space and time look like near a spinning black hole. The Kerr metric predicts effects such as space being 'dragged' around and light looping to make multiple copies of objects.

Publishing their findings in Physical Review Letters, the international group of researchers note that GW250114 was detected with a signal-to-noise ratio of 80. This clarity enabled precise tests of general relativity and black hole thermodynamics.

GW250114: testing Hawking's area law and the Kerr nature of black holes, Physical Review Letters (2025). DOI: 10.1103/kw5g-d732

'Potential biosignatures' found in ancient Mars lake

A new study suggests a habitable past and signs of ancient microbial processes on Mars. Led by NASA and featuring key analysis from Imperial College London, the work has uncovered a range of minerals and organic matter in Martian rocks that point to an ancient history of habitable conditions and potential biological processes on the Red Planet.

This is a very exciting discovery of a potential biosignature but it does not mean we have discovered life on Mars. We now need to analyze this rock sample on Earth to truly confirm if biological processes were involved or not.

While driving through the valley, called Neretva Vallis, Perseverance came across a thick succession of fine-grained mudstones and muddy conglomerates. Here, it conducted a detailed analysis of these rocks, using instruments such as the Planetary Instrument for X-ray Lithochemistry (PIXL) and Scanning Habitable Environments with Raman & Luminescence for Organics & Chemicals (SHERLOC).

By mapping the types and distributions of different sedimentary rocks, researchers were able to reconstruct the environment in which these mudstones were deposited.

Their analysis revealed a range of sedimentary structures and textures indicative of lake margin and lake bed environments, including a composition rich in minerals like silica and clays—the opposite to a river scenario, where fast-moving water would carry these tiny particles away.

This pointed to a surprising conclusion: they had found lake deposits in the bottom of a river valley.

The finding may suggest a period in the history of Jezero Crater where the valley itself was flooded, giving rise to this potentially habitable lake.

With the lake habitat scenario pinned down, the Perseverance science team turned their attention to the mudstones themselves. It was inside these rocks that they discovered a group of tiny nodules and reaction fronts, with chemical analysis revealing that these millimeter-scale structures are highly enriched in iron-phosphate and iron-sulfide minerals (likely vivianite and greigite).

These appear to have formed through redox reactions involving organic carbon, a process that could have been driven by either abiotic or—interestingly—biological chemistry. Importantly, this sets the stage for everything that happened next: the formation of this specific type of oxidized, iron- and phosphorus-rich sediment was the essential prerequisite for creating the ingredients for subsequent reactions.

Since these ingredients mirror by-products of microbial metabolism seen on Earth, it can be considered a compelling potential biosignature, raising the possibility that there was once microbial life on Mars.

Ultimately, the only way for the true origin of these structures to be determined is by returning the samples to Earth, a possibility that rests on when future missions will manage to successfully collect the samples from Mars' surface.

Joel Hurowitz, Redox-driven mineral and organic associations in Jezero Crater, Mars, Nature (2025). DOI: 10.1038/s41586-025-09413-0. www.nature.com/articles/s41586-025-09413-0

Climate change is driving fish stocks from countries' waters to the high seas, study finds

Fish and other marine organisms, though deeply affected by human activities, don't respect human borders. The ranges of many commercially important species in fact straddle the borders of countries' exclusive economic zones (EEZs) and international waters, known as the high seas. This arrangement, which makes fisheries management difficult, is set to get even more complicated as climate change continues to heat up the ocean, a new study says.

The study, published July 30 in the journal Science Advances, found that more than half of the world's straddling stocks will shift across the maritime borders between EEZs and the high seas by 2050. Most of these shifts will be into the high seas, where fisheries management is much more challenging and stocks are more likely to be overexploited.

Juliano Palacios-Abrantes et al, Climate change drives shifts in straddling fish stocks in the world's ocean, Science Advances (2025). DOI: 10.1126/sciadv.adq5976

Kamal Azmi et al, Putting Regional Fisheries Management Organisations' Climate Change House in Order, Fish and Fisheries (2025). DOI: 10.1111/faf.70015

Maternal gut microbiome composition may be linked to preterm births

Researchers have found that the presence of certain bacteria in the maternal gut microbiome during early pregnancy is linked to a higher risk of preterm birth. Published in the journal Cell Host & Microbe on September 10, the study reports that one particular species, Clostridium innocuum (C. innocuum), contains a gene that can degrade estradiol—an important pregnancy hormone.

This study suggests that for pregnant women or women preparing to become pregnant, it may be important to monitor their gut microbiome to prevent potential adverse pregnancy outcomes.

The researchers used samples and data from two large pregnancy cohorts—the Tongji-Huaxi-Shuangliu Birth cohort from southwest China and the Westlake Precision Birth cohort from southeast China.
For the first cohort, the team collected stool samples from 4,286 participants in early pregnancy, at an average of 10.4 gestational weeks. For the second cohort, they collected stool samples from 1,027 participants in mid-pregnancy, or around 26 gestational weeks. They also collected blood samples from all participants, which were used to measure human genetic variations and hormone metabolism.

After working with the first cohort, the researchers were able to establish a comprehensive database containing rRNA-based microbial genera data, metagenome-based species data, and phenotype data such as preterm delivery status.

They used several statistical models to screen the annotated gut microbial genera and species and their relationship to preterm birth status or gestational duration .Through that work, they identified 11 genera and 1 species that had a statistically significant link.

The results, which were validated with the second cohort, showed that bacterial species C. innocuum—a small, rod-shaped bacteria—had the strongest connection to preterm birth. Further study of C. innocuum revealed that this species makes an enzyme that degrades estradiol—a form of estrogen that plays a pivotal role during pregnancy.

Estradiol regulates critical pathways that sustain pregnancy and initiate the process of childbirth.

Part1

The researchers propose that dysregulated estradiol levels induced by a high prevalence of C. innocuum could be the mechanism that links the gut microbiome to preterm birth.
The researchers note that because their study was based on two China-based cohorts with a relatively low prevalence of preterm birth, the findings may not be generalizable to other populations and should be authenticated by more work with them.

In the future, they hope to further elucidate the molecular mechanisms by which C. innocuum modulates preterm birth risk and potentially identify optimal intervention strategies to mitigate the bacteria's impact on pregnancy. They also seek to characterize the interaction between C. innocuum and host estrogen metabolism more generally, beyond pregnancy.

Maternal gut microbiome during early pregnancy predicts preterm birth, Cell Host & Microbe (2025). DOI: 10.1016/j.chom.2025.08.004. www.cell.com/cell-host-microbe … 1931-3128(25)00330-0

Part 2

Donor-egg births may carry more risks

More women than ever are carrying babies conceived with someone else's egg—but few are told that this might carry greater health risks.

Pregnancies involving an embryo that doesn't share the pregnant woman's DNA are becoming more common. For many, it's a path to parenthood that would otherwise be closed.
But emerging evidence suggests that these pregnancies may come with higher rates of complications, including preeclampsia, gestational diabetes and preterm birth, and that women are often not given the full picture before treatment.

As the fertility industry expands and diversifies, it's time to ask whether patients are being adequately informed about the risks of carrying another woman's egg—and whether more caution is needed in how these options are presented.

There are three situations in which a woman may carry another woman's egg in her uterus.

The most common is when a woman cannot produce her own eggs but has a functioning uterus. In this case, donor eggs and in-vitro fertilization (IVF) offer the only route to pregnancy.

The other two situations involve fertile women carrying a donated egg on behalf of someone else. This happens in cases of gestational surrogacy, where a surrogate carries a baby genetically unrelated to her, or in reciprocal IVF, also known as ROPA or co-IVF. In the latter, one woman in a same-sex couple (or a trans man) donates her egg to her partner, so that both have a biological connection to the child.

In IVF, fertilization occurs outside the body and the resulting embryo is transferred into the uterus. But what happens when the egg in the uterus has no genetic similarity to the woman carrying it? Could this cause complications for her or the baby?

To answer that question, we need to compare outcomes in these situations to pregnancies where the egg shares approximately 50% of the mother's DNA, either through natural conception or own-egg IVF. Early evidence suggests that having someone else's egg in the uterus is associated with a higher risk of obstetric complications, including preeclampsia, gestational diabetes and preterm birth.

There are three key comparisons to make. First, donor-egg IVF v own-egg IVF. For infertile women using donor eggs, the most relevant comparison is IVF with their own eggs.
Second, gestational v traditional surrogacy. In gestational surrogacy, the surrogate carries a donor egg, while in traditional surrogacy, she uses her own. Outcomes can also be compared with the surrogate's previous natural pregnancies.

Third, reciprocal IVF v own-egg IVF. In same-sex couples, reciprocal IVF can be compared to own-egg IVF to assess risks.
Part1

A review of 11 studies comparing donor-egg IVF to own-egg IVF found that donor-egg pregnancies had significantly higher rates of hypertensive disorders in the mother, as well as preterm birth and babies that were small for their gestational age.

A separate review focusing on preeclampsia in singleton IVF pregnancies found the condition occurred in 11.2% of donor-egg pregnancies, compared to 3.9% of own-egg pregnancies.

For women who can only become pregnant using a donor egg, these risks may be worth accepting. But it's important that women are made aware of the potential complications, especially if carrying twins, which further increases risks.

Women deserve full, unbiased information about the risks. That includes knowing that carrying someone else's egg may increase the likelihood of pregnancy complications. They can then make informed decisions about whether the potential benefits outweigh the risks.

Phoebe Barry et al, The outcomes of surrogate pregnancy using a donor egg compared to the surrogate's egg: a systematic review, Preprints (2025). DOI: 10.22541/au.174919886.60741282/v1

Part2

DNA cassette tapes could solve global data storage problems

Our increasingly digitized world has a data storage problem. Hard drives and other storage media are reaching their limits, and we are creating data faster than we can store it. Fortunately, we don't have to look too far for a solution, because nature already has a powerful storage medium with DNA (deoxyribonucleic acid). It is this genetic material that researchers are using to create DNA storage cassettes.

DNA is the ultimate data storage solution because it is compact, dense and durable. It can hold an enormous amount of information in a microscopic space and preserve that data for thousands of years without needing electricity. Theoretically, the DNA in a single human cell has a capacity of approximately 3.2 gigabytes, which equates to roughly 6,000 books, 1,000 pieces of music or two movies.

Scientists have known about DNA's potential as a storage solution for a long time, but the challenge up until now has been to create a viable system that we can use. In a new study published in the journal Science Advances, researchers describe how they made a DNA cassette similar to cassette tapes that were staples in personal and car stereos in the 1980s.

The team first created the physical tape from a polyester-nylon blend. Then they printed barcode patterns on it to make millions of tiny, separate sections, similar to folders on a computer. This lets the system find the exact spot where the data is stored. Accessing information has been one of the problems of previous DNA storage techniques.
To store a file, digital data is first translated into a DNA sequence. The four bases, or building blocks of DNA (A, G, C, and T) act as a code, similar to the zeroes and ones that computers use. The researchers also coated the tape with a protective crystalline layer to protect the DNA bonds from breaking down.
Finally, they proved the system works by converting a digital image into DNA, then successfully and quickly retrieving it from the tape.

DNA cassette tape provides a strategy for fast, compact, large-scale DNA-based cold (infrequently accessed) or warm (needed on demand) data storage,  wrote the scientists in their paper.

Jiankai Li et al, A compact cassette tape for DNA-based data storage, Science Advances (2025). DOI: 10.1126/sciadv.ady3406

Medications leave lasting mark on gut microbiome, even years after use

Medications taken years ago can continue to shape the human gut microbiome, according to a large-scale study.

Analyzing stool samples and prescription records from over 2,500 Estonian Biobank participants in the Estonian Microbiome cohort, researchers found that the majority of drugs studied were linked to microbiome changes, with a substantial number of them also showing long-term effects detectable years after patients stopped taking them.

The impact was not limited to antibiotics: antidepressants, beta-blockers, proton pump inhibitors, and benzodiazepines all left microbial "fingerprints."

Most microbiome studies only consider current medications, but our results show that past drug use can be just as important as it is a surprisingly strong factor in explaining individual microbiome differences. 

This highlights that it is critical to account for drug usage history when studying links between the microbiome and disease. The research is published in the journal mSystems.

Interestingly, benzodiazepines—commonly prescribed for anxiety—had microbiome effects comparable to broad-spectrum antibiotics. The results also show that drugs from the same class that might be used for the same condition, e.g. diazepam and alprazolam, may differ in how much they disrupt the microbiome.

Follow-up samples from a subset of participants confirmed that starting or stopping certain drugs caused predictable microbial shifts, suggesting causal effects. Despite the small sample size of the second time-point analysis, the authors were able to verify long-term effects of proton pump inhibitors, selective serotonin reuptake inhibitors and antibiotics, such as penicillins in combination and macrolides.

Oliver Aasmets et al, A hidden confounder for microbiome studies: medications used years before sample collection, mSystems (2025). DOI: 10.1128/msystems.00541-25

Breathlessness increases long-term mortality risk, finds a study in Malawi

Research led by Liverpool School of Tropical Medicine and the Malawi-Liverpool-Wellcome Program shows that over half of hospital patients with breathlessness had died within a year of admission (51%), as opposed to just 26% of those without the symptom.

Most of these patients had more than one condition that caused breathlessness, including pneumonia, anemia, heart failure and TB.

The findings demonstrate the importance of integrated, patient-centered care, researchers say, to tackle the burden of high mortality for people with breathlessness, particularly in low-income countries. The work appears in Thorax.

Most of these patients live with more than one condition at the same time, which the researchers found to be a factor linked to higher mortality, such as those with TB or pneumonia. This suggests that treating diseases in isolation is not enough, and health care models that have traditionally focused on single presenting conditions may overlook important concurrent diseases.

Acute breathlessness as a cause of hospitalisation in Malawi: a prospective, patient-centred study to evaluate causes and outcomes, Thorax (2025). DOI: 10.1136/thorax-2025-223623

A pathological partnership between Salmonella and yeast in the gut

Researchers have found that a common gut yeast, Candida albicans, can help Salmonella typhimurium take hold in the intestine and spread through the body. When interacting, a Salmonella protein called SopB prompts the yeast to release arginine, which turns on Salmonella's invasion machinery and quiets the body's inflammation signals.

Gut microbes shape human health across colonization resistance, immune training, digestion, and signaling that reaches distant organs. Bacteria dominate both abundance and research attention, while roles for viruses and fungi remain less defined.

Altered mycobiome composition appears in multiple gastrointestinal diseases, and integration of fungi into gut ecology and into interactions with commensal and pathogenic bacteria remains largely unknown.

Non-typhoidal Salmonella ranks among the best-studied enteric pathogens, infecting an estimated 100 million people each year. Healthy individuals typically experience localized inflammatory diarrhea, while immunocompromised patients face risks of spread to peripheral organs.

Establishing gut colonization requires competition with resident microorganisms, and commensal fungi occur across tested mammalian species, yet mycobiome contributions during enteric infection remain largely unexplored.

Candida albicans is a frequent colonizer of human mucosal surfaces, present in the gut of more than 60% of healthy humans. Usual behavior is commensal, with pathogenic potential particularly in immunocompromised hosts. A key virulence trait is morphology switching from yeast to epithelium-penetrating hyphae.

Associations with inflammatory bowel disease, specifically Crohn's disease, have been reported. C. albicans cannot induce gut inflammation and has been shown to exacerbate it. Both Salmonella and C. albicans thrive under inflammatory gut conditions, and C. albicans likely resides in the gut of many patients at the time Salmonella infection occurs.

In the study, "Commensal yeast promotes Salmonella Typhimurium virulence," published in Nature, researchers investigated cross-kingdom interactions to determine how Candida albicans influences Salmonella colonization, systemic dissemination, and host inflammatory responses.

In the experiments conducted in mice, Candida in the gut led to higher Salmonella loads in the large intestine and more bacteria reaching the spleen and liver, with co-infected mice losing more weight. Candida also boosted Salmonella entry into human colon cell lines. Gene readouts showed Salmonella's invasion machinery switched on near Candida.

Co-cultures contained millimolar arginine, and adding L-arginine alone increased invasion in a dose-dependent way, while an arginine-transporter mutant did not respond to Candida. Candida lacking arginine production also failed to boost Salmonella invasion or gut colonization, and an ARG4 revertant restored the effect.

Researchers conclude that C. albicans colonization represents a susceptibility factor for Salmonella infection, with arginine acting as a pivotal metabolite connecting fungus, bacterium, and host. Findings point to SopB-driven arginine production in Candida that boosts Salmonella's invasion program while softening host inflammatory signals.

 Kanchan Jaswal et al, Commensal yeast promotes Salmonella Typhimurium virulence, Nature (2025). DOI: 10.1038/s41586-025-09415-y

The sound of crying babies makes our faces hotter, according to new research

Hearing a baby cry can trigger a range of responses in adults, such as sympathy, anxiety and a strong urge to help. However, new research suggests that a deeper physical reaction is also occurring. A baby's cry, particularly if it is in pain or distress, makes our faces physically warmer.

Since they can't speak yet, babies cry to communicate their needs, whether they're in pain or want some attention. When a baby is in distress, they forcefully contract their ribcage, which produces high-pressure air that causes their vocal cords to vibrate chaotically. This produces complex disharmonious sounds known as nonlinear phenomena (NLP).

To study how adults respond to crying babies, scientists played 23 different recordings to 41 men and women with little to no experience with young infants. At the same time, a thermal infrared imaging camera measured subtle changes to their facial temperatures. A rise in temperature in this part of the body is governed by the autonomic nervous system, a network of nerves that controls unconscious processes such as breathing and digestion. After each cry, the participants rated whether the baby was in discomfort or in pain.

The study found that adults' facial temperatures change when they hear a baby cry, a clear sign that the autonomic nervous system has been activated. This suggests that people unconsciously pick up on acoustic features in a baby's cry. The higher the level of NLP (meaning a baby is in more pain or distress), the stronger and more in sync the listener's facial temperature became. In other words, as the cry grew louder, a person's face grew warmer. This physiological reaction was the same for both men and women.

Lény Lego et al, Nonlinear acoustic phenomena tune the adults' facial thermal response to baby cries with the cry amplitude envelope, Journal of the Royal Society Interface (2025). DOI: 10.1098/rsif.2025.0150

Scientists engineer plants to double carbon uptake ability and produce more seeds and lipids

Typically, plants rely on the Calvin-Benson-Bassham (CBB) cycle to convert carbon dioxide in the atmosphere to usable organic matter for growth. Although this cycle is the main pathway for carbon fixation in all plants on Earth, it is surprisingly inefficient—losing one third of carbon in the cycle when synthesizing the molecule acetyl–coenzyme A (CoA) to generate lipids, phytohormones, and metabolites. Plants also lose carbon during photorespiration, which limits their growth. This is largely due to the inefficiency of an enzyme called RuBisCO.

In efforts to increase carbon uptake and reduce carbon loss in plants to boost biomass and lipid production, scientists have experimented with ways to increase the efficiency of RuBisCO, overexpress CBB cycle enzymes, introduce carbon-concentrating mechanisms, and reduce photorespiration losses. But, a new study published in Science, focuses on a novel approach—creating an altogether new pathway for carbon uptake.

The researchers involved in the study introduced a synthetic CO₂ uptake cycle into the plant Arabidopsis thaliana. They refer to the engineered cycle as the malyl-CoA-glycerate (McG) cycle, which works in conjunction with the CBB cycle to create a dual-cycle CO₂ fixation system. The new cycle increases efficiency by using previously wasted carbon.

"In the McG cycle, one additional carbon is fixed when 3PG is the input, or no carbon is lost when glycolate is the input. In both cases, acetyl-CoA is produced more efficiently, which is expected to enhance the production of lipids and other important plant metabolites, including phytohormones," the authors write.

 Kuan-Jen Lu et al, Dual-cycle CO₂ fixation enhances growth and lipid synthesis in Arabidopsis thaliana, Science (2025). DOI: 10.1126/science.adp3528

Scientists discover how nanoplastics disrupt brain energy metabolism

Scientists have discovered how nanoplastics—even smaller than microplastics—disrupt energy metabolism in brain cells. Their findings may have implications for better understanding neurodegenerative diseases characterized by declining neurological or brain function, and even shed new light on issues with learning and memory.

The study has revealed the specific mechanism by which these tiny nanoplastics can interfere with energy production in the brain in an animal model. The findings, recently published in the Journal of Hazardous Materials: Plastics, provide fresh insights into the potential health risks posed by environmental plastics.

Polystyrene nanoplastics (PS-NPs) are produced when larger plastics break down in the environment. These particles have been detected in multiple organs in the body, including the brain, sparking growing concerns about their possible role in neurological disease.

The researchers focused on mitochondria, which are critical for producing the energy needed for brain function. Mitochondrial dysfunction is a well-known feature of neurodegenerative diseases such as Parkinson's and Alzheimer's, as well as normal aging.

By isolating mitochondria from brain cells, the researchers showed that exposure to PS-NPs specifically disrupted the "electron transport chain," a simplified term for the set of protein complexes that work together to help generate cellular energy in the form of ATP. While individual mitochondrial complexes I and II were not directly impaired, electron transfer between complexes I–III and II–III, as well as the activity of complex IV, was significantly inhibited.

The scientists found that electron transfer between complex I–III and complex II–III was potently inhibited at much lower concentrations, suggesting environmentally relevant exposures could also impair bioenergetic function over chronic timeframes.

Interestingly, the same broad effects were seen in synaptic mitochondria, which are essential for communication between brain cells. This suggests that nanoplastics could also interfere with synaptic plasticity, a process fundamental to learning and memory.

D.M. Seward et al, Polystyrene nanoplastics target electron transport chain complexes in brain mitochondria, Journal of Hazardous Materials: Plastics (2025). DOI: 10.1016/j.hazmp.2025.100003

The death of the dinosaurs reengineered Earth

Dinosaurs had such an immense impact on Earth that their sudden extinction led to wide-scale changes in landscapes—including the shape of rivers—and these changes are reflected in the geologic record, according to a new study.

Scientists have long recognized the stark difference in rock formations from just before dinosaurs went extinct to just after, but chalked it up to sea level rise, coincidence, or other abiotic reasons. But the new study shows that once dinosaurs were extinguished, forests were allowed to flourish, which had a strong impact on rivers.

Studying these rock layers, the researchers suggest that dinosaurs were likely enormous "ecosystem engineers," knocking down much of the available vegetation and keeping land between trees open and weedy. The result was rivers that spilled openly, without wide meanders, across landscapes. Once the dinosaurs perished, forests were allowed to flourish, helping stabilize sediment and corralling water into rivers with broad meanders.

Their results, published in the journal Communications Earth & Environment, demonstrate how rapidly the Earth can change in response to catastrophic events.

Very often when we're thinking about how life has changed through time and how environments change through time, it's usually that the climate changes and, therefore, it has a specific effect on life, or this mountain has grown and, therefore, it has a specific effect on life. It's rarely thought that life itself could actually alter the climate and the landscape. The arrow doesn't just go in one direction, the researchers say.

 Dinosaur extinction can explain continental facies shifts at the Cretaceous-Paleogene boundary, Communications Earth & Environment (2025). DOI: 10.1038/s43247-025-02673-8

Ants defend plants from herbivores, but can hinder pollination by bees

Around 4,000 plant species from different parts of the world secrete nectar outside their flowers, such as on their stems or leaves, through secretory glands known as extrafloral nectaries. Unlike floral nectar, extrafloral nectar does not attract pollinators; rather, it attracts insects that defend plants, such as ants. These insects feed on the sweet liquid and, in return, protect the plant from herbivores. However, this protection comes at a cost.

A study published in the Journal of Ecology points out that the presence of ants can reduce the frequency and duration that bees visit the flowers of plants with extrafloral nectaries.

Pollination is only impaired when extrafloral nectaries are close to the flowers. Plants with these glands in other locations, such as on their leaves or branches, had increased reproductive success, likely due to the protection against herbivores provided by ants.

On the other hand, butterflies, another group of pollinators, are not affected by ants. This may be due to the way these two groups feed. Butterflies use a long, straw-like organ called a proboscis to suck nectar from a distance, keeping them safe from ants.

Bees, on the other hand, need to get very close to the flower to collect pollen and floral nectar, but ants don't allow them to stay for long. Not surprisingly, the new analysis showed that the presence of ants is detrimental to pollination when extrafloral nectaries are close to flowers, but has a positive effect on plant reproduction when they're located further away.

The conclusions are the result of an analysis of data from 27 empirical studies on the relationships between ants, pollinators, and plants with extrafloral nectaries. The articles were selected from an initial screening of 567 studies after applying inclusion and exclusion criteria. The data were compiled and analyzed with computational tools.

Amanda Vieira da Silva et al, Ants on flowers: Protective ants impose a low but variable cost to pollination, moderated by location of extrafloral nectaries and type of flower visitor, Journal of Ecology (2025). DOI: 10.1111/1365-2745.70087

Culture is overtaking genetics in shaping human evolution, researchers argue

Some Researchers are theorizing that human beings may be in the midst of a major evolutionary shift—driven not by genes, but by culture.

In a paper published in BioScience, they argue that culture is overtaking genetics as the main force shaping human evolution.

"When we learn useful skills, institutions or technologies from each other, we are inheriting adaptive cultural practices. On reviewing the evidence, we find that culture solves problems much more rapidly than genetic evolution. This suggests our species is in the middle of a great evolutionary transition", they say.

Cultural practices—from farming methods to legal codes—spread and adapt far faster than genes can, allowing human groups to adapt to new environments and solve novel problems in ways biology alone could never match. According to the research team, this long-term evolutionary transition extends deep into the past, it is accelerating, and may define our species for millennia to come.

Cultural evolution eats genetic evolution for breakfast, they argue. 

 In the modern environment cultural systems adapt so rapidly they routinely "preempt" genetic adaptation. For example, eyeglasses and surgery correct vision problems that genes once left to natural selection.

Medical technologies like cesarean sections or fertility treatments allow people to survive and reproduce in circumstances that once would have been fatal or sterile. These cultural solutions, researchers argue, reduce the role of genetic adaptation and increase our reliance on cultural systems such as hospitals, schools and governments.

Today, your well-being is determined less and less by your personal biology and more and more by the cultural systems that surround you—your community, your nation, your technologies. And the importance of culture tends to grow over the long term because culture accumulates adaptive solutions more rapidly.

Over time, this dynamic could mean that human survival and reproduction depend less on individual genetic traits and more on the health of societies and their cultural infrastructure.

But, this transition comes with a twist. Because culture is fundamentally a shared phenomenon, culture tends to generate group-based solutions.

Using evidence from anthropology, biology and history, Waring and Wood argue that group-level cultural adaptation has been shaping human societies for millennia, from the spread of agriculture to the rise of modern states. They note that today, improvements in health, longevity and survival reliably come from group-level cultural systems like scientific medicine and hospitals, sanitation infrastructure and education systems rather than individual intelligence or genetic change.
The researchers argue that if humans are evolving to rely on cultural adaptation, we are also evolving to become more group-oriented and group-dependent, signaling a change in what it means to be human.
Part1

In the history of evolution, life sometimes undergoes transitions which change what it means to be an individual. This happened when single cells evolved to become multicellular organisms and social insects evolved into ultra-cooperative colonies. These individuality transitions transform how life is organized, adapts and reproduces. Biologists have been skeptical that such a transition is occurring in humans.

But the researchers suggest that because culture is fundamentally shared, our shift to cultural adaptation also means a fundamental reorganization of human individuality—toward the group.
Cultural organization makes groups more cooperative and effective. And larger, more capable groups adapt—via cultural change—more rapidly. It's a mutually reinforcing system, and the data suggest it is accelerating.
For example, genetic engineering is a form of cultural control of genetic material, but genetic engineering requires a large, complex society. So, in the far future, if the hypothesized transition ever comes to completion, our descendants may no longer be genetically evolving individuals, but societal "superorganisms" that evolve primarily via cultural change.
The researchers emphasize that their theory is testable and lay out a system for measuring how fast the transition is happening. The team is also developing mathematical and computer models of the process and plans to initiate a long-term data collection project in the near future. They caution, however, against treating cultural evolution as progress or inevitability.
They are not suggesting that some societies, like those with more wealth or better technology, are morally 'better' than others. Evolution can create both good solutions and brutal outcomes. They think this might help our whole species avoid the most brutal parts.
The goal of this work goal is to use their understanding of deep patterns in human evolution to foster positive social change.
Still, the new research raises profound questions about humanity's future. "If cultural inheritance continues to dominate, our fates as individuals, and the future of our species, may increasingly hinge on the strength and adaptability of our societies.
And if so, the next stage of human evolution may not be written in DNA, but in the shared stories, systems, and institutions we create together, the researchers conclude.

Timothy M Waring et al, Cultural inheritance is driving a transition in human evolution, BioScience (2025). DOI: 10.1093/biosci/biaf094. academic.oup.com/bioscience/ad … osci/biaf094/8230384

Part 2

Scientists uncover how cellular receptors trigger inflammation and sensory changes

In two new studies, scientists have uncovered detailed blueprints of how certain molecular "gates" in human cells work—findings that could open doors to new treatments for conditions ranging from certain cancers and brain diseases to hearing loss and atherosclerosis, or plaque build-up in the arteries.

They studied a group of proteins known as P2X receptors, which sit on the surface of cells and detect ATP—a molecule best known as the body's energy source inside of cells.

When ATP leaks outside of cells, often as a sign of stress or damage, P2X receptors act like alarm bells, triggering responses related to inflammation, pain and sensory processing.

Extracellular ATP is a universal danger signal. When it builds up outside cells, P2X receptors sense it and change how the cells respond. Understanding these receptors at the atomic level is key to designing drugs that can either calm them down or fine-tune their activity.

In a study published in Nature Communications, researchers examined the molecular structure of the human P2X7 receptor, a protein linked to inflammatory diseases such as cancer, Alzheimer's and atherosclerosis. Despite years of effort, no drugs targeting P2X7 have reached the clinical market, partly because drugs that have worked well in animal models have not had the same success in humans.

Building on a previous study, where they determined how to turn the rat P2X7 receptor off, the team has now mapped how drugs turn off the human P2X7 receptor for the first time. They now know what makes the human receptor different from the receptor that is present in animal models. This is important for understanding how to better customize drugs to fit the binding pockets within the human receptor.

Using that information, the researchers, in collaboration with groups from around the world, designed a new compound referred to as UB-MBX-46. The compound complements the binding pocket in the human receptor, translating to a molecule that blocks the human receptor with high precision and strength.

This is the first time scientists have visualized the human P2X7 receptor and really understood how it is different from others. With that knowledge, they can now create a drug candidate that perfectly fits binding pockets within the human receptor, much like how a key fits in a lock. It gives us hope for developing therapies that have better chances to reach the clinic.

Part 1

A second study published in Proceedings of the National Academy of Sciences examined the human P2X2 receptor, a protein in the same family as the P2X7 receptor, but is predominantly found in the cochlea, the hearing organ of the inner ear.

The P2X2 receptor is involved in hearing processes and in the ear's adaptation to loud noise. Certain genetic mutations of this receptor have been linked to hearing loss. Currently, there are no drugs that target this receptor effectively, and until now, scientists had limited insight into how it functions.

Researchers  used cryo-electron microscopy—a powerful imaging method—to capture 3D structures of the human P2X2 receptor in two states: in a resting state and in a state bound to ATP but desensitized, meaning it's not active anymore. The team discovered unique structural features and pinpointed areas where hearing-related mutations occur.

Together, the studies mark a leap forward in understanding how P2X receptors contribute to a wide range of diseases by triggering inflammation and sensory changes.

Adam C. Oken et al, A polycyclic scaffold identified by structure-based drug design effectively inhibits the human P2X7 receptor, Nature Communications (2025). DOI: 10.1038/s41467-025-62643-8

Franka G. Westermann et al, Subtype-specific structural features of the hearing loss–associated human P2X2 receptor, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2417753122

Part2

 

Scientists shoot lasers into brain cells to uncover how illusions work

An illusion is when we see and perceive an object that doesn't match the sensory input that reaches our eyes.

In a new study published in Nature Neuroscience, researchers identified the key neural circuit and cell type that plays a pivotal role in detecting these illusions—more specifically, their outer edges or "contours"—and how this circuit works.

They discovered a special group of cells called IC–encoder neurons that tell the brain to see things that aren't really there as part of a process called recurrent pattern completion.

Because IC–encoder neurons have this unique capacity to drive pattern completion, the researchers think that they might have specialized synaptic output connectivity that allows them to recreate this pattern in a very effective manner.

They also also know that they receive top-down inputs from higher visual areas. The representation of the illusion arises in higher visual areas first and then gets fed back to the primary visual cortex; and when that information is fed back, it's received by these IC–encoders in the primary visual cortex.

 In the context of the brain and vision—using the above shape diagram—higher levels of the brain interpret the image as a square and then tell the lower-level visual cortex to "see a square" even though the visual stimulus consists of four semi-complete black circles.

They made the discovery by observing the electrical brain activity patterns of mice when they were shown illusory images like the Kanizsa triangle. They then shot beams of light at the IC-encoder neurons, in a process called two-photon holographic optogenetics, when there was no illusory image present.

When this happened, they noticed that even in the absence of an illusion, IC-encoder neurons triggered the same brain activity patterns that exist when an illusory image was present. They successfully emulated the same brain activity by stimulating these specialized neurons.

The findings shed light on how the visual system and perception work in the brain and have implications for diseases where this system malfunctions. In certain diseases you have patterns of activity that emerge in your brain that are abnormal, and in schizophrenia these are related to object representations that pop up randomly.

If you don't understand how those objects are formed and a collective set of cells work together to make those representations emerge, you're not going to be able to treat it; so understanding which cells and in which layer this activity occurs is helpful.

Recurrent pattern completion drives the neocortical representation of sensory inference, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02055-5.

Geologists discover where energy goes during an earthquake

The ground-shaking that an earthquake generates is only a fraction of the total energy that a quake releases. A quake can also generate a flash of heat, along with a domino-like fracturing of underground rocks. But exactly how much energy goes into each of these three processes is exceedingly difficult, if not impossible, to measure in the field.

Earthquakes are driven by energy that is stored up in rocks over millions of years. As tectonic plates slowly grind against each other, stress accumulates through the crust. When rocks are pushed past their material strength, they can suddenly slip along a narrow zone, creating a geologic fault. As rocks slip on either side of the fault, they produce seismic waves that ripple outward and upward.

We perceive an earthquake's energy mainly in the form of ground shaking, which can be measured using seismometers and other ground-based instruments. But the other two major forms of a quake's energy—heat and underground fracturing—are largely inaccessible with current technologies.

Now  geologists have traced the energy that is released by "lab quakes"—miniature analogs of natural earthquakes that are carefully triggered in a controlled laboratory setting. For the first time, they have quantified the complete energy budget of such quakes, in terms of the fraction of energy that goes into heat, shaking, and fracturing.

They found that only about 10% of a lab quake's energy causes physical shaking. An even smaller fraction—less than 1%—goes into breaking up rock and creating new surfaces. The overwhelming portion of a quake's energy—on average 80%—goes into heating up the immediate region around a quake's epicenter. In fact, the researchers observed that a lab quake can produce a temperature spike hot enough to melt surrounding material and turn it briefly into liquid melt.

The geologists also found that a quake's energy budget depends on a region's deformation history—the degree to which rocks have been shifted and disturbed by previous tectonic motions. The fractions of quake energy that produce heat, shaking, and rock fracturing can shift depending on what the region has experienced in the past.

The team's lab quakes are a simplified analog of what occurs during a natural earthquake. Down the road, their results could help seismologists predict the likelihood of earthquakes in regions that are prone to seismic events.

 Daniel Ortega‐Arroyo et al, "Lab‐Quakes": Quantifying the Complete Energy Budget of High‐Pressure Laboratory Failure, AGU Advances (2025). DOI: 10.1029/2025av001683

Scientists use AI to decode protein structures behind bitter taste detection

Receptor proteins, expressed on the cell surface or within the cell, bind to different signaling molecules, known as ligands, initiating cellular responses. Taste receptors, expressed in oral tissues, interact with tastants, the molecules responsible for the sensation of taste.

Bitter taste receptors (T2Rs) are responsible for the sensation of bitter taste. However, apart from oral tissue, these receptors are also expressed in the neuropod cells of the gastrointestinal tract, which are responsible for transmitting signals from the gut to the brain. Thus, T2Rs might play a crucial role in maintaining the gut-brain axis.

25 types of human T2Rs have been identified to date. However, due to certain complexities, the structure of most of these receptors is not yet elucidated. In recent times, AI-based prediction models have been used to understand protein structure accurately. Previously, a Nobel Prize-winning artificial intelligence (AI)-based model, AlphaFold2 (AF2), was utilized to decipher the structures of T2Rs. However, with the advancement in technology, the model has been updated to its latest version, AlphaFold3 (AF3). The latest model allows a more detailed structural prediction compared to the previous version.

In this study, a group of researchers decided to analyze the structure of T2Rs using the AF3 model and compare the accuracy with the results from the AF2-based prediction study and the available three-dimensional structures of the two T2Rs, T2R14 and T2R46.

The expression of bitter taste receptors in the gastrointestinal tract indicates that they are involved in maintaining the gut-brain axis, glucose tolerance, and appetite regulation. Hence, understanding the structure can provide a better insight into its function.

The researchers obtained the amino acid sequences of all human T2Rs from the UniProt database and used the AF3 model to predict their three-dimensional structures. For comparison, previously generated AF2 prediction data were retrieved from the AlphaFold database. The experimentally determined structures of T2R14 and T2R46 were sourced from the Protein Data Bank (PDB). Various software tools were employed for structure visualization, alignment, and accuracy assessment.

The analysis revealed that AF3 provided consistently more accurate structural predictions than AF2. For T2R14, predictions were benchmarked against 115 cryo-EM structures, and AF3 showed a higher agreement with experimental data. Similarly, for T2R46, comparisons with three experimentally resolved structures confirmed that AF3 achieved the closest match in all cases.

Part1

Similarities in the structure of the T2Rs were also analyzed for this study. For these receptors, part of the protein remains inside the cell, known as the intracellular region, while another part stays outside the cell (extracellular region). The interaction with signal molecules happens in the extracellular region. The study demonstrated that there are more structural similarities and consistencies among the intracellular regions of the T2Rs. The extracellular region of the receptors shows significant structural variation.
"Clustering of proteins is based on their structural similarity and dissimilarity. Based on their findings, the researchers divided the T2Rs into three different clusters.
The structure of T2Rs probably allows them to recognize the thousands of different bitter substances via interaction with another taste receptor-specific G protein, α-gustducin.

"With the receptors' involvement in detecting bitter tastants and maintaining the gut-brain axis, this can play an important role in health and pharmaceutical-based research, specifically targeting lifestyle diseases like diabetes.

 Takafumi Shimizu et al, The three-dimensional structure prediction of human bitter taste receptor using the method of AlphaFold3, Current Research in Food Science (2025). DOI: 10.1016/j.crfs.2025.101146

Part 2

**

Kidney transplant rejection associated with changes in lymphatic vessels, new research shows

Scientists have uncovered how lymphatic vessels—the kidney's "plumbing system"—undergo dramatic changes during chronic transplant rejection, becoming structurally disorganized and spreading to unusual parts of the kidney.

Researchers used single-cell sequencing combined with powerful 3D imaging to look at small lymphatic vessels in kidney tissue, comparing healthy kidneys with transplanted kidneys that had been rejected.

Published in the Journal of Clinical Investigation, the research sheds new light on a major unsolved challenge in kidney transplantation and could open the door to new treatments that help transplants last longer.
Kidney transplantation is the most common form of solid organ transplant worldwide. Although the short-term outcomes of kidney transplantation—within a year after surgery—are very good, the long-term outcomes are poorer. Within 10 years, and depending on what country patients are treated in, roughly 50% of kidney grafts will fail.

Researchers know that a big component of why kidney transplant failure occurs is that the patient's immune system attacks parts of the new kidney—such as the blood vessels within it. However, the role of the lymphatic vessels is far less understood. In healthy kidneys, lymphatic vessels act as the organ's plumbing system—playing a vital role in draining excess fluid and helping to regulate immune activity. Therefore, the researchers sought to gain a deeper understanding of the lymphatic system during transplant rejection.

Part 1

Researchers used two different and powerful methods—single cell RNA sequencing and advanced 3D imaging. They studied samples from both healthy and transplant rejection patients.

Single-cell sequencing allows scientists to study the activity of genes in individual cells, one at a time. The researchers did this on a very large scale to generate a huge amount of data. Then the team stained large chunks of kidney tissue while still intact and used a procedure to make it transparent. This 3D imaging helped validate the predictions from the single-cell genetic analysis.

The researchers found that during kidney transplant rejection, the lymphatic vessels within the transplant change their shape and organization. The vessels spread into deeper parts of the kidney known as the medulla, which normally has no lymphatic vessels within it. At the same time, the cell junctions, which are protein anchors that connect cells, go from looking like loose buttons to tightening up like zippers. This is a change that in other contexts is associated with immune cells getting trapped and unable to escape.

Additionally, the researchers found that the balance of T cells inside and around the vessels was disrupted. These T cells released signals that made the vessels switch on molecules acting like "brakes" for the immune system, in an attempt to calm inflammation. However, this protective response was not enough, as other immune cells and antibodies were seen to be directly attacking the kidney. Strikingly, the vessels themselves were also carrying signs that they too were being targeted by the same harmful antibodies.
These findings challenge the view that lymphatic vessels are simply good or bad in transplant rejection. This study suggests that the lymphatic system is normally protective but impaired in transplant rejection as the findings show the vessels change in ways that could encourage rejection by altering their structure and fueling immune responses. The results pave the way for research to focus on regenerating or protecting the lymphatic system in chronic kidney rejection.

Daniyal J. Jafree et al, Organ-specific features of human kidney lymphatics are disrupted in chronic transplant rejection, Journal of Clinical Investigation (2025). DOI: 10.1172/jci168962

Part 2

Man's COVID Infection Lasted 2 Years, Setting a New Record

An immunocompromised man endured ongoing acute COVID-19 for more than 750 days. During this time, he experienced persistent respiratory symptoms and was hospitalized five times.
In spite of its duration, the man's condition differs from long COVID as it wasn't a case of symptoms lingering once the virus had cleared out, but the viral phase of SARS-CoV-2 that continued for over two years.

While this record may be easy to dismiss as something that occurs only to vulnerable people, persistent infections have implications for us all, researchers warn in their new study.

https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(25)00050-3/fulltext

A new explanation for Siberia's giant exploding craters

Scientists may be a step closer to solving the mystery of Siberia's giant exploding craters. First spotted in the Yamal and Gydan peninsulas of Western Siberia in 2012, these massive holes, known as giant gas emission craters (GECs) can be up to 164 feet deep. They seem to appear randomly in the permafrost and are formed when powerful explosions blast soil and ice hundreds of feet into the air.

For more than a decade, researchers have been coming up with theories about the origin of these craters, ranging from meteor impacts to gas explosions. However, none of these have been able to explain why the craters are only found in this specific area and not in the permafrost elsewhere in the Arctic.

Now, research published in the journal Science of the Total Environment proposes a new and more complete explanation that links the craters to specific factors unique to the two peninsulas, the vast gas reserves in this region and the effects of climate change.

"We propose that the formation of GECs is linked to the specific conditions in the area, including abundant natural gas generation and seepage and the overall limited thickness of the continuous permafrost," wrote the researchers in their paper.

According to their model, GECs form when gas and heat rise from deep underground. The heat melts the permafrost seal (a layer of permanently frozen ground that acts as a lid), making it thinner. Meanwhile, the gas builds up underneath it, and with nowhere to go, the pressure rises. As the climate warms, the permafrost thaws even more, making the lid thinner. Eventually, pressure becomes too great and causes an explosive collapse that creates a large crater.

 Helge Hellevang et al, Formation of giant Siberian gas emission craters (GECs), Science of The Total Environment (2025). DOI: 10.1016/j.scitotenv.2025.180042

Exploding Siberian Craters

Study provides first evidence that plastic nanoparticles can accumulate in the edible parts of vegetables

Plastic pollution represents a global environmental challenge, and once in the environment, plastic can fragment into smaller and smaller pieces.

A new study shows for the first time that some of the tiniest particles found in the environment can be absorbed into the edible sections of crops during the growing process.

The research used radishes to demonstrate, for the first time, that nanoplastics—some measuring as little as one millionth of a centimeter in diameter—can enter the roots, before spreading and accumulating into the edible parts of the plant.

The researchers say the findings reveal another potential pathway for humans and animals to unintentionally consume nanoplastics and other particles and fibers that are increasingly present in the environment.

It also underscores the need for further research to investigate what is an emerging food safety issue, and the precise impacts it could have on environmental and human health.

This study provides clear evidence that particles in the environment can accumulate not only in seafood but also in vegetables. This work forms part of our growing understanding on accumulation, and the potentially harmful effects of micro- and nanoparticles on human health.

Nathaniel J. Clark et al, Determining the accumulation potential of nanoplastics in crops: An investigation of 14C-labelled polystyrene nanoplastic into radishes, Environmental Research (2025). DOI: 10.1016/j.envres.2025.122687

Estimated 16,500 climate change deaths during Europe summer: Study

Scientists estimated this week that rising temperatures from human-caused climate change were responsible for roughly 16,500 deaths in European cities this summer, using modeling to project the toll before official data is released.

The rapidly produced study is the latest effort by climate and health researchers to quickly link the death toll during heat waves to global warming—without waiting months or years to be published in a peer-reviewed journal.

The estimated deaths were not actually recorded in the European cities, but instead were a projection based on methods such as modeling used in previously peer-reviewed studies.

Death tolls during heat waves are thought to be vastly underestimated because the causes of death recorded in hospitals are normally heart, breathing or other health problems that particularly affect the elderly when the mercury soars.

researchers used climate modeling to estimate that global warming made temperatures an average of 2.2 degrees Celsius hotter in 854 European cities between June and August.

Using historical data indicating how such soaring temperatures drive up mortality rates, the team estimated there were around 24,400 excess deaths in those cities during that time.

They then compared this number to how many people would have died in a world that was not 1.3C warmer due to climate change caused by humans burning fossil fuels.

Nearly 70%—16,500—of the estimated excess deaths were due to global warming, according to the rapid attribution study.

This means climate change could have tripled the number of heat deaths this summer, said the study from scientists at Imperial College London and epidemiologists at the London School of Hygiene & Tropical Medicine.

The estimates did reflect previous peer-reviewed research, such as a Nature Medicine study which determined there were more than 47,000 heat-related deaths during the European summer of 2023.

Numerous prominent climate and health researchers also backed the study.

What makes this finding even more alarming is that the methods used in these attribution studies are scientifically robust, yet conservative.

The actual death toll could be even higher, warn the researchers. And what about if the figures for the entire world taken into account! Extremely alarming.

Source: Nature Medicine

Some small asteroids can abruptly explode

Some asteroids are more dangerous than others, according to a report published in Nature Astronomy by an international team of researchers.

The team had presented their findings of an investigation into the impact of small asteroid 2023 CX1 over France in February 2023. This new paper revealed that small asteroids can explode on atmospheric entry.

The researchers confirmed the existence of a new population of asteroids linked to L-type chondrites, capable of fragmenting abruptly in the atmosphere and releasing almost all their energy at once. 

Such asteroids must be accounted for in planetary defense strategies, as they pose an increased risk to populated areas, they say.

Auriane Egal et al, Catastrophic disruption of asteroid 2023 CX1 and implications for planetary defence, Nature Astronomy (2025). DOI: 10.1038/s41550-025-02659-8.

Coral reefs set to stop growing as climate warms

Most coral reefs will soon stop growing and may begin to erode—and almost all will do so if global warming hits 2°C, according to a new study in the western Atlantic. 

The study, published in the journal Nature, projects that more than 70% of the region's reefs will stop growing by 2040—and over 99% will do so by 2100 if warming reaches 2°C or more above pre-industrial levels. The paper is titled "Reduced Atlantic reef growth past 2°C warming amplifies sea-level impacts."

Climate change—along with other issues such as coral disease and deteriorating water quality—reduces overall reef growth by killing corals and impacting colony growth rates, the study concludes.

 Chris Perry, Reduced Atlantic reef growth past 2°C warming amplifies sea-level impacts, Nature (2025). DOI: 10.1038/s41586-025-09439-4. www.nature.com/articles/s41586-025-09439-4

Ostrich and emu ancestor could fly, scientists discover

How did the ostrich cross the ocean?

We have long been puzzled by how the family of birds that includes African ostriches, Australian emus and cassowaries, New Zealand kiwis and South American rheas spread across the world—given that none of them can fly.

However, a study published this week may have found the answer to this mystery: the family's oldest-known ancestors were able to take wing.

The only currently living member of this bird family—which is called paleognaths—capable of flight is the tinamous in Central and South America. But even then, the shy birds can only fly over short distances when they need to escape danger or clear obstacles.

Researchers analyzed the specimen of a lithornithid, the oldest paleognath group for which fossils have been discovered. They lived during the Paleogene period 66–23 million years ago.

The fossil of the bird Lithornis promiscuus was first found in the US state of Wyoming, but had been sitting in the Smithsonian museum's collection.

Because bird bones tend to be delicate, they are often crushed during the process of fossilization, but this one was not. 

Crucially for this study, it retained its original shape. This allowed the researchers to scan the animal's breastbone, which is where the muscles that enable flight would have been attached.

They determined that Lithornis promiscuus was able to fly—either by continuously beating its wings or alternating between flapping and gliding.

But  why did these birds give up the power of flight?

Birds tend to evolve flightlessness when two important conditions are met: they have to be able to obtain all their food on the ground, and there cannot be any predators to threaten them.

Part 1

Research has also recently revealed that lithornithids may have had a bony organ on the tip of their beaks which made them excel at foraging for insects.

But what about the second condition—a lack of predators?

Researchers suspect that paleognath ancestors likely started evolving towards flightlessness after dinosaurs went extinct around 65 million years ago.

With all the major predators gone, ground-feeding birds would have been free to become flightless, which would have saved them a lot of energy.

The small mammals that survived the event that wiped out the dinosaurs would have taken some time to evolve into predators.

This would have given flightless birds "time to adapt by becoming swift runners" like the emu, ostrich and rhea—or even "becoming themselves dangerous and intimidating, like the cassowary.

Quantitative analysis of stem-palaeognath flight capabilities sheds light on ratite dispersal and flight loss, Biology Letters (2025). DOI: 10.1098/rsbl.2025.0320. royalsocietypublishing.org/doi … .1098/rsbl.2025.0320

Part 2

How an essential vitamin B-derived nutrient concentrates in mitochondria

There's a molecule that our body makes from vitamin B₅ that is critical for all of the metabolic processes essential for human life. And when something goes wrong in that molecule's production, it affects nearly every organ system in our body and causes a number of diseases.

Researchers have discovered that up to 95% of this molecule—called essential cofactor coenzyme A (CoA)—is located inside mitochondria, organelles that supply cellular energy and regulate cellular metabolism. But what has not been clear is how CoA gets there.

Reporting in Nature Metabolism, researchers have now uncovered that CoA is trafficked into mitochondria and have identified the mechanisms responsible.

This information, the researchers say, is important for future considerations about when and where to target treatments for diseases in which CoA is implicated.

The researchers were able to identify 33 different CoA conjugates in whole cells as well as 23 CoA conjugates in mitochondria.

The question then was whether the CoA conjugates in the mitochondria were made there or brought in from elsewhere.

In additional experiments, the researchers discovered that the enzyme required to make CoA largely exists outside of mitochondria. Further, when they made cells that lacked the molecular transporters that can move CoA around, mitochondria had far less CoA.

These findings strongly support the idea that CoA is being imported into mitochondria, and these transporters are required for that to happen.

This study advances the fundamental understanding of CoA and how it gets to where it needs to be in order to perform its essential functions. That, in turn, sheds light on how disruptions of this process might contribute to illness.

For instance, mutations in the genes that produce CoA transporters are associated with diseases such as encephalomyopathy, a disorder that can include neurodevelopmental delay, epilepsy, and decreased muscle tone. Mutations in the enzymes that produce CoA have been implicated in neurodegeneration.

In the context of brain disorders, such as neurodegeneration and psychiatric disorders, there's an emerging idea that dysregulated mitochondrial metabolism is a contributor.

Ran Liu et al, Cellular pan-chain acyl-CoA profiling reveals SLC25A42/SLC25A16 in mitochondrial CoA import and metabolism, Nature Metabolism (2025). DOI: 10.1038/s42255-025-01358-y