Even though the glass looks clean when cleaned with detergent, its ability to transmit light is significantly impaired. Therefore, a clean-looking end result does not guarantee optimal performance.
The study provides information on solar panel maintenance for users of solar power.

 Aapo Poskela et al, Impact of Textured Surfaces and Cleaning on Solar Panel Glass Transmittance, (2024). DOI: 10.4229/eupvsec2024/3av.1.17

Part 2

Dopamine acts on motivation and reinforcement learning via distinct cellular processes

Dopamine is a key neurotransmitter known to modulate motivation and reinforcement learning. While the role of dopamine in these reward-related processes is well-established, the cellular and neural circuit-level mechanisms underpinning its involvement in these processes is not yet fully understood.

So researchers  carried out a study investigating the cellular processes via which dopamine supports motivation and the reinforcement of specific behaviours.

Their findings, published in Nature Neuroscience, suggest that different aspects of reward-related behaviour are supported by two distinct dopamine receptors, namely D3 and D1.

The previous literature clearly showed that dopamine is important for motivation and reinforcement. 

This is an important topic since deficits in motivation or excessive motivation are cardinal symptoms in many mental disorders. The nucleus accumbens, a brain region where dopamine is thought to exert its effects, is uniquely enriched with a molecule that recognizes dopamine, the D3 receptor.

As an initial step in addressing the role of D3,the researchers developed a new mouse strain that enables cell-type-selective deletion of D3 receptors, including in the nucleus accumbens.

The results show that specifically, D3 receptors were found to regulate motivation, while D1 receptors appeared to regulate reinforcement.

These  findings provide the first evidence that dopamine exerts its actions on motivation and reinforcement through separable cellular processes in neurons that are part of the brain's reward circuitry.

There are important implications because medications that act on D3 receptors are used for the treatment of mood disorders.

Juan Enriquez-Traba et al, Dissociable control of motivation and reinforcement by distinct ventral striatal dopamine receptors, Nature Neuroscience (2024). DOI: 10.1038/s41593-024-01819-9

Nicolas X. Tritsch, Motivating interest in D3 dopamine receptors, Nature Neuroscience (2024). DOI: 10.1038/s41593-024-01820-2

Archaeologists reveal 8,000-year-old bone powder cooking practice in ancient China

A new study by archaeologists published in the International Journal of Osteoarchaeology, provides insights into some of the earliest forms of humans processing bones into powder for cooking, dating back nearly 8,000 years (6,085 and 6,369 BC).

The finding was made at the Xielaozhuang (XLZ) site in the Henan province of North China. The site belonged to the Peiligang culture (ca. 9,000–7,000 BP), which was one of North China's most significant Neolithic cultures. It was known for being among the earliest producers of fermented beverages, creators of the oldest tonal flutes, basic textile weavers and sewers, and possibly one of the earliest users of the Chinese script.

Using a multidisciplinary approach that combined Scanning Electron Microscopy with Energy-Dispersive X-ray (SEM-EDS), Fourier Transform Infrared Spectroscopy (FTIR), X-Ray Diffraction (XRD), and starch analysis, the researchers were able to analyze the chemical, mineral, and microscopic composition of the crust-residue.

More specifically, the research team found certain compounds and minerals, including hydroxyapatite, magnesium whitlockite, phosphate (PO₄^3-), and carbonate (CO₃^2-) groups, as well as key elements, including carbon, oxygen, phosphorus, calcium, and magnesium, all of which are typical components found in bone.

They concluded that bone powder was likely ground up and cooked together with various wild plants, including acorns and Job's tears.

This was particularly interesting because, despite agriculture having been developed in China around 10,000 years ago, the Peiligang culture made limited use of cultivated crops and animals, including foxtail millet, common millet, rice, and pigs. In fact, no domesticated crops were found in the crust-residue at XLZ, and from previous zooarchaeological analyses, it was known that domesticated animals, such as pigs, only made up around 10% of all remains.

The researchers speculate that bone powder processing at XLZ represented an important survival strategy during the transition from hunting-gathering to farming. It has long been hypothesized that various Paleolithic societies used bone grease extraction methods to extract extra fat (grease) and nutrients from otherwise inedible resources.

This research contributes to a growing body of evidence showing how early Neolithic societies developed sophisticated subsistence strategies during the transition from hunter-gatherer to farm-based societies.

 Xingtao Wei et al, Bone Powder and Wild Plants: Subsistence Strategies of Early Neolithic Settlers in North China, International Journal of Osteoarchaeology (2024). DOI: 10.1002/oa.3376

Octopus arms have segmented nervous systems to power extraordinary movements

Octopus arms move with incredible dexterity, bending, twisting, and curling with nearly infinite degrees of freedom. New research revealed that the nervous system circuitry that controls arm movement in octopuses is segmented, giving these extraordinary creatures precise control across all eight arms and hundreds of suckers to explore their environment, grasp objects, and capture prey.

Octopus arms move with incredible dexterity, bending, twisting, and curling with nearly infinite degrees of freedom. Credit: Cassady Olson

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Using cellular markers and imaging tools to trace the structure and connections from the ANC, the researchers  saw that neuronal cell bodies were packed into columns that formed segments, like a corrugated pipe. These segments are separated by gaps called septa, where nerves and blood vessels exit to nearby muscles. Nerves from multiple segments connect to different regions of muscles, suggesting the segments work together to control movement.

The best way to set up a control system for this very long, flexible arm would be to divide it into segments.

Part 1

Nerves for the suckers also exited from the ANC through these septa, systematically connecting to the outer edge of each sucker. This indicates that the nervous system sets up a spatial, or topographical, map of each sucker.

Octopuses can move and change the shape of their suckers independently. The suckers are also packed with sensory receptors that allow the octopus to taste and smell things that they touch—like combining a hand with a tongue and a nose. The researchers think the "suckeroptopy," as they called the map, facilitates this complex sensory-motor ability.

 Neuronal segmentation in cephalopod arms, Nature Communications (2025). DOI: 10.1038/s41467-024-55475-5

Part 2

Marine animals consume microplastic particles and excrete them in feces, posing risks to marine environment

A new  study has uncovered alarming findings about the spread of microplastic particles in the marine food web. In recent years, numerous studies have examined the dangers of marine animals and more specifically, filter-feeding organisms, ingesting non-degradable microplastic particles.

In the current study, the research team sought to understand how the biological filtration by filter-feeding organisms affects the microplastics in their environment. The findings indicate that the particles are excreted in the feces of marine animals, causing them to be unidentifiable as plastic to the marine environment, but potentially as other organic matter suitable for consumption.

Additionally, the presence of microplastic within feces affects feces dispersal, which causes the accumulation of feces and plastic particles. This may increase carbon and nitrogen levels on the seafloor and lead to algal blooms, which have a critical impact on the balance of the marine food web.

Eden Harel et al, Effects of biological filtration by ascidians on microplastic composition in the water column, Chemosphere (2024). DOI: 10.1016/j.chemosphere.2024.143589

AI-designed proteins neutralize toxins found in snake venom

A study by this year's Nobel Laureate in Chemistry reveals a possible game-changer in snakebite treatment. Researchers have created new proteins that neutralize lethal toxins found in snake venom, potentially offering a safer and more effective alternative to traditional antivenoms.

According to the WHO, venomous snakebites affect between 1.8 and 2.7 million people each year, leading to roughly 100,000 annual deaths and three times as many permanent disabilities, including lost limbs. Most injuries happen in Africa, Asia, and Latin America, where weak health systems aggravate the issue.

Currently, the only antivenoms used to treat snakebite victims are derived from animal plasma and often come with high costs, limited efficacy, and adverse side effects. Venoms also differ widely across snake species, necessitating custom treatments in different parts of the world.

In recent years, however, scientists have gained a deeper understanding of snake toxins and developed new ways to combat their effects. One such development was published on 15 January in Nature.

A team led by 2024 Nobel Laureate in Chemistry David Baker from the University of Washington School of Medicine and Timothy Patrick Jenkins from DTU (the Technical University of Denmark) used deep learning tools to design new proteins that bind to and neutralize toxins from deadly cobras.

The study focuses on an important class of snake proteins called three-finger toxins, which are often the reason antivenoms based on immunized animals fail. While not yet protecting against full snake venom—which is a complex mixture of different toxins unique to each snake species—the AI-generated molecules provide full protection from lethal doses of three-finger toxins in mice: 80–100% survival rate, depending on the exact dose, toxin and designed protein.

These toxins tend to evade the immune system, rendering plasma-derived treatments ineffective. This research thus demonstrates that AI-accelerated protein design can be used to neutralize harmful proteins that have otherwise proven difficult to combat.

David Baker, De novo designed proteins neutralize lethal snake venom toxins, Nature (2025). DOI: 10.1038/s41586-024-08393-x. www.nature.com/articles/s41586-024-08393-x

Mosquitoes defy droughts by drinking blood, ensuring survival and disease spread

Mosquitoes are able to survive prolonged droughts by drinking blood, which helps to explain how their populations quickly rebound when it finally rains, biologists found. 

A study examined how two species of mosquito known for infecting people with diseases such as malaria were able to survive nearly three weeks without rain.

The findings could help explain why the incidence of infection from mosquito-borne illness does not always decline during droughts. While there may be fewer mosquitoes, those that survive bite more often.

And mosquitoes appear to be benefiting from climate change as winters get warmer by biting people more!

 Christopher J. Holmes et al, Multiple blood feeding bouts in mosquitoes allow for prolonged survival and are predicted to increase viral transmission during dry periods, iScience (2025). DOI: 10.1016/j.isci.2025.111760

India achieves 'historic' space docking mission

India docked two satellites in space Thursday, a key milestone for the country's dreams of a space station and a manned moon mission, the space agency said.

The satellites, weighing 220 kilograms (485 pounds) each, blasted off in December on a single rocket from India's Sriharikota launch site. Later they separated.

The two satellites were maneuvered back together on Thursday in a "precision" process resulting in a "successful spacecraft capture", the Indian Space Research Organisation (ISRO) said, calling it a "historic moment".

India became the fourth country to achieve the feat—dubbed as SpaDeX, or Space Docking Experiment—after Russia, the United States and China.

The aim of the mission was to "develop and demonstrate the technology needed for rendezvous, docking, and undocking of two small spacecraft", ISRO said.

ISRO said the technology is "essential" for India's moon mission.

Source: ISRO

Damage to RNA, not DNA, found to be main cause of acute sunburn

We have all been told to avoid direct sunlight between 12 noon and 3 p.m., seek out shade and put on sunscreen and a hat. Nevertheless, most of us have experienced sunburn at least once. The skin turns bright red, feels irritated and needs cooling.

You may also have been told that sunburn damages the DNA. But that is not the full truth, according to researchers responsible for a new study conducted . The findings are published in the journal Molecular Cell.

Sunburn damages the DNA, leading to cell death and inflammation. So the textbooks say. But in this study researchers were surprised to learn that this is a result of damage to the RNA, not the DNA that causes the acute effects of sunburn!

RNA is similar to DNA, but whereas DNA is long lived, RNA is a more transient molecule. A type of RNA, known as messenger RNA (mRNA), functions as the intermediate 'messenger' that carries information from DNA to make proteins—the basic building blocks of cellular components.

DNA damage is serious as the mutations will get passed down to progenies of the cells, RNA damage happens all the time and does not cause permanent mutations. Therefore, we used to think that the RNA is less important, as long as the DNA is intact. But in fact, damages to the RNA are the first to trigger a response to UV radiation.

The new study was conducted on mice as well as human skin cells, and the objective was to describe the impact of UV radiation on the skin and what causes these damages. The researchers found the same skin response to UV radiation exists in both mice and human cells.

mRNA damage triggers a response in ribosomes (protein complexes that "read" the mRNA to synthesize protein), orchestrated by a protein known as ZAK-alpha—the so-called ribotoxic stress response—the new study shows. The response can be described as a surveillance system within the cells, which registers the RNA damage, leading to inflammatory signaling and recruitment of immune cells, which then leads to inflammation of the skin.

Researchers  found that the first thing the cells respond to after being exposed to UV radiation is damage to the RNA, and that this is what triggers cell death and inflammation of the skin. In mice exposed to UV radiation they found responses such as inflammation and cell death, but when they removed the ZAK gene, these responses disappeared, which means that ZAK plays a key role in the skin's response to UV-induced damage.

So you could say that everything depends on this one response, which monitors all protein translations occurring. The cells respond to the RNA damage, realizing that something is wrong, and this is what leads to cell death.

Part 1

The result of the study changes our understanding of sunburn and the skin's defense mechanisms: that RNA damage triggers a faster and more effective response, protecting the skin from further damage.
The fact that the DNA does not control the skin's initial response to UV radiation, but that something else does and that it does so more effectively and more quickly, is quite the paradigm shift.
We need to understand the function of RNA damage, as it may in the long term change our entire approach to prevention and treatment of sunburn."

"Many inflammatory skin diseases are worsened by sun exposure. Thus, understanding how our skin responds at the cellular level to UV damage opens the door to innovative treatments for certain chronic skin conditions.

Now rewrite the text books!

Anna Constance Vind et al, The ribotoxic stress response drives acute inflammation, cell death, and epidermal thickening in UV-irradiated skin in vivo, Molecular Cell (2024). DOI: 10.1016/j.molcel.2024.10.044

Part 2

Wildfires ignite infection risks by weakening the body's immune defenses and spreading bugs in smoke

We know fire can harm directly, causing injuries and death.

But wildfires, or bushfires, can also have indirect consequences for human health. In particular, they can promote the incidence and spread of a range of infections.

Most people appreciate that fires can cause burns and smoke inhalation, both of which can be life-threatening in their own right. What's perhaps less well known is that both burns and smoke inhalation can cause acute and chronic changes in the immune system. This can leave those affected vulnerable to infections at the time of the injury, and for years to come.

Burns induce profound changes in the immune system. Some parts go into overdrive, becoming too reactive and leading to hyper-inflammation. In the immediate aftermath of serious burns, this can contribute to sepsis and organ failure.

Finding Clues to Oxygen Production on Early Earth

Possible link between Earth’s rotation rate and oxygenation

Earth's Rotation Is Slowing Down, And Could Explain Why We Have Oxygen

Ever since its formation around 4.5 billion years ago, Earth's rotation has been gradually slowing down, and its days have gotten progressively longer as a result.

While Earth's slowdown is not noticeable on human timescales, it's enough to work significant changes over eons. One of those changes is perhaps the most significant of all, at least to us: lengthening days are linked to the oxygenation of Earth's atmosphere, according to a study from 2021.

Specifically, the blue-green algae (or cyanobacteria) that emerged and proliferated about 2.4 billion years ago would have been able to produce more oxygen as a metabolic by-product because Earth's days grew longer.

There are two major components to this story that, at first glance, don't seem to have a lot to do with each other. The first is that Earth's spin is slowing down. The reason Earth's spin is slowing down is because the Moon exerts a gravitational pull on the planet, which causes a rotational deceleration since the Moon is gradually pulling away. We know, based on the fossil record, that days were just 18 hours long 1.4 billion years ago, and half an hour shorter than they are today 70 million years ago. Evidence suggests that we're gaining 1.8 milliseconds a century.

The second component is something known as the Great Oxidation Event – when cyanobacteria emerged in such great quantities that Earth's atmosphere experienced a sharp, significant rise in oxygen. Without this oxidation, scientists think life as we know it could not have emerged; so, although cyanobacteria may cop a bit of side-eye today, the fact is we probably wouldn't be here without them.

https://www.nature.com/articles/s41561-021-00784-3

A chain reaction: HIV vaccines can lead to antibodies against antibodies

Many vaccines work by introducing a protein to the body that resembles part of a virus. Ideally, the immune system will produce long-lasting antibodies recognizing that specific virus, thereby providing protection.

But scientists have now discovered that for some HIV vaccines, something else happens: after a few immunizations the immune system begins to produce antibodies against immune complexes already bound to the viral protein alone.

They don't yet know whether this chain reaction, described in Science Immunology, hurts or helps the immune system's ability to fight HIV, but say that understanding it better could lead to improvements in HIV vaccines. The research was published in the journal on January 17, 2025.

Understanding these responses could lead to smarter vaccine designs and immunotherapeutics. It's an exciting step forward in fine-tuning antibody and vaccine-based strategies against HIV and other diseases.

Sharidan Brown et al, Anti-Immune Complex Antibodies are Elicited During Repeated Immunization with HIV Env Immunogens, Science Immunology (2025). DOI: 10.1126/sciimmunol.adp5218. www.science.org/doi/10.1126/sciimmunol.adp5218

Study provides insight into how some species thrive in dark, oxygen-free environments

Most life on Earth relies on the sun's energy for survival, but what about organisms in the deep sea that live beyond the reach of its rays? A new study led by Woods Hole Oceanographic Institution (WHOI), published in The ISME Journal, sheds light on how a species of foraminifera, single-celled organisms found in almost all marine habitats, thrives in a dark, oxygen-free environment.

For this foraminifera species, the answer is chemoautotrophy, a metabolic process that utilizes inorganic energy sources, perhaps sulfide, to take up carbon, enabling it to survive in oxygen-free environments. Chemoautotrophy has been observed within Bacteria and Archaea, which are microbial organisms without a true nucleus. However, foraminifera are eukaryotes, meaning they have a well-defined nucleus, which houses an organism's genetic material.

 Fatma Gomaa et al, Array of metabolic pathways in a kleptoplastidic foraminiferan protist supports chemoautotrophy in dark, euxinic seafloor sediments, The ISME Journal (2024). DOI: 10.1093/ismejo/wrae248

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Brains of people with sickle cell disease appear older, study finds

Individuals with sickle cell disease—a chronic illness where misshapen, sticky blood cells clump together, reducing oxygen delivery to organs—are at a higher risk for stroke and resulting cognitive disability. But even in the absence of stroke, many such patients struggle with remembering, focusing, learning and problem solving, among other cognitive problems, with many facing challenges in school and in the workplace.

Now a multidisciplinary team of researchers and physicians at Washington University School of Medicine in St. Louis has published a study that helps explain how the illness might affect cognitive performance in sickle cell patients without a history of stroke.

The researchers found such participants had brains that appeared older than expected for their age. Individuals experiencing economic deprivation, who struggle to meet basic needs, even in the absence of sickle cell disease, had more-aged-appearing brains, the team also found.

The study was published January 17 in JAMA Network Open.

Brain age modelling and cognitive outcomes in young adults with and without sickle cell anemia., JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2024.53669

Neuroimaging reveals 94% of gray matter in brains of mothers undergoes changes during pregnancy

A study led by the UAB has analyzed the brains of women during pregnancy for the first time using neuroimaging techniques. The study included non-pregnant mothers, whose partners were pregnant, to distinguish biological effects from those caused by the experience of being a mother. The research shows that there is a reduction and partial recovery of almost 5% of gray matter in 94% of the total gray matter volume of the brain, especially in regions linked to social cognition.

The researchers have published the first longitudinal neuroimaging (Magnetic Resonance Imaging) study in a cohort of more than a hundred women seeking to become mothers for the first time.

In total, the researchers have analyzed the brain of 179 women to study the structural changes that occur during the second and third trimester of pregnancy and the first six months postpartum, using a scan taken before conception as a baseline. For the first time, this cohort includes a group of non-gestational mothers as a control group: women whose partners underwent pregnancy during the study. The inclusion of this group of women made it possible to determine that the trajectory of brain changes is mainly attributed to the biological process of pregnancy, rather than to the experience of becoming a mother.

The findings reveal a dynamic trajectory in the brain during pregnancy and postpartum, significantly linked to the steroid hormone fluctuations inherent to pregnancy, and to the psychological well-being of the mothers.

This work has revealed that, during the first pregnancy, gray matter volume in the brain is reduced by up to 4.9%, with a partial recovery during the postpartum period. These changes are observed in 94% of the brain, being particularly prominent in regions linked to social cognition.

The study also demonstrates, for the first time, that the evolution of these morphological changes in the brain is associated with fluctuations in two estrogens (estriol-3-sulfate and estrone-sulfate), hormones that increase exponentially during pregnancy and return to basal levels after delivery. Specifically, the researchers observed that a greater increase and subsequent decrease in estrogen levels is associated with a greater decrease and subsequent recovery of brain gray matter volume.

Finally, in analyzing the possible influence of brain changes on maternal behaviour, this study discovered that women with a higher percentage of grey  matter volume recovery during postpartum reported a greater bond with their infant at 6 months postpartum, and that maternal well-being is a key factor that positively enhances the association between brain changes and maternal-filial bonding.

This study, which comprehensively characterizes normative brain changes during pregnancy and postpartum, stands out for both its sample size and rigorous methodological control, including carefully selected groups that allowed the distinguishing of pregnancy-specific changes from those linked to the experience of motherhood.

The data obtained not only establishes a key reference for understanding the neurobiology of the maternal brain, but also serves as a basis for future studies analyzing other neuroimaging modalities and more diverse samples, including women with clinical conditions such as postpartum depression , allowing progress towards a more complete and applied understanding of the brain in this vital period.

Camila Servin-Barthet et al, Pregnancy entails a U-shaped trajectory in human brain structure linked to hormones and maternal attachment, Nature Communications (2025). DOI: 10.1038/s41467-025-55830-0

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Sepsis molecule discovery could lead to improved treatments for critically ill patients

Researchers have uncovered how a molecule found on certain bacteria may drive blood clotting in sepsis, a life-threatening condition that causes about 8 million deaths per year.

The team in the cardiovascular engineering lab at OHSU has focused on the role of specific blood clotting mechanisms in sepsis, with hopes of improving treatments for critically ill patients.

 The immune system's response to bacteria can spiral out of control sometimes.

Your blood normally forms tiny clots to contain certain bacteria to clear them from the bloodstream. But if there are too many bacteria, the system gets overwhelmed, using up all the platelets and clotting factors. The result is catastrophic—you can't stop clotting or bleeding.

The team's newest study, published in this month's issue of the Journal of Biological Chemistry, focused on lipopolysaccharide, or LPS, a molecule found on the surface of certain bacteria like E. coli. The researchers found that LPS can directly activate proteins in the blood that trigger clotting, which can block blood flow and damage vital organs.

This process, known as the "contact pathway," involves a chain reaction where proteins in the blood work together to form clots. The researchers showed that one specific type of LPS, called O26:B6, is particularly good at setting off this reaction, making it more likely to cause clotting problems.

Sepsis is a dangerous condition where the body's response to an infection spirals out of control, leading to widespread inflammation, organ failure and problems like excessive blood clotting. Gram-negative bacteria, such as E. coli, are common culprits in sepsis because they release LPS when they invade the bloodstream.

Part 1

Sepsis can be incredibly challenging to treat in such cases. The systems that control blood clotting and bleeding become dangerously unbalanced.

The study, conducted in nonhuman primates, found that when bacteria containing LPS entered the bloodstream, it quickly activated the clotting system. This included coagulating proteins like factor XII, which seems to initiate the clotting process, causing a chain reaction.

Even when we know the bacteria causing the infection, different strains can behave differently. By understanding this,  scientists hope to develop precision therapies.

André L. Lira et al, The physicochemical properties of lipopolysaccharide chemotypes regulate activation of the contact pathway of blood coagulation, Journal of Biological Chemistry (2024). DOI: 10.1016/j.jbc.2024.108110

Part 2

AI to stop stampedes at world's biggest gathering -Kumbhmela

Science assisting spirituality

Keen to improve India's abysmal crowd management record at large-scale religious events, organizers of the world's largest human gathering are using artificial intelligence to try to prevent stampedes.

Organizers predict up to 400 million pilgrims will visit the Kumbh Mela, a millennia-old sacred show of Hindu piety and ritual bathing that began Monday and runs for six weeks.

Deadly crowd crushes are a notorious feature of Indian religious festivals, and the Kumbh Mela, with its unfathomable throngs of devotees, has a grim track record of stampedes.

More than 400 people died after being trampled or drowned at the Kumbh Mela on a single day of the festival in 1954, one of the largest tolls in a crowd-related disaster globally. Another 36 people were crushed to death in 2013, the last time the festival was staged in the northern city of Prayagraj.

So AI is helping the police avoid reaching that critical mass in sensitive places.

This time, authorities say the technology they have deployed will help them gather accurate estimates of crowd sizes, allowing them to be better prepared for potential trouble. Police say they have installed around 300 cameras at the festival site and on roads leading to the sprawling encampment, mounted on poles and a fleet of overhead drones. Not far from the spiritual center of the festival at the confluence of the Ganges and Yamuna rivers, the network is overseen in a glass-paneled command and control room by a small army of police officers and technicians.

The footage fed into an AI algorithm that gives its handlers an overall estimate of a crowd stretching for miles in every direction, cross-checked against data from railways and bus operators.

They are using AI to track people flow, crowd density at various inlets, adding them up and then interpolating from there. The system sounds the alarm if sections of the crowd get so concentrated that they pose a safety threat.

Organizers say the scale of this year's festival is that of a temporary country -- with numbers expected to total around the combined populations of the United States and Canada.

Organizers have been eager to tout the technological advancements of this year's edition of the Kumbh Mela and their attendant benefits for pilgrims. Even the Pilgrims think  that the fact that there are cameras and drones makes them feel safe!

Yes, science and tech makes people feel safe!

Source: News agencies

Extinction threatens nearly a quarter of all freshwater species

Freshwater ecosystems cover less than 1% of Earth's surface, but are vital for life on this planet. New research reveals that damage to these environments is pushing freshwater animals to the edge of extinction, with 24% of species in danger of being wiped out.

Thousands of fish, crab and dragonfly species could become extinct in the coming decades—and many more could follow.

A landmark assessment of the health of nearly 24,000 fresh water species found that just under a quarter are at risk of extinction. Of these, almost 1,000 species are considered Critically Endangered, with 200 having potentially been lost already.

These numbers may only represent the tip of the iceberg, with scientists lacking the information needed to properly understand the extinction risk of thousands of species. The authors of the study, says that urgent action is needed to understand and protect these animals.

"Lack of data on freshwater biodiversity can no longer be used as an excuse for inaction," they say. "Freshwater landscapes are home to 10% of all known species on Earth and key for billions of people's safe drinking water, livelihoods, flood control and climate change mitigation, and must be protected for nature and people alike."

While fresh, clean water is vital for all life on land, freshwater ecosystems are some of the most threatened on Earth. Freshwater environments are being put under pressure as demand for food, water and resources increases.

Wetlands in particular, including bogs, mangroves and saltmarshes, are bearing the brunt of these losses. It's estimated that an area the size of India—a staggering 3.4 million square kilometers—of wetland has been lost since 1700.

The loss of wetlands harms far more than just the animals and plants that live there, as it also limits our ability to fight climate change and stop flooding.

Freshwater sources are also suffering from a cocktail of different challenges. An increase in water abstraction and dams on rivers are reducing the available habitat for wildlife. Some rivers, like the Colorado River, no longer even reach the sea.

The animals that persist in these reduced habitats are then impacted by sewage, industrial and plastic pollution. Yet, despite the rising risk to these species, freshwater environments are significantly understudied compared to the oceans.

While around 10% of all species depend on freshwater, the study was particularly concerned with four groups that are intimately linked to it—the decapods, odonates, mollusks and fishes.

Catherine A. Sayer et al, One-quarter of freshwater fauna threatened with extinction, Nature (2025). DOI: 10.1038/s41586-024-08375-z

In times of uncertainty, the brain takes the easy route by following the crowd

In uncertain situations where information is lacking, individuals often find themselves imitating the choices of others. 

This behaviour highlights a tendency to conform to others when faced with ambiguity. Computational neuroscience research has shown that the decision to follow others unconditionally serves as an alternative strategy that activates certain brain processes in uncertain environments.

Researchers investigated how the decisions of others influence individual decision-making in uncertain contexts.

Decision-making in social situations typically involves a value judgment process that integrates both personal preferences and the choices of others. This study uncovers the strategies the brain employs when access to individual preferences is compromised.

According to the research findings, now published in PLOS Computational Biology, the brain employs a "heuristic" strategy that reflects social information from the choices of others during decision-making. When value judgments based on individual preferences are not possible, individuals tend to take the shortcut of imitating the decisions made by others.

The research team arrived at these conclusions through experiments conducted on participants with partial damage to the brain's insula or dorsal anterior cingulate cortex (dACC), regions known to play critical roles in processing uncertain information.

The research team noted that the implications of these findings could extend to adolescents, whose individual preferences may be in flux. Both situations of uncertainty and the lack of established personal preferences render value judgments based on individual preferences challenging.

This study sheds light on why individuals with unclear personal preferences may be particularly sensitive to the opinions of those around them. Therefore, the importance of creating a supportive environment and implementing educational approaches to help establish individual preferences as a means of addressing social issues such as addiction.

Mark A. Orloff et al, Social conformity is a heuristic when individual risky decision-making is disrupted, PLOS Computational Biology (2024). DOI: 10.1371/journal.pcbi.1012602

Neuronal subtypes study uncovers parallel gut-to-brain pathways that regulate feeding behaviours

The ability to regulate one's own food intake is essential to the survival of both humans and other animals. This innate ability ensures that the body receives the nutrients it needs to perform daily activities, without significantly exceeding calorie intake, which could lead to health problems and metabolic disorders.

Past neuroscience studies suggest that the regulation of food intake is supported by specific regions in the brain, including the hypothalamus and caudal nucleus of the solitary tract (cNTS), which is part of the brainstem. This key region in the brainstem is known to integrate sensory signals originating from the gut and then transform them into adaptive feeding behaviours.

While previous research has highlighted the key role of the cNTS in food intake regulation, the unique contribution of the different neuron subtypes within this brainstem region and the mechanisms by which they regulate feeding remain poorly understood. Better understanding these neuron-specific mechanisms could help to devise more effective therapeutic interventions for obesity and eating disorders.

Researchers recently carried out a study aimed at identifying neuronal subtypes in the mouse cNTS that are involved in how mice control their feeding behaviors. Their findings, published in Nature Neuroscience, show that different types of cNTS neurons process gut-originating signals via distinct sensory pathways, collectively contributing to the regulation of feeding.

The cNTS in the brainstem serves as a hub for integrating interoceptive cues from diverse sensory pathways. Understanding  the mechanisms by which cNTS neurons transform these signals into behaviours is vital too.

So the researchers systematically analyzed the brains and feeding behaviors of mice that were genetically intervened upon to turn "off" and "on" nine types of neurons in the cNTS. The researchers found that two key neuron populations, namely Th⁺ (tyrosine hydroxylase-expressing) and Gcg⁺ (glucagon-like peptide 1-expressing) neurons encoded different aspects of food intake.

Th⁺ cNTS neurons encode esophageal mechanical distension and transient gulp size via vagal afferent inputs, providing quick feedback regulation of ingestion speed.

By contrast, Gcg+ cNTS neurons monitor intestinal nutrients and cumulative ingested calories and have long-term effects on food satiation and preference. These nutritive signals are conveyed through a portal vein–spinal ascending pathway rather than vagal sensory neurons.

New studies could explore the unique contribution of the two broad neuron populations outlined by the researchers (i.e., Th⁺ and Gcg⁺ neurons), as well as their interactions with other brain regions in regulating feeding behaviours.

Hongyun Wang et al, Parallel gut-to-brain pathways orchestrate feeding behaviors, Nature Neuroscience (2024). DOI: 10.1038/s41593-024-01828-8

Why our biological clock ticks: Research reconciles major theories of aging

Researchers have published results that shed new light on an old question: what causes aging at the molecular level? Their findings, published in Nature Aging, describe a never-before-seen link between the two most accepted explanations: random genetic mutations and predictable epigenetic modifications. The latter, also known as the epigenetic clock theory, has been widely used by scientists as a consistent, quantitative measure of biological aging.

The new research suggests that the process may not be so simple.

Major research institutions and companies are betting on turning back the epigenetic clock as a strategy to reverse the effects of aging, but this new research suggests that this may only be treating a symptom of aging, not the underlying cause.

If mutations are in fact responsible for the observed epigenetic changes, this fact could fundamentally change the way we approach anti-aging efforts in the future.

There are two prevailing theories about the relationship between aging and DNA. The somatic mutation theory suggests that aging is caused by the accumulation of mutations, permanent changes in our DNA sequence that occur randomly. The epigenetic clock theory suggests that aging occurs due to the accumulation of epigenetic modifications, minor changes to the chemical structure of DNA that do not alter the underlying sequence, but instead change which genes are on or off. Unlike mutations, epigenetic modifications can also be reversed in some cases.

Because epigenetic modifications only occur at specific sites on our genome rather than at random locations, they are easier to quantify and have become a go-to way for scientists to determine the "biological age" of cells. However, scientists have long wondered about the source of these epigenetic changes.

Part 1

To answer this fundamental question, researchers analyzed data from 9,331 patients cataloged in the Cancer Genome Atlas and the Pan-Cancer Analysis of Whole Genomes. By comparing genetic mutations to epigenetic modifications, they found that mutations were predictably correlated with changes in DNA methylation, one type of epigenetic modification.
They found that a single mutation could cause a cascade of epigenetic changes across the genome, not just where the mutation occurred. Using this relationship, the researchers were able to make similar predictions of age using either mutations or epigenetic changes.

Epigenetic clocks have been around for years, but scientists are only now beginning to answer the question of why epigenetic clocks tick in the first place.

This study demonstrates for the first time that epigenetic changes are intricately and predictably tied to random genetic mutations.
The study's authors note that further research is needed to fully understand the relationship between somatic mutations and epigenetic changes in aging. However, the study's findings provide a major breakthrough in our understanding of the aging process and have important implications for the development of new therapies aimed at preventing or reversing aging.
If somatic mutations are the fundamental driver of aging and epigenetic changes simply track this process, it's going to be a lot harder to reverse aging than we previously thought, say the authors of this study.
This shifts our focus from viewing aging as a programmed process to one that's largely influenced by random, cumulative changes over time.

Zane Koch et al, Somatic mutation as an explanation for epigenetic aging, Nature Aging (2025). DOI: 10.1038/s43587-024-00794-x

Part 2

What's behind preterm birth? Scientists discover a molecular timer

A typical human pregnancy lasts 40 weeks, but most parents know this number is only a rough estimate. Babies are born on a seemingly unpredictable timeline, with a normal pregnancy ranging from 38 to 42 weeks. And 10% of all births are preterm, meaning they occur before 37 weeks of gestation, which puts babies at risk of a host of complications.

Now  researchers have discovered a molecular timer in mice that plays a role in controlling when they give birth. Surprisingly, the timer is activated in the very first days of pregnancy and operates within the uterus.

If the same set of molecules is found to be important in human pregnancies, it could lead to new tests to identify women who are at risk of preterm labour, as well as interventions to delay it.

DNA packaging during pregnancy

Throughout pregnancy, the female body undergoes massive biological shifts, with the activity of hundreds of genes going up or down within the uterus.

Researchers were studying a protein called KDM6B which regulates gene activity. They suspected that during pregnancy, KDM6B could help regulate the genes involved in the transition to labor.

KDM6B works by removing methyl chemical groups from histones—structures that help organize and package DNA within cells. In response to KDM6B, DNA becomes more accessible to other factors that regulate gene expression, turning on the activity of nearby genes.

The team noticed that when they blocked KDM6B, pregnancies in the mice became longer, and their babies were born later than usual.

At first, the scientists suspected that, late in pregnancy, KDM6B must be activating genes in the uterus's epithelial cells, which produce hormones known to trigger labor.

But when they carried out detailed analyses on different cell types, they found that KDM6B's effects on pregnancy length were tied to a different cell type called fibroblasts. These structural cells are not typically considered to play a role in the regulation of labor. Moreover, KDM6B regulated these fibroblasts during the first days of pregnancy.

These findings highlight a surprising role for uterine fibroblasts in regulating birth timing.

Part 1

Further experiments on mice revealed that shortly after conception, more methyl groups appear on histones near certain genes in uterine fibroblasts. In response, these genes remain inactive, which enables the uterus to support pregnancy.

Over the course of pregnancy, levels of methylation on these histones fade in a slow and steady way, eventually reaching low enough levels that the nearby genes—related to pregnancy events like labor—are activated. This erosion, which does not require KDM6B, functions as a timer.

Essentially, what appears to happen is this timer gets wound up right at the beginning of pregnancy, and then progressively winds down. When histone methylation erodes enough, nearby genes flip on.

When the researchers blocked KDM6B, histones near certain genes accumulated too much methylation early in pregnancy. This increased "setpoint" meant that, despite erosion, these genes were not activated on time, delaying labour.
While the new study did not directly study preterm births, the newly discovered molecular timer could help control pregnancy length in humans.

If the newly studied molecular signals are disrupted in humans, they could be linked to preterm birth risk, his team hypothesizes. For instance, some women could begin pregnancy with lower than usual levels of histone methylation; and this could lead to the erosion of the methylation to turn on labor-related genes too quickly.

 KDM6B-dependent epigenetic programming of uterine fibroblasts in early pregnancy regulates parturition timing in mice, Cell (2025). DOI: 10.1016/j.cell.2024.12.019. www.cell.com/cell/fulltext/S0092-8674(24)01432-6

Part 2

Biotin may shield brain from manganese-induced damage, study finds

While manganese is an essential mineral involved in many bodily functions, both deficiency and excessive exposure can cause health issues. Maintaining a balanced diet typically provides sufficient manganese for most individuals; however, high levels of exposure can be toxic, particularly to the central nervous system.

Chronic manganese exposure may result in a condition known as manganism, characterized by symptoms resembling Parkinson's disease, including tremors, muscle stiffness, and cognitive disturbances.

New research published in Science Signaling employs model systems and human nerve cells to show the mechanisms by which manganese inflicts damage to the central nervous system. The study also suggests that the vitamin biotin may have a protective effect, potentially mitigating manganese-induced damage.

Exposure to neurotoxic metals like manganese has been linked to the development of Parkinsonism. In this study, researchers applied untargeted metabolomics using high-resolution mass spectrometry and advanced cheminformatics computing in a newly developed model of parkinsonism, leading them to the discovery of biotin metabolism as a modifier in manganese-induced neurodegeneration.

Chronic occupational and environmental exposure to manganese, commonly from welding fumes and some sources of rural drinking water, increases the risk of Parkinsonian syndrome, which involves similar but distinct neurological symptoms of Parkinson's disease. Manganese has been previously shown to bind with the protein alpha-synuclein, causing it to misfold and accumulate in the brain.

Using the fruit fly Drosophila, researchers developed a model that mimics occupational manganese exposure in humans and found that manganese induced motor deficits, mitochondrial and lysosomal dysfunction, neuronal loss, and reduced lifespan in flies.

The team validated these findings using human dopaminergic neurons derived from induced pluripotent stem cells (iPSC) and demonstrated that manganese exposure selectively damages these cells. The loss of dopamine-producing cells is a hallmark of Parkinson's disease and Parkinsonian syndrome.

The research indicates that B vitamin biotin, a micronutrient synthesized by gut bacteria, enhances dopamine production in the brain. Biotin supplementation reversed neurotoxicity in flies and iPSC-derived neurons, improving mitochondrial function and reducing cell loss.

This finding aligns with a growing scientific recognition that Parkinson's is a multisystem disorder, with early symptoms often emerging in the gut, and that changes in the gut microbiome may contribute to the disease.

"Biotin supplementation shows potential as a therapeutic strategy to mitigate manganese-induced neurodegeneration, and the safety and tolerability of biotin in humans make it a promising candidate for further exploration," say the researchers.

Biotin-rich prebiotics or biotin-producing probiotics could provide non-pharmacological intervention options.

Biotin rescues manganese-induced Parkinson's disease phenotypes and neurotoxicity, Science Signaling (2025). DOI: 10.1126/scisignal.adn9868

Scientists create world's first fully-3D printed microscope in under three hours

Scientists  have created the world's first fully 3D printed microscope in under three hours and for less than £50—a fraction of the cost of traditional devices.

Using a publicly available design from the website OpenFlexure the scientists produced the microscope's frame—and clear plastic lenses they designed themselves—using low-cost, accessible 3D printers.

The microscope was completed by adding a shop-bought camera and a light, with the whole device controlled by a Raspberry Pi computer processor.

The researchers have presented their results in a paper submitted for publication in the Journal of Microscopy which is currently in pre-print on the server bioRxiv ahead of publication following peer review.

To test the imaging performance of the system, the scientists used standard test samples: a stained blood smear and a stained, thin section of mouse kidney. The microscope demonstrated sub-cellular resolution, clearly imaging individual red blood cells and detailed structures in the kidney sample.

This opens the doors to democratized access, rapid prototyping, and bespoke design of microscopes and optics at a fraction of the price of traditional microscopes. It could help scientists and medics in low-income countries around the world, as well as enabling students to learn more about science through accessible, cheap kit.

Jay Christopher et al, A fully 3D-printed optical microscope for low-cost histological imaging, bioRxiv (2024). DOI: 10.1101/2024.12.16.628684

Discovery shows oyster blood proteins improve antibiotic effectiveness

While slurping oysters is not likely to replace popping a pill, they could help in the fight against superbugs. A groundbreaking find by researchers has shown oysters might be able to help treat a growing worldwide public health problem: antibiotic-resistant bacteria.

In a study published in PLOS ONE, the researchers demonstrate a protein in the blood, or hemolymph, of a Sydney Rock Oyster not only kills bacteria but increases the effectiveness of some conventional antibiotics against a range of clinically important bacteria.

This new research supports the potential use of natural products from oysters to treat bacterial infections. Importantly, the oyster hemolymph proteins were not toxic to human lung cells, suggesting it should be possible to optimize a safe, effective dose. 

 Antimicrobial proteins from oyster hemolymph improve the efficacy of conventional antibiotics, PLOS ONE (2025). DOI: 10.1371/journal.pone.0312305. journals.plos.org/plosone/arti … journal.pone.0312305

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Scientists finally know how cells build a structure that lets them migrate

Some of the body's cells stay put for life, while others are free to roam. To move, these migratory cells rely on filopodia—sensitive, finger-like protrusions that reach out from the cell membrane into the local environment. In a healthy cell, this can be a lifesaver: say, when an immune cell is speeding to the site of an infection. But filopodia can also wreak havoc: metastatic cancer cells use them to invade new regions of the body.

Filopodia are composed of hexagonal bundles of proteins that give them structure and strength. How these intricate bundles come together has been a puzzle for more than 40 years. A major piece of that puzzle has now been solved by Rockefeller University's Laboratory of Structural Biophysics and Mechanobiology, which developed advanced imaging technology to reveal how underlying proteins build these cohesive assemblies.

The findings, published in Nature Structural & Molecular Biology, may improve some cancer treatments already in development, as understanding the structure of filopodia and the changes they undergo may help to refine these therapies or inspire new ones.

The study marks the first time such a complex higher-order protein assembly has been imaged at the atomic level—a technological advance that other scientists can now use to study similarly complex configurations.

 Rui Gong et al, Fascin structural plasticity mediates flexible actin bundle construction, Nature Structural & Molecular Biology (2025). DOI: 10.1038/s41594-024-01477-2

New effective treatment for deadly pancreatic cancer may be on its way

Pancreatic cancer is one of the deadliest of all cancers. Only 12% of men diagnosed with pancreatic cancer are alive five years after diagnosis; for women it is 14%.

In pancreatic cancer, symptoms are unclear and often emerge late in its progression. It is difficult to treat once the cancer has spread, as it cannot be removed completely with surgery.

Now researchers  have made significant advances in developing a treatment for pancreatic cancer and a new study published in Science Advances depicts how it is done. The study is based on the ADC (antibody drug conjugates) technique, which is being used to treat other types of cancers.

This study shows promising results with a new type of drug that can fight the cancer on several fronts. The treatment directly kills the cancer cells and the support cells that the cancer uses to grow and shield itself.

By targeting the support cells, the treatment also releases toxins that can kill neighboring cancer cells. Additionally, destroying the support cells weakens the tumor structure, making it easier for the body's immune system to attack and eliminate it.

The ADC consists of three main components: an antibody, a chemical linker that ties the antibody to the drug, and a strong chemotherapeutic drug. Once the ADC has located and entered the cancer cell, the linker decomposes, activating the chemotherapy and killing the cancer cell from the inside. This Trojan horse strategy offers targeted treatment without affecting the healthy cells.

Because ADC treatment is extremely accurate and causes minimal damage to healthy cells, it is a likely candidate for treatment of the more difficult cancers.

As part of the process, the researchers have humanized the ADC antibody, which means that we have changed its structure to resemble antibodies naturally occurring in the human body. This adjustment ensures that the body's immune system does not recognize the antibody as foreign and attack it. Humanization is a critical step in making the treatment both safe and effective for patients and represents a key milestone on the path towards clinical trials.

The researchers are now working to further develop the drug and get it ready for clinical testing on humans with pancreatic cancer.

Virginia Metrangolo et al, Targeting uPAR with an antibody-drug conjugate suppresses tumor growth and reshapes the immune landscape in pancreatic cancer models, Science Advances (2025). DOI: 10.1126/sciadv.adq0513

An energy trap for tumor cells: Researchers find enzyme blockade halts liver cancer growth

Glycolysis is a central metabolic pathway by which cells obtain energy from sugar. Cancer cells in particular have long been thought to depend on the energy obtained through glycolysis, a phenomenon known as the Warburg effect. Today we know that cancer cells can use energy sources more flexibly than previously thought. Even when glycolysis is blocked, they survive by obtaining their energy through the respiratory chain.

This makes results published by Almut Schulze and colleagues from the German Cancer Research Center (DKFZ) all the more surprising: When the researchers blocked the enzyme aldolase A, which catalyzes an important step in glycolysis, liver cancer cells experienced "energy stress" and ceased their division activity. The team demonstrated this both in mouse liver cancer cells and in several human cancer cell lines.

The findings are published in the journal Nature Metabolism.

However, when the researchers blocked an earlier step in glycolysis, the enzyme glucose-6-phosphate isomerase, this had no effect on the growth of the cancer cells.

The glycolytic enzyme aldolase is essential for liver cancer cells, although the glycolytic pathway itself is apparently dispensable.

At first glance, the result seems surprising, since the enzyme blockade inhibits the sugar degradation pathway in both cases. However, a closer look at the biochemical steps of glycolysis provides clarity: The metabolic pathway, which involves many reactions, is divided into two parts. First, the cell has to invest energy to generate the highly energetic intermediate fructose-bisphosphate.

This is where aldolase A comes in. If it is switched off, fructose bisphosphate accumulates in the cell, and the energy bound in it remains unused, trapped as it is. The cell cannot reap the energy profit from the steps that would normally follow. Glycolysis has reversed from an energy-producing to an energy-consuming process. What's more, the lack of energy further stimulates the production of fructose bisphosphate, creating a vicious circle.

Sooner or later, this leads to energy consumption exceeding energy production. In liver cancer cells, this results in a massive energy deficiency, the cell cycle is stopped and tumor growth is inhibited. The team also demonstrated this in liver cancer-bearing mice: If the animals' aldolase A was genetically switched off, the cancer growth was reduced and the mice survived significantly longer.

By switching off Aldolase A, we can overcome the metabolic plasticity of cancer cells. We not only block energy production through glycolysis, but also prevent the cell from switching to other metabolic pathways, because the energy is trapped in the fructose bisphosphate. Targeted inhibition of aldolase A could therefore be a promising strategy for combating cancer cells.

Part 1

However, the only aldolase A inhibitor currently available has so far only been tested experimentally and is not approved as a drug. The Heidelberg team is now testing the substance for its potential in cancer therapy.

It is important to note that even a slight reduction in the activity of aldolase A could be enough to drive cancer cells into the energy trap.

Normal cells should tolerate this because they take up smaller amounts of glucose and produce less energy-rich fructose bisphosphate. The Warburg effect is therefore a weak point of cancer cells that makes them more sensitive to a blockade of aldolase A.

The results show how a deeper understanding of tumor metabolism can enable innovative approaches to cancer treatment. These findings could pave the way for new, highly specific therapies that target the weaknesses of cancer metabolism while sparing healthy cells.

Marteinn T. Snaebjornsson et al, Targeting aldolase A in hepatocellular carcinoma leads to imbalanced glycolysis and energy stress due to uncontrolled FBP accumulation, Nature Metabolism (2025). DOI: 10.1038/s42255-024-01201-w

Part 2

Paralysed man flies virtual drone using brain implant

Paralysed man flies virtual drone
Researchers have developed a device that let a 69-year-old man with paralysis fly a virtual drone using only his thoughts. The brain–computer interface (BCI) decoded the man’s brain activity as he imagined moving three groups of digits in real time. By associating neural signals with the movements of multiple fingers, the work builds on previous BCI research, most of which has focused on moving a single computer cursor or whole virtual hand.

https://www.nature.com/articles/d41586-025-00167-3?utm_source=Live+...

Frequent social media use tied to higher levels of irritability

A survey led by researchers has analyzed the association between self-reported social media use and irritability among US adults. Frequent social media use, especially among active posters, was correlated with higher levels of irritability.

Existing studies on social media and mental health predominantly focus on depressive symptoms, with limited attention to other negative emotions such as irritability. Irritability, defined as a tendency toward anger and frustration, has been linked to functional impairments, poorer mental health outcomes, and suicidal behaviours.

While prior research has established connections between social media use and depressive symptoms, the extent to which social media engagement is associated with irritability or its influence on depression and anxiety has remained uncertain.

In the study, "Irritability and Social Media Use in US Adults," published in JAMA Network Open, the research team used data from two waves of the COVID States Project, a nationwide nonprobability web-based survey conducted between November 2, 2023, and January 8, 2024, which included questions about social media use and irritability.

Researchers evaluated the relationship between social media use and irritability by analyzing responses from 42,597 participants using multiple linear regression models.

Part 1

The survey collected sociodemographic data, self-reported social media usage, and measures of irritability. Participants completed the Brief Irritability Test (BITe), which consists of five statements evaluating irritability symptoms over the previous two weeks. Scores range from 5 to 30, with higher scores indicating higher levels of irritability. The analysis also included depression and anxiety metrics to account for overlapping psychological symptoms.

Social media use was categorized based on frequency: never, less than once per week, once per week, several times per week, once per day, several times per day, or most of the day. Platforms analyzed included Facebook, Instagram, TikTok, and Twitter/X. Frequency of active posting, political engagement, and political affiliation were also examined to identify potential confounding factors.

Participants had a mean age of 46 years, with 58.5% identifying as women, 40.4% as men, and 1.1% as nonbinary. Among respondents, 78.2% reported daily use of at least one social media platform. Frequent social media use correlated with higher irritability scores, even after adjusting for anxiety and depression.

For example, participants using social media most of the day scored 3.37 points higher on the BITe in unadjusted models. After adjusting for anxiety and depression, the increase remained significant at 1.55 points.

Platform-specific analyses revealed a dose-response relationship between posting frequency and irritability. Posting multiple times per day was associated with the highest irritability levels across all platforms, with TikTok users showing the largest increase (1.94 points; 95% CI, 1.57-2.32 points).

Political engagement variables, such as frequent political posting or consuming political news, were associated with increased irritability. Political engagement did not diminish the observed relationship between social media use and irritability, though following political news "not very closely" was associated with a slight decrease.

High social media engagement levels, particularly frequent posting, were associated with greater irritability in US adults. While the study could not establish direct causation, findings suggest a potential feedback loop relationship, where irritability may both influence a desire to engage and increase irritation from social media use.

 Roy H. Perlis et al, Irritability and Social Media Use in US Adults, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2024.52807

Part 2

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Fighting experience plays key role in brain chemical's control of male aggression

Like humans, mice will compete over territory and mates, and show increased confidence in their fighting skills the more they win. At first, a brain chemical called dopamine is essential for young males to master this behavior. But as they gain experience, the chemical grows less important in promoting aggression, a new study shows.

Dopamine has been linked to male aggression for decades. How past experiences might influence this relationship, however, had until now been unclear.

In experiments in rodents, a team led by researchers at NYU Langone Health boosted activity in dopamine-releasing cells in a part of the brain called the ventral tegmental area. The findings revealed that in inexperienced male fighters, this led the animals to attack for twice as long as they would have fought naturally. When the cells were blocked, the novice mice would not fight at all.

By contrast, this pattern did not hold true in males that had extensive fighting experience. Whether or not dopamine-releasing cells were boosted or blocked, the duration of the attack did not change. Notably, though, the more clashes a mouse won, the more fights it would start in the future.

These findings show that while aggression is an innate behaviour, dopamine—and fighting experience—is essential for its maturation during adulthood.

A report on the findings was published online Jan. 22 in the journal Nature.

Dayu Lin, Experience-dependent dopamine modulation of male aggression, Nature (2025). DOI: 10.1038/s41586-024-08459-w. www.nature.com/articles/s41586-024-08459-w

Silver nanoparticles in packaging can contaminate dry foods, testing shows

A team of research scientists has found evidence of silver nanoparticles embedded in packaging used as an antimicrobial agent seeping into the dry food it is meant to protect. In their paper published in the journal ACS Food Science & Technology, the group describes how they created their own packaging with embedded silver nanoparticles and tested it with various foods, and what they learned by doing so.

Silver has been a known antimicrobial agent for centuries, but it has only recently been made into nanoparticle-sized grains for use in food packaging. Prior research has shown that when such packaging is used for liquid or gelatinous foods or beverages, the nanoparticles can easily seep into and permeate the food. It is still not known if such particles can cause harm to people who consume them—testing is still ongoing, which is why they are banned in many countries. In this new effort, the research team wanted to know if such particles also find their way into dry foods.

To find out, the team created samples of silver nanoparticles and embedded them in polyethylene film wraps, which could hold various types of food items. They tested wheat flour, slices of cheese, ground rice and spinach leaves. They then stored the packages in ways normal to consumers' homes.

The team then brought the packages into their lab for testing with mass spectrometry. In so doing, they found that the nanoparticles had made their way to all the foods, though to varying degrees. They found, for example, that there was far more contamination of the cheese than there was with the spinach leaves. They noted that the more surface contact between the food and the packaging, the more contamination. They also noted that most of the contamination was confined to the surface of the food, which meant that most of it could be easily rinsed away.

 Laxmi Adhikari et al, Silver Migrates to Solid Foods and Abiotic Surfaces from Model Plastic Packaging Containing Silver Nanoparticles, ACS Food Science & Technology (2025). DOI: 10.1021/acsfoodscitech.4c00813

Insulin-producing cells avoid immune attack

Gene-edited insulin-producing beta cells have survived for a month after being injected into a man with type 1 di.... These tweaked cells have a protein called CD47 on their surface, which tells the immune system not to destroy them. Only a small number of cells were injected into the man’s arm, but they have produced insulin and avoided his immune system’s crosshairs so far, suggesting that they could become an effective treatment for diabetes.

https://ir.sana.com/news-releases/news-release-details/sana-biotech...

https://www.newscientist.com/article/2463508-gene-edited-cells-that...

Uncovering the role of Y chromosome genes in male fertility in mice

Researchers at the Crick have uncovered which genes on the Y chromosome regulate the development of sperm and impact fertility in male mice. This research could help us understand why some men don't produce enough sperm and are infertile.

Males typically have one copy of the Y chromosome and one copy of the X chromosome, whereas females typically have two X chromosomes. Scientists know that the Y chromosome is essential for male fertility, but which genes are the most important and how they work is less clear till now.

In research published in Science, a research team at the Crick resolved this question by generating 13 different mouse models, each with different Y genes removed, and investigated their fertility.

The researchers studied the ability of these adult mice to reproduce, including looking at the number of offspring, number of sperm produced and the appearance and motility of the sperm.

They found that several Y genes were critical for reproduction. If these genes were removed, the mice couldn't produce young, due to absence or reduced number of sperm, failure to produce a reservoir of sperm stem cells or abnormal sperm shape or movement.

Interestingly, some other genes had no impact when removed individually, but did lead to the production of abnormal sperm when removed together.

This was the case for a group of three genes which model a region of the chromosome called AZFa in humans. AZFa deletions are a common cause of the most severe cases of male infertility, but it has been hard to tell which genes in the region are responsible.

Jeremie Subrini et al, Systematic identification of Y-chromosome gene functions in mouse spermatogenesis, Science (2025). DOI: 10.1126/science.ads6495. www.science.org/doi/10.1126/science.ads6495

Smart fabric can heat up by 30°C after 10 minutes of sun exposure

A new type of cloth developed by researchers at the University of Waterloo can heat up when exposed to the sun thanks to innovative nanoparticles embedded in the fabric's fibers. This advance represents an innovative and environmentally friendly option for staying warm in the winter.

Wearable heated clothing typically relies on metals or ceramic heating elements to heat up and an external power source, which could pose safety risks for users.

This new cloth incorporates conductive polymer nanoparticles that can heat up to 30°C when exposed to sunlight. The design requires no external power and can also change color to visually monitor temperature fluctuations. The study was recently published in Advanced Composites and Hybrid Materials.

The magic behind the temperature-sensitive color change lies in the combination of nanoparticles embedded in the polymer fibers. The nanoparticles are activated by sunlight, enabling the fabric to absorb heat and convert it into warmth.

The fiber is created using a scalable wet-spinning process, combining polyaniline and polydopamine nano particles to enhance light absorption and improve photothermal conversion. Thermoplastic polyurethane serves as the spinning matrix, while thermochromic dyes enable the reversible color-changing feature. The resultant fiber can be woven into fabric for wearable applications.

In addition to its temperature-changing capability, the Waterloo researchers' new fabric can stretch out by as much as five times its original shape and withstand as much as two-dozen washings while still maintaining its function and appearance. Its reversible color-changing ability provides a built-in temperature monitoring feature to ensure the wearer's safety and convenience.

The fabric's potential applications include aiding in cold rescue situations and solar-powered pet clothing to help keep them comfortable when outside during the winter.

 Fangqing Ge et al, Color tunable photo-thermochromic elastic fiber for flexible wearable heater, Advanced Composites and Hybrid Materials (2024). DOI: 10.1007/s42114-024-00994-4

An underestimated source of methane found in shallow coastal waters

Shallow coastal waters are hotspots for methane emissions, releasing significant amounts of this potent greenhouse gas into the atmosphere and contributing to global warming. New research highlights how tides, seasons, and ocean currents strongly influence methane emissions and how tiny microorganisms, called methanotrophs, help reduce their impact.

While human-made sources of methane are well-studied, natural sources like coastal waters remain less understood. These shallow, dynamic ecosystems are rich in methane, and because the water is not very deep, methane-eating microbes (methanotrophs) have little time to break it down before it escapes into the atmosphere.

The study investigated three regions: the Doggerbank seep area in the North Sea, the Dutch Wadden Sea, and coastal waters near Svalbard in the Arctic. Findings revealed that methane emissions are highly influenced by natural factors like tides and seasonal changes, which also affect the activity of methane-eating microbes.

In the Wadden Sea, methane levels and emissions were higher during warmer seasons when microbial activity was stronger. However, even in colder seasons, methane concentrations remained high, with windy conditions contributing to significant atmospheric releases. Tidal currents transported methane into neighboring waters, where it could still escape into the atmosphere, highlighting the broader impact of coastal methane dynamics.
At the Doggerbank seep area, falling tides triggered bursts of methane release while also stimulating microbial activity in deeper waters. However, during cooler autumn months, when water mixed, microbial activity decreased, leading to more methane escaping into the atmosphere compared to summer.

In the Arctic near Svalbard, methane concentrations were highest near the seafloor, where diverse and abundant microbial communities were present. Ocean currents played a key role in spreading methane and microbes, limiting their ability to fully break down the gas before it reached the atmosphere.
Part 1

In addition to fieldwork, laboratory experiments revealed that methanotrophic microbes are remarkably adaptable. They thrive in a range of environmental conditions, including shifts in temperature, salinity, and methane levels.
As ecosystems change, methane-eating microbes adapt. When one group struggles, another takes over, keeping nature's methane filter running even in a warming world.

Tim de Groot. Environmental controls on microbial methane oxidation in the coasta... ( PhD Dissertation)

Part 2

Mane attraction: Molecular 'switch' may control long scalp hair

Treating hair loss may be as simple as developing therapies to flip a molecular "switch," according to a new study by researchers .

The researchers reviewed the biological and social evolution of human scalp hair. Based on their analysis, they proposed a novel theory that points to a molecular basis underlying the ability to grow long scalp hair. In short, human ancestors may have always had the ability to grow long scalp hair, but the trait remained dormant until certain environmental and biological conditions—like walking upright on two legs—turned on the molecular program.

The team published their findings, which they said could serve as the basis for future experimental work, in the British Journal of Dermatology.

Humans grow extremely long scalp hair.

Likewise, attributes of scalp hair—its length, shape, color and loss of hair—play an essential role in social communication. They signify our ancestry, age, health, sexual maturity and social status, to name but a few. And yet, despite the importance of having long scalp hair, we know very little about how this feature of human skin came about and how it is regulated.

Previous research had shown that tightly curled hair, in particular, served as an effective shield against the sun, reducing the need for excessive sweating that can cause dangerous dehydration. 

Building on this work, the researchers proposed that long scalp hair initially evolved to protect early human ancestors in equatorial Africa from the intense heat and solar radiation of their environment, and then it came to have meaning in many other spheres of life, such as signaling age, health, maturity and social status.

Long, tightly curled hair was a crucial adaptation that allowed our ancestors to thrive in hot, open environments. Understanding when long scalp hair evolved will help to better appreciate when it acquired its essential non-biological purposes.

While long hair is rare among mammals, it is not entirely unique to humans. Animals like male lions, orangutans and even now-extinct wooly mammoths also grew remarkably long hair, albeit for different reasons, according to the researchers.

What these examples tell us is that the molecular blueprint for growing very long hair has always existed, albeit often in a 'silenced' state. When human ancestors evolved their ability to grow extremely long scalp hair, it was likely accomplished by just a few genetic tweaks that reactivated a dormant program rather than via the evolution of an entirely new molecular mechanism.

The findings have broader implications for medical research, particularly in addressing hair loss, a condition that impacts millions worldwide. Understanding how human scalp hair follicles normally grow very long hair will naturally result in novel molecular targets for more efficacious therapies for hair loss.

This knowledge could lead to treatments that help restore hair growth and alleviate the emotional distress that often accompanies hair loss.

Lo-Yu Chang et al, Evolution of long scalp hair in humans, British Journal of Dermatology (2025). DOI: 10.1093/bjd/ljae456

Mitochondria may be a promising therapeutic target for inflammatory diseases

Scientists have discovered how mitochondria influence the body's immune response through modulating specific cell signaling pathways, according to a study published in Science Advances.

The findings highlight the potential of targeting mitochondrial function specifically in immune cells to treat a range of inflammation-related diseases.

Therapies aimed at improving mitochondrial activity could benefit inflammatory diseases such as inflammatory bowel disease, sepsis, and chronic infections by enhancing the immune system's ability to regulate inflammation.

Mitochondria contain the mitochondrial electron transport chain (ETC), or a series of protein complexes in which electrons pass through and produce ATP, or energy, for the cell. Mitochondrial ETC function also controls macrophages, or specialized immune cells that are essential for fighting infections and regulating inflammation in the body.

Macrophages also release an anti-inflammatory protein called IL-10, which reduces inflammation and prevents excess immune responses that can harm the body. The underlying mechanisms that allow mitochondrial ETC to control macrophage immune responses, however, have remained poorly understood.

Using bulk-RNA sequencing to study mice with macrophages deficient in mitochondria ETC complex III, the scientists discovered that a type of reactive oxygen species (ROS), or unstable molecules that contain oxygen and easily react with other molecules in a cell, that is produced by mitochondrial complex III, called superoxide, is critical for macrophages to release IL-10.

The scientists also discovered those mice with the defective mitochondrial complex also struggled to recover from infection and inflammation because their cells released less IL-10. However, activating a specific ROS dependent signaling pathway in the cells restored IL-10 release, according to the study.

This finding highlights a previously unknown connection between mitochondrial activity, inflammation control and the signaling pathways that regulate it.

Overall, the findings underscore mitochondria's essential role beyond energy production and suggest that mitochondria may be a promising therapeutic target for treating a range of inflammatory diseases and enhancing current therapies, according to the researchers.

Boosting IL-10 levels through mitochondrial pathways offers promise for managing autoimmune disorders like rheumatoid arthritis and lupus, where the immune system mistakenly attacks the body. Enhancing the function of mitochondrial complex III, or mimicking its effects, may also improve recovery from severe infections. Additionally, inhibiting mitochondrial complex III would decrease IL-10 suppression of inflammation, and could cooperate with existing immunotherapies.

 Joshua S. Stoolman et al, Mitochondria complex III–generated superoxide is essential for IL-10 secretion in macrophages, Science Advances (2025). DOI: 10.1126/sciadv.adu4369

Eight psychiatric disorders share the same genetic causes, study says

Psychiatric disorders often overlap and can make diagnosis difficult. Depression and anxiety, for example, can coexist and share symptoms. Schizophrenia and anorexia nervosa. Autism and attention deficit/hyperactivity disorder, too. But, why?

Life experiences, environment, and genetics can all influence psychiatric disorders, but much of it comes down to variations in our genetics. Over the past few years, scientists in the field of psychiatric genetics have found that there are common genetic threads that may be linking and causing coexisting psychiatric disorders.

In 2019, researchers at the Psychiatric Genomics Consortium, Harvard University, and the UNC School of Medicine identified 136 "hot spots" within the genome that are associated with eight psychiatric disorders. Among them, 109 hot spots were shared among multiple disorders, or "pleiotropic."

A new genetic study has successfully delineated the functional consequences of genetic variants into two groups. Their findings, which were published in Cell, suggest that pleiotropic variants may be optimal targets for treatment, due to their extended roles in development and sensitivity to change.

Pleiotropy was traditionally viewed as a challenge because it complicates the classification of psychiatric disorders. However, if we can understand the genetic basis of pleiotropy, it might allow us to develop treatments targeting these shared genetic factors, which could then help treat multiple psychiatric disorders with a common therapy.

The human genome acts as the body's operating manual, containing the instructions that helped us develop from a single cell into a whole person. However, everyone's genetic foundation is unique. There are specific regions of the genome that are prone to genetic variations.

Specific genetic variants can impact biological processes, like protein overproduction or altered synapse formation, affecting brain development and contributing to psychiatric disorder. But researchers are armed with tools to track these variants and learn more about the origins of disease.

In 2019, an international team of researchers at the UNC School of Medicine and the Psychiatric Genomics Consortium conducted genome-wide association studies (GWAS) on eight disorders: autism spectrum disorder, attention deficit/hyperactivity disorder (ADD), schizophrenia, bipolar disorder, major depressive disorder, Tourette syndrome, obsessive-compulsive disorder (OCD), and anorexia nervosa, to better understand the shared genetic underpinnings between psychiatric disorders. The analysis previously revealed 136 "hot spots" on the genome that have a causal effect on one or more of the eight psychiatric disorders. Of those, 109 of these locations were identical across more than one disorder.

As part of their latest study, researchers wanted to pry more information from the genetic variants embedded within these 136 "hot spots." Using a powerful technology, called a massively parallel reporter assay, they sought to determine which causal variants could be interfering with gene regulation.

Gene regulation controls how and when proteins are produced in the body, allowing the tiny machines to carry out a wide array of functions in the body. If certain variants are interfering with this important process, researchers can use that information to home in on the variants of interest and use them as new targets for treatment.

Part 1

Researchers first took all 17,841 genetic variants from the 136 "hot spots" and inserted them into human neural cells to see how they acted in a living system. After putting the variants through the massively parallel reporter assay, researchers found that 683 of the 17,841 genetic variants had a measurable effect on gene regulation.
The researchers then categorized the 683 variants into two groups: those shared across multiple disorders (pleiotropic variants) and those specific to a single disorder (disorder-specific variants). After dividing them into categories, researchers performed a tried-and-true scientific method: compare and contrast.

Pleiotropic variants were found to be more active and more sensitive to change compared to disorder-specific variants. Researchers noted that pleotropic variants were active for much longer during brain development, compared to disease-specific ones. This extended activity suggests that pleiotropic variants may be influencing multiple stages of neurodevelopment and potentially contributing to various observable traits and disorders.

Additionally, the genes affected by these pleiotropic variants appear to be more sensitive to changes, meaning disruptions in these genes could have a bigger impact on human health.

The proteins produced by these genes are also highly connected to other proteins. Changes to these proteins in particular could ripple through the network, potentially causing widespread effects on the brain.
These findings mark an important step toward understanding how genetics contributes to shared symptoms across psychiatric disorders. Targeting these variants, their associated genes, and pathways could pave the way for treatments that address multiple conditions at once.

Sool Lee et al, Massively parallel reporter assay investigates shared genetic variants of eight psychiatric disorders, Cell (2025). DOI: 10.1016/j.cell.2024.12.022

Part 2

Microplastics block blood flow in the brain, mice study reveals

In mice, immune cells carry microplastics — specks of plastic less than 5 millimetres long — through the bloodstream, where they eventually become lodged in blood vessels in the brain. The plastic-packed cells appeared in the mice’s brains just hours after they were given polystyrene-laced water and piled up “like a car crash in the blood vessels”, says biomedical researcher and study author Haipeng Huang. The obstructions sometimes cleared eventually, but others stayed stuck for the entire month-long observation period and had effects including impairing the mice’s mobility. It’s not clear whether such blockages occur in people.

https://www.nature.com/articles/d41586-025-00178-0?utm_source=Live+...

https://www.science.org/doi/10.1126/sciadv.adr8243

Cancer cells ‘poison’ the immune system with tainted mitochondria

Cancer cells can sabotage immune cells that try to attack them by filling them with ..., the organelles that cells rely on to make energy. In samples from three people with cancer, researchers noticed that mitochondria in both the tumour cells and immune cells called tumour-infiltrating lymphocytes (TILs) shared the same mutations. When they grew cancer cells with fluorescent-tagged mitochondria alongside TILs, the TILs had taken on some faulty mitochondria after only 24 hours. By 15 days, their native mitochondria had been replaced almost entirely. Tainted TILs were less able to divide and more likely to commit cell ‘suicide’.

https://www.nature.com/articles/s41586-024-08439-0?utm_source=Live+...

https://www.nature.com/articles/d41586-025-00176-2?utm_source=Live+...