Researchers from the laboratory of Roberta Gualdani at the University of Louvain in Brussels identified an unexpected role for a molecule known as TRPV4 in itch triggered by mechanical stimulation, such as scratching.

“We were initially studying TRPV4 in the context of pain,” Gualdani explained. “But instead of a pain phenotype, what emerged very clearly was a disruption of itch, specifically, how scratching behavior is regulated.”

TRPV4 and the Nervous System

TRPV4 is part of a family of ion channels that function like tiny molecular gateways in sensory nerve cells. These channels allow ions to move through cell membranes in response to physical or chemical changes. They help the nervous system detect sensations including temperature, pressure, and tissue stress.

Scientists have suspected for years that TRPV4 plays a role in sensing mechanical stimulation, but its involvement in itch, particularly chronic itch, has remained unclear and heavily debated.

To investigate more precisely, Gualdani’s team created genetically engineered mice in which TRPV4 was removed only from sensory neurons. Earlier studies had deleted the molecule throughout the entire body, making it difficult to determine exactly where it was acting.

Using genetic analysis, calcium imaging, and behavioral testing, the researchers found that TRPV4 appears in touch sensitive neurons known as Aβ low-threshold mechanoreceptors (Aβ-LTMRs). The channel was also present in certain sensory neurons connected to itch and pain pathways, including neurons expressing TRPV1.

Why Scratching Sometimes Does Not Stop

The team then created a chronic itch condition in mice that resembled atopic dermatitis. The results surprised the researchers. Mice missing TRPV4 in sensory neurons scratched less often overall, but each scratching episode lasted much longer than normal.

“At first glance, that seems paradoxical,” Gualdani said. “But it actually reveals something very important about how itch is regulated.”

According to the study, TRPV4 does not simply create the sensation of itch. Instead, it appears to help activate a negative feedback signal in mechanosensory neurons. This signal informs the spinal cord and brain that scratching has provided enough relief.

Without that feedback system, the sense of satisfaction from scratching becomes weaker, causing scratching to continue for extended periods. Researchers say TRPV4 may therefore function as part of the nervous system’s internal “stop scratching” mechanism.

“When we scratch an itch, at some point we stop because there’s a negative feedback signal that tells us we’re satisfied,” Gualdani explained. “Without TRPV4, the mice don’t feel this feedback, so they continue scratching much longer than normal.”

Implications for Chronic Itch Treatments

The findings also suggest that TRPV4 has a more complicated role in itch than previously believed. In skin cells, the channel may help trigger itch sensations. In neurons, however, it appears to help control and limit scratching behavior.

That distinction could be important for future drug development.

“This means that broadly blocking TRPV4 may not be the solution,” Gualdani noted. “Future therapies may need to be much more targeted — perhaps acting only in the skin, without interfering with the neuronal mechanisms that tell us when to stop scratching.”

Chronic itch affects millions of people living with conditions such as eczema, psoriasis, and kidney disease, but treatment options remain limited. Researchers believe that understanding how the body controls itch, including the signals that tell us when to stop scratching, could eventually lead to more effective therapies.

Using satellite observations, scientists detected unusually high levels of formaldehyde inside the enormous volcanic plume created by the eruption. That discovery immediately caught their attention because formaldehyde is produced when methane breaks down in the atmosphere.

“When we analyzed the satellite images, we were surprised to see a cloud with a record-high concentration of formaldehyde. We were able to track the cloud for 10 days, all the way to South America. Because formaldehyde only exists for a few hours, this showed that the cloud must have been destroying methane continuously for more than a week,” explains Dr. Maarten van Herpen from Acacia Impact Innovation BV, first author of the study, which has just been published in Nature Communications.

“It is known that volcanoes emit methane during eruptions, but until now it was not known that volcanic ash is also capable of partially cleaning up this pollution,” he adds.

Volcano Ash, Sea Salt, and Sunlight Triggered Chemical Reaction

The researchers believe the eruption activated a rare chemical process that they had previously identified in an entirely different environment.

In earlier research published in 2023, scientists discovered that dust blowing from the Sahara Desert across the Atlantic Ocean can combine with salt from sea spray to create tiny particles called iron salt aerosols. When sunlight strikes these particles, chlorine atoms are released. Those chlorine atoms react with methane and help break it apart in the atmosphere. The discovery significantly changed scientists’ understanding of atmospheric chemistry in the troposphere.

“What is new — and completely surprising — is that the same mechanism appears to occur in a volcanic plume high up in the stratosphere, where the physical conditions are entirely different,” says Professor Matthew Johnson from the Department of Chemistry at the University of Copenhagen, one of the researchers behind both discoveries.

During the Tonga eruption, massive amounts of salty seawater were blasted into the stratosphere together with volcanic ash. Researchers think sunlight interacting with this mixture created highly reactive chlorine that then helped destroy methane released during the eruption. The unusually high formaldehyde levels detected by satellites served as evidence that methane breakdown was taking place.

Scientists Say Global Methane Estimates May Need Revision

The discovery also suggests that scientists may need to rethink the global methane budget, which estimates how much methane enters and leaves Earth’s atmosphere.

“We now know that atmospheric dust — for example from a volcanic eruption — impacts the methane budget, meaning the budget of how much methane is added to the atmosphere and how much is removed. Because dust has not previously been taken into account, it is important that we correct the data on which these estimates are based,” says Matthew Johnson.

Why Methane Matters for Climate Change

Methane is responsible for about one third of current global warming. Over a 20-year period, methane traps roughly 80 times more heat than CO₂. Unlike carbon dioxide, however, methane does not remain in the atmosphere for centuries. It typically breaks down within about 10 years.

Because methane has a shorter atmospheric lifetime, reducing methane pollution could produce climate benefits relatively quickly. Scientists sometimes describe methane reduction as an “emergency brake” for climate change because lowering methane levels could help slow warming within the next decade and potentially reduce the risk of climate tipping points. Researchers stress, however, that cutting CO₂ emissions remains critical for long-term climate stability.

Discovery Could Inspire Future Climate Technologies

The team says the findings may help advance efforts to artificially accelerate methane removal from the atmosphere. Scientists around the world are currently exploring several possible approaches, but accurately measuring methane removal has been a major challenge.

“How do you prove that methane has been removed from the atmosphere? How do you know your method works? It’s very difficult. But here we address that problem by showing that methane breakdown can in fact be observed using satellites,” says Dr. Jos de Laat from the Royal Netherlands Meteorological Institute, senior author of the study.

The research relied on the TROPOMI instrument aboard the European Space Agency’s Sentinel-5P satellite, which tracks greenhouse gases and air pollution around the globe every day.

“Retrieving formaldehyde from TROPOMI in a stratospheric volcanic plume is far outside the instrument’s standard operating conditions — we had to carefully correct the satellite’s sensitivity for the unusual altitude of the signal and account for interference from the high sulfur dioxide concentrations. Getting these corrections right was essential to confirm that what we were seeing was real,” said Dr. Isabelle De Smedt, Royal Belgian Institute for Space Aeronomy.

Researchers believe the discovery could eventually inspire practical engineering solutions aimed at reducing methane pollution.

“It’s an obvious idea for industry to try to replicate this natural phenomenon ­ — but only if it can be proven to be safe and effective. Our satellite method could offer a way to help figure out how humans might slow global warming,” concludes Matthew Johnson.

About the Study

• Researchers estimate that the Tonga eruption released roughly 300 gigagrams (Gg) of methane, an amount comparable to the annual methane emissions produced by more than two million cows. At the same time, the volcanic plume removed about 900 megagrams (Mg) of methane per day, equal to the daily emissions from approximately two million cows.
• The study was published in Nature Communications.
• The research team included Maarten van Herpen (Acacia Impact Innovation BV, Netherlands); Isabelle De Smedt (Royal Belgian Institute for Space Aeronomy, Belgium); Daphne Meidan and Alfonso Saiz-Lopez (CSIC, Spain); Matthew Johnson (University of Copenhagen, Denmark); Thomas Röckmann (Utrecht University, Netherlands); and Jos de Laat (Royal Netherlands Meteorological Institute, Netherlands).
• The work was supported by Spark Climate Solutions.

The findings come from a mouse study focused on the microbiome, the vast community of bacteria and other microbes living in the digestive system. Researchers found that giving older mice back their own younger gut microbes produced striking effects throughout the body, especially in the liver.

Young Gut Microbiome Protected Aging Mice

To test the idea, scientists collected fecal samples from eight young mice and preserved them for later use. As the mice aged, the researchers transplanted the stored samples back into the same animals through a process known as fecal microbiota transplantation, or FMT.

Another group of eight aging mice served as controls and received sterilized fecal material instead. Researchers also included a small group of young mice to provide baseline comparisons.

By the end of the study, none of the mice that received their restored youthful microbiome developed liver cancer. In contrast, liver cancer appeared in 2 out of 8 untreated aging mice. The treated mice also showed lower levels of inflammation and reduced liver injury.

“We’re learning from this work that the aging microbiome actively contributes to liver dysfunction and cancer risk rather than simply reflecting the aging process,” said Qingjie Li, PhD, associate professor in the Division of Gastroenterology and Hepatology at The University of Texas Medical Branch, and lead researcher on the study. “The microbiome has a broader influence on the body’s cancer defenses than previously understood.”

Researchers Found Changes in a Cancer Related Gene

After completing the in vivo study, the research team closely examined liver tissue from the mice. They discovered important differences involving MDM2, a gene already associated with liver cancer development.

Young mice showed low levels of the MDM2 protein, while untreated older mice had much higher levels. Older mice that received the restored microbiome had suppressed MDM2 levels that more closely resembled those seen in younger animals.

“Restoring a more youthful microbiome can reverse several core features of aging at both the molecular and functional level, including inflammation, fibrosis, mitochondrial decline, telomere attrition, and DNA damage,” Dr. Li said.

Earlier Heart Research Led to the Discovery

The liver findings emerged unexpectedly from previous research examining the microbiome’s effects on heart health. In that earlier cardiac study, scientists observed that altering gut bacteria appeared to improve heart function.

However, when the researchers later analyzed tissue samples, they noticed even stronger effects in the liver. That observation prompted the team to investigate the connection more deeply.

To reduce the chances of immune complications or infection, the researchers used each mouse’s own preserved microbiome rather than relying on donor samples. They said this approach also creates a clearer proof of concept for possible future human studies.

Dr. Li stressed that the findings are limited to animal research and cannot yet be applied to people. Still, he said the team hopes to begin first in human clinical trials in the near future.

But researchers uncovered something unexpected. HSL was not just working on the surface of fat droplets inside fat cells. It was also operating deep inside the nucleus of those cells, where DNA is stored and important genetic activity is controlled. The discovery revealed an entirely different side to a protein scientists had studied since the 1960s.

The findings, published in Cell Metabolism, helped solve a long-standing mystery in obesity research and opened new directions for understanding diabetes, heart disease, and other metabolic disorders.

Fat Cells Do Far More Than Store Calories

Fat cells, also called adipocytes, are often viewed as passive storage containers for excess calories. In reality, they are highly active cells that help regulate the body’s entire energy system.

Inside adipocytes, fat is stored in structures called lipid droplets. When the body needs fuel between meals or during fasting, hormones such as adrenaline trigger the release of that stored energy. HSL plays a central role in this process by breaking down triglycerides into fatty acids that other organs can use for fuel.

Scientists long assumed that removing HSL would prevent fat breakdown and lead to obesity. Surprisingly, that is not what happened.

Studies in both mice and people with mutations in the HSL gene showed the opposite effect. Instead of accumulating extra fat, they developed lipodystrophy, a rare condition in which the body loses healthy fat tissue.

That contradiction puzzled researchers for years.

Obesity and Dangerous Fat Loss Share Similar Problems

Although obesity and lipodystrophy seem completely different, they can produce many of the same health complications.

In obesity, fat tissue becomes enlarged and dysfunctional. In lipodystrophy, the body lacks enough properly functioning fat tissue. In both cases, adipocytes fail to regulate energy normally, which can contribute to insulin resistance, type 2 diabetes, fatty liver disease, inflammation, and cardiovascular problems.

This overlap suggested that healthy fat tissue is not simply about how much fat the body carries. The quality and function of fat cells may be just as important.

Researchers at the Institute of Cardiovascular and Metabolic Diseases (I2MC) at the University of Toulouse wanted to understand why the loss of HSL caused fat tissue to break down instead of build up. What they found changed the scientific picture of fat metabolism.

Scientists Discover HSL Inside the Cell Nucleus

The research team, led by Dominique Langin, discovered that HSL was located in an unexpected place inside adipocytes: the nucleus.

The nucleus acts as the cell’s control center. It contains DNA and regulates which genes are switched on or off. Proteins found in the nucleus often help control cell growth, repair, metabolism, and communication.

“In the nucleus of adipocytes, HSL is able to associate with many other proteins and take part in a program that maintains an optimal amount of adipose tissue and keeps adipocytes ‘healthy’,” explained Jérémy Dufau, co-author of the study.

Researchers found that nuclear HSL appears to help regulate important cellular systems, including mitochondrial activity and the extracellular matrix, which provides structural support for tissues.

Mitochondria are often called the power plants of cells because they generate energy. The extracellular matrix helps maintain the shape and integrity of tissues. Problems in either system have been linked to obesity, inflammation, and metabolic disease.

A Protein With Two Very Different Jobs

The study showed that HSL behaves differently depending on where it is located inside the cell.

On lipid droplets, HSL acts as an enzyme that helps release stored fat during fasting or exercise. In the nucleus, however, it appears to work more like a regulator that helps maintain healthy adipose tissue.

Researchers also discovered that the amount of HSL inside the nucleus changes in response to the body’s metabolic state.

During fasting, adrenaline activates HSL and pushes it out of the nucleus so it can help mobilize fat stores. In obese mice fed a high-fat diet, nuclear HSL levels increased.

The protein’s movement appears to be controlled by signaling pathways involving TGF-β and SMAD3, molecules already known to influence inflammation, tissue remodeling, and metabolic disease.

Scientists also found evidence that nuclear HSL interacts with proteins involved in gene expression and RNA processing, suggesting it may directly influence how fat cells function at a genetic level.

Why the Discovery Matters

The findings helped explain why complete HSL deficiency causes lipodystrophy instead of obesity. Without HSL in the nucleus, fat cells may lose their ability to stay healthy and properly maintain adipose tissue.

“HSL has been known since the 1960s as a fat-mobilizing enzyme. But we now know that it also plays an essential role in the nucleus of adipocytes, where it helps maintain healthy adipose tissue,” Langin said.

The discovery may also help researchers better understand why some obesity treatments succeed while others fail. Many current therapies focus mainly on reducing fat mass. But the study suggests preserving healthy fat tissue function could be equally important.

Scientists are increasingly recognizing that adipose tissue acts as a complex endocrine organ that communicates with the brain, liver, muscles, and immune system through hormones and signaling molecules. Dysfunctional fat tissue can disrupt the body far beyond weight gain alone.

Obesity Remains a Global Health Challenge

The research arrives as obesity rates continue to rise worldwide. According to global estimates, billions of people are now overweight or obese, increasing the risk of diabetes, heart disease, stroke, sleep apnea, and some cancers.

Researchers hope that understanding how proteins like HSL regulate fat cell health could eventually lead to more targeted therapies for metabolic disease.

Instead of simply trying to eliminate fat, future treatments may focus on restoring the normal function of adipocytes and protecting the biological systems that keep fat tissue healthy in the first place.

Researchers at Tohoku University Graduate School of Medicine uncovered an unexpected possibility involving a drug that has long been used to treat constipation. In a clinical trial, the medication lubiprostone appeared to slow the decline of kidney function in patients with moderate CKD, raising hopes for an entirely new approach to kidney disease treatment.

“We noticed that constipation is a symptom that often accompanies CKD, and decided to investigate this link further,” explains Abe. “Essentially, constipation disrupts the intestinal microbiota, which worsens kidney function. Working backwards, we hypothesized that we could improve kidney function by treating constipation.”

The Surprising Gut Kidney Connection

Doctors have increasingly focused on what researchers call the “gut kidney axis,” the complex relationship between intestinal bacteria and kidney health. People with CKD often experience constipation and imbalances in gut microbes, which can contribute to inflammation and the buildup of harmful compounds in the body.

Earlier research had hinted that improving gut health might help protect the kidneys, but evidence in humans remained limited. To explore the idea further, researchers launched the multicenter Phase II clinical trial known as the LUBI-CKD TRIAL across nine medical institutions in Japan.

The study enrolled 150 patients with moderate chronic kidney disease. Participants received either lubiprostone or a placebo, allowing scientists to compare how the treatment affected kidney function over time.

The results surprised the researchers. Patients who received either 8 µg or 16 µg doses of lubiprostone showed a slower decline in kidney function compared with those in the placebo group. Kidney performance was measured using estimated glomerular filtration rate (eGFR), one of the most widely used indicators of kidney health.

Researchers reported that the protective effect appeared dose dependent, meaning higher doses were linked to greater benefits. The 16 µg group showed particularly promising preservation of kidney function signals during the 24 week trial period.

How a Constipation Drug May Protect the Kidneys

Scientists then investigated why the drug appeared to help the kidneys.

Their analysis pointed to changes in the gut microbiome. Lubiprostone increased the production of spermidine, a naturally occurring compound tied to healthier mitochondrial activity. Mitochondria are often described as the power plants of cells because they generate the energy cells need to function properly.

The researchers found that improved mitochondrial function may help shield kidney tissue from further damage. They also identified changes in bacterial pathways connected to polyamine production, adding more evidence that gut microbes may directly influence kidney health.

Interestingly, the treatment did not significantly reduce certain uremic toxins that scientists originally expected to change. Instead, the kidney benefits seemed tied more closely to microbiome remodeling and mitochondrial support. That finding could reshape how researchers think about treating CKD in the future.

Why Researchers Are Excited About the Findings

The study has drawn attention because lubiprostone is already an approved medication for chronic constipation, potentially making future clinical use faster than developing a completely new drug from scratch.

Researchers also believe the discovery may have implications beyond kidney disease. Because mitochondrial dysfunction is involved in many chronic illnesses, scientists are exploring whether similar gut targeted approaches could eventually help other disorders as well.

The research team is now planning larger Phase 3 trials to confirm whether the benefits hold up in broader patient populations. Scientists are also searching for biomarkers that could predict which patients are most likely to respond to treatment.

Although more research is still needed, the findings have added momentum to a rapidly growing area of medicine focused on the connection between gut bacteria, cellular energy production, and chronic disease progression. For people living with CKD, even modest slowing of kidney decline could potentially delay dialysis and improve quality of life.

Inside the human mouth, bacteria are in near constant communication. Roughly 700 bacterial species live there, and many exchange chemical messages through a process called quorum sensing. Some of these microbes communicate using signaling molecules known as N-acyl homoserine lactones (AHLs).

Researchers from the College of Biological Sciences and the School of Dentistry set out to investigate how these bacterial signals shape the oral microbiome and whether interrupting those signals could help prevent harmful plaque buildup while preserving healthy bacteria. Their findings, published in npj Biofilms and Microbiomes, could eventually influence treatments far beyond dentistry.

Scientists Target Bacterial Communication

The research team discovered several important patterns in how mouth bacteria interact:

• Bacteria living in dental plaque produce AHL signals in aerobic environments (such as above the gumline), and those signals can still affect bacteria in anaerobic environments (beneath the gumline).
• Removing AHL signals using specialized enzymes called lactonases increased populations of bacteria associated with good oral health.
• The findings suggest that carefully selected enzymes may be able to reshape dental plaque communities and support a healthier oral microbiome.

“Dental plaque develops in a sequence, much like a forest ecosystem,” said Mikael Elias, associate professor in the College of Biological Sciences and senior author of the study. “Pioneer species like Streptococcus and Actinomyces are the initial settlers in simple communities — they’re generally harmless and associated with good oral health. Increasingly diverse late colonizers include the ‘red complex’ bacteria like Porphyromonas gingivalis, which are strongly linked to periodontal disease. By disrupting the chemical signals bacteria use to communicate, one could manipulate the plaque community to remain or return to its health-associated stage.”

Oxygen Levels Change Bacterial Behavior

The researchers also found that oxygen plays a surprisingly important role in determining how these bacterial messages influence plaque growth.

“What’s particularly striking is how oxygen availability changes everything,” said lead author Rakesh Sikdar. “When we blocked AHL signaling in aerobic conditions, we saw more health-associated bacteria. But when we added AHLs under anaerobic conditions, we promoted the growth of disease-associated late colonizers. Quorum sensing may play very different roles above and below the gumline, which has major implications for how we approach treatment of periodontal diseases.”

This discovery suggests that bacterial communication works differently depending on where bacteria live inside the mouth. That insight could help researchers design more targeted approaches to controlling gum disease and maintaining a healthier balance of microbes.

Future Treatments Could Protect Healthy Bacteria

The next phase of the research will examine how bacterial signaling differs across various areas of the mouth and in people with different stages of periodontal disease.

“Understanding how bacterial communities communicate and organize themselves may ultimately give us new tools to prevent periodontal disease — not by waging war on all oral bacteria, but by strategically maintaining a healthy microbial balance,” said Elias.

Researchers believe this strategy could eventually be expanded beyond oral health. Imbalances in the microbiome, known as dysbiosis, have been linked to numerous diseases throughout the body, including certain cancers. Scientists hope these findings could help lay the groundwork for future therapies that guide microbial communities toward healthier states rather than eliminating bacteria altogether.

Funding for the study was provided by the National Institutes of Health.

The study, published in Science Advances in 2023, builds on earlier work by physicist Kostya Trachenko and colleagues showing that liquid viscosity is tied directly to fundamental physical constants. That finding established a lower limit for how “runny” liquids can be. The newer research extended the idea into biology, asking whether the same physical rules that shape the cosmos may also quietly determine whether cells can function.

Why Liquid Flow Matters for Life

Life depends on movement at microscopic scales. Nutrients must travel through cells, proteins need to fold correctly, and molecules constantly diffuse through watery environments. All of this relies on viscosity, the property that determines how easily a liquid flows.

According to the researchers, the Universe appears to operate within a surprisingly narrow “bio-friendly” window where viscosity and diffusion remain suitable for life. If the constants governing physics shifted by only a few percent, liquids essential to biology could become dramatically thicker or thinner.

“Understanding how water flows in a cup turns out to be closely related to the grand challenge to figure out fundamental constants. Life processes in and between living cells require motion and it is viscosity that sets the properties of this motion. If fundamental constants change, viscosity would change too impacting life as we know it. For example, if water was as viscous as tar life would not exist in its current form or not exist at all. This applies beyond water, so all life forms using the liquid state to function would be affected.”

The team says the consequences would extend far beyond drinking water or oceans. Human blood, cellular fluids, and the chemistry that powers life all rely on carefully balanced flow properties.

“Any change in fundamental constants including an increase or decrease would be equally bad news for flow and for liquid-based life. We expect the window to be quite narrow: for example, viscosity of our blood would become too thick or too thin for body functioning with only a few per cent change of some fundamental constants such as the Planck constant or electron charge.” Professor of Physics Kostya Trachenko said.

A New Twist on Cosmic Fine-Tuning

Physicists have long debated why the Universe’s constants appear finely tuned. Tiny differences in values such as the electron charge or the strength of fundamental forces could prevent stars from forming heavy elements needed for planets and life.

What makes this research unusual is that it shifts the discussion from stars and galaxies down to the level of living cells. Previous fine-tuning arguments often focused on nuclear reactions inside stars. This work argues that even if stars and heavy elements still formed, life might remain impossible if liquids could not flow properly inside organisms.

That introduces a second layer of fine-tuning. The constants not only appear compatible with a universe full of matter, but also with biological systems that depend on delicate liquid dynamics.

The researchers even suggest that multiple stages of tuning may have occurred. In the paper, Trachenko compares the possibility to biological evolution, where traits emerge independently over time. The idea remains speculative, but it raises the possibility that nature may favor stable physical structures in ways scientists do not yet fully understand.

Later Research Expanded the Idea

Since the original publication, scientists have continued exploring how viscosity, diffusion, and fluid behavior connect to fundamental physics. Follow-up theoretical work reviewed how liquid motion inside cells may place additional limits on the values of physical constants, especially in systems involving biochemical “machines” such as molecular motors.

Other researchers have also examined how viscosity itself may arise from deeper physical laws. A 2023 analysis highlighted growing evidence that liquid viscosity may be linked to universal physical limits rather than simply being a property measured in laboratories.

Together, these studies are helping reshape an old scientific mystery. Instead of viewing the constants of nature only through the lens of cosmology and particle physics, scientists are increasingly asking whether the conditions needed for flowing liquids and functioning cells should also be part of the equation.

Could Physics and Biology Be More Connected Than We Thought?

The idea remains highly theoretical, and many physicists would caution that there is still no accepted explanation for why the constants of nature have their observed values. But the research opens an unexpected path for thinking about one of science’s biggest questions.

For decades, the mystery of fundamental constants was mostly explored through black holes, stars, and subatomic particles. This work suggests the answer may also involve something much closer to everyday life: the simple ability of liquids to flow through living cells.