Microplastics in the air may be leading to lung and colon cancers

Tires and degrading garbage shed tiny pieces of plastic into the air, creating a form of air pollution that  researchers suspect may be causing respiratory and other illnesses.

A review of some 3,000 studies implicates these particles in a variety of serious health problems. These include male and female infertility, colon cancer and poor lung function. The particles also may contribute to chronic pulmonary inflammation, which can increase the risk of lung cancer.

These microplastics are basically particulate matter air pollution, and we know this type of air pollution is harmful, say the researchers.

Microplastics are less than 5 millimeters—smaller than a grain of rice—and they are ubiquitous in the environment. Each year, companies around the world produce nearly 460 million metric tons of plastic. That is projected to reach 1.1 billion by 2050.

A major source of plastic in the air is driving. Friction wears down tires along with the road surface, sending plastic fragments into the air.

This new paper is the first systematic review of microplastics using gold standard methods approved by the National Academy of Sciences.

Researchers  urge regulatory agencies and policy leaders to consider the growing evidence of health harms from microplastics, including colon and lung cancer.

 Environmental Science & Technology (2024). 

Effects of Microplastic Exposure on Human Digestive, Reproductive, and Respiratory Health: A Rapid Systematic Review

doi.org/10.1021/acs.est.3c09524

What is metformin's secret sauce? New study shows how this drug works in living animals

Millions of people take metformin, a type 2 diabetes medication that lowers blood sugar. The drug has also been shown to slow cancer growth, improve COVID outcomes and reduce inflammation. So scientists are trying to determine how, exactly, the drug works.

A new study has provided direct evidence in mice that the drug reversibly cuts the cell's energy supply by interfering with mitochondria to lower glucose levels. More specifically, metformin blocks a specific part of the cell's energy-making machinery called mitochondrial complex I. In doing so, the drug can target cells that may be contributing to disease progression without causing significant harm to normal, healthy cells.

Colleen Reczek et al, Metformin targets mitochondrial complex I to lower blood glucose levels, Science Advances (2024). DOI: 10.1126/sciadv.ads5466. www.science.org/doi/10.1126/sciadv.ads5466

Your lifestyle may be aging your brain faster than you think

New research has found a relationship between lifestyle choices that affect dementia risk and early signs of aging in the brain.

Researchers discovered reduced white matter volume and an imbalance in electrical activity in the brains of participants whose lifestyle factors were linked to a higher risk of dementia.

It appeared factors like dietary habits, sleep patterns and physical activity levels, could already be affecting the brain before any signs of cognitive decline.

In the same way that sun safety choices can present on your skin and affect your future cancer risk, the researchers found a relationship between a person's lifestyle choices, their brain health, and their future dementia risk.

Even in very healthy older adults, higher modifiable dementia risk was connected to two major indicators of brain health—white and the brain's ability to balance its electrical activity.

It appears that the dementia risk of your daily choices is "painted" onto the canvas of your brain. The good news? The paint is still wet, and you're holding the brush.

Thomas Pace et al, Modifiable dementia risk associated with smaller white matter volume and altered 1/f aperiodic brain activity: cross-sectional insights from the LEISURE study, Age and Ageing (2024). DOI: 10.1093/ageing/afae243

This new  sunscreen uses TiO₂ nanoparticles to cool skin while blocking UV rays

Wearing sunscreen is important to protect your skin from the harmful effects of UV radiation but doesn't cool people off. However, a new formula, described in Nano Letters, protects against both UV light and heat from the sun using radiative cooling. The prototype sunblock kept human skin up to 11 degrees Fahrenheit (6 degrees Celsius) cooler than bare skin, or around 6 °F (3 °C) cooler than existing sunscreens.

Radiative cooling involves either reflecting or radiating heat away from something, cooling whatever's underneath. It is already used to create cooling fabrics and coatings that could both cool and heat homes, among other applications.

Some passive radiative cooling technologies rely on an ingredient called titanium dioxide (TiO2) because the whitish substance reflects heat. TiO2 particles are also used in mineral sunscreens to reflect UV light, but the particles aren't the right size to produce a cooling effect. So, researchers  wanted to tune the size of TiO2 nanoparticles to create a sunscreen that works both as a UV protector and a radiative cooler.

The team created their sunblock by combining six ingredients: TiO2 nanoparticles, water, ethanol, moisturizing cream, pigments, and a common silicone polymer used in cosmetics called polydimethylsiloxane. By carefully adjusting the sizes of the TiO2 nanoparticles, they produced a material that reflects both UV light and solar heat, imparting the cooling ability.

The new formulation demonstrated an SPF of about 50, water resistance and continued efficacy after 12 hours of simulated sunlight exposure with a xenon lamp. Additionally, when applied to both animal and human skin, the product didn't cause irritation.

In tests on people in a hot and humid outdoor environment, the new radiative cooling sunscreen was found to keep the participants' skin up to 10.8 °F (6.0 °C) cooler than bare skin, and up to 11.0 °F (6.1 °C) cooler than commercially available sunscreens. The formulation is inexpensive, costing only $0.92 for 10 grams of the mixture—on par with sunblocks already on the market.

Jiaqi Xu et al, High-Performance Radiative Cooling Sunscreen, Nano Letters (2024). DOI: 10.1021/acs.nanolett.4c04969

Climate change could trigger more earthquakes, study suggests

A recent  study published in the journal Geology demonstrates that climate change can affect the frequency of earthquakes, adding to a small but growing body of evidence showing that climate can alter the seismic cycle.

Geoscientists analyzed the Sangre de Cristo Mountains in southern Colorado, a range with an active fault along its western edge. Their results indicate that the fault had been held in place under the weight of glaciers during the last ice age, and as the ice melted, slip along the fault increased. This suggests that earthquake activity along a fault could increase as glaciers recede.

Climate change is happening at a rate that is orders of magnitude faster than we see in the geologic record.

We see this in the rapid mountain glacial retreats in Alaska, the Himalayas and the Alps. In many of these regions, there are also active tectonics, and this work demonstrates that as climate change alters ice and water loads, tectonically active areas might see more frequent fault movements and earthquakes due to rapidly changing stress conditions.

It is well known that climate adjusts to seismic changes in the Earth's surface. The tectonic uplift of mountain ranges alters atmospheric circulation and rainfall, for example.

The Sangre de Cristo Mountains were covered with glaciers during the last ice age. Using remote-sensing and field data, the researchers reconstructed where the ice was, calculated the load that would have been pushing on the fault, and then measured displacement of the fault, or how much it had shifted.

The study found that fault slip rates have been five times faster since the last ice age than during the time the range was covered in glaciers. This research may preview how other glacier-adjacent faults will respond to a warming climate.

And this is compelling evidence. 

The research adds to our understanding of what drives earthquakes, which is important for hazard assessment. Faults in areas with rapidly retreating glaciers or evaporating large bodies of water may need to be monitored for increasing earthquake activity.

Cecilia Hurtado et al, Exploring the impact of deglaciation on fault slip in the Sangre de Cristo Mountains, Colorado, USA, Geology (2024). DOI: 10.1130/G52661.1

Adding sweetener to coffee enhances 'night-owl' effects of caffeine, research reveals

Adding sugar or artificial sweeteners to coffee disrupted the body clocks in mice more than coffee on its own, researchers have found, with it causing day and night to be reversed in some mice. If this holds for humans as well, adding sweetener to coffee would have significant health ramifications.

If you need to perk yourself up in the morning, or stay up late to get some work or a school assignment done, most people will make themselves a cup of coffee or grab an energy drink containing caffeine. These "night-owl" effects of that perky chemical are far from unknown.

A myriad of epidemiological studies have demonstrated how night-oriented people tend to drink more caffeinated beverages than morning people, and experiments on animals and cells have shown how caffeine works to extend the waking period of the internal body clock.

But a group of researchers accidentally discovered that changes in the activity rhythms of mice were affected even more strongly when they mixed caffeine with sugar or other sweeteners.

The mice that had consumed the caffeine-sweetener mix experienced a very long "free-running" sleep-wake period of 26–30 hours, and some even switched from a nocturnal circadian rhythm to a daytime-based one.

These effects continued to happen even when the mice were subjected to persistent darkness. This latter phenomenon suggests that the caffeine-sweetener effect is operating independently of the central regulator of the internal body clock, the suprachiasmatic nucleus (SCN), which lies in the hypothalamus in the brain. That central regulator itself is normally governed by light and the natural day-night cycle, and it in turn ensures a synchronization of clocks situated in organ tissue elsewhere in the body.

The researchers think that the combination of caffeine and sweetness may be creating a conflicting signal within the body possibly mediated by another famous chemical, dopamine. Both caffeine and sweeteners activate the reward system in the brain, leading to the release of dopamine. It is this double hit of dopamine that could be contributing to the emergence of the long-period activity rhythms.

The researchers now aim to investigate further the possible dopamine link and see whether the boost to caffeine produced by a sweetener is replicated in humans. While this initial study only looked at the effects in mice, the findings may have important implications for our understanding of how sweetened caffeine affects human health.

 Yu Tahara et al, Sweetened caffeine drinking revealed behavioral rhythm independent of the central circadian clock in male mice, npj Science of Food (2024). DOI: 10.1038/s41538-024-00295-6

New discovery pinpoints when good cholesterol becomes harmful

We have heard till now that good cholesterol is good. But wait ....

Researchers have discovered that certain components of so-called "good" cholesterol—high-density lipoproteins (HDL)—may be associated with an increased prevalence of cardiovascular disease.

Surprized? Yes, new data asks for revisits.

Yes, not all cholesterol is born the same. What is not commonly recognized is that each type of cholesterol has two forms—free cholesterol, which is active and involved in cellular functions, and esterified, or bound, cholesterol, which is more stable and ready to be stored in the body. Too much free cholesterol, even if it is in HDL, could contribute to heart disease. Hmmm!

In pre-clinical studies, the research team discovered that HDL with a high content of free cholesterol is likely dysfunctional. To validate their findings and prove their hypothesis, they are currently at the halfway point of the Houston Heart Study in which they will be studying 400 patients with a range of plasma HDL concentrations.

The most surprising finding from  this new study thus far is that there is a strong link between the amount of free cholesterol in HDL and how much of it accumulates in white blood cells called macrophages, which can contribute to heart disease.

While it was previously thought that the transfer of free cholesterol to HDL was beneficial for heart health by removing excess cholesterol from tissues, the new data shows that in the context of high plasma HDL concentrations, the reverse is true, wherein free cholesterol transfer from HDL to the white blood cells in blood and tissues could actually raise one's risk for cardiovascular disease.

The researchers say once they reach their immediate goal of showing that excess free cholesterol in HDL is associated with excess cardiovascular disease, they plan to develop new diagnostics and treatments for managing heart disease, as well as use HDL-free cholesterol as a biomarker to identify patients requiring HDL-lowering therapies.

Now that you are confused, what should you do?

Wait for more clarification and confirmation studies while still taking care of your heart's health.

Dedipya Yelamanchili et al, HDL-free cholesterol influx into macrophages and transfer to LDL correlate with HDL-free cholesterol content, Journal of Lipid Research (2024). DOI: 10.1016/j.jlr.2024.100707

Squirrels Have Developed a Taste For Meat in Surprise Discovery
Squirrels might look like adorable, nut-hoarding furballs, but some are ruthless predators that hunt, tear apart, and devour voles.

That's the startling finding of a new study published this week in the Journal of Ethology – the first to document widespread carnivorous behavior in these seemingly innocent creatures.
The observations were made this summer, during the 12th year of a long-term study conducted at Briones Regional Park in Contra Costa County, California.

Between June and July, researchers recorded 74 interactions involving California ground squirrels and voles, with 42 percent of them involving active hunting of their fellow rodents.
It was previously known that as many as 30 species of squirrels opportunistically consume meat, ranging from small fish to birds. However, it was unclear whether this behavior stemmed from scavenging or active predation.

The new study is the first to confirm that hunting is, in fact, a common behavior.

Researchers observed squirrels crouching low to the ground before ambushing their prey, though more often, they chased voles, pounced, and delivered a neck bite followed by vigorous shaking.

The study also found that the squirrels' carnivorous behavior peaked during the first two weeks of July, coinciding with a surge in vole populations.

https://link.springer.com/article/10.1007/s10164-024-00832-6

Dark energy 'doesn't exist' so can't be pushing 'lumpy' universe apart, physicists say

One of the biggest mysteries in science—dark energy—doesn't actually exist, according to researchers looking to solve the riddle of how the universe is expanding.

Their analysis has been published in the journal Monthly Notices of the Royal Astronomical Society Letters.

For the past 100 years, physicists have generally assumed that the cosmos is growing equally in all directions. They employed the concept of dark energy as a placeholder to explain unknown physics they couldn't understand, but the contentious theory has always had its problems.

Now a team of physicists and astronomers are challenging the status quo, using improved analysis of supernovae light curves to show that the universe is expanding in a more varied, "lumpier" way.

The new evidence supports the "timescape" model of cosmic expansion, which doesn't have a need for dark energy because the differences in stretching light aren't the result of an accelerating universe but instead a consequence of how we calibrate time and distance.

It takes into account that gravity slows time, so an ideal clock in empty space ticks faster than inside a galaxy.

The model suggests that a clock in the Milky Way would be about 35 percent slower than the same one at an average position in large cosmic voids, meaning billions more years would have passed in voids. This would in turn allow more expansion of space, making it seem like the expansion is getting faster when such vast empty voids grow to dominate the universe.

These findings show that we do not need dark energy to explain why the universe appears to expand at an accelerating rate. Dark energy is a misidentification of variations in the kinetic energy of expansion, which is not uniform in a universe as lumpy as the one we actually live in.

The research provides compelling evidence that may resolve some of the key questions around the quirks of our expanding cosmos.

With new data, the universe's biggest mystery could be settled by the end of the decade, the physicists say.

Part 1

Dark energy is commonly thought to be a weak anti-gravity force which acts independently of matter and makes up around two thirds of the mass-energy density of the universe.

The standard Lambda Cold Dark Matter (ΛCDM) model of the universe requires dark energy to explain the observed acceleration in the rate at which the cosmos is expanding.

Scientists base this conclusion on measurements of the distances to supernova explosions in distant galaxies, which appear to be farther away than they should be if the universe's expansion were not accelerating.

However, the present expansion rate of the universe is increasingly being challenged by new observations.

Firstly, evidence from the afterglow of the Big Bang—known as the Cosmic Microwave Background (CMB)—shows the expansion of the early universe is at odds with current expansion, an anomaly known as the "Hubble tension."

In addition, recent analysis of new high precision data by the Dark Energy Spectroscopic Instrument (DESI) has found that the ΛCDM model does not fit as well as models in which dark energy is "evolving" over time, rather than remaining constant.

Both the Hubble tension and the surprises revealed by DESI are difficult to resolve in models which use a simplified 100-year-old cosmic expansion law—Friedmann's equation.

This assumes that, on average, the universe expands uniformly—as if all cosmic structures could be put through a blender to make a featureless soup, with no complicating structure. However, the present universe actually contains a complex cosmic web of galaxy clusters in sheets and filaments that surround and thread vast empty voids.

Part 2

We now have so much data that in the 21st century we can finally answer the question—how and why does a simple average expansion law emerge from complexity?

"A simple expansion law consistent with Einstein's general relativity does not have to obey Friedmann's equation."

The researchers say that the European Space Agency's Euclid satellite, which was launched in July 2023, has the power to test and distinguish the Friedmann equation from the timescape alternative. However, this will require at least 1,000 independent high quality supernovae observations.

When the proposed timescape model was last tested in 2017, the analysis suggested it was only a slightly better fit than the ΛCDM as an explanation for cosmic expansion, so the present  team worked closely with the Pantheon+ collaboration team who had painstakingly produced a catalog of 1,535 distinct supernovae.

They say the new data now provides "very strong evidence" for timescape. It may also point to a compelling resolution of the Hubble tension and other anomalies related to the expansion of the universe.

Further observations from Euclid and the Nancy Grace Roman Space Telescope are needed to bolster support for the timescape model, the researchers say.

 Antonia Seifert et al, Supernovae evidence for foundational change to cosmological models, Monthly Notices of the Royal Astronomical Society: Letters (2024). DOI: 10.1093/mnrasl/slae112

Part 3

**

Hidden hazards of chemical mixtures in rivers

Artificial intelligence can provide critical insights into how complex mixtures of chemicals in rivers affect aquatic life—paving the way for better environmental protection.

A new approach, developed by researchers  demonstrates how advanced artificial intelligence (AI) methods can help identify potentially harmful chemical substances in rivers by monitoring their effects on tiny water fleas (Daphnia).

International researchers from various countries  analyzed water samples from the Chaobai River system near Beijing. This river system is receiving chemical pollutants from a number of different sources, including agricultural, domestic and industrial.

There is a vast array of chemicals in the environment. Water safety cannot be assessed one substance at a time. Now we have the means to monitor the totality of chemicals in sampled water from the environment to uncover what unknown substances act together to produce toxicity to animals, including humans, say the researchers.

The results, published in Environmental Science and Technology, reveal that certain mixtures of chemicals can work together to affect important biological processes in aquatic organisms, which are measured by their genes. The combinations of these chemicals create environmental hazards that are potentially greater than when chemicals are present individually.

The research team used water fleas (Daphnia) as test organisms in the study because these tiny crustaceans are highly sensitive to water quality changes and share many genes with other species, making them excellent indicators of potential environmental hazards.

Part 1

Typically, aquatic toxicology studies either use a high concentration of an individual chemical to determine detailed biological responses or only determine apical effects like mortality and altered reproduction after exposure to an environmental sample.

"However, this study breaks new ground by allowing us to identify key classes of chemicals that affect living organisms within a genuine environmental mixture at relatively low concentration while simultaneously characterizing the biomolecular changes elicited.

The findings could help improve environmental protection by identifying previously unknown chemical combinations that pose risks to aquatic life, enabling more comprehensive environmental monitoring, and supporting better-informed regulations for chemical discharge into waterways.

Bioactivity Profiling of Chemical Mixtures for Hazard Characterization, Environmental Science & Technology (2024). DOI: 10.1021/acs.est.4c11095

Part 2

**

First demonstration of quantum teleportation over busy internet cables

Researchers and engineers successfully demonstrated quantum teleportation over a fiber-optic cable already carrying internet traffic.

The discovery introduces the new possibility of combining quantum communication with existing internet cables—greatly simplifying the infrastructure required for distributed quantum sensing or computing applications.

The study is published on the arXiv preprint server and is due to appear in the journal Optica.

Only limited by the speed of light, quantum teleportation could make communications nearly instantaneous. The process works by harnessing quantum entanglement, a technique in which two particles are linked, regardless of the distance between them. Instead of particles physically traveling to deliver information, entangled particles exchange information over great distances—without physically carrying it.

In optical communications, all signals are converted to light. While conventional signals for classical communications typically comprise millions of particles of light, quantum information uses single photons.

The researchers found a way to help the delicate photons steer clear of the busy traffic. After conducting in-depth studies of how light scatters within fiberoptic cables, the researchers found a less crowded wavelength of light to place their photons. Then, they added special filters to reduce noise from regular internet traffic.

They carefully studied how light is scattered and placed their photons at a judicial point where that scattering mechanism is minimized.  They found they could perform quantum communication without interference from the classical channels that are simultaneously present.

To test the new method, the research team set up a 30 kilometer-long fiberoptic cable with a photon at either end. Then, they simultaneously sent quantum information and regular internet traffic through it. Finally, they measured the quality of the quantum information at the receiving end while executing the teleportation protocol by making quantum measurements at the mid-point. The researchers found the quantum information was successfully transmitted—even with busy internet traffic whizzing by.

 Quantum teleportation coexisting with classical communications in optical fiber, Optica (2024).

Preprint: Jordan M. Thomas et al, Quantum teleportation coexisting with classical communications in optical fiber, arXiv (2024). DOI: 10.48550/arxiv.2404.10738

Intense ribbons of rain also bring the heat, scientists say

The environmental threat posed by atmospheric rivers—long, narrow ribbons of water vapor in the sky—doesn't come only in the form of concentrated, torrential downpours and severe flooding characteristic of these natural phenomena. According to a new  study, they also cause extreme warm temperatures and moist heat waves.

The atmospheric rivers—horizontal plumes that transport water vapour from the warm subtropics to cooler areas across midlatitude and polar regions of the world—are also transporting heat. As a result, atmospheric rivers may have a greater effect on global energy movement than previously recognized. 

We're seeing temperature anomalies associated with atmospheric rivers that are 5 to 10 degrees Celsius [9 to 18 degrees Fahrenheit] higher than the climatological mean. The numbers are astounding, say the researchers.

The findings are published in the journal Nature.

Scientists began using the term "atmospheric river" in the 1990s. Today, there are three to five of them winding their way through each hemisphere at any given time.

They can be thousands of miles long, but only a few hundred miles wide; the amount of water vapor they carry is about 7–15 times greater than the equivalent amount of water discharged each day by the Mississippi River. The heavy rains that often result can cause major damage and disruption.

The researchers analyzed 40 years of global weather data from NASA's MERRA-2 reanalysis, as well as seven publicly available algorithms that track atmospheric rivers worldwide. Specifically, they looked at temperature increases related to atmospheric rivers on two timescales: hourly temperature spikes and heat waves of three or more days of moist heat.

"There was no doubt—atmospheric rivers are really impactful for both timescales", they conclude.

The researchers noted that the phenomenon has a more dramatic effect in the winter than it does in summer.

The new study shows that when atmospheric rivers occur, they change the balance of energy on the surface in several ways, the researchers say. For example, while cloudy conditions block incoming sunlight, those clouds also trap more thermal radiation near the surface, creating a transient enhanced greenhouse effect. This heating balances out the loss of sunlight—but is not the cause of temperature spikes.

Instead, the main cause of warm temperatures in atmospheric rivers is simply the transport of warm air, located near the water's surface, from one region to another.

Serena R. Scholz et al, Atmospheric rivers cause warm winters and extreme heat events, Nature (2024). DOI: 10.1038/s41586-024-08238-7

How human eyelashes promote water drainage

Throughout human evolution, body and facial hair have notably diminished, yet eyelashes have remained a distinguishing feature. The physiological or functional purpose of eyelashes—traditionally thought to be for catching dust or filtering air—has long been debated.

However, a team of  researchers has recently elucidated the characteristics of human eyelashes. Their study reveals that eyelashes consist of a hydrophobic, curved, flexible fiber array, featuring surface micro-ratchets and a macro-curvature approximating the Brachistochrone curve. This structure enables eyelashes to rapidly and directionally expel incoming liquid, thereby preserving clear vision.

The hydrodynamic advantages of eyelashes, particularly their ability to expel unwanted liquids from the eye to maintain visual clarity, have received little attention. For instance, during facial washing or intense physical activity, the eyes are exposed to significant amounts of water or sweat without compromising clear vision.

The study is published in Science Advances on Dec. 20

The research team aimed to investigate the interaction between water and the flexible fiber array of eyelashes. They began by characterizing the structure, wettability, and water drainage process of human eyelashes. Next, they explored how the flexibility, wettability, and curvature of the fiber array influence water drainage.
Based on their findings, the researchers revealed the control mechanism governing transfer direction and contact time, which arise from the multi-scale asymmetric structures and heterogeneous elastic deformations of the fiber array. They also developed a quantitative computational model to calculate the elastic forces acting on the fiber array.
This research has also led to the design of eyelash-mimetic rapid liquid transfer edges, including aesthetically pleasing and protective false eyelashes, waterproof imaging devices, and ventilated structures.

Shan Zhou et al, Rapid water drainage on human eyelashes of a hydrophobic Brachistochrone fiber array, Science Advances (2024). DOI: 10.1126/sciadv.adr2135. www.science.org/doi/10.1126/sciadv.adr2135

Sea snakes regain advanced color vision, recovering a complex trait once lost to evolutionary time

Nine species of sea snakes have now been identified as having regained the genetic requirements for advanced color vision, demonstrating that once a complex trait has been lost to evolutionary time, it may be regained in some way.

A new study found the genetic trait may have existed in a common ancestor of the nine species, which all belong to the Hydrophis genus, dating back three million years.

Researchers previously identified one species of sea snake that had re-elaborated the visual function—the fully marine Hydrophis cyanocinctus, which did so in response to its spectrally complex environment.

With the re-elaboration now identified in so many species, the researchers say there is sufficient evidence to suggest evolutionary losses can be somewhat reversed.

We often think of evolution as a force that moves in just one direction—forward. But really, an organism's ecological circumstances are continuously dynamic, and sometimes becoming the 'fittest' means revisiting traits that were once less beneficial.

The re-elaboration of Hydrophis cyanocinctus' visual function was in response to its bright underwater environment—which differed from the low-light habitats of some of its ancestors.

Snakes descended from lizard-like ancestors which had a full visual opsin complement, which makes sense as they inhabited bright, colorful environments.

The earliest snakes underwent a period of dim-light living, and consequently lost two visual opsin genes, which caused them to lose much of their ability to distinguish colours.

Descendants of these earlier snakes inhabit a diverse variety of light environments today, including bright and colorful marine ecosystems. This opsin expansion showcases how new sensory innovations can more or less re-elaborate visual functions previously thought to be lost.

Though the species of sea snakes identified in this new research have regained the genetic requirements for advanced colour vision, the functions these expanded visual opsins have conferred upon the snakes is unclear and have to be investigated thoroughly now.

 Isaac H Rossetto et al, Dynamic Expansions and Retinal Expression of Spectrally Distinct Short-Wavelength Opsin Genes in Sea Snakes, Genome Biology and Evolution (2024). DOI: 10.1093/gbe/evae150

Removing toxins from potatoes

Scientists have discovered a way to remove toxic compounds from potatoes, making them safer to eat and easier to store. The breakthrough could cut food waste and enhance crop farming in space and other extreme environments.

Potato plants naturally produce chemicals that protect them from insects. The chemicals, called steroidal glycoalkaloids, or SGAs, are found in high quantities in the green parts of potato peels, and in the sprouting areas. They render the potatoes unsafe for insects as well as humans.

These compounds are critical for plants to ward off insects, but they make certain parts of these crops inedible. 

Now that scientists have uncovered the biosynthetic pathway, they can potentially create plants that produce these compounds only in the leaves while keeping the edible parts safe.

Sunlight can induce the production of SGAs in potato "tubers"—the part of the potato plant that is eaten—even after they've been harvested. By identifying a key genetic mechanism in SGA production, researchers may be able to reduce potatoes' toxicity while preserving the plants' natural defenses. Taking SGA out of potatoes will also make them easier to store and transport in open air.

The research, published in Science, focuses on a protein dubbed "GAME15," which plays a key role in directing the plant's production of SGAs. This protein acts both as an enzyme and a scaffold, organizing other enzymes into a "conversion factory" that efficiently produces SGAs while preventing toxic compounds from leaking into other parts of plant cells, where they would wreak havoc.

Tomatoes also produce SGAs, primarily in the green, unripe fruit, as well as in the leaves, stems, and roots of the plants. When the researchers silenced the GAME15 gene in tomatoes, they eliminated SGA production but also made the plants highly susceptible to pests.

By engineering plants to control when and where SGAs are produced, for example, in the leaves but not the potatoes themselves, the researchers envision crops that can be stored without the risk of toxicity from sunlight exposure.

The team achieved these insights by initially recreating the SGA production process in tobacco plants. Surprisingly, they found that during evolution, the process redirected protein from the plasma membrane or Golgi apparatus, where it is responsible for the production of cell wall components crucial for cell growth, to the endoplasmic reticulum, a part of the cell where toxin production begins.

Green, unripe fruit may be toxic, but during ripening these molecules convert to something edible. By limiting SGAs to non-edible parts of plants, farmers and consumers alike could benefit from safer, more versatile crops.

This work demonstrates that plants have evolved ingenious ways to balance growth, reproduction, and defense. Understanding these systems allows us to redesign crops to meet modern needs without compromising their ability to thrive.

 Adam Jozwiak et al, A cellulose synthase–like protein governs the biosynthesis of Solanum alkaloids, Science (2024). DOI: 10.1126/science.adq5721

Scientists steer the development of stem cells to regenerate and repair organs

Investigators have identified a new way to deliver instructions that tell stem cells to grow into specific bodily structures, a critical step in eventually regenerating and repairing tissues and organs.

The scientists engineered cells that form structures called "synthetic organizers." These organizers provided instructions to the stem cells through biochemical signals called morphogens, which stimulated and enabled the stem cells to grow into specific complex tissues and organ-like assemblies.

The research was conducted with mouse embryonic stem cells, and the findings were published in Cell.

Scientists now can use these synthetic organizers to push the stem cells toward making different parts of the early embryo or toward making a heart or other organs.

In one instance, scientists were able to induce the stem cells to begin to form a mouse body that stretched from head to tail, similar to regular embryonic development in the womb. In another instance, the scientists were able to spur the stem cells to generate a large heart-like structure complete with a central chamber and a regular beat, along with a network of early blood vessels.

This type of synthetic organizer cell platform provides a new way to interface with stem cells and to program what they develop into.

By controlling and reshaping how stem cells differentiate and develop, it might allow us to grow better organs for transplantation or organoids for disease modeling and eventually utilize it to drive tissue regeneration in living patients.

Part 1

To steer organizer cells and control stem cell development, the scientists uploaded genetic codes into the cells and engineered two key features in the cells.

First, they instructed the cells to stick to the stem cells in the form of a node or a shell clustering around the clump of stem cells. Second, the investigators engineered the organizer cells to produce specific biochemical signals crucial to inducing early embryonic development.

To effectively and precisely control the organizer cells, researchers developed a chemical switch within the cells, allowing scientists to turn the delivery of instructions to stem cells on or off. Additionally, they installed a "suicide" switch to eliminate the organizer cells when needed.

These synthetic organizers show that we can provide more refined developmental instructions to stem cells by engineering where and when specific morphogen signals are provided.

The organizer cells carry both spatial information and biochemical information, thus giving us an incredible amount of control that we have not had before.

The use of engineered synthetic organizer cells could ultimately allow the team to build real-world applications in the future. The remarkable science of programming instructions to coax stem cells could one day open the door to tackle complex diseases.

Toshimichi Yamada et al, Synthetic organizer cells guide development via spatial and biochemical instructions, Cell (2024). DOI: 10.1016/j.cell.2024.11.017

Part 2

Commercial tea bags release millions of microplastics, entering human intestinal cells

Do you know why I never use these tea bags? Because my instinct told me they don't have good vibes! And I am right!

Research has characterized in detail how polymer-based commercial tea bags release millions of nanoplastics and microplastics when infused. The study shows for the first time the capacity of these particles to be absorbed by human intestinal cells, and are thus able to reach the bloodstream and spread throughout the body.

Plastic waste pollution represents a critical environmental challenge with increasing implications for the well-being and health of future generations. Food packaging is a major source of micro and nanoplastic (MNPLs) contamination and inhalation and ingestion is the main route of human exposure.

A study by the Mutagenesis Group of the UAB Department of Genetics and Microbiology has successfully obtained and characterized micro and nanoplastics derived from several types of commercially available tea bags. The paper is published in the journal Chemosphere.

The researchers observed that when these tea bags are used to prepare an infusion, huge amounts of nano-sized particles and nanofilamentous structures are released, which is an important source of exposure to MNPLs.

The tea bags used for the research were made from the polymers nylon-6, polypropylene and cellulose. The study shows that, when brewing tea, polypropylene releases approximately 1.2 billion particles per milliliter, with an average size of 136.7 nanometers; cellulose releases about 135 million particles per milliliter, with an average size of 244 nanometers; while nylon-6 releases 8.18 million particles per milliliter, with an average size of 138.4 nanometers.

To characterize the different types of particles present in the infusion, a set of advanced analytical techniques such as scanning electron microscopy (SEM), transmission electron microscopy (TEM), infrared spectroscopy (ATR-FTIR), dynamic light scattering (DLS), laser Doppler velocimetry (LDV), and nanoparticle tracking analysis (NTA) were used.

Interactions with human cells observed for the first time.

The particles were stained and exposed for the first time to different types of human intestinal cells to assess their interaction and possible cellular internalization. The biological interaction experiments showed that mucus-producing intestinal cells had the highest uptake of micro and nanoplastics, with the particles even entering the cell nucleus that houses the genetic material.

The result suggests a key role for intestinal mucus in the uptake of these pollutant particles and underscores the need for further research into the effects that chronic exposure can have on human health.

As the use of plastic in food packaging continues to increase, it is vital to address MNPLs contamination to ensure food safety and protect public health, the researchers add.

Gooya Banaei et al, Teabag-derived micro/nanoplastics (true-to-life MNPLs) as a surrogate for real-life exposure scenarios, Chemosphere (2024). DOI: 10.1016/j.chemosphere.2024.143736

Having Your Tonsils removed as a Child May Have a Drastic Impact on Your Life

Thousands of children around the world   have their tonsils surgically removed each year to improve breathing while sleeping or reduce recurrent infection.

A study by an international team of researchers now suggests this relatively common procedure could increase a patient's risk of developing an anxiety-related disorder later in life.

Scientists analyzed data on over a million people held in a Swedish health registry, finding that a tonsillectomy was linked to a 43 percent increased risk of developing conditions such as post-traumatic stress disorder (PTSD), depression, or anxiety. 

Being an observational study, the research can't determine the cause of this outcome, however the increased risk was present even after accounting for the sex of the participants, the age at which they had their tonsils out, any family history of stress-related disorders, and the education level of the parents (an indicator of socioeconomic status).

These findings suggest a potential role of adenotonsillar diseases or associated health conditions in the development of stress-related disorders, the researchers write in their published paper.

Of the conditions identified, PTSD presented the greatest risk increase; a rise of some 55 percent was shown for those who had tonsillectomies earlier in life, compared with those who hadn't.

The researchers compared siblings in some families to control for certain genetic and environmental factors. Even among this sample there was a 34 percent greater risk of anxiety disorders for those family members who had their tonsils removed.

If our findings here are validated in future studies of independent study populations, mechanistic studies would be needed to disentangle the role of human tonsils and their diseases, via inflammation or other associated health conditions, in the development of psychiatric disorders in general and stress-related disorders specifically," write the researchers.

https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2827613

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Antarctica's tipping points threaten global climate stability

Antarctica is approaching a series of cascading tipping points that could reshape ecosystems and intensify global climate disruptions, according to a new study by an international team of scientists.

The study identifies eight potential tipping points spanning physical, biological, chemical, and governance systems. The research is published in the journal Ambio.

These include collapsing ice sheets, invasive species, ocean acidification, and pressures on the Antarctic Treaty System (ATS), which oversees human activity in the region.

The findings highlight the region's critical role in global climate stability.

Antarctica's ice sheets are vital to regulating the Earth's climate and oceans. If they collapse, we'll see significant sea-level rise, impacting millions of people living in coastal areas.

The study warns that these tipping points are interconnected, creating a risk of cascading effects. Melting ice sheets, for example, not only contribute to sea-level rise but also disrupt ocean circulation, which is crucial for transporting heat, carbon, and nutrients around the globe. Such disruptions threaten marine ecosystems, global fisheries, and food security.

The Antarctic Treaty System has been a cornerstone in preserving this fragile environment. But it's increasingly under pressure from geopolitical tensions and expanding human activity. Strengthening it is critical to mitigating these cascading impacts.

Ida Kubiszewski et al, Cascading tipping points of Antarctica and the Southern Ocean, Ambio (2024). DOI: 10.1007/s13280-024-02101-9

Scientists observe 'negative time' in quantum experiments

Scientists have long known that light can sometimes appear to exit a material before entering it—an effect dismissed as an illusion caused by how waves are distorted by matter.

Now, researchers through innovative quantum experiments, say they have demonstrated that "negative time" isn't just a theoretical idea—it exists in a tangible, physical sense, deserving closer scrutiny.

The findings, posted on the preprint server arXiv but not yet published in a peer-reviewed journal, have attracted both global attention and skepticism.

The researchers emphasize that these perplexing results highlight a peculiar quirk of quantum mechanics rather than a radical shift in our understanding of time.

While the term "negative time" might sound like a concept lifted from science fiction, some physicists defend its use, hoping it will spark deeper discussions about the mysteries of quantum physics.

Years ago, the research team began exploring interactions between light and matter.

When light particles, or photons, pass through atoms, some are absorbed by the atoms and later re-emitted. This interaction changes the atoms, temporarily putting them in a higher-energy or "excited" state before they return to normal.

The team now set out to measure how long these atoms stayed in their excited state. "That time turned out to be negative" —meaning a duration less than zero.

Part 1

The explanation lies in quantum mechanics, where particles like photons behave in fuzzy, probabilistic ways rather than following strict rules.

Instead of adhering to a fixed timeline for absorption and re-emission, these interactions occur across a spectrum of possible durations—some of which defy everyday intuition.

Critically, the researchers say, this doesn't violate Einstein's theory of special relativity, which dictates that nothing can travel faster than light. These photons carried no information, sidestepping any cosmic speed limits.
The concept of "negative time" has drawn both fascination and skepticism, particularly from prominent voices in the scientific community.

German theoretical physicist Sabine Hossenfelder, for one, criticized the work in a YouTube video viewed by over 250,000 people, noting, "The negative time in this experiment has nothing to do with the passage of time—it's just a way to describe how photons travel through a medium and how their phases shift."

Angulo and Steinberg, the researchers who did this work, pushed back, arguing that their research addresses crucial gaps in understanding why light doesn't always travel at a constant speed.

Steinberg acknowledged the controversy surrounding their paper's provocative headline but pointed out that no serious scientist has challenged the experimental results.

"We've made our choice about what we think is a fruitful way to describe the results," he said, adding that while practical applications remain elusive, the findings open new avenues for exploring quantum phenomena.

"I'll be honest, I don't currently have a path from what we've been looking at toward applications," he admitted. "We're going to keep thinking about it, but I don't want to get people's hopes up."

Daniela Angulo et al, Experimental evidence that a photon can spend a negative amount of time in an atom cloud, arXiv (2024). DOI: 10.48550/arxiv.2409.03680 , arxiv.org/abs/2409.03680

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How does being born preterm affect long-term health?

Research has found that adults who were born preterm showed no statistically significant differences in diabetes, prediabetes, or dyslipidemia and had fewer cardiovascular events compared with adults born at term. A higher likelihood of developing high blood pressure by age 50 was seen among the preterm group.

Preterm birth occurs before 37 weeks gestation and affects an estimated one in 10 births worldwide. Outcomes in adulthood have previously been associated with elevated risk for cardiovascular disorders, including hypertension and stroke. These earlier investigations rarely included individuals who reached midlife in the modern era of improved neonatal care.

Long-term consequences for people born preterm are therefore lacking a contemporary research evaluation to identify potential age-related health risks.

In the study, "Health Outcomes 50 Years After Preterm Birth in Participants of a Trial of Antenatal Betamethasone," published in Pediatrics, researchers performed a follow-up of individuals originally enrolled in a double-blind, placebo-controlled trial of antenatal betamethasone at the National Women's Hospital in Auckland.
Participants completed a health questionnaire and provided consent for administrative health data review. Clinical endpoints measured included hypertension, diabetes mellitus, prediabetes, treated dyslipidemia, and major adverse cardiovascular events. Secondary outcomes covered respiratory, mental health, educational, and additional health metrics.

More than one-third of preterm-born adults showed higher reported rates of high blood pressure (34.7% vs. 19.8%), yet the overall risk of major adverse cardiovascular events was lower in this group than in term-born peers (2.8% vs. 6.9%).

Rates of diabetes, prediabetes, and treated dyslipidemia were not significantly different. Respiratory outcomes were generally comparable, and no significant differences were observed in chronic kidney disease prevalence.
Part 1

Mental health disorders were less common in preterm participants (38.2% vs. 52.9%). Self-reported depression was less common in the preterm group. Educational attainment and mortality after the first year of life did not vary significantly.

The results suggest that worsened cardiovascular outcomes are not universal for all individuals born preterm, particularly for those born at moderate gestation. These findings offer nuanced insights into the long-term impacts of preterm birth in the era of antenatal corticosteroid use.

Anthony G. B. Walters et al, Health Outcomes 50 Years After Preterm Birth in Participants of a Trial of Antenatal Betamethasone, Pediatrics (2024). DOI: 10.1542/peds.2024-066929

Part 2

Digest this: Ants prove superior to humans in group problem-solving maze experiment

Anyone who has dealt with ants in the kitchen knows that ants are highly social creatures; it's rare to see one alone. Humans are social creatures too, even if some of us enjoy solitude. Ants and humans are also the only creatures in nature that consistently cooperate while transporting large loads that greatly exceed their own dimensions.

Researchers have used this shared trait to conduct a fascinating evolutionary competition that asks the question: Who will be better at maneuvering a large load through a maze? The surprising results, published in the Proceedings of the National Academy of Sciences, shed new light on group decision making, as well as on the pros and cons of cooperation versus going it alone.

To enable a comparison between two such disparate species, the research team  created a real-life version of the "piano movers puzzle," a classical computational problem from the fields of motion planning and robotics that deals with possible ways of moving an unusually shaped object—say, a piano—from point A to point B in a complex environment.

Instead of a piano, the participants were given a large T-shaped object that they had to maneuver across a rectangular space divided into three chambers connected by two narrow slits.

The researchers created two sets of mazes that differed only in size, to match the dimensions of ants and humans, as well as groups of different sizes. Recruiting study participants was easier in the case of humans, who volunteered simply because they were asked to participate, and probably because they liked the idea of a competition. Ants, on the other hand, are far from competitive. They joined because they were misled into thinking that the heavy load was a juicy edible morsel that they were transporting into their nest.

The ants chosen to compete against Homo sapiens were Paratrechina longicornis. They are called this because of their long antennae, though they are sometimes referred to as "crazy ants" for their tendency to dash around. This familiar species of black ant, about 3 mm long, is common around the world.

Part 1

The ants tackled the maze challenge in three combinations: a single ant, a small group of about seven ants and a large group of about 80. Humans handled the task in three parallel combinations: a single person, a small group of six to nine individuals and a large group of 26.

To make the comparison as meaningful as possible, groups of humans were in some cases instructed to avoid communicating through speaking or gestures, even wearing surgical masks and sunglasses to conceal their mouths and eyes. In addition, human participants were told to hold the load only by the handles that simulated the way in which it is held by ants. The handles contained meters that measured the pulling force applied by each person throughout the attempt.

The researchers repeated the experiment numerous times for each combination, then meticulously analyzed the videos and all the advanced tracking data while using computer simulations and various physics models.

Unsurprisingly, the cognitive abilities of humans gave them an edge in the individual challenge, in which they resorted to calculated, strategic planning, easily outperforming the ants.
In the group challenge, however, the picture was completely different, especially for the larger groups. Not only did groups of ants perform better than individual ants, but in some cases they did better than humans. Groups of ants acted together in a calculated and strategic manner, exhibiting collective memory that helped them persist in a particular direction of motion and avoid repeated mistakes.

Humans, on the contrary, failed to significantly improve their performance when acting in groups. When communication between group members was restricted to resemble that of ants, their performance even dropped compared to that of individuals. They tended to opt for "greedy" solutions—which seemed attractive in the short term but were not beneficial in the long term, and—according to the researchers—opted for the lowest common denominator.
An ant colony is actually a family. All the ants in the nest are sisters, and they have common interests. It's a tightly knit society in which cooperation greatly outweighs competition. That's why an ant colony is sometimes referred to as a super-organism, sort of a living body composed of multiple 'cells' that cooperate with one another.

These new findings validate this vision. Researchers shown that ants acting as a group are smarter, that for them the whole is greater than the sum of its parts. In contrast, forming groups did not expand the cognitive abilities of humans. The famous 'wisdom of the crowd' that's become so popular in the age of social networks didn't come to the fore in these experiments.

Tabea Dreyer et al, Comparing cooperative geometric puzzle solving in ants versus humans, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2414274121

Part 2

 Preventing Christmas tree fires, with science

Perceptein, a protein-based artificial neural network in living cells

Researchers have designed a protein-based system inside living cells that can process multiple signals and make decisions based on them.

The researchers have also introduced a unique term, "perceptein," as a combination of protein and perceptron. Perceptron is a foundational artificial neural network concept, effectively solving binary classification problems by mapping input features to an output decision.

By merging concepts from neural network theory with protein engineering, "perceptein" represents a biological system capable of performing classification computations at the protein level, similar to a basic artificial neural network. This "perceptein" circuit can classify different signals and respond accordingly, such as deciding to stay alive or undergo programmed cell death.

In the study, "A synthetic protein-level neural network in mammalian cells," published in Science, researchers showed that perceptein circuits could distinguish signal inputs with tunable decision boundaries, offering the possibility of controlling complex cellular responses without transcriptional regulation.

 Zibo Chen et al, A synthetic protein-level neural network in mammalian cells, Science (2024). DOI: 10.1126/science.add8468

Salt-seeking behavior traced to specific brain neurons

Salt, or more precisely the sodium it contains, is very much a "Goldilocks" nutrient. Low sodium levels cause a drop in blood volume, which can have serious, sometimes deadly, health consequences. Conversely, too much salt can lead to high blood pressure and cardiovascular disease.

Given the critical importance of sodium for body and brain functions, evolution has developed a powerful drive to consume salt in situations where there is a deficiency.

Aldosterone triggers salt-appetite neurons.

Researchers made their discovery by teasing out the actions of aldosterone, a key hormone for controlling sodium levels.

Normally, aldosterone is produced when body fluid volume (including blood volume) is low, for example, after sweating without drinking enough fluid, or blood loss, or during an illness with vomiting or diarrhea. Aldosterone tells the kidney and other organs to retain sodium, which helps maintain the existing fluid in the body.

However, when aldosterone is inappropriately high, a condition called primary aldosteronism, blood pressure can rise to dangerous levels. Aldosteronism is the cause of hypertension in as many as 10-30% of all patients with high blood pressure, and the risk of stroke, heart failure, and abnormal heart rhythms is three times higher in these patients than in other patients with hypertension, although it is not clear why.

The research team focused on an unappreciated aspect of aldosteronism—a tendency to eat more salt. Almost a century ago, studies showed that aldosterone and related hormones cause salt appetite to go up in rats. More recent human studies have also found that patients with aldosteronism consume more salt than other patients with hypertension.

The team first confirmed that lack of sodium in the diet of mice increases aldosterone production and salt intake. It also increases the activity of a tiny group of neurons in the brainstem known as HSD2 neurons. The researchers had previously discovered these HSD2 neurons and had circumstantial evidence suggesting they were responsible for salt appetite.

Researchers used genetically targeted cell deletion to show that the HSD2 neurons were required for aldosterone-driven salt consumption. Moreover, they showed that humans also have a small population of HSD2 neurons in the same part of the brainstem, indicating that the same neural circuit may be relevant to people with elevated aldosterone.

Overall, the findings suggest that aldosterone acts on the tiny population of HSD2 neurons (there are roughly 200 HSD2 neurons in mice and 1,000 in humans) to induce the highly specific behavior of seeking and consuming sodium. The team's findings suggest that boosting sodium appetite may be the only central function of HSD2 neurons.

Silvia Gasparini et al, Aldosterone-induced salt appetite requires HSD2 neurons, JCI Insight (2024). DOI: 10.1172/jci.insight.175087

Unclogging the immune system: Scientists use immunotherapy to remove aging cell buildup

 As we age, our bodies are flooded by aging, or senescent cells, which have stopped dividing but, instead of dying, remain active and build up in body tissues. Recent studies have shown that getting rid of these cells might delay age-related diseases, reduce inflammation and extend lives. Despite the great potential, however, there is currently no drug that can target these cells directly and efficiently.

researchers suggest an alternative approach. In a new study published in Nature Cell Biology, they reveal that senescent cells  build up in the body by clogging up the immune system, thereby preventing their own removal.

The scientists demonstrated in mice how to unclog this blockage using immunotherapy, the new generation of treatments that is revolutionizing cancer therapy.  These findings could pave the way for innovative treatment of age-related diseases and other chronic disorders.

Julia Majewska et al, p16-dependent increase of PD-L1 stability regulates immunosurveillance of senescent cells, Nature Cell Biology (2024). DOI: 10.1038/s41556-024-01465-0

How gold reaches Earth's surface

A research team has discovered a new gold-sulfur complex that helps researchers understand how gold deposits are formed.

Gold in ore deposits associated with volcanoes around the Pacific Ring of Fire originates in Earth's mantle and is transported by magma to its surface. But how that gold is brought to the surface has been a subject of debate. Now, the research team has used numerical modeling to reveal the specific conditions that lead to the enrichment of gold in magmas that rise from the Earth's mantle to its surface.

Specifically, the model reveals the importance of a gold-trisulfur complex whose existence has been vigorously debated.

The presence of this gold-trisulfur complex under a very specific set of pressures and temperatures in the mantle 30 to 50 miles beneath active volcanoes causes gold to be transferred from the mantle into magmas that eventually move to the Earth's surface. The team's results are published in the Proceedings of the National Academy of Sciences.

This offers the most plausible explanation for the very high concentrations of gold in some mineral systems in subduction zone environments.

Gold deposits associated with volcanoes form in what are called subduction zones. Subduction zones are regions where a continental plate—the Pacific plate, which lies under the Pacific Ocean—is diving under the continental plates that surround it. In these seams where continental plates meet each other, magma from Earth's mantle has the opportunity to rise to the surface.

On all of the continents around the Pacific Ocean, from New Zealand to Indonesia, the Philippines, Japan, Russia, Alaska, the western United States and Canada, all the way down to Chile, we have lots of active volcanoes. All of those active volcanoes form over or in a subduction zone environment. The same types of processes that result in volcanic eruptions are processes that form gold deposits.

Part 1

Gold is present in Earth's mantle above the subducting ocean plate. But when the conditions are just right that a fluid containing the trisulfur ion is added from the subducting plate to the mantle, gold strongly prefers to bond with trisulfur to form a gold-trisulfur complex. This complex is highly mobile in magma.

Scientists have previously known that gold complexes with various sulfur ions, but this study is the first to present a robust thermodynamic model for the existence and importance of the gold-trisulfur complex.

To identify this new complex, the researchers developed a thermodynamic model based on lab experiments in which the researchers control pressure and temperature of the experiment, then measure the results of the experiment. Then, the researchers developed a thermodynamic model that predicts the results of the experiment. This thermodynamic model can then be applied to real-world conditions.

These results provide a really robust understanding of what causes certain subduction zones to produce very gold-rich ore deposits.

Deng-Yang He et al, Mantle oxidation by sulfur drives the formation of giant gold deposits in subduction zones, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073/pnas.2404731121

Part 2

From Earth to alien worlds: The fundamental limits to life

Extraterrestrial and artificial life have long captivated the human mind. Knowing only the building blocks of our own biosphere, can we predict how life may exist on other planets? What factors will rein in the Frankensteinian life forms we hope to build in laboratories here on Earth?

An open-access paper published in Interface Focus and co-authored by several SFI researchers takes these questions out of the realm of science fiction and into scientific laws.

Reviewing case studies from thermodynamics, computation, genetics, cellular development, brain science , ecology and evolution, the paper concludes that certain fundamental limits prevent some forms of life from ever existing.

Requirements include entropy reduction (which includes, for instance, the ability to heal and repair), closed-compartment cells as the inevitable units of life, and a system—such as brains—that integrates information and makes decisions using neuron-like units.

The authors point to historical examples where people predicted some complex feature of life that biologists later confirmed. Examples include the Schrodinger view of information molecules as "aperiodic crystals," or mid-century simulations predicting that parasites are inevitable when complex life evolves.

That such correct predictions were possible with almost no available evidence suggests all living systems follow an underlying universal logic.

 Ricard Solé et al, Fundamental constraints to the logic of living systems, Interface Focus (2024). DOI: 10.1098/rsfs.2024.0010

Scientists discover a 'Goldilocks' zone for DNA organization, opening new doors for drug development

In a discovery that could redefine how we understand cellular resilience and adaptability, scientists  have unlocked the secret interactions between a primordial inorganic polymer of phosphate known as polyphosphate (polyP), and two basic building blocks of life: DNA and the element magnesium. These components formed clusters of tiny liquid droplets–also known as condensates–with flexible and adaptable structures.

PolyP and magnesium are involved in many biological processes. Thus, the findings could lead to new methods for tuning cellular responses, which could have impactful applications in translational medicine.

The ensuing study, published in Nature Communications on October 26, 2024, reveals a delicate "Goldilocks" zone—a specific magnesium concentration range—where DNA wraps around polyP-magnesium ion condensates. Similar to a thin eggshell covering a liquid-like interior, this seemingly simple structure may help cells organize and protect their genetic material.

The microscopy images revealed that DNA wraps itself around a condensate, creating a thin eggshell-like barrier. This shell could affect molecule transportation and also slow down fusion: the process where two condensates merge into one. Without DNA shells, polyP-magnesium ion condensates readily fused—like how oil drops and vinegar fuse in a salad dressing bottle when shaken. However, careful examination showed that fusion overall slowed to varying extents, depending on DNA length. Longer DNA, the researchers suspected, caused greater entanglement on condensate surfaces—similar to how long hair tangles more than short hair.

Another crucial discovery: DNA shell formation only occurred within a specific magnesium concentration range—too much or too little, and the shell wouldn't materialize. This "Goldilocks" effect highlights how cells can regulate condensate structure, size and function simply by tuning control parameters.

 Ravi Chawla et al, Reentrant DNA shells tune polyphosphate condensate size, Nature Communications (2024). DOI: 10.1038/s41467-024-53469-x

The Risk of Cancer Fades as We Get Older

Aging brings two opposing trends in cancer risk: first, the risk climbs in our 60s and 70s, as decades of genetic mutations build up in our bodies. But then, past the age of around 80, the risk drops again – and a new study may explain a key reason why.

The international team of scientists behind the study analyzed lung cancer in mice, tracking the behavior of alveolar type 2 (AT2) stem cells. These cells are crucial for lung regeneration, and are also where many lung cancers get started.

What emerged was higher levels of a protein called NUPR1 in the older mice. This caused cells to act as if they were deficient in iron, which in turn limited their regeneration rates – putting restrictions on both healthy growth and cancerous tumors.

The aging cells actually have more iron, but for reasons we don't yet fully understand, they function like they don't have enough. Aging cells lose their capacity for renewal and therefore for the runaway growth that happens in cancer.

The same processes were found to be happening in human cells too: more NUPR1 leads to a drop in the amount of iron available to cells. When NUPR1 was artificially lowered or iron was artificially increased, cell growth capabilities were boosted again.

That potentially gives researchers a way of exploring treatments that target iron metabolism – especially in older people. 

These findings also have implications for cancer treatments based on a type of cell death called ferroptosis, which is triggered by iron. This cell death is less common in older cells, the researchers found, because of their functional iron deficiency.

This perhaps also makes them more resistant to cancer treatments based on ferroptosis that are in development– so the earlier a ferroptosis treatment can be tried, the better it's likely to work.

https://www.nature.com/articles/s41586-024-08285-0

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Novel biomarker catches aging cells in the act

Researchers have identified interleukin-23 receptor (IL-23R) as a significant biomarker of cellular senescence and aging in both mice and humans. Experiments show that IL-23R levels in the bloodstream increase with age and can decrease, reflecting senescent cell clearing, with senolytic therapies.

Cellular senescence occurs when cells stop dividing but do not trigger apoptosis mechanisms that would allow them to die naturally. Instead, they are stuck in a zombie-like state, where they still have the urge to feed and carry out metabolic activities, but with increasingly incoherent cell signaling and increased pro-inflammatory cytokine secretions.

Senescent cell activity has been linked to several age-related diseases, including those of the immune, cardiovascular, metabolic, pulmonary, musculoskeletal and neurological systems.
Scientists have been searching for a biomarker that reliably estimates the levels of active senescent cells in the body. If found, this biomarker could inform clinical interventions, potentially intervening before disease conditions present themselves.

In the study "IL-23R is a senescence-linked circulating and tissue biomarker of aging," published in Nature Aging, researchers sought to identify senescence-related biomarkers and measure their responsiveness to different therapeutics in mice of various ages.

The team tested 92 plasma proteins through the Olink Target 96 Mouse Exploratory panel and ultimately analyzed 67 (25 were excluded due to low or no detection).

Tissues, including kidney, liver, spleen, cerebral cortex, adipose and lung, were examined with real-time PCR for 21 gene expressions related to senescence secretions and inflammation markers.
Part 1

Applying short-term interventions with drugs that clear senescent cells, including venetoclax, navitoclax, fisetin and luteolin, as well as transgenic clearance methods targeting p16-positive senescent cells, mice were examined for changes in plasma proteins and tissue transcripts.

Analyses showed that three of the tested plasma proteins, IL-23R, CCL5 and CA13, displayed age-related alterations in circulation and tissues, indicating potential biomarker marker viability.

Age-dependent increases in IL-23R and CCL5 were reversed by senolytic treatment, and CA13 levels, which normally decline with age, were restored to more youthful levels.

Researchers identified IL-23R as the most promising plasma protein biomarker due to its obvious and consistent association with aging across multiple tissue parameters. IL-23R increased with age in both mice and humans and had a robust change response to senolytic interventions.

The strong correlation between IL-23R and other well-defined senescence tissue markers makes it a potential reliable biomarker of systemic senescent cell burden, offering an important new tool for probing and possibly preventing age-related diseases.

Chase M. Carver et al, IL-23R is a senescence-linked circulating and tissue biomarker of aging, Nature Aging (2024). DOI: 10.1038/s43587-024-00752-7

Part 2

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New genetic mutation found to suppress cancer growth

 Researchers have identified a genetic mutation that slows the growth of melanoma and potentially other cancers by harnessing the power of the immune system. Their findings, published in the Journal of Experimental Medicine, could lead to new treatments that improve outcomes from existing cancer immunotherapies.

Researchers have identified many genes, known as oncogenes, that initiate and drive cancer when mutated. Although scientists have long speculated that mutations protecting against cancer also exist in the human genome but finding them by studying human subjects has been difficult because people carrying these genetic variants don't show any obvious differences compared to others.

To search for genes that confer tumor resistance, researchers created mouse models with various genetic mutations and then searched for mice that didn't develop tumors or had limited cancer growth. Next, they used a method recently developed  called automated meiotic mapping (AMM), which traces unusual features of interest in mutant mice to the causative mutations.

Part 1

The researchers quickly homed in on a gene called H2-Aa. Mice carrying two mutated copies of this gene, causing them to completely lack the H2-Aa protein, often showed no tumor growth after exposure to melanoma cells. Those carrying one mutant copy had significantly reduced growth compared with mice carrying strictly the "wild type" form of the gene. H2-Aa is responsible for producing part of an immune protein called MHC class II, which helps the immune system distinguish self-proteins from non-self-proteins, readying it to attack potential invaders.
Using genetic engineering, the researchers narrowed H2-Aa's cancer-supporting function to its presence on the surface of a subclass of immune cells called dendritic cells. Eliminating H2-Aa in only these cells was enough to mimic having the absence of H2-Aa throughout the body. When the researchers compared tumors that developed in wild-type mice and those in mice lacking H2-Aa, the tumors in mutant mice were infiltrated with more dendritic cells as well as more tumor-fighting CD8 T cells, and far fewer regulatory T cells that suppress anticancer immune activity.

Seeking a pharmaceutical that could produce the same effects as mutant H2-Aa, the researchers developed a monoclonal antibody—a protein that blocks the effects of other proteins—against H2-Aa. Although the antibody had a considerable anticancer effect when delivered to mice with melanoma tumors, its effect was greatly enhanced when the researchers also treated the same mice with a checkpoint inhibitor drug, a type of immunotherapy. On the other hand, without monoclonal antibodies against H2-Aa, checkpoint inhibitors had no effect on cancer growth.
Monoclonal antibodies targeting the human form of this and other closely related proteins could have a similar effect, serving as a viable cancer treatment on its own or as a boost to immunotherapy treatments. This idea might eventually be tested in clinical trials.

Hexin Shi et al, Suppression of melanoma by mice lacking MHC-II: Mechanisms and implications for cancer immunotherapy, Journal of Experimental Medicine (2024). DOI: 10.1084/jem.20240797

Part 2

 Bacteria in human gut rarely update their CRISPR defense systems

Within the human digestive tract are trillions of bacteria from thousands of different species. These bacteria form communities that help digest food, fend off harmful microbes, and play many other roles in maintaining human health.

These bacteria can be vulnerable to infection from viruses called bacteriophages. One of bacterial cells' most well-known defenses against these viruses is the CRISPR system, which evolved in bacteria to help them recognize and chop up viral DNA.

A new study  has yielded new insight into how bacteria in the gut microbiome adapt their CRISPR defenses as they encounter new threats. The researchers found that while bacteria grown in the lab can incorporate new viral recognition sequences as quickly as once a day, bacteria living in human gut add new sequences at a much slower rate—on average, one every three years.

The findings suggest that the environment within the digestive tract offers many fewer opportunities for bacteria and bacteriophages to interact than in the lab, so bacteria don't need to update their CRISPR defenses very often. It also raises the question of whether bacteria have more important defense systems than CRISPR.

This finding is significant because we use microbiome-based therapies like fecal microbiota transplant to help treat some diseases, but efficacy is inconsistent because new microbes do not always survive in patients. Learning about microbial defenses against viruses helps us to understand what makes a strong, healthy microbial community.

In bacteria, CRISPR serves as a memory immune response. When bacteria encounter viral DNA, they can incorporate part of the sequence into their own DNA. Then, if the virus is encountered again, that sequence produces a guide RNA that directs an enzyme called Cas9 to snip the viral DNA, preventing infection.

These virus-specific sequences are called spacers, and a single bacterial cell may carry more than 200 spacers. These sequences can be passed onto offspring, and they can also be shared with other bacterial cells through a process called horizontal gene transfer.

Previous studies have found that spacer acquisition occurs very rapidly in the lab, but the process appears to be slower in natural environments.

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The researchers looked at how CRISPR sequences changed over time in two different datasets obtained by sequencing microbes from the human digestive tract. One of these datasets contained 6,275 genomic sequences representing 52 bacterial species, and the other contained 388 longitudinal "metagenomes," that is, sequences from many microbes found in a sample, taken from four healthy people.
By analyzing those two datasets, the researchers found out that spacer acquisition is really slow in human gut microbiome: On average, it would take 2.7 to 2.9 years for a bacterial species to acquire a single spacer in our gut, which is super surprising because our gut is challenged with viruses almost every day from the microbiome itself and in our food.
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The researchers then built a computational model to help them figure out why the acquisition rate was so slow. This analysis showed that spacers are acquired more rapidly when bacteria live in high-density populations. However, the human digestive tract is diluted several times a day, whenever a meal is consumed. This flushes out some bacteria and viruses and keeps the overall density low, making it less likely that the microbes will encounter a virus that can infect them.
Another factor may be the spatial distribution of microbes, which the researchers think prevents some bacteria from encountering viruses very frequently.

Sometimes one population of bacteria may never or rarely encounter a phage because the bacteria are closer to the epithelium in the mucus layer and farther away from a potential exposure to viruses.
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Among the populations of bacteria that they studied, the researchers identified one species—Bifidobacteria longum—that had gained spacers much more recently than others. The researchers found that in samples from unrelated people, living on different continents, B. longum had recently acquired up to six different spacers targeting two different Bifidobacteria bacteriophages.
This acquisition was driven by horizontal gene transfer—a process that allows bacteria to gain new genetic material from their neighbors. The findings suggest that there may be evolutionary pressure on B. longum from those two viruses.
Analyzing microbes' immune defenses may offer a way for scientists to develop targeted treatments that will be most effective in a particular patient, the researchers say. For example, they could design therapeutic microbes that are able to fend off the types of bacteriophages that are most prevalent in that person's microbiome, which would increase the chances that the treatment would succeed.

An-Ni Zhang et al. CRISPR-Cas spacer acquisition is a rare event in human gut microbiome, Cell Genomics (2024). DOI: 10.1016/j.xgen.2024.100725. www.cell.com/cell-genomics/ful … 2666-979X(24)00354-9

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Microplastics found in multiple human organ tissues correlated with lesions

Researchers have recently performed a metadata investigation into the presence of microplastics in humans. They report a concerning relationship between micro and nanoplastic (MNP) concentrations in damaged tissues and links with multiple health conditions.

With the increased use in consumer products came elevated microscopic plastic pollution circulating in soil and waterways, eventually accumulating in the environment, food webs and human tissues.

In the study, "Mapping micro(nano)plastics in various organ systems: Their emerging links to human diseases?" published in TrAC Trends in Analytical Chemistry, investigators collected 61 available research articles for MNP detection in human tissues, plus 840 articles on MNP toxicological mechanisms.

Data came from spectroscopy, microscopy, and pyrolysis-gas chromatography/mass spectrometry investigations to identify polymer types in different tissues. Toxicological studies employed cell models and animal experiments to examine oxidative stress, inflammatory responses, and related signaling pathways.

The studies documented particles detected in skin, arteries, veins, thrombi, bone marrow, testes, semen, uterus, and placenta. MNPs were found in the digestive system, from saliva to feces, liver, and gallstones.

Within the respiratory system, MNPs were everywhere, including lung tissue, with microscopic fibers common in bronchoalveolar lavage fluid and sputum. Positive correlations emerged between particle abundance and specific disorders, such as inflammatory bowel disease, thrombosis, cervical cancer, and uterine fibroids.

Toxicological tests showed possible MNP-triggered oxidative stress, mitochondrial dysfunction, inflammatory responses, and apoptosis in various cell types, along with organ-level concerns like neurodegenerative disease onset when crossing the blood-brain barrier.

A critically important signal in the metadata discovered by the researchers was that measured levels of MNPs tended to be higher in tissues with lesions than in non-lesioned tissues. These included inflamed intestines, fibrotic lungs, or cancerous growths, suggesting a potential link between MNP buildup and local pathology.

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what came first, the lesion or the microplastic," it is possible that MNPs contribute to inflammation, oxidative stress, and cellular damage, which can cause or worsen tissue lesions. But it is also possible that these lesions accumulate more MNPs in already damaged tissue areas. While the current findings do not provide a direct cause-and-effect relationship, they offer good targets for further study.
There are no conventional methods for removing microplastics from the environment or human tissues. While efforts are underway to discover methods of environmental mitigation, developing such strategies to handle diverse particle sizes and chemistries of the particles embedded in living tissues presents an immense and potentially unattainable challenge.

Yating Luo et al, Mapping micro(nano)plastics in various organ systems: Their emerging links to human diseases?, TrAC Trends in Analytical Chemistry (2024). DOI: 10.1016/j.trac.2024.118114

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Analysis of 160,000 films shows rise in 'murderous verbs' since 1970

The amount of murdering and killing in movies has increased overall over the past 50 years, according to a study that analyzed a massive database of film dialogue.

Researchers used machine learning to search a database of subtitles from more than 160,000 English-language movies produced from 1970 to 2000. They calculated the amount of dialogue from characters using variations of the words "murder" or "kill" in each of the films.

While the total use of these "murderous verbs" varied widely from year to year, there was a clear increasing trend over the five-decade period.

And not just in crime movies, where violence might be expected. Characters in noncrime movies are also talking more about killing and murdering today than they did 50 years ago.

It is still happening. Researchers found increases in violence cross all genres.

These findings suggest that references to killing and murder in movie dialogue not only occur far more frequently than in real life but are also increasing over time.

Movies are trying to compete for the audience's attention and research shows that violence is one of the elements that most effectively hooks audiences."

That means we need to promote "mindful consumption and media literacy to protect vulnerable populations, especially children," the researchers wrote in the study.

Why only in English movies, we find this trend in all Indian language movies too!

Trends of Violence in Movies During the Past Half Century, JAMA Pediatrics (2024). DOI: 10.1001/jamapediatrics.2024.5741

Preclinical study finds surges in estrogen promote binge drinking in females

The hormone estrogen regulates binge drinking in females, causing them to "pregame," or consume large quantities of alcohol in the first 30 minutes after it's offered, according to a preclinical study led by scientists at Weill Cornell Medicine. The study establishes—for what is thought to be the first time—that circulating estrogen increases binge alcohol consumption in females and contributes to known sex differences in this behaviour.

The findings, published Dec. 30 in the journal Nature Communications, could lead to novel approaches for treating alcohol use disorder.

In a 2021 study, researchers showed that a specific subpopulation of neurons in a brain region called the bed nucleus of the stria terminalis (BNST) were more excitable in female mice than in males. This enhanced activity correlated with their binge-drinking behaviour.

But what makes this neural circuit more excitable in females? Estrogen has such powerful effects on so many behaviors, particularly in females. So, it makes sense that it would also modulate drinking.

To assess estrogen's potential involvement, the researchers began by monitoring the hormone levels throughout the estrous cycle of female mice. Then, they served up the alcohol. They found that when a female has a high level of circulating estrogen, she drinks much more than on days when her estrogen is low.

That enhanced binging behaviour was reflected in heightened activity in those same neurons in the BNST. When a female takes her first sip from the bottle containing alcohol, those neurons go crazy. And if she's in a high-estrogen state, they go even crazier. That extra boost of neural activity means the mice hit the bottle even harder, particularly within the first 30 minutes after the alcohol was made available, a behavior researchers refer to as "front-loading."
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