Climate change emerges as third major threat to global wildlife, scientists warn

New research published in BioScience reveals that climate change is rapidly emerging as a third major threat to Earth's wild animals, joining habitat alteration and overexploitation in what scientists call a shift from "twin to triple threats."

The research team analyzed data for 70,814 animal species from 35 classes, using two publicly available biodiversity datasets to assess climate change vulnerability among the world's wild animal populations.

Their findings indicate that 5.1% of all assessed animal species are threatened by climate change, with six animal classes having at least 25% of assessed species at risk. The researchers note that these figures likely underestimate the true scale of the crisis.

"We are entering an existential crisis for the world's wild animals," say the authors. Although some species might benefit, increases in global temperature can lead to a variety of impacts on wild animals, including changes in their physiology, behavior, life cycle, distribution, and interactions among species.

"Rapid and effective climate mitigation is crucial now more than ever for saving the world's biodiversity," the researchers conclude.

 William Ripple et al, Climate change threats to Earth's wild animals, BioScience (2025). DOI: 10.1093/biosci/biaf059

Color-correcting algorithm removes the effect of water in underwater scenes

The ocean is teeming with life. But unless you get up close, much of the marine world can easily remain unseen. That's because water itself can act as an effective cloak: Light that shines through the ocean can bend, scatter, and quickly fade as it travels through the dense medium of water and reflects off the persistent haze of ocean particles. This makes it extremely challenging to capture the true color of objects in the ocean without imaging them at close range.

Now, a team has developed an image-analysis tool that cuts through the ocean's optical effects and generates images of underwater environments that look as if the water had been drained away, revealing an ocean scene's true colors. The team paired the color-correcting tool with a computational model that converts images of a scene into a three-dimensional underwater "world," that can then be explored virtually.

The researchers have dubbed the new tool SeaSplat, in reference to both its underwater application and a method known as 3D Gaussian splatting (3DGS), which takes images of a scene and stitches them together to generate a complete, three-dimensional representation that can be viewed in detail, from any perspective.

Daniel Yang et al, SeaSplat: Representing Underwater Scenes with 3D Gaussian Splatting and a Physically Grounded Image Formation Model, arXiv (2024). DOI: 10.48550/arxiv.2409.17345

Stopping infections before they can start: Promising approach blocks bacteria from binding to cells

As concerns about waning antibiotic effectiveness grow, researchers are using unique tools to search for new ways to keep bacteria from causing infections in both humans and animals.

Researchers used the Canadian Light Source (CLS) at the University of Saskatchewan to visualize the structure of long, thin proteins called adhesins, which most bacteria have, and which bind to a sugar molecule on the surface of a cell. Once attached, the bacteria start to form a colony and then eventually a biofilm. This is how they get started in an infection.

The goal of the research, recently published in the journal mBio, is to find a way to interrupt that attachment process—to "put something in there that would fool them (bacteria) and not allow them to bind to the host cells."

Researchers  learned how to recognize those parts of the protein that stick to the surface of cells and begin causing infections. The researchers noted one spot on the protein that attaches to a simple sugar called fucose found on human blood cells and other organisms.

Special imaging at the CLS—called crystallography—confirmed the model and revealed a possible way to inhibit bacteria from binding to cells. 

Adding more fucose in with the bacterium disrupts the binding process "because they're confused by all of this free fucose floating around" . The protein sensorsrs "that are looking out for the sugar on our cells" are unable to bind "because we're flooding the market with fucose."

The next steps in the research will be to produce compounds that mimic fucose "but that cannot be metabolized by either the bacteria or by the human cells that scientists are trying to protect" .  We won't have to put so much sugar in the system.

Qilu Ye et al, Aeromonas hydrophila RTX adhesin has three ligand-binding domains that give the bacterium the potential to adhere to and aggregate a wide variety of cell types, mBio (2025). DOI: 10.1128/mbio.03158-24

Markers in blood and urine may reveal how much ultra-processed food we are eating

Molecules in blood and urine may reveal how much energy a person consumes from ultra-processed foods, a key step to understanding the impact of the products, a new study finds.

It's the first time that scientists have identified biological markers that can indicate higher or lower intake of the foods, which are linked to a host of health problems. The study is published   this week in the journal PLOS Medicine.

It can potentially give us some clues as to what the underlying biology might be between an ultraprocessed food association and a health outcome.

Ultraprocessed foods—sugary cereals, sodas, chips, frozen pizzas and more—are products created through industrial processes with ingredients such as additives, colours and preservatives not found in home kitchens. 

The scientists found that hundreds of metabolites—products of digestion and other processes—corresponded to the percentage of energy a person consumes from ultra-processed foods. From those, they devised a score of 28 blood markers and up to 33 urine markers that reliably predicted ultra-processed food intake in people consuming typical diets.

The researchers  found this signature that was sort of predictive of this dietary pattern that's high in ultra-processed food and not just a specific food item here and there.

A few of the markers, notably two amino acids and a carbohydrate, showed up at least 60 times out of 100 testing iterations. One marker showed a potential link between a diet high in ultraprocessed foods and type 2 diabetes, the study found.

The research team found that they could use the metabolite scores to tell when the individual participants were eating a lot of ultra-processed foods and when they weren't eating those foods.

The results suggested the markers were "valid at the individual level".

With more research, these metabolic signatures can begin to untangle the biologic pathways and harms of UPF and also differences in health effects of specific UPF food groups, processing methods and additives.

Abar L, et al. Identification and validation of poly-metabolite scores for diets high in ultra-processed food: An observational study and post-hoc randomized controlled crossover-feeding trial.PLOS Medicine (2025). DOI: 10.1371/journal.pmed.1004560

Could Mitochondria Be Rewriting the Rules of Biology?

Why are men usually taller than women?

A recent study, analyzing genetic data from nearly a million individuals, sheds light on why men are typically taller than women. Researchers focused on the SHOX gene, located on both X and Y chromosomes, and its role in height determination.

While scientists have long suspected that genetics contribute to these differences, the biological mechanisms behind this sexual dimorphism independent of hormones remained unclear, until a team of researchers from the U.S. shed some light onto it with their study published in PNAS.

The team analyzed a large-scale dataset with 928,605 adult participants, including 1,225 adults with sex chromosome aneuploidies (SCAs)—genetic conditions where individuals have an abnormal number of X or Y chromosomes, either extra or missing.

They found that having an extra Y chromosome led to a greater increase in height compared to an additional X chromosome, regardless of the influence of male hormones.

The sex chromosomes X and Y are non-homologous, meaning they do not share many gene sequences or structures, but both contain a gene called SHOX located in pseudoautosomal region 1 (PAR1), a small section where X and Y chromosomes share sequence identity and work like a regular chromosome. The SHOX gene is a key player in influencing height.

In human females, most of the X chromosome is inactivated, except for PAR1, which escapes X-inactivation, and both human males and females typically have two active copies of PAR1 genes.

Research indicated that the SHOX and other genes in the PAR1 region have lower levels of expression in the inactive X chromosome (Xi), suggesting they are only partially protected from silencing.

This partial silencing means that males (46,XY) may have higher levels of SHOX since it is expressed in both the X and Y chromosomes, compared to females (46,XX) with two X chromosomes. This difference in gene expression is especially noticeable in musculoskeletal tissues, thus explaining sex differences in growth and height.

The findings indicated that the height contribution of the Y chromosome was larger than that of a second X chromosome, irrespective of hormonal differences.

The researchers highlight that understanding genetic underpinnings of sex dimorphisms is crucial not just for traits like height, but also for uncovering the biological mechanisms behind sex-based disparities in the occurrence of autoimmune, neuropsychiatric, and other medical conditions.

Alexander S. F. Berry et al, X and Y gene dosage effects are primary contributors to human sexual dimorphism: The case of height, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2503039122

Engineered bacteria can deliver antiviral therapies and vaccines

New research  demonstrates how specially engineered bacteria taken orally can operate as a delivery system for antiviral therapies and vaccines. The research is published in the journal Gut Microbes.

The work focuses on engineering probiotic bacteria to accomplish a wide variety of functions, from breaking down cancer's defenses to imaging and diagnosing lung infections.

A few years ago, researchers asked whether the same chassis, using the bacterium E.coli Nissle 1917, could ferry antiviral therapeutic agents or vaccine antigens directly to the gut, a major portal of viral entry. They focused on the COVID-19 virus, SARS-CoV-2, for the proof-of-concept research.

Oral delivery lets us target the mucosal surfaces where pathogens first gain a foothold while avoiding needles and cold-chain logistics.

Most engineered bacteria keep their therapeutic cargo inside the cell, but vaccines work best when antigens are presented to the immune system. The researchers therefore displayed viral proteins on the bacterial surface and harnessed outer-membrane vesicles (OMVs)—nano-sized spheres that bacteria naturally shed—to act as self-propelled delivery vehicles. Once released, OMVs traffic through the gut epithelium, enter blood circulation and distribute their payload to distant tissues.

The researchers systematically screened anchor motifs and expression cassettes to optimize antigen density on the probiotic surface. For the vaccine version, the bacteria was designed to express the spike protein found on the surface of the virus that causes COVID-19. This same spike protein is currently delivered through mRNA COVID-19 vaccines.

Current vaccines are safe and effective at providing what is called systemic immunity, as antibodies move throughout the whole body in the bloodstream. But there are gateways in the body where viruses typically enter—through mucosal lining in the gastrointestinal system, lungs and other organs—that can be targeted to provide what is called mucosal immunity.

Part 1

In preclinical animal studies, a two-dose oral regimen generated blood-borne (systemic) antibody levels comparable to intramuscular mRNA vaccination. Notably, it produced markedly higher levels of secretory immunoglobulin A (IgA) in the gut and airways—the antibodies that underlie mucosal immunity, considered critical for blocking infection at the point of entry.
While vaccines are delivered before a person is infected with a virus, antiviral therapies such as monoclonal antibodies are given as a treatment after infection.

The team developed another version of engineered E.coli Nissle 1917 to display therapeutic proteins on the surface. To create a post-exposure therapy, the team encoded anti-spike nanobodies: antibodies that are one-tenth the size of conventional monoclonal antibodies.

Although full viral-challenge studies are pending, nanobodies released from the engineered bacteria reached the bloodstream, likely facilitated by OMVs, and accumulated in lung tissue, where they neutralized SARS-CoV-2 in ex-vivo assays.
Clinical trials will validate the safety and efficacy of this delivery system for new engineered bacteria targeting other viruses.
So far the engineered bacteria have been found to be safe to use and do not generate any adverse immune response or side effects in animal models. Moreover, the parent strain of bacteria has decades of safe use as a probiotic.

Nitin S. Kamble et al, Engineered bacteria as an orally administered anti-viral treatment and immunization system, Gut Microbes (2025). DOI: 10.1080/19490976.2025.2500056

Part 2

Newfound mechanism rewires cellular energy processing for drastic weight loss

Mice genetically engineered to lack the ability to make the amino acid cysteine, and fed a cysteine-free diet, lost 30% of their body weight in just one week, a new study shows.

Published online in Nature, the work found that cysteine depletion disrupts the normal metabolic pathways used by mammalian to convert food into energy, forcing the animals to rapidly burn fat stores in a futile attempt to meet energy demands.

 The study reveals key details about how cells process fuels like carbohydrates and fats (metabolism), and how cysteine depletion affects tissues. Experiments showed that lowering cysteine levels caused a drop in levels of the small molecule called coenzyme A (CoA), which rendered inefficient mechanisms that convert carbohydrates and fats into energy.

Despite CoA being involved in more than 100 intermediate metabolic reactions and serving as a partner (cofactor) for 4% of all enzymes in the body, scientists had previously been unable to study its function directly. This is because mice with defective CoA synthesis typically do not survive beyond three weeks of age. The current findings detail, for the first time, how CoA shapes metabolism in adult mice.

The current finding does not immediately suggest a new approach to weight loss, the authors caution, as cysteine is found in nearly all foods.

Achieving a truly cysteine-free diet would require patients to consume a specially formulated solution that would be challenging for most. Moreover, because cysteine is involved in numerous cellular pathways, eliminating it—such as through a drug that inhibits cysteine production—could make organs more vulnerable to everyday toxins, including medications.

That said, the study authors say it is worth considering that fruits, vegetables, and legumes contain much lower levels of cysteine and its precursor, the sulfur-containing amino acid methionine, than red meat. While earlier studies have linked low sulfur amino acid intake to health benefits, this study clarifies that these benefits are due to cysteine depletion specifically, and not methionine restriction.

Part 1

The study is the first to examine the effects of removing cysteine, or any of the nine of the essential amino acids, which must be obtained through diet and are required for building proteins that make up most of the body's enzymes, tissues, and signaling molecules. The findings revealed that eliminating cysteine from the mammalian body led to far greater weight loss than the removal of any other essential amino acid.

Specifically, cysteine deprivation disrupted oxidative phosphorylation, the main process for producing adenosine triphosphate (ATP), the molecule that serves as cells' energy currency. Oxidative phosphorylation is known to be tightly dependent on CoA.

As a result, sugar-derived intermediate molecules (carbon skeletons) such as pyruvate, orotate, citrate, and α-ketoglutarate were no longer used efficiently, and were instead lost in the urine. In response, the body turned to stored lipids (fats) to make energy.

Further, the team found that cysteine restriction activates both the integrated stress response (ISR), a signaling network that restores cellular balance after stress, and the oxidative stress response (OSR), which is triggered by higher levels of reactive oxygen species (ROS) following depletion of glutathione, the body's primary antioxidant. ROS can oxidize (take away electrons from) and damage sensitive cell parts like DNA.

Remarkably, this simultaneous activation of ISR and OSR—previously observed only in cancer cells—was shown to occur in normal tissues in mice in the cysteine-restriction group, with the two stress responses reinforcing each other.

The study also shows that ISR and OSR, acting independently of CoA depletion, increase production of the stress hormone GDF15, which contributes to food aversion and degradation of acetyl-CoA-carboxylase, a key enzyme in lipid synthesis. This increased weight loss further in the study mice by preventing the replenishment of their fat stores.

Evgeny Nudler, Unravelling cysteine-deficiency-associated rapid weight loss, Nature (2025). DOI: 10.1038/s41586-025-08996-y. www.nature.com/articles/s41586-025-08996-y

Part 2

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How the placebo effect tricks the mind into relieving pain

The detailed mechanism of how the placebo effect reduces the perception of pain in rats has been uncovered by  neuroscientists. These findings, published in Science Advances, could potentially lead to ways to harness the placebo effect in therapy.

If you're convinced you are taking a powerful painkiller, it could well reduce your perception of pain, even if the painkiller turns out to be a sham.

That's the power of the placebo effect. The brain, tricked into anticipating a benefit, produces the benefit itself.

Harnessing the placebo effect for pain relief could help to reduce dosages of painkillers, lowering the risk of both side effects and becoming dependent on medication.

Because it's a psychological effect, the placebo effect is much easier to induce and monitor in humans than in animals. But since only relatively noninvasive techniques can be used on people, it's hard to determine what's happening on a neural-circuit level.

The researchers conditioned rats by injecting them with a painkiller over four days. The animal came to associate injections with pain relief, so that when they were injected with a saline solution, the placebo effect kicked in. Many researchers didn't think that animals could experience the placebo effect. But the researchers succeeded in inducing it in rodents by using Pavlovian conditioning.

About a third of the rats exhibited the full placebo effect, another third had a partial placebo effect, and the remaining third hardly experienced any pain relief.

The research team was then able to study what was going on in the animal brains using neuroimaging methods that are too invasive to use on people.

Several brain regions were found to activate in response to placebo in neuropathic animals. That's very similar to results in humans. 

The team found that the placebo effect occurred as a result of brain signals related to the endogenous opioid system in the medial prefrontal cortex, a region at the front of the brain, which in the presence of the placebo injections set off the descending pain inhibitory system.

They strongly suspect that the same mechanism operates in people. The mechanism is similar to how pain relief occurs in humans.

Hiroyuki Neyama et al, Opioidergic activation of the descending pain inhibitory system underlies placebo analgesia, Science Advances (2025). DOI: 10.1126/sciadv.adp8494

How a mold can unbalance the lungs

An invisible intruder puts the delicate balance in our lungs to the test: the mold Aspergillus fumigatus, harmless in nature, can become a serious danger if the immune system is weakened—and change the entire bacterial world in the lungs. But that's not all: The intestines and metabolism also appear to be affected by a lung infection.

Aspergillus fumigatus can be found almost everywhere—in soil, compost or in the air. It is usually harmless for healthy people. However, in patients with a weakened immune system, it can cause severe lung infection, known as invasive aspergillosis.

The fungus may potentially alter the oxygen levels in the lungs to a degree that it creates a more suitable environment for certain bacteria—such as Ligilactobacillus murinus, typically found in the intestines, oral cavity and lungs of mice—to better survive and potentially thrive. This interaction could possibly influence disease progression and enable new treatment strategies.

It has long been known that the gut and lungs are closely connected. New data from a research team in Jena has now deepened this understanding.

Researchers found evidence that not only the lung microbiome, but also the gut microbiome and certain metabolic products in the blood change during infection of the lungs with Aspergillus fumigatus. This so-called "gut-lung axis" could play an important role in future therapy.

A key finding of the study was that the fungal infection unbalances both the lung and gut microbiome. In the lungs, this leads to an accumulation of anaerobic bacteria. Particularly striking was the increased growth of Ligilactobacillus murinus, suggesting that the fungus creates a microaerophilic niche (low oxygen concentrations) that favors this bacterium.

Fungal infections are a serious problem, especially for immunocompromised people or those who are already seriously ill—for example in intensive care units or with cancer. The new findings provide important information on how such infections can be better understood and possibly prevented.

In the future, it may be possible to specifically influence the microbiome in order to support the body in its fight against the fungus—or to develop new drugs that target precisely this area.

Liubov Nikitashina et al, The murine lung microbiome is disbalanced by the human-pathogenic fungus Aspergillus fumigatus resulting in enrichment of anaerobic bacteria, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.115442

Lethal mutations cause 1 in 136 in pregnancy losses, study estimates

In a study published in Nature recently "Sequence diversity lost in early pregnancy," scientists from deCODE genetics, estimate that around one in 136 pregnancies are lost due to new mutations in the fetus. In other words, millions of pregnancies worldwide are lost because of mutations every year.

The human genome varies between individuals, but there are some locations in the genome where there seems to be little or no sequence variation between individuals. This raises the question of whether the sequences at these locations are essential for human development.

It is known that mutations in essential genomic sequences are major contributors to neurodevelopmental disorders. The question remains, do they also contribute to pregnancy loss? As part of a Nordic collaboration, scientists from deCODE genetics sought to answer these questions by sequencing 467 samples from pregnancy losses from a prospective study. Interestingly, by comparing the genomes of the fetuses from pregnancy losses to their parents, the scientists found that the fetuses harbored a similar number of new mutations as adults. Despite the similar numbers, they discovered that the main difference between the lost fetuses and adults was that the mutations in the fetuses occurred in essential genomic sequences. Moreover, they managed to pinpoint when, in the development of the fetus, some of the mutations occurred.

In addition to mapping new mutations in the lost fetuses, they also showed that some couples are at a higher risk of pregnancy loss due to genetic compatibility issues. You inherit one copy of a gene from each parent, and most of the time, you are fine with one defective copy, but problems can arise if you inherit a defective copy from both parents.

Along with recombination, the continuous generation of mutations enables us to evolve as a species. However, this continuous influx of new mutations comes at the expense of rare diseases. This study demonstrates the contribution of mutations to pregnancy loss and sheds new light on conserved sequences in the human genome.

Gudny A. Arnadottir et al, Sequence diversity lost in early pregnancy, Nature (2025). DOI: 10.1038/s41586-025-09031-w

Small molecules in plant-based foods may reduce efficacy of anti-cancer drugs

A Cancer Research study has uncovered a surprising link between diet, intestinal microbes and the efficacy of cancer therapy.

The study could help explain why drugs known as PI3 kinase (PI3K) inhibitors—which disrupt an abnormally activated biochemical signaling pathway that spurs cancer cell proliferation—haven't led to consistent, durable cancer control in patients with solid tumors.

Many cancer x drugs don't work equally well for all patients, and one emerging possibility is that diet plays a role in this variability.

This study showed that diet can indeed alter cancer treatment outcomes in preclinical models and can do so in an unexpected way, unrelated to its immediate nutritional effects. It turns out that certain small molecules in plant-based foods are transformed in mice by commensal gut bacteria into compounds that activate the liver to clear PI3K inhibitors more quickly, lowering the efficacy of the drug.

The liver enzymes involved in clearing these drugs break down many others as well. This suggests these findings could be of relevance to multiple classes of drugs used to treat cancer and other diseases.

Asael Roichman et al, Microbiome metabolism of dietary phytochemicals controls the anticancer activity of PI3K inhibitors, Cell (2025). DOI: 10.1016/j.cell.2025.04.041

Rather, experiments revealed that the key determinant was the molecular complexity of the diet—whether it was made of "whole foods" versus highly processed ones.

The ketogenic food consumed by mice in preclinical studies is a highly processed formulation lacking the complex mix of plant-derived chemicals (phytochemicals), especially from legumes and soy, that are present in standard chow. It turned out that gut microbes break down phytochemicals, namely soyasaponins derived from soybeans, into molecules that induce the expression of a detoxifying liver enzyme, cytochrome P450.

Experiments revealed that elevated production of these hepatic enzymes in the chow-fed mice led to rapid clearance of PI3K inhibitors, reducing the anti-cancer efficacy of the regimen. In line with these findings, the researchers demonstrated that a high-carbohydrate but low-phytochemical diet—as well as antibiotics that suppressed the gut microbiome—enhanced PI3K inhibitor activity in the mice.

Part 2

Infrared contact lenses allow people to see in the dark, even with their eyes closed

Neuroscientists and materials scientists have created contact lenses that enable infrared vision in both humans and mice by converting infrared light into visible light. Unlike infrared night vision goggles, the contact lenses, described in the journal Cell, do not require a power source—and they enable the wearer to perceive multiple infrared wavelengths. Because they're transparent, users can see both infrared and visible light simultaneously, though infrared vision was enhanced when participants had their eyes closed.

The contact lens technology uses nanoparticles that absorb infrared light and convert it into wavelengths that are visible to mammalian eyes (e.g., electromagnetic radiation in the 400–700 nm range). The nanoparticles specifically enable the detection of "near-infrared light," which is infrared light in the 800–1600 nm range, just beyond what humans can already see.

To create the contact lenses, the team combined the nanoparticles with flexible, nontoxic polymers that are used in standard soft contact lenses. After showing that the contact lenses were nontoxic, they tested their function in both humans and mice.

They found that contact lens-wearing mice displayed behaviors suggesting that they could see infrared wavelengths. For example, when the mice were given the choice of a dark box and an infrared-illuminated box, contact-wearing mice chose the dark box whereas contact-less mice showed no preference.

The mice also showed physiological signals of infrared vision: the pupils of contact-wearing mice constricted in the presence of infrared light, and brain imaging revealed that infrared light caused their visual processing centers to light up.

In humans, the infrared contact lenses enabled participants to accurately detect flashing Morse code-like signals and to perceive the direction of incoming infrared light.

It's totally clear-cut: without the contact lenses, the subject cannot see anything, but when they put them on, they can clearly see the flickering of the infrared light.

The researchers also found that when the subject closes their eyes, they're even better able to receive this flickering information, because near-infrared light penetrates the eyelid more effectively than visible light, so there is less interference from visible light.

Near-Infrared Spatiotemporal Color Vision in Humans Enabled by Upconversion Contact Lenses, Cell (2025). DOI: 10.1016/j.cell.2025.04.019. www.cell.com/cell/fulltext/S0092-8674(25)00454-4

Ancient DNA used to map evolution of fever-causing bacteria

Researchers  have analyzed ancient DNA from Borrelia recurrentis, a type of bacteria that causes relapsing fever, pinpointing when it evolved to spread through lice rather than ticks, and how it gained and lost genes in the process.

This transition may have coincided with changes in human lifestyles, like living closer together and the beginning of the wool trade.

B. recurrentis bacteria cause relapsing fever, an illness with many recurring episodes of fever, which is typically found today in areas with poor sanitation or overcrowding, such as refugee camps. It is a distant cousin of the bacteria that today cause Lyme disease.

Only three known species of bacteria, including B. recurrentis, have transitioned from being carried primarily by ticks to lice, changing the potential severity of the disease. Until now, it was unknown when B. recurrentis made the jump from ticks to lice and what impact this had on disease transmission and severity in humans.

In research published in Science, the scientists sequenced the whole genome from four samples of B. recurrentis. Ranging from 2,300 to 600 years ago, their samples include the oldest B. recurrentis genome to date. These ancient samples were obtained from the skeletons of people who were infected hundreds of years ago. The DNA is a shadow of the bacteria that once circulated in their blood and has been captured in bones and teeth.

The individuals' teeth contained traces of B. recurrentis DNA. Two samples had relatively high amounts of the pathogen, suggesting these individuals may have died from a severe, acute infection, or that the DNA was particularly well preserved.

The researchers looked at differences in the ancient genomes and modern-day B. recurrentis to map how the bacteria have changed over time, finding that the species likely diverged from its nearest tick-borne cousin, B. duttonii, about 6,000 to 4,000 years ago.

They compared the B. recurrentis genomes with B. duttonii, finding that much of the genome was lost during the tick-to-louse transition but that new genes were also gained over time. These genetic changes affected the bacteria's ability to hide from the immune system and also share DNA with neighboring bacteria, suggesting B. recurrentis had specialized to survive within the human louse.
Part 1

Based on these ancient and modern genomes, the divergence from the bacteria's tick-borne ancestor happened during the transition from the Neolithic period to the Early Bronze Age. This was a time of change in human lifestyles, as people began to domesticate animals and live in more dense settlements. This may have helped B. recurrentis spread from person to person more easily.
The researchers also raise the possibility that the development of sheep farming for wool at this time may have given an advantage to louse-borne pathogens, as wool has better conditions for lice to lay eggs.
They conclude that the evolution of B. recurrentis highlights that a combination of genetic and environmental changes can help pathogens spread and infect populations more easily.

Ancient Borrelia genomes document the evolutionary history of louse-borne relapsing fever., Science (2025). DOI: 10.1126/science.adr2147

Part 2

Climate change may make it harder to reduce smog in some regions

Global warming will likely hinder our future ability to control ground-level ozone, a harmful air pollutant that is a primary component of smog, according to a new  study.

The results could help scientists and policymakers develop more effective strategies for improving both air quality and human health. Ground-level ozone causes a host of detrimental health impacts, from asthma to heart disease, and contributes to thousands of premature deaths each year.

The researchers' modeling approach reveals that, as the Earth warms due to climate change, ground-level ozone will become less sensitive to reductions in nitrogen oxide emissions in eastern North America and Western Europe. In other words, it will take greater nitrogen oxide emission reductions to get the same air quality benefits.

The researchers found that eastern North America and Western Europe are especially sensitive to increases in nitrogen oxide emissions from the soil, which are natural emissions driven by increases in temperature.

Due to that sensitivity, as the Earth warms and more nitrogen oxide from soil enters the atmosphere, reducing nitrogen oxide emissions from human activities will have less of an impact on ground-level ozone.

However, the study also shows that the opposite would be true in northeast Asia, where cutting emissions would have a greater impact on reducing ground-level ozone in the future.

The researchers combined a climate model that simulates meteorological factors, such as temperature and wind speeds, with a chemical transport model that estimates the movement and composition of chemicals in the atmosphere.

By generating a range of possible future outcomes, the researchers' ensemble approach better captures inherent climate variability, allowing them to paint a fuller picture than many previous studies.

Future air quality planning should consider how climate change affects the chemistry of air pollution. We may need steeper cuts in nitrogen oxide emissions to achieve the same air quality goals, say the researchers.

Emmie J. Le Roy et al, Impact of Climate Variability and Change on the Surface Ozone Response to NO_x Emissions Reductions, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c01347

Hawaiian volcanic rocks reveal Earth's core contains vast hidden gold reserves

Earth's largest gold reserves are not kept inside Fort Knox, the United States Bullion Depository. In fact, they are hidden much deeper in the ground than one would expect. More than 99.999% of Earth's stores of gold and other precious metals lie buried under 3,000 km of solid rock, locked away within Earth's metallic core and far beyond the reaches of humankind.

Now, researchers  have found traces of the precious metal ruthenium (Ru) in volcanic rocks on the islands of Hawaii that must ultimately have come from Earth's core. The findings were published in Nature.

Compared to Earth's rocky mantle, the metallic core contains a slightly higher abundance of a particular Ru isotope: 100Ru. This is because part of the Ru, which was locked in Earth's core together with gold and other precious metals when it formed 4.5 billion years ago, came from a different source than the scarce amount of Ru that is contained in the mantle today. These differences in 100Ru are so tiny that it was impossible to detect them in the past.

Now, new procedures developed by researchers  make it possible to resolve them. The unusually high 100Ru signal they found in lavas on Earth's surface can only mean that these rocks ultimately originated from the core-mantle boundary.

New  data confirmed that material from the core, including gold and other precious metals, is leaking into Earth's mantle above. 

This means that at least some of the precarious supplies of gold and other precious metals that we rely on for their value and importance in so many sectors such as renewable energy, may have come from Earth's core.

Nils Messling et al, Ru and W isotope systematics in ocean island basalts reveals core leakage, Nature (2025). DOI: 10.1038/s41586-025-09003-0

Ammonia made from air, water and sunlight: Catalysts mimic photosynthesis for cleaner production

Ammonia is a chemical essential to many agricultural and industrial processes, but its mode of production comes with an incredibly high energy cost. Various attempts have, and are, being made to produce ammonia more efficiently.

For the first time, a group including researchers from the University of Tokyo combined atmospheric nitrogen, water and sunlight, and, using two catalysts, produced sizable quantities of ammonia without a high energy cost. Their processes mirror natural processes found in plants utilizing symbiotic bacteria.

The work has been published in Nature Communications

They succeeded in developing a novel catalytic system for producing ammonia from abundant molecules found on Earth, including atmospheric nitrogen and water. The key lies in a combination of two kinds of catalysts, intermediate compounds which enable or speed up reactions without contributing to the final mixture, made especially for ammonia production, and which are driven by sunlight.

Yasuomi Yamazaki et al, Catalytic ammonia formation from dinitrogen, water, and visible light energy, Nature Communications (2025). DOI: 10.1038/s41467-025-59727-w

Microplastics are 'silently spreading from soil to salad to humans'

According to a new  review work agricultural soils now hold around 23 times more microplastics than oceans. Among the revelations in the comprehensive evaluation is that plastics in soil may be exposed to up to 10,000 chemical additives, most of which are unregulated in agriculture.

These microplastics are turning food-producing land into a plastic sink.

Both microplastics and nanoplastics have now been found in lettuce, wheat and carrot crops. This happens through various means, from plastic mulching, fertilizers and even through being dropped by clouds.

This is particularly concerning when combined with findings of these plastics in the human lungs, brain, heart, blood, and even placenta.

And BPA-free does not equal risk-free. Replacement chemicals like BPF and BPS show comparable or greater endocrine-disrupting activity. 

The challenge is that regulations are slower than science, and industry is faster than both.

In addition to this, assessing additive toxicity is often overlooked  due to the lack of transparency in the plastic industry and the large number of additives produced.

 This makes the plastic crisis unchecked, and human health exposed.

Alongside endocrine disruptors, the review pinpointed other additives in soil such as phthalates (linked to reproductive issues), and PBDEs (neurotoxic flame retardants).

These additives have been linked with neurodegenerative disease, increased risks of stroke and heart attack and early death.

These are not distant possibilities—they are unfolding within biological systems—silently and systematically, say the reviewers. 

This review highlights the urgent need for coordinated scientific and regulatory efforts.

 Joseph Boctor et al, Microplastics and nanoplastics: fate, transport, and governance from agricultural soil to food webs and humans, Environmental Sciences Europe (2025). DOI: 10.1186/s12302-025-01104-x

A soil predator’s death is boosting drug resistance, without antibiotics

Skin bacteria protect us from sun damage

Some People think that the bacteria on our skin is bad. Body odor is largely caused by bacteria on your skin interacting with sweat. While sweat itself is odorless, the bacteria that live on your skin metabolize the sweat and produce the smells we perceive as body odor.

While most bacteria are harmless, some can be pathogenic and cause infections when they enter the body.

A balanced skin microbiome is important for healthy skin, and it can be disrupted by factors like harsh skincare products or environmental pollution, leading to issues like dryness, redness, or breakouts.

Bacteria on our skin could have a protective effect against a type of ultraviolet (UV) radiation in sunlight. When UV-B radiation hits our skin, it converts a molecule called trans-urocanic acid into another form: cis-urocanic acid. This form dampens the activity of immune cells in our skin’s outer layer, which can leave it more vulnerable to infections or cancer-causing mutations. Researchers found that bacteria such as Staphylococcus epidermidis in the human skin microbiome can break down cis-urocanic acid, which curbs the molecule’s immunosuppressive effects.

https://www.jidonline.org/article/S0022-202X(25)00405-1/fulltext

Skin fungus keeps bacteria at bay with acid

Malassezia sympodialis — a fungus found in our skin microbiome — produces a type of fatty acid that keeps Staphylococcus aureus bacteria at bay. S. aureus is a normal resident of our skin microbiome, but it can cause dangerous infections if it isn’t kept in check. Researchers found that the fungus-produced molecule, called 10-HP, isn’t toxic to bacteria under normal lab conditions, but has antibacterial properties in a more acidic environment such as the surface of healthy skin.

https://www.cell.com/current-biology/abstract/S0960-9822(25)00371-9?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0960982225003719%3Fshowall%3Dtrue

Science Alert 

AI linked to boom in suspect health papers
Analysis flags hundreds of studies that seem to follow a template, reporting correlations between complex health conditions and single variables based on publicly available data sets.
A flood of papers making misleading health claims is probably the product of artificial intelligence tools scraping openly available data. In an analysis of papers that used data from the US National Health and Nutrition Examination Survey, researchers spotted over 300 papers that linked one variable, such as vitamin D levels or sleep quality, with a complex disorder, such as depression or heart disease, ignoring the fact that these conditions have many contributing factors. The papers were “extremely formulaic”, says biomedical scientist and study co-author Matt Spick, and “could easily have been generated by large language models”.

The scientific literature is at risk of becoming flooded with papers that make misleading health claims based on openly available data that are easy to process using artificial intelligence (AI) tools, researchers have warned.

In a study published in PLoS Biology recently, scientists analysed more than 300 papers that used data from the US National Health and Nutrition Examination Survey (NHANES), an open data set of health records. The papers all seemed to follow a similar template, associating one variable — for example, vitamin D levels or sleep quality — with a complex disorder such as depression or heart disease, ignoring the fact that these conditions have many contributing factors.

They  found that the associations in many of the papers did not hold up to statistical scrutiny, and that some studies seemed to have cherry-picked data.

And Youtubers and Tic-Tokers are using this data to make silly claims!

https://journals.plos.org/plosbiology/article?id=10.1371/journal.pb...

Vitamin D supplements help slow telomere shortening linked to biological aging

Results from the VITAL randomized controlled trial reveal that vitamin D supplementation helps maintain telomeres, protective caps at the ends of chromosomes that shorten during aging and are linked to the development of certain diseases.

The new report, published in The American Journal of Clinical Nutrition, is based on data from a VITAL sub-study by researchers  and supports a promising role in slowing a pathway for biological aging.

VITAL is the first large-scale and long-term randomized trial to show that vitamin D supplements protect telomeres and preserve telomere length.

This is of particular interest because VITAL had also shown the benefits of vitamin D in reducing inflammation and lowering risks of selected chronic diseases of aging, such as advanced cancer and autoimmune disease.

Telomeres are made of repeating sequences of DNA, or base pairs, that prevent chromosome ends from degrading or fusing with other chromosomes. Telomere shortening is a natural part of aging and is associated with an increased risk of various age-related diseases.

A few short-term, small-scale studies have suggested that vitamin D or omega-3 fatty acid supplementation may help support telomeres, but results have been inconsistent. VITAL is a randomized, double-blind, placebo-controlled trial of vitamin D3 (2,000 IU/day) and omega-3 fatty acid (1 g/day) supplementation that tracked U.S. females aged 55 years and older and males aged 50 years and older for five years. The VITAL Telomere sub-study included 1,054 of these participants, whose telomere length in white blood cells was assessed at baseline and at Year 2 and Year 4.

Compared with taking placebo, taking vitamin D3 supplements significantly reduced telomere shortening over four years, preventing the equivalent of nearly three years of aging compared with placebo. Omega-3 fatty acid supplementation had no significant effect on telomere length throughout follow-up.

 Vitamin D3 and Marine Omega-3 Fatty Acids Supplementation and Leukocyte Telomere Length: 4-Year Findings from the VITAL Randomized Controlled Trial, American Journal of Clinical Nutrition (2025). DOI: 10.1016/j.ajcnut.2025.05.003
ajcn.nutrition.org/article/S00 … (25)00255-2/fulltext

**

Environmental SOS: Rare birds crunch from bellies full of plastic

Birds on a remote Australian island are so full of plastic they crunch, British researchers report.

They found plastic in the bellies of chicks less than 3 months old and a dead bird with 778 individual pieces of plastic packed into its tummy "like a brick," according to ecologist Alex Bond, principal curator at Britain's National History Museum.

"This isn't microplastics," he told The Washington Post. "We're talking items up to and including the size of bottle caps and tetra pack lids, cutlery, clothes pegs, the takeaway soy sauce fish bottle that you get from restaurants."

A major 2023 study reported that mankind had filled the world's oceans with more than 170 trillion pieces of plastic, creating a "plastic smog" that doubles roughly every six years.

The team suspects the birds fish pieces of plastic from the ocean and feed them to their chicks, according to The Post.

Researchers combed the shores for dead birds and examined their stomach contents. They also flushed the tummies of live birds with water. In some, as much as a fifth of their total weight—up to 2 ounces—was plastic.

This is because a chemical signal emitted by the plastic causes adult birds to mistake it for food while fishing in the Tasman Sea.

The plastic in the bird  belly makes a "crunching sound" that can be heard by pressing the bird.

The bellies of some have "laminated into solid, compact bricks—likely due to their oily marine diet".

The plastic affects "nearly every organ system" of the birds, he said, especially the brain. Birds less than 6 months old exhibit signs of brain damage similar to those of dementia.

The plastic crisis is accelerating—and demanding more from all of us.

"Oh, please do something about it, the world is sending an SOS, Homo sapiens!"

Source: News Agencies

What would we see at the speed of light?

What does the speed of light look like on earth?

New high-resolution laser device reads millimeter-scale text from a mile away

According to the study published in Physical Review Letters, the developed setup includes multiple laser emitters that enable super-resolution imaging of targets as small as millimeters in scale from a 1.36 kilometers (0.85 miles) distance in an outdoor urban environment. The device successfully images letter-shaped physical targets measuring 8×9 mm, with letter widths of 1.5 mm, placed at the far end of its imaging range.

Interferometry is a widely used imaging technique in astronomy which works by merging light from different sources to create an interference pattern. These interference patterns are formed when light waves interact to either reinforce or cancel each other depending on their phase differences. These patterns carry detailed information about the object or phenomenon being studied.
Intensity interferometry, on the other hand, does not rely on combining light amplitudes or maintaining phase information but on light from a single source being measured separately by two detectors or telescopes, and the variations in their recorded intensities are compared.

Studying intensity fluctuations, correlations and their changes with the distance between the detectors can help extract spatial details about the object being studied.

What makes intensity interferometry stand out? It can cut through atmospheric turbulence and ignore flaws in telescope optics—making it ideal for long-distance, high-resolution imaging. Yet, its applications have mostly been limited to observing bright stars or objects that can be lit up with nearby light sources.

Part 1

Scientists have attempted to expand its scope to active imaging applications such as light detection and ranging or LiDAR, but the lack of suitable thermal light sources and robust image reconstruction algorithms make the process challenging.

To overcome these issues, the researchers created an intensity interferometer setup with pseudothermal illumination achieved by superimposing light from 8-phase-independent multiple laser emitters. This setup included two telescopes and an infrared laser system on a shared optical bench.

The laser system produced thermal illumination, and reconstructed sparse, noisy data being collected into a high-resolution image with the help of a computational algorithm.

To test the super-resolution capabilities of the device, the letters "USTC" were crafted out of hollowed-out blackened aluminum sheets which were then covered in retroreflective sheets and used as a complex imaging target positioned over a kilometer away.
Using the designed active intensity interferometer, the researchers successfully demonstrated super-resolution imaging of millimeter-scale targets at a distance of 1.36 km in an outdoor urban environment. The imaging system achieved a resolution of 3 mm, which is 14 times higher than the diffraction limit of a single telescope, typically around 42.5 mm.

Once scaled for use beyond the laboratory, this device could significantly accelerate advancements in long-range, high-resolution remote sensing, surveillance, and non-invasive imaging in challenging environments.

Lu-Chuan Liu et al, Active Optical Intensity Interferometry, Physical Review Letters (2025). DOI: 10.1103/PhysRevLett.134.180201

Part 2

Silent X chromosome awakens with age: New explanation for sex differences in age-related diseases

Women age differently from men when it comes to health—particularly in conditions like cardiovascular disease and neurodegenerative disorders such as dementia and Parkinson's.

A research team proposed a new explanation for this. In aging female mice, genes on the previously silenced second X chromosome become active again. This mechanism might also influence women's health later in life. The study is published in the journal Nature Aging.

Unlike men, who carry one X and one Y chromosome, women have two X chromosomes in each cell. However, one of the two X chromosomes is effectively silenced. It folds into a compact structure known as the Barr body and can no longer be read. Without this mechanism, the genes on the X chromosome would be read twice as often in women as in men.

Scientists have known for some time that some genes can escape inactivation in the Barr body, resulting in higher gene activity in women. These genes are suspected to influence disease.

Researchers have now shown for the first time that with increasing age, more and more genes escape the inactivation of the Barr body.

The researchers examined the major organs of mice at different stages of life. In the older animals, the proportion of genes that had escaped was on average twice as high as in adult animals—6% instead of 3% of the genes on the X chromosome. In some organs, the numbers were even higher: in the kidneys, for instance, nearly 9%.

With aging, epigenetic processes gradually loosen the tightly packed structure of the inactive X chromosome. This mainly happens at the ends of the chromosome, allowing for genes located in those regions to be read again.

Many of the genes that become active again with age are associated with disease. These new  findings are based on mice, but since the X chromosome is very similar in humans,  the same may happen in aging women. 

According to the researchers, this doubled gene activity could have positive effects in some cases and negative effects in others.

ACE2, for example—a gene that escapes in the lungs with age—can help limit pulmonary fibrosis. Increased activity of the gene TLR8 in old age, however, may play a role in autoimmune diseases such as late-onset lupus.

Sex differences in age-related disease are incredibly complex.

So far, scientific explanations have mostly focused on hormonal or lifestyle factors. While the role of the X chromosome and some escape genes have been studied before, the discovery that many genes on the inactive X can reactivate with age opens up entirely new lines of research.

Sarah Hoelzl et al, Aging promotes reactivation of the Barr body at distal chromosome regions, Nature Aging (2025). DOI: 10.1038/s43587-025-00856-8

Trees May Be Able to Warn Us When a Volcano Is About to Erupt

The science of predicting volcanic eruptions can genuinely save lives – potentially, a lot of lives – and researchers have shown that tree leaf colors can act as warning signals around a volcano that's about to blow. As volcanoes get more active and closer to an eruption, they push magma up closer to the surface, releasing higher levels of carbon dioxide. That in turn can boost the health of the surrounding trees, making leaves greener. And those changes – specifically in the measurement known as the normalized difference vegetation index (NDVI) – can be spotted by satellites in space. We could be looking at an early warning system for eruptions that doesn't require any local field work or ground sensors, so it could work in remote and difficult-to-access areas.

https://www.sciencedirect.com/science/article/abs/pii/S003442572400...

Size matters when it comes to antibiotics. Obese patients may need customized doses of certain drugs

Obesity can have a distinct impact on the absorption, effectiveness and excretion of antibiotics, medications that have been in use for more than 80 years, but only now have consensus guidelines been proposed on prescribing the drugs for patients with substantial fat mass.

The new research arrives amid two major global health crises: In 2022, the World Health Organization declared that 43% of the global adult population is overweight, and an estimated 16% of adults are considered obese, some severely so. Also, in recent years, the WHO has stressed the need for more efficient use of antibiotics to preserve their usefulness as drug-resistant superbugs become an increasingly lethal threat.

Now, an international team of medical investigators reports that obesity can interfere with antibiotics, resulting in too much or too little drug exposure to treat infections. And because dosages that effectively work in normal weight individuals don't seem to treat the obese, the research team has developed obesity-specific antibiotic dosing guidelines for certain classes of the drugs.

Writing in The Lancet Infectious Diseases, the team describes its research as an in-depth systematic review of the medical literature on dosing and antibiotics. Conclusions drawn from the research created the framework for the guidelines.

Obesity can alter antibiotic pharmacokinetics due to physiological changes, such as body composition and organ dysfunction that result in increased or decreased drug exposures in plasma or at the site of infection, say the researchers.

Researchers used the standard definition of obesity, a BMI of 30 or higher, and underscored that "substantial changes can occur in the volume of [systemic antibiotic] distribution due to increased fat and muscle mass." In other words, obesity can alter how antibiotics are absorbed, distributed and excreted from the body.

The team began its systematic investigation with a review of 6,113 studies on obesity and antibiotic dosing. After eliminating duplicate studies, the team narrowed that number to 128 studies from which conclusions in the study were drawn.

A pictorial chart in the study illustrated problems facing the obese when it comes to taking antibiotics: increased fat mass, impaired kidney and/or liver function. Of special concern in the liver is the dysfunction of cytochrome P450, the group of enzymes responsible for metabolizing drugs.

Part 1

The researchers studied a number of antibiotic classes and how body weight affects the drugs' metabolism. Drug classes analyzed in the study included β-lactams, aminoglycosides, glycopeptides, lipoglycopeptides, and quinolones, among others. Yet, not all antibiotics require special guidelines for the obese.
Obesity modestly alters the pharmacokinetics of β-lactam antibiotics, so evidence does not support routine dose adjustments [because of body weight].
For aminoglycosides and glycopeptides, the impact of obesity on pharmacokinetics is evident and weight-based dosing is recommended.
β-lactam antibiotics include such widely prescribed drugs as the penicillins, cephalosporins, carbapenems and monobactams. They are chemically characterized by a β-lactam ring in their chemical structure. The drugs are used against a wide range of bacterial infections, including Gram-positive and Gram-negative species. But there's no need to treat obese patients differently when it comes to β-lactam medications.

Doctors, meanwhile, frequently turn to aminoglycosides to treat extremely serious infections, especially those caused by Gram-negative bacteria. Aminoglycosides include such medications as gentamicin, streptomycin, and neomycin. These drugs work by disrupting critical protein production activity inside the bacterial cell. The drugs enter bacteria and bind to the 30S ribosomal subunit, resulting in flawed protein synthesis and death of the pathogens.

Guidelines were recommended for the use of this class in the obese as well as for glycopeptide antibiotics, which include the highly potent cell-wall-disrupting drug vancomycin.
Maintenance doses [of vancomycin] should be individualized and guided by therapeutic drug monitoring to increase the probability of achieving therapeutic yet non-toxic drug exposures, the researchers say.
The team did not provide a guideline based on total body weight for the quinolones, the drug class that includes the fluoroquinolones. However, the team's recommendations stressed special consideration for administering fluoroquinolones.
Higher or more frequent dosing resulting in higher systemic exposure should be considered for patients with obesity and severe deep-seated infections to reach adequate tissue concentration," the team asserted.

Data were sparse for other antibiotic classes and will require additional study, according to findings from the research.
When making decisions on dosing in obesity, the severity of illness, site of infection, susceptibility of the pathogen, and potential toxicity of the antibiotics should be considered, they concluded.

Anne-Grete Märtson et al, The pharmacokinetics of antibiotics in patients with obesity: a systematic review and consensus guidelines for dose adjustments, The Lancet Infectious Diseases (2025). DOI: 10.1016/S1473-3099(25)00155-0

Part 2

Humans are seasonal creatures, according to our circadian rhythms

It's natural to think that, with our fancy electric lights and indoor bedrooms, humanity has evolved beyond the natural influence of sunlight when it comes to our sleep routines.

But new research  shows that our circadian rhythms are still wild at heart, tracking the seasonal changes in daylight. Humans really are seasonal, even though we might not want to admit that in our modern context. 

Day length, the amount of sunlight we get,  really influences our physiology. The study shows that our biologically hardwired seasonal timing affects how we adjust to changes in our daily schedules.

This finding could enable new ways to probe and understand seasonal affective disorder, a type of depression that's connected to seasonal changes. It could also open new areas of inquiry in a range of other health issues that are connected to the alignment of our sleep schedules and circadian clocks.

Researchers have previously shown that our moods are strongly affected by how well our sleep schedules align with our circadian rhythms. 

This work may have deeper implications for mental health issues, like mood and anxiety, but also metabolic and cardiovascular conditions as well.

The research also showed there is a genetic component of this seasonality in humans, which could help explain the vast differences in how strongly individuals are affected by changes in day length.

For some people they might be able to adapt better, but for other people it could be a whole lot worse.

Exploring this genetic component will help researchers and doctors understand where individuals fall on that spectrum, but getting to that point will take more time and effort. For now, this study is an early but important step that reframes how we conceive of human circadian rhythms.

A lot of people tend to think of their circadian rhythms as a single clock. What  the researchers are showing is that there's not really one clock, but there are two. One is trying to track dawn and the other is trying to track dusk, and they're talking to each other.

The fact that circadian rhythms  in people exhibited a seasonal dependence is a compelling argument for just how hardwired this feature is in humans, which isn't altogether surprising, the researchers say.

Seasonal timing and interindividual differences in shiftwork adaptation, npj Digital Medicine (2025). DOI: 10.1038/s41746-025-01678-z

Filtered car emissions still turn toxic after sunlight exposure, study reveals

A new international study reveals that emissions from modern gasoline cars—despite meeting the currently strictest European emission standards EURO 6d—can become significantly more harmful after being released into the atmosphere. The findings, published in Science Advances, challenge the assumption that filtered exhaust from EURO 6d-compliant vehicles is inherently safe.

The research focused on a gasoline vehicle equipped with a gasoline particulate filter (GPF), designed to drastically reduce primary particulate emissions. Freshly emitted exhaust showed no detectable cytotoxic effects on human lung cells. However, once the exhaust underwent "photochemical aging"—a natural transformation process driven by sunlight and atmospheric oxidants—it became substantially more toxic.

The aged emissions caused notable DNA damage and oxidative stress in both cancerous alveolar and normal bronchial epithelial cells. This toxicity was not only associated with newly formed particles, known as secondary organic and inorganic aerosols (SOA and SIA), but also with oxygenated volatile compounds, such as carbonyls, generated during their residence in the atmosphere.

 These findings point to a critical shortfall in current vehicle emissions testing and regulation.

While EURO 6d standards ensure low emissions at the tailpipe, they do not account for the chemical transformations those emissions undergo once released into the environment.

This new study shows that we are missing a big part of the picture by not considering how exhaust gases change—and become more harmful—after they leave the car.

The results have important implications for how air quality standards are set and monitored. Current regulations focus primarily on the emissions measured directly after combustion, without factoring in how these emissions interact with sunlight and atmospheric chemicals to form new, more harmful pollutants.

Mathilde N. Delaval et al, The efficiency of EURO 6d car particulate filters is compromised by atmospheric aging: In vitro toxicity of gasoline car exhaust, Science Advances (2025). DOI: 10.1126/sciadv.adq2348

Science behind the surge in northern lights

If you feel like you've seen more of the northern lights painting the night sky lately, you'd be right. 

We're currently in a period of solar maximum, which is good news for aurora borealis enthusiasts. If you want to watch beautiful shows of the dancing northern lights, solar max is an ideal time to do that, say the experts.

The sun operates on a roughly 11-year cycle of magnetic activity. 

As the sun's magnetic field flips its north and south poles over this time, it switches between periods of lower magnetic activity (solar minimum) and periods of higher magnetic activity (solar maximum).

Surrounding the north and south magnetic poles of Earth are regions referred to as the "auroral ovals"—areas where aurora displays typically happen. During periods of solar max, these zones tend to expand a bit closer towards the equator, moving into areas where more people live.

There's more energy available, so they're more powerful, but they also move so they're at locations where they're more visible. 

Before any colors appear in the night skies over Earth, things need to turn explosive—literally—on the sun. The sun's surface is permeated by bundles of strong magnetic fields which poke out into the solar atmosphere. The ends of such magnetic loops represent cooler regions of the solar surface called sunspots. 

Loops can be stable for days and then suddenly they'll explode and launch a whole mass of charged particles into space—that's called a coronal mass ejection. It's basically a rapid release of the energy in these magnetic loops, but in the form of charged particles, which get a lot of kinetic energy and exceed the escape velocity of the sun's gravity field, blasting outwards into the solar system. 

Part 1

Earth's magnetic field typically deflects the majority of these blasts of charged particles, but during periods of intense activity, some manage to get through. Merging of the magnetic fields in the solar wind, arriving from the sun as a result of the expansion of its atmosphere into space, with the magnetic fields of Earth inject energy into near-Earth space and power space weather and the dancing northern (and southern) lights.

In order to generate the aurora, accelerated particles, mostly electrons, rain down towards Earth and then collide with atoms and molecules in the upper atmosphere, between 100 and 250 kilometers above Earth's surface. In the period after these collisions, when the particles drop back down into a lower-energy state, "they spit out a photon of light."
You have these energy conversion processes occurring at the solar surface, but then you also have something similar occurring in Earth's magnetic field. That's ultimately the origin of the energy for accelerating the charged particles that rain into Earth's atmosphere and cause this sort of glowing effect.
The palette of brilliant colors we see from the ground is a result of different gases involved in the collisions. Green, by far the most common hue, comes from particles colliding with oxygen atoms. Higher-energy collisions involving oxygen can have a red hue, and nitrogen is the gas responsible for blue and purple-tinted displays.
Part 2

**

Intestinal bacteria influence aging of blood vessels

The aging of the innermost cell layer of blood vessels leads to cardiovascular diseases. Researchers at UZH have now shown for the first time that intestinal bacteria and their metabolites contribute directly to vascular aging.

As people age, the bacterial composition in their gut changes, resulting in fewer "rejuvenating" and more harmful substances in the body.

Cardiovascular diseases are the most common cause of death worldwide. Even if known traditional risk factors such as diabetes or high blood pressure are treated, the disease worsens in half of all cases, especially in older patients.

In a study published in Nature Aging, researchers at UZH have now shown for the first time that intestinal bacteria and their metabolites can accelerate the aging of blood vessels and trigger cardiovascular disease.

The human body consists of around 30 to 100 trillion bacteria that reside in our organs. Ninety percent of these bacteria live in the intestine, processing the food we eat into metabolic products, which in turn affect our bodies.

Half of these substances have not yet been recognized. 

Using data from more than 7,000 healthy individuals aged between 18 and 95 as well as a mouse model of chronological aging, the researchers found that the breakdown product of the amino acid phenylalanine—phenylacetic acid—accumulates with age.

In several series of experiments, researchers were able to prove that phenylacetic acid leads to senescence of endothelial cells, in which the cells that line the inside of blood vessels do not proliferate, secrete inflammatory molecules, and exhibit an aging phenotype. As a result, the vessels stiffen up and their function is impaired.

By conducting a comprehensive bioinformatic analysis of the microbiome of mice and humans, the researchers were able to identify the bacterium Clostridium sp.ASF356, which can process phenylalanine into phenylacetic acid.

When the researchers colonized young mice with this bacterium, they subsequently showed increased phenylacetic acid levels and signs of vascular aging. However, when the bacteria were eliminated with antibiotics, the concentration of phenylacetic acid in the body decreased.

However, the microbiome in the gut also produces substances that are beneficial to vascular health. Short-chain fatty acids such as acetate, which are produced by fermentation of dietary fibers and polysaccharides in the intestine, act as natural rejuvenating agents.

The research group used in-vitro experiments to show that adding sodium acetate can restore the function of aged vascular endothelial cells. When analyzing intestinal bacteria, they found that the number of bacteria that produce such rejuvenating agents decreases with age.

"The aging process of the cardiovascular system can therefore be regulated via the microbiome", say the researchers.

The researchers are also working on ways to reduce phenylacetic acid in the body through medication.

Seyed Soheil Saeedi Saravi et al, Gut microbiota-dependent increase in phenylacetic acid induces endothelial cell senescence during aging, Nature Aging (2025). DOI: 10.1038/s43587-025-00864-8

Neural circuit mechanism may explain why people have different fear levels

In a study published in Neuron, a research team revealed the neural circuit underlying individual differences in visual escape habituation.

Emotional responses, such as fear behaviors, are evolutionarily conserved mechanisms that enable organisms to detect and avoid danger, ensuring survival. Since Darwin's "On the Origin of Species" (1859) proposed that individual differences drive natural selection, understanding behavioral adaptation has become essential for unraveling biodiversity and survival strategies.

Repeated exposure to predators can elicit divergent coping strategies—habituation or sensitization—that are dependent on sensory inputs, internal physiological states, and prior experiences. However, the neural circuits underlying individual variability in the regulation of internal states and habituation to repeated threats remain poorly understood.

To address this question, researchers employed advanced techniques such as in vivo multichannel recording, fiber photometry, pupillometry and optogenetic manipulation to investigate how individual differences in arousal and internal states influence visual escape habituation.

Researchers found that distinct subcortical pathways from the superior colliculus to the amygdala and insula cortical pathways that govern two visual escape behaviors in two groups of mice. They identified two distinct defensive behaviors—sustained rapid escape (T1) and rapid habituation (T2).

T1 involves the superior colliculus (SC)/insular cortex-ventral tegmental area (VTA)-basolateral amygdala (BLA) pathway, whereas T2 relies on the SC/insula-dorsomedial thalamus (MD)-BLA circuit. The MD integrates inputs from the SC and insula to regulate arousal and fear responses, while beta oscillations in BLA modulate fear states.
Dysregulation of innate fear circuits is closely linked to many mental health conditions, including phobias, anxiety, and post-traumatic stress disorder (PTSD). Elucidating the neural circuitry underlying innate fear not only enhances our understanding of emotional disorders but also provides promising therapeutic targets for clinical interventions.

By elucidating the neural basis of individual differences in fear plasticity, this study highlights the central role of brain states in stress adaptation.

Xuemei Liu et al, Neural circuit underlying individual differences in visual escape habituation, Neuron (2025). DOI: 10.1016/j.neuron.2025.04.018

Part 2

Artificial cell-like structures mimic self-reproduction and release polymeric spores

Life on Earth possesses an exceptional ability to self-reproduce, which, even on a simple cellular level, is driven by complex biochemistry. But can self-reproduction exist in a biochemistry-free environment?

A study by researchers  demonstrated that the answer is yes.

The researchers designed a non-biochemical system in which synthetic cell-like structures form and self-reproduce by ejecting polymeric spores.

The PNAS paper reports a one-pot reaction in which chemically active polymer protocells began their journey as a uniform mixture of molecules that usually do not self-assemble. However, when placed under green light (530 nm), they formed vesicle-like structures that grew and divided as the reaction proceeded.

Living organisms produce offspring from their own cellular material, giving rise to new, independent life forms which interact with their environment to obtain food, energy, and information needed for survival. If all goes well, the internal chemical networks of these new systems also enable them to self-reproduce, leading to future generations. As Rudolf Virchow, father of cellular pathology, stated in 1858, "every cell comes from a pre-existing cell."

In biochemistry-based life, even single-celled organisms like bacteria depend on a chain of well-coordinated complex chemical processes to run the life-sustaining processes and reproduction.

It is known that biochemistry is sufficient for driving self-reproduction, but is it essential? Or can we build artificial, compartmentalized chemical systems in the lab that can self-assemble and reproduce on their own?

Part 1

Previous studies have shown reproduction-like behaviors such as polymerization-induced self-assembly (PISA) in micelles and vesicles. However, these processes were neither biochemistry-free nor did they demonstrate true autonomous self-reproduction.

To explore the unknown, the team designed a one-pot PISA batch reactor consisting of strictly non-biochemical molecules with an aim to synthesize amphiphiles that can self-organize, self-assemble, and self-initiate into chemically active entities.

The reaction vial included an aqueous solution of a hydrophilic polymer with a hydrophobic chain transfer agent molecule (CTA) attached to its end, along with the monomer to be polymerized and a photocatalyst in a nitrogen-filled inert environment. This mixture was then allowed to sit under green LED light for 90 minutes at 33°C.

They observed that the mixture of chemicals undergoes photo-Reversible Addition-Fragmentation Chain Transfer (RAFT) photopolymerization in water to transform the starting molecules into amphiphilic block copolymers. These block copolymers then gave rise to non-biochemical polymer vesicles or synthetic cells that displayed self-reproduction behavior via PISA.

The vesicles not only formed and sustained themselves but also released polymeric "spores" that seeded a nonlinear, exponential increase in vesicle numbers, with each new generation inheriting certain properties from their "parent" vesicles.

The behavior shown in this study mimics self-reproduction—a key feature of living systems—arising from simple chemistry without the need for complex biochemical processes.

The researchers note that the findings not only offer insights into how life might have begun but also open new possibilities for creating a wide range of abiotic, life-like systems.

Sai Krishna Katla et al, Self-reproduction as an autonomous process of growth and reorganization in fully abiotic, artificial and synthetic cells, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2412514122

Part 2

Researchers say emulsifiers may cause a variety of health problems

The difference between commerce and science: Commerce wants to sell its products by showing you eye and attention catching ads and videos, while  science tries to see what lies behind the masks and makes people alert. 

Which one do you listen to and which one do you follow?

Ice cream that resists melting. Great, you would think and buy  the thing that  can make this possible.

'But, wait', says science. Why?

This is the actual scene playing out before you:

 In a video explaining the science behind it, a seller of food chemicals shows scoops of ice cream holding their shape under hot lights. The super ingredient? Polysorbate 80.

Polysorbate 80 is an emulsifier, a chemical used to control the consistency of thousands of supermarket products. Other widely used emulsifiers or stabilizers include carboxymethyl cellulose, carrageenan, and maltodextrin.

Emulsifiers and thickening agents play an important role in improving food texture and consistency.

Recently, such ingredients have been showing up in scientific studies for another reason: Researchers say they may cause a variety of health problems.

Studies have found that emulsifiers can alter the mix of bacteria in the gut, known as the microbiome or microbiota; damage the lining of the gastrointestinal tract; and trigger inflammation, potentially contributing to problems elsewhere in the body.

Emulsifiers and stabilizers are among the most common ingredients in ultraprocessed foods. But could you ban them?

This is the complexity of the war on food additives. 

The researchers show how, when it comes to food science, regulators are chronically playing catch-up. In the meantime, for many ingredients, regulators and consumers alike are left in a gray zone between suspicion and proof of harm in humans.

Emulsifiers' assault on the microbiome could help explain inflammatory bowel diseases such as Crohn's disease and ulcerative colitis, metabolic disorders, and even cancer, the studies suggest.

"There is a lot of data showing that those compounds are really detrimental to the microbiota and that we should stop using them," say the several studies on them.

But solid proof?!

Yet much larger and more ambitious clinical trials in humans are needed to get it.

Wait, we  some evidence from doctors and patients. 

For people who  suffered from gastrointestinal illness, the research fits their own experience as a consumer. Changing their diet to avoid emulsifiers has made a shocking difference, easing symptoms that were debilitating. 

Clinically, many patients have reported an improvement in symptoms with such changes, say the gastroenterologists.

Part 1

The scientific findings come with caveats. For instance, much of the research has been done in mice, or by mimicking the human gut in a tube. There are many unknowns. Not all emulsifiers have bad effects, or the same effects, and some people are thought to be much more vulnerable than others.

Even some researchers who have co-authored papers say that it's too soon to say regulators should ban them.

Still, the research poses a challenge.

 When emulsifiers began spreading through the food supply, controllers weren't focusing on the gut microbiome, a relatively recent scientific frontier, researchers say. The scenario changed now as science progressed. We cannot use old excuses.

There's a body of research now that suggests concern with some of these ingredients. These chemicals are creating an inflammatory response in the gastrointestinal tract, and with an altered microbiome lining that GI tract, kids feel sick, report the medical doctors.

Same is true for petroleum-based food dyes too. 

As far back as 2020, an international organization for the study of inflammatory bowel diseases advised that, for people with those conditions, it "may be prudent to limit intake" of maltodextrin, carrageenan, carboxymethyl cellulose, and polysorbate 80.

Emulsifiers are developed from a variety of sources, including plants and bacteria.

Some ingredients that might affect the microbiome show up in foods because they were deemed "generally recognized as safe.

But new information does at any time require reconsideration. Doesn't it?

Earlier these  substances "fell within the standards" when they were greenlighted.

These chemicals were "never considered before for the potential effect on the microbiota".

Part 2

For a consumer, trying to steer clear of emulsifiers can be difficult. Without realizing it, people can consume a variety of emulsifiers from a variety of foods—and the same chemicals from multiple sources.

Polysorbate 80 alone was listed as an ingredient on the labels of 2,311 products!
Carrageenan was listed on 8,100 product labels; maltodextrin, 12,769; and xanthan gum, 17,153.
Some emulsifiers have multiple names, making them harder to recognize. Some names can apply to more than one emulsifier. Controllers find it difficult to identify them.
Carboxymethyl cellulose—not to be confused with methyl cellulose—is also known as carboxymethylcellulose and cellulose gum. Maltodextrin can be derived from substances such as cornstarch, rice starch, and wheat starch—but the FDA doesn't consider it synonymous with the term "modified food starch."

The naming practices can frustrate efforts to track the chemicals in food, to measure how much of the stuff people are taking in, and even to figure out precisely which chemicals a scientific study evaluated, researchers say.
And there is a hell lot of confusion everywhere!
The very term "emulsifier" is problematic. By strict definition, emulsifiers create an emulsion—a stable blend of liquids that would not otherwise mix, such as oil and water. However, the term is used broadly, encompassing chemicals such as maltodextrin that thicken, stabilize, or alter texture.

Emulsifiers can be found in foods marketed as natural or healthy as well as ones that look artificial. Some products contain multiple emulsifiers.

Research on emulsifiers has been building in recent years.

For instance, a study published in January this year by the Journal of Crohn's and Colitis concluded that a diet low in emulsifiers is an effective treatment for mild or moderate Crohn's disease. 

A study published in February 2024 in the journal PLOS Medicine found that higher intakes of carrageenan and mono- and diglycerides of fatty acids were associated with higher risks of cancer. The study observed 92,000 French adults for an average of 6.7 years.

A study published in September 2023 in The BMJ, formerly known as the British Medical Journal, found that intake of several types of emulsifiers was associated with the risk of cardiovascular disease. The study observed more than 95,000 French adults for a median of 7.4 years.

A series of earlier studies found that emulsifiers "can promote chronic intestinal inflammation in mice"; that two in particular, carboxymethyl cellulose and polysorbate 80, "profoundly impact intestinal microbiota in a manner that promotes gut inflammation and associated disease states"; and that, based on a laboratory study of human samples, "numerous, but not all, commonly used emulsifiers can directly alter gut microbiota in a manner expected to promote intestinal inflammation," as recounted in a 2021 paper in the journal Microbiome.

Part 3

But when conflicts of interest take hold, even researchers cook up research results.

Will the companies that make these products stop using these 'chemicals'?

we are in the twilight zone now, neither here, not there. After knowing this, we have to take our own decisions now.

I am making my own ice creams now, without using any harmful chemicals.  I am making my own other things too. They might not be like the ones we buy outside. But  they are good for my health.  That is enough for me.

What about you? 

Sources: Microbiome, British medical journal, PLoS Medicine and medical express with inputs from Sci-Art Lab.

Part 4

Harmful effects of gas cookers on health and the environment reviewed in report

Researchers put the magnitude of the problem into perspective by providing figures on the number of children with asthma and premature deaths associated with the use of gas cookers, and highlighted the need for measures and policies to reduce emissions from these appliances.

Environmental pollution is combined with fumes from gas cookers during normal use, and are believed to be the cause of  thousands of premature deaths.

They recommend electric cooking and induction cookers. 

 Assessment of the health impacts and costs associated with indoor nitrogen dioxide exposure related to gas cooking in the European Union and the United Kingdom, repositori.uji.es/items/156fbd … a4-9856-9415513d505f

The sleep switch: How one brain signal turns sleep on and off

Researchers showed that a single brain signal acts like a biological switch—both triggering sleep and ending it.

Their findings, published in the journal Current Biology, were made possible by studying a tiny roundworm, C. elegans, a powerful model organism in biology.

We know that falling asleep and waking up is controlled by a special set of brain cells, called sleep neurons. However, we don't know how exactly they control the downstream molecular pathways to make us fall asleep and wake up again until now.

Researchers turned to C. elegans to answer these questions. In contrast to humans, who have thousands of sleep neurons that control sleep, C. elegans needs just one neuron to do this job. This simplicity makes it a perfect model organism to study the principal molecular pathways controlling sleep.

This research sheds light on one of the fundamental questions in biology: how organisms regulate sleep and wakefulness. By understanding the fundamental molecular machinery behind sleep, researchers can better understand sleep disorders such as narcolepsy and insomnia that have a major impact on quality of life. The findings also add to the growing body of evidence that even simple model organisms can reveal fundamental mechanisms that govern life.

The team focused on a chemical messenger called FLP-11. When a sleep neuron activates, it releases FLP-11. Such chemical messengers work like molecular "notes" that are passed between brain cells to deliver different commands.

Through genetic screening, the researchers identified a key receptor, called DMSR-1, that FLP-11 binds to deliver its message. If this receptor was missing from the brain, researchers observed that the worms slept significantly less. DMSR-1 turned out to be present in different types of neurons. Depending on which neuron received the message, the results were dramatically different.

They discovered that FLP-11 activates DMSR-1 receptors in two completely different types of neurons.  They found the receptor present in neurons that promote wakefulness. When activated by FLP-11, the receptor turns off the wakefulness neurons. This, in turn, helps the worm fall asleep. On the other hand, the receptor is also present in the sleep neuron itself. Here, it also turns it off, which ultimately wakes the animal back up.

In other words, the same chemical that puts the worm to sleep also helps wake it up again, simply by targeting different cells in the brain. It is an efficient mechanism that controls the start of sleep while also keeping its duration in check.

Unlike humans, C. elegans have much shorter sleep phases that last only around 20 minutes. However, sleep is such a fundamental biological process that many molecules and mechanisms involved in sleep are shared across species. We don't yet know if the same sleep switch exists in humans, but it provides a promising clue in the search for mechanisms that control sleep in our species

Lorenzo Rossi et al, The neuropeptide FLP-11 induces and self-inhibits sleep through the receptor DMSR-1 in Caenorhabditis elegans, Current Biology (2025). DOI: 10.1016/j.cub.2025.03.039