The surprising new ways bacteria spread without propellers

 New research from Arizona State University shows that bacteria can travel in unexpected ways even when their usual propulsion system fails. Normally, bacteria move using flagella, slender, whip-like structures that spin to push the cells forward. The new studies reveal that microbes can still spread across surfaces without these structures.

Movement is critical for bacteria. It allows them to gather into communities, explore new environments, and escape harmful conditions. Learning how bacteria move may help scientists design better strategies to prevent infections.

In the first study, researcher Navish Wadhwa and his team found that salmonella and E. coli can migrate across moist surfaces even when their flagella are disabled. The bacteria generate motion through their metabolism. When they ferment sugars, they create tiny outward flowing currents across the wet surface. These flows slowly push the bacterial colony outward, similar to leaves drifting along a thin stream.

Researchers named this newly identified movement "swashing." The discovery could help explain how disease causing microbes manage to colonize medical devices, wounds, and food processing equipment. By understanding how bacterial metabolism drives this type of motion, scientists may be able to slow or stop it by altering environmental conditions such as pH or sugar levels.

"We were amazed by the ability of these bacteria to migrate across surfaces without functional flagella. In fact, our collaborators originally designed this experiment as a 'negative control,' meaning that we expected (once rendered) flagella-less, the cells to not move," Wadhwa says. "But the bacteria migrated with abandon, as if nothing were amiss, setting us off on a multiyear quest to understand how they were doing it.

"It just goes to show that even when we think we've got something figured out, there are often surprises waiting just under the surface, or in this case, above it."

Wadhwa is a researcher with the Biodesign Center for Mechanisms of Evolution and assistant professor with the Department of Physics at ASU. The study appears in the Journal of Bacteriology and was selected as an Editor's Pick, highlighting its significance.

Sugar Fueled Swashing

The swashing effect begins when bacteria consume fermentable sugars such as glucose, maltose, or xylose. During fermentation, the microbes release acidic by products including acetate and formate. These compounds pull water toward the colony from the surrounding surface, creating tiny currents that push the cells outward.

Fermentable sugars are required for this movement. Without them, bacteria cannot produce the fluid flows needed for swashing. Sugar rich environments inside the body, such as mucus, could therefore make it easier for harmful bacteria to spread and trigger infections.

Scientists also tested what happens when surfactants, detergent-like molecules, are added to the colonies. These compounds stopped swashing completely. However, the same chemicals did not interfere with swarming, another type of bacterial movement powered by flagella that enables microbes to rapidly spread across wet surfaces. This difference suggests the two behaviors rely on separate physical mechanisms. It also hints that surfactants might someday be used to control bacterial movement depending on whether microbes are swashing or swarming.

The discovery that bacteria can colonize surfaces even when their normal swimming machinery fails has important health implications. Some microbes could spread across medical catheters, implants, or hospital equipment through swashing. Simply blocking flagella might not prevent that spread. Instead, treatments may need to target the metabolic processes that drive the fluid currents.

E. coli and salmonella are both well known causes of foodborne illness. Recognizing that these bacteria can spread through passive fluid flows may help improve sanitation strategies in food processing facilities. Because swashing depends on fermentation and acidic by products, altering factors such as surface pH or sugar levels could limit bacterial growth. The study found that even modest changes in acidity could influence how bacteria move.

Similar conditions may also exist inside the human body. Moist environments such as gut mucus, wound fluids, or the urinary tract provide surfaces where bacteria could spread through swashing, even when their flagella are not functioning effectively.

A Molecular Gear System for Bacterial Movement

A second study examined a different group of microbes called flavobacteria. Unlike E. coli, these bacteria do not swim. Instead, they travel along environmental and host surfaces using a specialized machine known as the type 9 secretion system, or T9SS. This system powers a molecular conveyor belt that moves along the surface of the cell.

Under normal conditions, the T9SS allows flavobacteria to glide across surfaces. The mechanism works by moving an adhesive coated belt around the outside of the cell, pulling the bacterium forward in a motion that resembles a microscopic snowmobile.

Source: ScienceDaily

Severe COVID or flu may raise lung cancer risk years later

 Serious cases of COVID-19 and influenza may do more than cause short term illness. New research from UVA Health's Beirne B. Carter Center for Immunology Research and the UVA Comprehensive Cancer Center suggests that severe viral infections can create conditions in the lungs that help cancer develop and progress more quickly. The study also found that vaccination can prevent many of these harmful effects.

Researchers led by UVA School of Medicine scientist Jie Sun, PhD, discovered that severe respiratory infections can alter immune cells in the lungs in ways that support tumor growth months or even years later. Based on these findings, the scientists recommend that doctors closely watch patients who recover from severe COVID, flu, or pneumonia so lung cancer can be detected early, when treatment is most effective.

"A bad case of COVID or flu can leave the lungs in a long-lasting 'inflamed' state that makes it easier for cancer to take hold later," said Sun, co-director of UVA's Carter Center and a member of UVA's Division of Infectious Diseases and International Health. "The encouraging news is that vaccination largely prevents those harmful changes for cancer growth in the lung."

Severe Respiratory Infections and Long Term Lung Damage

Respiratory illnesses such as influenza and COVID are among the most common sources of lung injury. However, scientists have not fully understood how this type of damage might influence cancer risk years later. To explore this question, Sun and his team studied the effects of severe lung infections in both laboratory mice and human patients.

The findings were striking. Mice that experienced severe lung infections were more likely to develop lung cancer later and were also more likely to die from the disease. When the researchers analyzed patient data, they found a similar pattern. People who had previously been hospitalized with COVID-19 showed a higher rate of lung cancer diagnoses.

The analysis revealed a 1.24-fold increase in lung cancer incidence among patients who had been hospitalized for COVID-19. This elevated risk was seen regardless of whether the individuals smoked or had other medical conditions, which doctors refer to as "comorbidities."

"These findings have important immediate implications for how we monitor patients after severe respiratory viral infection," said Jeffrey Sturek, MD, PhD, a UVA physician-scientist who collaborated on the study. "We've known for a long time that things like smoking increase the risk for lung cancer. The results from this study suggest that we may need to think about severe respiratory viral infection similarly. For example, in some patients who are at high risk for lung cancer based on smoking history, we recommend close monitoring with routine screening CT scans of the lungs to catch cancer early. In future studies, we may want to consider a similar approach after severe respiratory viral infection."

Immune Changes That Create a Pro Tumor Environment

Experiments in mice helped the researchers uncover why severe infections may increase cancer risk. The team observed major changes in immune cells known as neutrophils and macrophages, which normally help defend the lungs.

After severe infection, some neutrophils began behaving abnormally and contributed to a persistent inflammatory environment described as "pro-tumor," meaning it supports cancer growth. The scientists also found significant changes in epithelial cells that line the lungs and the tiny air sacs responsible for breathing.

Vaccination May Protect the Lungs

The study also produced encouraging findings about prevention. Prior vaccination appeared to block many of the lung changes linked to cancer development. Vaccines help the immune system respond more effectively to infections, which reduces how severe the illness becomes.

The researchers observed the increased cancer risk mainly in people who had severe COVID-19. Individuals who experienced only mild infections did not show this elevated risk and actually had a slight decrease in lung cancer incidence.

Even so, the scientists warn that many people who survived severe COVID-19 or other serious respiratory infections could face a higher risk of lung cancer in the future.

"With tens of millions of people globally experiencing long-term pulmonary [COVID-19] sequelae, these findings carry significant implications for clinical care," the researchers wrote in their scientific paper. "Individuals recovering from severe viral pneumonia, particularly those with smoking history, may benefit from enhanced lung cancer surveillance, and preventing severe infection through vaccination may confer indirect cancer protection benefits."

Source: ScienceDaily

Indoor Plants, HEPA Air Purifiers, or Open Window Ventilation: Simple Clean Air Tips for Household PM2.5 Reduction

 Indoor air quality has become a growing concern as people spend more time indoors in tightly sealed homes. Indoor plants' air quality benefits, HEPA air purifiers, and open window ventilation are three of the most common strategies people use when looking for simple clean air tips. Each approach works differently, and understanding their strengths and limits helps households choose the best mix for healthier breathing.

What Affects Household Air Quality?

Household air can contain dust, pet dander, mold spores, smoke, and tiny particles known as PM2.5. These fine particles are small enough to enter deep into the lungs and are linked to respiratory and cardiovascular issues, so household PM2.5 reduction is a key goal.

Indoor sources such as cooking, candles, cleaning products, and damp areas can increase pollution levels, while outdoor air pollution can enter through leaks, doors, and windows.

Do Indoor Plants Really Improve Air Quality?

Do Indoor Plants Actually Improve Indoor Air Quality?

Plants can absorb certain gases and volatile organic compounds (VOCs) through their leaves and roots. In controlled lab conditions this can reduce specific pollutants over time, but in real homes the effect is usually modest, especially for very small particles like PM2.5.

Even so, indoor plants' air quality benefits go beyond chemistry. Leaves can trap some dust on their surfaces, and plants can slightly increase humidity, which may reduce airborne dust. Greenery also improves mood and perceived freshness, making indoor spaces feel more pleasant and relaxing.

Best Indoor Plants for Cleaner Air

Some species are especially popular for indoor plants' air quality goals because they are hardy and have large leaf surfaces. Common choices include snake plant, spider plant, pothos, peace lily, rubber plant, and ZZ plant.

A practical approach is placing one to three medium-sized plants in rooms where people spend the most time, such as the living room, bedroom, or home office. Indoor plants are best treated as a supporting measure rather than a primary solution for household PM2.5 reduction.

Limitations of Indoor Plants for PM2.5 Reduction

Indoor plants are not a fast or powerful tool for fine particles. Unlike mechanical filtration, they do not actively pull large volumes of air through a filter, so they cannot quickly clear a smoky or heavily polluted room.

Source: Medical Daily

Scientists discover molecule that stops aggressive breast cancer in its tracks

 Researchers at Oregon Health & Science University have developed a new molecule that may open the door to treating difficult cases of triple-negative breast cancer, a particularly aggressive form of the disease that currently has few effective treatment options.

In a study published in the journal Cell Reports Medicine, the team describes how the experimental molecule, called SU212, blocks an enzyme that plays a key role in cancer progression. The findings come from experiments using a humanized mouse model designed to mimic human disease.

"It's an important step forward to treat triple-negative breast cancer," said senior author Sanjay V. Malhotra, Ph.D., co-director of the Center for Experimental Therapeutics in the OHSU Knight Cancer Institute. "Triple-negative breast cancer is an aggressive form of cancer and there are no effective drugs available right now."

The next stage of development would involve moving the molecule toward human clinical trials. That process requires significant resources to obtain Food and Drug Administration approval and to launch studies involving patients.

Malhotra, the Sheila Edwards-Lienhart Endowed Chair in Cancer Research and a professor of cell, developmental and cancer biology in the OHSU School of Medicine, said the same strategy could potentially be used to treat other types of cancer as well.

Triple-negative breast cancer makes up about 15% of all breast cancer cases.

Targeting a Key Enzyme That Fuels Cancer Growth

To test the new compound, researchers used a humanized mouse model of triple-negative breast cancer. The molecule SU212 attaches to an enzyme called enolase 1, or ENO1. This enzyme helps regulate glucose levels inside human cells and is produced in unusually high amounts by many cancer cells.

Once bound to ENO1, the molecule causes the enzyme to break down. This process ultimately reduced tumor growth and limited metastasis in the mice.

Under normal conditions, the enzyme plays a role in metabolism by helping cells convert glucose into energy. By disrupting this process in cancer cells, SU212 interferes with a critical pathway that tumors use to survive and spread.

Malhotra noted that this mechanism may be particularly relevant for patients who also have metabolic disorders such as diabetes, a chronic disease that leads to high blood sugar levels.

Potential for Treating Multiple Types of Cancer

The researchers believe that drugs targeting enolase 1 may have benefits beyond triple-negative breast cancer. Other cancers that are influenced by this enzyme include glioma, pancreatic cancer, and thyroid carcinoma.

"A drug that targets enolase 1 could help improve the treatment of these cancers too," he said.

Malhotra joined OHSU in 2020 after working at Stanford University, where his laboratory continued studying the molecule. The compound was originally developed during his earlier research at the National Cancer Institute in Bethesda, Maryland.

As co-director of OHSU's Center for Experimental Therapeutics, Malhotra works with colleagues to move laboratory discoveries toward clinical applications that can benefit patients treated in OHSU hospitals and clinics.

"There is definitely great science going on here, and we want to translate that science for the benefit of people," he said.

The research was supported by the National Cancer Institute, the National Institute of Aging and the National Heart, Lung and Blood Institute, all of the National Institutes of Health, under award numbers N91019D00024, RF1AG079890, and R01HL164729; the Department of Defense, award HT9425-23-1-0796; the Knight Cancer Institute and the Biomedical Innovation Program at OHSU; and Sheila Edwards-Lienhart endowment funds. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH or other funders.

Source: ScienceDaily

Scientists detect a sudden acceleration in global warming

 Global warming has been increasing at a faster pace since about 2015, according to a new study from the Potsdam Institute for Climate Impact Research (PIK). By adjusting global temperature records to remove known natural influences, researchers were able to identify a statistically significant rise in the rate of warming for the first time.

During the past decade, global temperatures have climbed at an estimated rate of about 0.35°C per decade, depending on the dataset analyzed. From 1970 through 2015, the average increase was just under 0.2°C per decade. The more recent trend represents the fastest warming observed in any decade since instrumental temperature records began in 1880.

"We can now demonstrate a strong and statistically significant acceleration of global warming since around 2015," says Grant Foster, a US statistics expert and co-author of the study, which was published today in the scientific journal Geophysical Research Letters.

"We filter out known natural influences in the observational data, so that the 'noise' is reduced, making the underlying long-term warming signal more clearly visible," Foster added.

Removing Natural Climate Variability From Temperature Data

Short term natural events can temporarily raise or lower global temperatures and make it harder to detect changes in long term climate trends. These influences include El Niño events, volcanic eruptions, and variations in solar activity.

To address this challenge, the researchers analyzed measurement data from five widely used global temperature datasets (NASA, NOAA, HadCRUT, Berkeley Earth, ERA5). By adjusting the data to account for these natural factors, the team was able to isolate the underlying warming trend more clearly.

"The adjusted data show an acceleration of global warming since 2015 with a statistical certainty of over 98 percent, consistent across all data sets examined and independent of the analysis method chosen," explains Stefan Rahmstorf, PIK researcher and lead author of the study.

Statistical Analysis Reveals a Shift in Warming Trends

The study focused on determining whether the pace of warming has changed, rather than identifying the causes behind that shift.

After accounting for the influence of El Niño and the recent solar maximum, the extremely warm years of 2023 and 2024 appear slightly cooler in the adjusted analysis. Even with these corrections, they still rank as the two warmest years recorded since instrumental measurements began. Across all datasets, the faster warming trend becomes visible around 2013 or 2014.

To evaluate whether the warming rate has changed since the 1970s, the researchers applied two statistical techniques: a quadratic trend analysis and a piecewise linear model that identifies when shifts in warming rates occur.

Implications for the Paris Agreement Climate Target

The study does not attempt to determine the specific reasons behind the acceleration in warming. However, the authors note that climate models already allow for the possibility that the rate of warming could increase over time.

"If the warming rate of the past 10 years continues, it would lead to a long-term exceedance of the 1.5°C limit of the Paris Agreement before 2030," says Stefan Rahmstorf. "How quickly the Earth continues to warm ultimately depends on how rapidly we reduce global CO2 emissions from fossil fuels to zero."

Source: ScienceDaily

Parents’ stress may be quietly driving childhood obesity, Yale study finds

 Childhood obesity has been increasing in recent years. According to the U.S. Centers for Disease Control, about one in five children and teenagers in the United States met the clinical definition of obesity in 2024.

Preventing obesity in children is not simple. For many years, the main approaches have focused on encouraging healthy eating and regular physical activity. Researchers at Yale now suggest that another important factor should be added to that list: reducing stress in parents.A research team led by Yale psychologist Rajita Sinha found evidence that lowering parental stress may help reduce the risk of obesity in young children.

"It's the third leg of the stool," said Sinha. "We already knew that stress can be a big contributor in the development of childhood obesity. The surprise was that when parents handled stress better, their parenting improved, and their young child's obesity risk went down."

The findings were published in the journal Pediatrics.

Parent Stress May Influence Children's Eating and Health

Earlier studies have shown that children are more likely to develop obesity if their parents are obese. Researchers have also suspected that parental stress may be another hidden contributor to obesity in early childhood.

Previous work has shown that stressed parents are more likely to depend on fast food and less healthy eating habits. These choices can influence children's behavior and food preferences. When parents feel overwhelmed, family routines can break down, unhealthy food choices may become more common, and positive parenting behaviors can decline.

Still, most current childhood obesity prevention programs focus mainly on nutrition education and physical activity. According to Sinha, these efforts often fail to create lasting improvements.

Sinha is the Foundations Fund Professor in Psychiatry and a professor in neuroscience and child study at Yale School of Medicine.

Testing a Stress Reduction Program for Parents

To explore the role of parental stress, researchers conducted a 12 week randomized prevention trial involving 114 parents from diverse ethnic and socioeconomic backgrounds. All participants had children between two and five years old who were overweight or obese.

Parents were assigned to one of two groups. One group participated in a stress focused program called Parenting Mindfully for Health (PMH). This program taught mindfulness techniques and behavioral self regulation skills while also providing guidance on healthy nutrition and physical activity.

Source: ScienceDaily

Scientists capture a magnetic flip in 140 trillionths of a second

 A team led by Ryo Shimano at the University of Tokyo has directly observed how electron spins flip inside an antiferromagnet, a material in which opposing spins cancel each other out. By capturing this process in action, the researchers identified two separate switching mechanisms. One of them outlines a practical path toward ultrafast, non-volatile magnetic memory and logic devices that could outperform today's technologies. The results were published in Nature Materials.

From punched paper cards and metal rods to vacuum tubes and transistors, modern computing has always relied on physical systems to represent 0s and 1s. As demand for processing power continues to rise, researchers are searching for faster and more efficient alternatives. Antiferromagnets offer a promising option. Although they appear magnetically neutral because their spins balance out, their internal magnetic structure can still be harnessed to store digital information in new ways."For many years," says Shimano, "scientists believed that antiferromagnets like Mn3Sn (manganese three tin) could switch their magnetization extremely quickly. However, it was unclear whether this non-volatile switching could complete within a few to several tens of picoseconds or how the magnetization really changed during the switching process."

Heat or Current? Solving the Switching Mystery

A central question was what actually drives the spin reversal. Does the electric current flip the spins directly, or does heat generated by the current cause the change?

To find out, the team designed an experiment to watch the process unfold in real time. They fabricated a thin film of Mn3Sn and sent brief electrical pulses through it. At the same time, they illuminated the sample with precisely timed ultrafast flashes of light, adjusting the delay between the current pulse and the light pulse. This approach allowed them to assemble a time resolved sequence showing how the magnetization evolved moment by moment.

"The most challenging part of the project," Shimano remembers, "was measuring the infinitesimal changes in the magneto-optical signal. However, we were surprised how clearly we could finally observe the switching process once we established the right method."

Two Distinct Spin Switching Mechanisms Revealed

The experiment produced something unprecedented: a frame by frame view of magnetic pattern changes during switching. The images showed that the behavior depends on the strength of the applied current.

When the current was strong, switching was driven by heating effects. Under weaker current conditions, however, the spins flipped with little to no heating involved. This second pathway is especially significant because it suggests a way to control magnetic states quickly and efficiently without wasting energy as heat.

That heat free switching mechanism could serve as the foundation for next generation spintronic devices used in computing, communications, and advanced electronics. For Shimano, the findings point to new scientific territory still waiting to be explored.

Pushing the Limits of Picosecond Switching

"Our present fastest time-resolved observation of electrical switching in Mn₃Sn is 140 picoseconds, mainly limited by how short the current pulses can be generated in our device setup. However, our findings suggest that the material itself could switch even faster under appropriate conditions. In the future, we aim to explore these ultimate limits by creating even shorter current pulses and by optimizing the device structure."

Although the current measurements are capped at 140 picoseconds, the material's true speed limit may be even shorter. By refining their experimental tools and device design, the researchers hope to uncover just how fast antiferromagnetic spin switching can ultimately go.

Source: ScienceDaily