Published in Cancer Discovery, the study was led by researchers at the Wellcome Sanger Institute and their collaborators. The team combined genetic analysis with detailed clinical records to investigate how chronic blood cancers can develop over several decades. The findings were also presented at the American Association of Cancer Research (AACR) Conference in San Diego.

How Chronic Blood Cancers Develop

Myeloproliferative neoplasms (MPNs) are a group of rare, long-lasting blood cancers that begin in the bone marrow, where blood cells are produced. In people with MPNs, the bone marrow makes certain blood cells in an uncontrolled way.

Around 40,000 people in the UK are living with MPNs, and approximately 4,000 new cases are diagnosed each year.[1] These cancers often progress slowly. They can begin with mutations, or changes in DNA, that arise very early in life, followed by additional mutations that accumulate over several decades.[2]

Most MPNs are associated with mutations in the JAK2, CALR or MPL genes. However, around 10 percent of patients do not have any of these common genetic changes.

In these cases, doctors may diagnose cancer largely by examining the appearance of cells in the bone marrow. As a result, some patients could receive cancer treatment, including chemotherapy, without definitive genetic evidence that they have an underlying blood cancer.

Why Some Cases Worsen

The course of chronic blood cancer varies widely between patients. Some people feel well for years and need only mild treatment while their disease remains stable. Others eventually develop more serious conditions, including leukemia or myelofibrosis, which causes scarring in the bone marrow.

Doctors cannot always determine in advance whose disease will remain stable and whose will progress. The researchers therefore investigated whether genetic changes could reveal which patients were at greater risk. They also examined whether people who lacked the common MPN mutations truly had blood cancer.

The team followed 30 patients with chronic blood cancers, primarily MPNs. They combined whole-genome sequencing with extensive clinical information, including nearly 8,000 blood test results, treatment records and disease data.[3]

More than 450 samples were examined through repeated genomic testing. Some patients were monitored through routine clinical care for as long as 25 years.

Building Family Trees of Blood Cells

The long follow-up period connected genomic research at the Sanger Institute with routine patient care at Cambridge University Hospitals NHS Foundation Trust. This allowed the scientists to observe how blood cell populations changed over time and provided a broader view of how cancers evolve.

Using DNA taken from blood cells, the researchers created genetic 'family trees'. These reconstructions allowed them to trace the origins of cancer clones, groups of genetically identical cells that later contributed to disease progression.

The analysis revealed distinct patterns of evolution among patients with MPNs.

People whose disease remained clinically stable tended to have genetically 'steady' blood cell populations that acquired few or no additional mutations. By contrast, patients whose disease progressed developed new DNA changes over time.

The results suggest that progression in chronic blood cancers may be biologically 'encoded' years before a patient's condition visibly deteriorates. Mutations linked to future progression may be detectable long before symptoms worsen or standard clinical tests reveal a major change.

Some Diagnoses May Reflect Normal Aging

The researchers also examined patients who lacked mutations in JAK2, CALR or MPL.

They reconstructed 'family trees' from around 200 blood cell genomes belonging to these patients. Instead of finding patterns typical of cancer, the scientists observed changes that were more consistent with normal aging.

This finding challenges the assumption that everyone with certain unusual bone marrow features has a true blood cancer. Some people currently placed in this disease category may instead have biological characteristics that are different from those seen in genuine MPNs.

The results suggest that doctors may need to reconsider how these patients are diagnosed and managed. They also support new British Society for Haematology guidelines for investigating people without JAK2, CALR or MPL mutations.[4,5]

These guidelines recommend that some patients initially be described as having thrombocytosis without JAK2, CALR or MPL mutations, rather than being immediately diagnosed with blood cancer. Thrombocytosis means a high platelet count without clear genetic evidence of cancer.

Toward Regular Genomic Monitoring

The study highlights several possible clinical benefits of using genomic information more routinely in cancer care. Genetic testing could help doctors distinguish stable disease from cancers that are likely to progress, refine uncertain diagnoses and guide the development of more precise treatments.

In the future, regular genomic tests could allow clinicians to identify high-risk patients years before their disease worsens. That could create opportunities to intervene earlier while avoiding unnecessary treatment for people whose blood changes may not be cancerous.

Dr. Daniel Leongamornlert, first author at the Wellcome Sanger Institute, said: "We followed patients with myeloproliferative neoplasms over many years and used genome sequencing and clinical history to trace how blood cell populations changed over time. By reconstructing the ancestry of cells, we were able to see different evolutionary patterns between patients who had stable disease compared to others who progressed."

Dr. Dani Skirrow, Research Information Manager at Cancer Research UK, who part-funded the study, said: "We're in a golden age of research where advances in technology mean we can rapidly read DNA to find the errors in the code that can lead to cancer. Collaboratively, our researchers have read huge amounts of DNA to build up a detailed picture of how certain blood cancers can start, grow and behave, revealing some changes that could help us predict cancer years in advance. This type of discovery research is essential to improve how we monitor people at risk of blood cancer, and to help us find better ways to prevent, detect and treat the disease so people can live longer, better lives."

Dr. Jyoti Nangalia, senior author at the Wellcome Sanger Institute and Honorary Consultant Haematologist at Cambridge University Hospitals NHS Foundation Trust, said: "These are patients we have cared for and followed in our clinic for over 15 years. It can be incredibly difficult to predict how their cancers might change over time. By combining long-term clinical care with regular genomic analysis, we've been able to watch how the genetic code of their disease evolves in advance of clinical changes. The patterns we have found will help doctors develop better monitoring strategies, refine diagnosis and lead to better patient outcomes in the long run."

One Patient's Decades-Long Experience

Alan Everitt, 77, has received care at Cambridge University Hospitals NHS Foundation Trust for more than three decades. He was diagnosed in 1992 with essential thrombocythemia (ET), a rare form of MPN that causes the body to produce too many platelets, the blood cells involved in clotting.

His condition later progressed to myelofibrosis, which causes scar tissue to develop in the bone marrow. He has also experienced recurrent skin cancers.

Alan Everitt, from Hardwick, Cambridgeshire, said: "It's been reassuring to be cared for over so many years by both the hematology and plastic surgery teams at Addenbrooke's Hospital in Cambridge. I have always felt well supported and I'm grateful for the care and feedback at every step. Living with a blood cancer for such a long time has come with many challenges, and I hope that taking part in this research will help make a difference for future patients whose cancer is likely to progress over time, as mine has."

Notes:

1. Blood Cancer UK. Myeloproliferative neoplasms (MPN). Available at: https://bloodcancer.org.uk/understanding-blood-cancer/myeloproliferative-neoplasms/ (Last accessed: April 2026)
2. N. Williams et al. (2022). 'Life histories of myeloproliferative neoplasms inferred from phylogenies.' Nature. DOI: 10.1038/s41586-021-04312-6
3. Blood and bone marrow samples were obtained from patients recruited at Cambridge University Hospitals NHS Foundation Trust. Clinical data regarding the patients including blood counts and treatment history were collected using the electronic health record (EHR) systems. Whole blood and skin biopsies were obtained during routine clinical visits with buccal swab or T-cell samples from patients for matched 'normal' material.
4. A. Godfrey et al. (2026). 'Investigation and management of thrombocytosis without JAK2, CALR or MPL mutations: A British Society for Haematology Guideline'. British Journal of Haematology. DOI: 10.1111/bjh.70260
5. New British Society for Haematology guidelines recommend describing some patients as having thrombocytosis without JAK2, CALR or MPL mutations -- meaning a high platelet count without clear genetic evidence of cancer -- rather than initially diagnosing them with a blood cancer.

This research was supported in part by Wellcome and Cancer Research UK.

Reporting from ScienceDaily contributed to this story.

The study, led by Dr. Keisuke Obara, Dr. Kento Yoshioka, and Professor Yoshio Tanaka of the Faculty of Pharmaceutical Sciences, found that ferulic acid (FA) can reduce intestinal smooth muscle contractions by blocking voltage-dependent calcium channels. The discovery could eventually support new dietary approaches for intestinal motility disorders such as irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD).

A Common Compound in Whole Grains

Ferulic acid is a polyphenol found in many plant-based foods, especially whole grains and rice bran. It is already known for its antioxidant and neuroprotective effects, and previous research has largely examined how it may benefit the body more broadly.

Much less was known, however, about its effects on gastrointestinal motility, the coordinated muscle activity that moves food and waste through the digestive system.

People with IBS and IBD can experience abnormal intestinal movement. In some cases, the gut contracts too much, while in others, movement is reduced. The researchers set out to determine whether FA could directly alter these contractions.

Ferulic Acid Reduced Intestinal Contractions

The team tested FA using guinea pig ileal longitudinal smooth muscle (ILSM). The compound significantly reduced contractions triggered by several signaling molecules, including acetylcholine, histamine, prostaglandin F2α, and serotonin.

The inhibitory effect was reversible, meaning normal contractions returned after FA was removed. It was also concentration-dependent, with stronger effects appearing at higher concentrations.

The researchers found that FA acted in a noncompetitive manner. This suggests that it did not simply block the receptors used by the signaling molecules. Instead, it appeared to interfere with a shared mechanism involved in muscle contraction.

Blocking Calcium Signals in Smooth Muscle

Additional experiments using vascular smooth muscle cell models offered a possible explanation. FA reduced the rise in intracellular calcium caused by potassium chloride.

Calcium entering smooth muscle cells plays a central role in triggering contraction. The results indicate that FA suppresses this process by inhibiting voltage-dependent calcium channels, reducing the calcium signals needed for the muscles to tighten.

Possible Benefits and Risks for Gut Disorders

The findings suggest that FA may act as a natural regulator of intestinal motility. By calming excessive smooth muscle activity, it could potentially help people with diarrhea-predominant IBD.

The same effect may not be beneficial for everyone. In people with constipation-predominant IBS, or in healthy individuals, further slowing intestinal movement could make constipation or related symptoms worse.

Human Studies Are Still Needed

The researchers emphasized that the concentrations of FA that produced an effect in vitro were higher than the blood levels usually reached through normal dietary intake.

However, FA concentrations inside the intestines may be higher after food or supplements are consumed because the compound comes into direct contact with the digestive tract. More research will be needed to determine whether the laboratory findings reflect what happens in the human body.

The study provides a foundation for investigating whether ferulic acid could eventually be used in dietary interventions or supplements designed to regulate gut movement. Clinical trials will be necessary to confirm its effects in people, identify which patients might benefit, and determine safe and effective intake levels.

Reporting from ScienceDaily contributed to this story.

The study, led by Houston Methodist researchers, examined how changes in body fat associated with obesity may send damaging signals to the brain. These signals appear to interfere with the brain's immune system and contribute to the biological damage linked to Alzheimer's disease.

The research was co-led by Stephen Wong, Ph.D., the John S. Dunn Presidential Distinguished Chair in Biomedical Engineering, and Li Yang, Ph.D., a research associate in the Chao Center for BRAIN at Houston Methodist. The findings were published in Molecular Neurodegeneration.

Fat Molecules May Connect Obesity and Alzheimer's

The researchers identified phosphatidylethanolamines (PEs) as a potentially important link between obesity and Alzheimer's disease. PEs are a class of lipid, or fat molecule, found in cell membranes throughout the body.

According to the study, obesity raises the amount of these molecules in body tissue. The PEs are then loaded into tiny particles that can travel through the body and reach the brain.

Once inside the brain, these particles can interfere with communication between brain cells, weaken immune protection, and encourage amyloid proteins to accumulate. Amyloid buildup is one of the major biological features associated with Alzheimer's disease.

"Obesity can change how signals travel to the brain," Wong said. "The good news is that this may be something we can treat. Instead of looking at Alzheimer's risk tied to obesity as just a metabolic problem, this research suggests we may be able to target the process that connects those changes to the brain."

Restoring Lipid Balance Improved Brain Function

The findings also suggest a possible direction for future treatments. When the researchers restored a healthier balance of PEs, they observed less disruption in lipid regulation.

Correcting the imbalance also improved brain function and cognitive performance in models of Alzheimer's disease. Cognitive performance refers to abilities such as learning, memory, attention, and problem solving.

These results suggest that targeting the fat molecules or the pathway that carries them to the brain could potentially reduce some of the damage associated with obesity and Alzheimer's.

A Growing Public Health Challenge

According to the Centers for Disease Control and Prevention, more than 6.5 million Americans are living with Alzheimer's. That total is expected to rise to nearly 14 million by 2060.

Yang emphasized that more research will be required before treatments aimed at PEs can be tested as prevention or therapy in people. Still, the findings introduce a possible strategy for intervening earlier in individuals whose metabolic health may place them at greater risk of Alzheimer's disease.

Study Collaborators and Funding

Other collaborators on the study include Li Yang, Jianting Sheng, Shaohua Qi, Zheng Yin, Michael Chan, Yuliang Cao, Hong Zhao, Zhihao Wan, Bill Chan, Ju Ahn, Xiaohui Yu, Matthew Vasquez and Shan Xu from Houston Methodist; Xianlin Han from the University of Texas, San Antonio; Weiming Xia from Boston University and Willa Hsueh from Ohio State University.

The study was funded by grants from the Cure Alzheimer's Fund, the T.T. and W.F. Chao Foundation, and the John S. Dunn Research Foundation.

Reporting from ScienceDaily contributed to this story.

The study, conducted by ECU's Centre for Precision Health (CPH), examined the aquaporin-4 (AQP4) gene. This gene helps control the movement of fluid through the brain, a function that supports the organ's natural waste-clearing system.

The Brain's Overnight Waste Removal System

The brain's waste-removal process becomes especially active during sleep. Scientists believe it helps clear potentially harmful proteins, including proteins associated with Alzheimer's disease.

Researchers found that the effects of sleep appeared to vary depending on which version of the AQP4 gene a person carried.

"Our study shows that individuals carrying certain AQP4 variants showed faster grey matter loss when they reported shorter sleep," researcher Dr. Ayeisha Milligan Armstrong said.

"It's not just which genes you carry -- it's how those genes interact with the world around you. The same variant can look protective or detrimental depending on how someone is sleeping. That's important, because sleep is one of the few modifiable factors people can actually act on."

Grey matter contains many of the brain cells involved in memory, decision-making, movement, and other essential functions. A decline in grey matter volume can be a sign of structural changes in the brain.

Sleep Effects Differed by Genetic Variant

The researchers analyzed 13 common AQP4 gene variants, along with participants' self-reported sleep patterns, brain scans, and cognitive test results.

Among some participants, sleeping for fewer hours was associated with a faster decline in grey matter. In others, taking longer to fall asleep was linked to structural brain changes involving lower brain volume.

Cognitive performance also changed differently over time among people who experienced sleep disturbances. Whether the effect appeared beneficial or harmful depended on the specific AQP4 variant each person carried.

"We've known for a while that poor sleep and Alzheimer's risk are linked," researcher Dr. Tenielle Porter said.

"What this shows is that rather than assuming everyone at risk follows the same pathway, a more targeted and personalized approach to Alzheimer's prevention may be needed. But we're not at the point of recommending genetic testing; our findings need replication in larger and more diverse cohorts."

Toward Personalized Alzheimer's Prevention

The findings suggest that two people with similar overall Alzheimer's risk may not respond to poor sleep in the same way. Genetic differences could help explain why brain decline progresses more quickly in some individuals than in others.

The researchers recommended conducting clinical trials that incorporate genetic information. Such studies could test whether improving sleep habits can reduce inherited vulnerability and change long-term brain outcomes associated with Alzheimer's disease.

"This moves us closer to understanding why some people decline faster than others, even when they have similar risk on paper," CPH Director Professor Simon Laws said.

"Identifying who is most vulnerable, and who is most likely to benefit from a particular lifestyle intervention, is where precision health needs to go rather than treating everyone at risk of Alzheimer's the same way."

The study, "Evidence for Direct and Sleep-Moderated Relationships between Aquaporin -4 Genetic Variants and Alzheimer's Disease Phenotypes" is published online in Alzheimer's & Dementia, the Journal of the Alzheimer's Association.

Reporting from ScienceDaily contributed to this story.

However, the new analysis suggests that the later increase in BMI is not caused by a rebound in fat. Instead, it may largely reflect the normal growth of muscle and other lean tissue.

The research, led by Professor Andrew Agbaje, a physician and associate professor of clinical epidemiology and child health at the University of Eastern Finland, Kuopio, Finland, was presented at this year's European Congress on Obesity in Istanbul, Turkey and published in The Journal of Nutrition.

Why the Adiposity Rebound Theory Matters

Questioning the existence of the "adiposity rebound" could have important consequences for childhood health care. Since the theory was introduced, some physicians, including pediatricians, have treated the pattern as a meaningful warning sign that might be prevented or modified through diet and lifestyle changes.

If the rise in BMI is actually a normal result of muscle development, however, efforts to stop it may be addressing a problem that does not exist.

The concept dates back to 1984, when French researcher Marie Françoise Rolland-Cachera and her colleagues described "adiposity rebound" in a paper published in The American Journal of Clinical Nutrition.

The researchers reported a connection between the age at which a child's BMI began rising again and the child's BMI adiposity at age 16 years. An early rebound (before age 5.5 years) was associated with greater adiposity later in adolescence than a rebound occurring after age 7 years. Some later studies reported similar associations.

How Children's BMI Normally Changes

BMI tends to follow a recognizable pattern during childhood. It rises quickly during infancy and reaches a high point at about age 1 year. It then gradually declines, reaching its lowest level at around age 4 years, before beginning to rise again.

By age 6 years, a child typically returns to the same BMI recorded at age 2 years. This pattern occurs across the childhood population and became known as the "rebound."

Researchers have often focused on the timing of the decline and subsequent rise. They proposed that children whose BMI begins climbing at a younger age may reach a higher BMI later in life and face a greater risk of BMI-obesity.

The theory was based partly on statistical models suggesting that when BMI reaches its lowest point earlier, it also begins rising earlier, potentially leading to a higher BMI in later childhood or adolescence.

A Statistical Link May Not Reflect Biology

Professor Agbaje argues that the BMI pattern should not be compared with major biological transitions such as puberty.

Puberty occurs in nearly every child who reaches adulthood, but unusually early puberty has been linked to health risks supported by known biological mechanisms. According to Agbaje, no comparable biological explanation supports the idea that an early "adiposity rebound" causes later obesity.

"Puberty is a defining moment in human biology that alters the whole body, but adiposity rebound is not; it is a natural growth process unattached to any problem, whether it is early rebound or late. So the previous associations relating early BMI-based adiposity rebound to later life obesity are misleading analyses. Positive statistical associations do not always equate to biological plausibility."

Over the past several decades, researchers have also conducted clinical trials intended to influence the timing of the supposed rebound. Agbaje says the results provide further evidence that the pattern is a fixed part of normal growth rather than a disease process.

A Long-Term Diet Trial Could Not Change the Pattern

One randomized controlled trial in Finland followed participants from 7 months of age until age 20 years.

Infants in the intervention group were introduced to a heart-healthy diet with a relatively low intake of saturated fat and cholesterol. Parents and children received dietary counseling and nutrition education from the time the children were 7 months old through early adulthood. The control group did not receive the intervention.

Despite the long-term nutritional program, there was no difference between the groups in the average age at which BMI declined and then began rising again by age 6.

"This is just one example showing clinical trials could not change the so-called 'adiposity rebound' because it is simply a normal part of life and not a disease process or risk."

Measuring Body Fat More Directly

To determine whether body fat truly rebounds, Agbaje examined a measurement that more closely reflects adiposity than BMI.

BMI is calculated using weight and height, but it cannot distinguish between fat, muscle, bone, and other tissues. A rise in BMI can therefore occur even when a person is gaining healthy muscle rather than excess fat.

The new study used waist circumference-to-height ratio (WHtR), which estimates body fat/adiposity with around 90% accuracy when compared with the gold standard (dual-energy X-ray absorptiometry) measure of fat mass.

Agbaje analyzed information from 2410 multiracial children aged 2 -- 19 years who participated in the US National Health and Nutrition Examination Survey (NHANES) 2021-2023 cycle. The analysis compared childhood patterns in both BMI and WHtR.

The average BMI at age 2 years was 17.1 kg/m2. After declining significantly between age 2 and age 6 years (see graph in full paper), BMI returned to that same average level by age 6 years. On its own, this result appeared to support the traditional adiposity rebound theory.

Body Fat Did Not Actually Rebound

The WHtR results told a different story.

The average WHtR at age 2 years was 0.54, but children never returned to that level at age 6 years or at any other point during childhood and adolescence.

WHtR continued to fall until about age 7 years. It then increased through the rest of childhood and late adolescence, but it never recovered to the level recorded at age 2 years.

According to Agbaje, this means there was no true rebound in fat mass. Instead, the increase in BMI seen between about ages 5 and 7 appears to be caused by the growth of muscle and other lean tissue.

"Children in effect undergo a body composition reset at the plateau around age 4 years, which prepares them for the growth stages after that age," he explains.

A BMI Pattern Mistaken for Fat Gain

Agbaje describes the adiposity rebound theory as a BMI-driven "false discovery." He compares it with the so-called "obesity paradox" reported in some adult studies.

The "obesity paradox" refers to findings suggesting that people living with obesity may, under certain circumstances, have lower mortality rates than people with a BMI in the normal range. In studies of heart failure and mortality, BMI has sometimes produced a U-shaped pattern that appears to suggest that a higher BMI protects against heart disease.

Later research indicated that the apparent protection may come from greater muscle mass rather than excess body fat. Because BMI counts muscle as part of total weight, it can create misleading associations.

When WHtR was examined in randomized clinical trials involving heart failure, the relationship was linear. Greater fat mass was consistently associated with worse cardiovascular disease. Agbaje argues that this makes WHtR more useful than BMI for identifying excess fat and the health risks connected with it.

Researchers Call the Rebound a BMI Fallacy

"We do not need to push the adiposity rebound theory in pediatric literature any further because it is not a real disease state or a critical period that warrants clinical intervention. It is a statistical anomaly. Fat-free mass or lean mass growth is likely the accurate physiological explanation for the body composition reset that occurs in early childhood. It is a natural phenomenon for survival, which we have erroneously considered a disease process, and we have been trying to treat or prevent it for 42 years. So, the term 'adiposity rebound' is wrong; it is a BMI fallacy; it is simply muscle mass build-up or growth."

Agbaje believes the findings could change how excess body fat is identified in young people.

"This is a pivotal moment in history in the definition and accurate diagnosis of childhood excess body fat, with the possibility of adopting WHtR as a practical and clinically useful universal tool in diagnosing excess fat in children and adolescents."

Normal Muscle Growth May Need No Intervention

The analysis suggests that the familiar rise in childhood BMI is not necessarily evidence of an obesity-related process. It may instead represent a healthy transition as children build muscle and prepare for later stages of growth.

"Our new analysis suggests that this adiposity rebound phenomenon is not an obesity problem; this is an increase in muscle mass, and it is a good thing for healthy, normal growth. No clinical intervention is needed to address a non-existent problem in children. Let's allow children to grow in peace."

Agbaje also reports that his research team has released a freely accessible WHtR calculator designed to help detect excess fat in children and adolescents.

Reporting from ScienceDaily contributed to this story.

Researchers at McMaster University have now identified a biological pathway that could help explain why these muscle symptoms develop. The finding may eventually lead to treatments that make statins easier to tolerate without reducing their important cardiovascular benefits.

Published in Science Advances, the study points to a previously unrecognized interaction between the immune system and muscle cell metabolism. The mechanism appears to contribute to muscle damage caused by statins and challenges earlier ideas about the origins of these side effects.

Why Statin Side Effects Matter

"Statins are among the most effective medications we have for reducing cardiovascular disease risk and preventing early death," said Jonathan Schertzer, professor in McMaster's Department of Biochemistry and Biomedical Sciences and senior author of the study.

"Unfortunately, muscle side-effects lead some people to reduce their dose or stop taking the medication altogether. We wanted to understand why this happens and whether it might be possible to separate the side-effects from the benefits."

An estimated seven to 29 percent of statin users experience muscle-related symptoms. Although the connection between statins and muscle problems has been recognized for years, scientists have not fully understood the biological processes responsible.

Statins Can Disrupt Muscle Cell Energy

The research was led by first authors Nazli Robin and Nicole Barra of the Schertzer Lab at McMaster. Their team found that statins can interfere with the way muscle cells generate energy.

That disruption appears to activate an immune response inside the muscle cells, leading to tissue damage. In experiments involving muscle cells and mouse models, the researchers prevented much of the damage by blocking the immune response.

"One of the most exciting findings of the research is that the mechanism causing muscle side-effects appears to be separate from the mechanism that lowers cholesterol," said Schertzer. "That suggests it may one day be possible to target the side-effects without interfering with the cardiovascular benefits that make statins so valuable."

A Surprising Connection Between Immunity and Metabolism

The findings also uncovered an unexpected relationship between metabolism and the immune system. Changes in the way muscle cells processed energy caused the cells to activate their own immune response.

This discovery offers new insight into how inflammation may contribute to medication side effects. It also suggests that scientists could potentially protect muscle tissue by targeting the immune pathway while leaving the cholesterol-lowering effects of statins intact.

More research is needed before the findings can be developed into treatments for patients. Still, the newly identified pathway provides several possible targets for medications designed to prevent statin intolerance.

"These findings give us a clearer understanding of why some patients experience muscle symptoms and provide promising directions for making these important medications safer and more effective in the future," added Schertzer.

An International Research Collaboration

The project involved researchers from the Centre International de Recherche en Infectiologie (CIRI) in Lyon, France; the Centre for Muscle Research at the University of Melbourne, Australia; the Murdoch Children's Research Institute and The Royal Children's Hospital in Australia; York University in Canada; and McMaster's Department of Pathology and Molecular Medicine.

The research was funded by the Natural Sciences and Engineering Research Council of Canada (NSERC).

Reporting from ScienceDaily contributed to this story.

The researchers found that daily avocado consumption was linked to a lower concentration of low-density lipoprotein (LDL) particles in the blood. These particles carry cholesterol throughout the body. The size of the reduction was associated with an estimated 4% decrease in heart disease risk.

"If people want to improve the quality of their diet, making one small change might be a more feasible strategy than attempting to change their entire diet," said Janhavi Damani, postdoctoral scholar at Penn State and first author of the study. "For people with obesity, including avocados in their daily diet might be a good starting place."

LDL Particle Count Can Reveal Hidden Heart Risk

LDL particles are not the same measurement as LDL cholesterol, often called "bad cholesterol." Both are associated with cardiovascular disease, but particle concentration can reveal risk that a standard cholesterol test may not show. The researchers noted that this risk is often greater in people with abdominal obesity.

LDL cholesterol cannot travel through the bloodstream on its own. It must be carried by protein particles. A person with more LDL carrying particles may face a greater risk of heart disease, even when their total amount of LDL cholesterol is the same as someone with fewer particles.

"Imagine two people with the same high levels of LDL cholesterol," Damani said. "Person A carries their cholesterol in fewer, larger LDL particles, and Person B carries their cholesterol in more, smaller LDL particles. Person B's heart disease risk would be higher because their overall particle count is higher even though a test of their LDL cholesterol would look identical."

Smaller LDL particles can more easily enter artery walls and contribute to plaque buildup, Damani explained. Plaque narrows blood vessels and makes them less flexible, increasing the strain on the cardiovascular system.

When the heart must work harder because of exercise, heat, stress or another cause, stiffened blood vessels may be less able to accommodate the increased blood flow. Blood pressure can then rise more sharply, potentially contributing to a cardiac event such as a heart attack.

Testing One Avocado a Day

For the new analysis, the team examined data from 786 participants enrolled in the Habitual Diet and Avocado Trial. The six-month study included adults ages 25 and older.

Men qualified for the study if their waist circumference was greater than 40 inches, while women were eligible if their waist circumference exceeded 35 inches.

Half of the participants were asked to continue their usual diets and physical activity. The remaining participants also maintained their normal routines but received one avocado to eat every day.

Earlier results from the Habitual Diet and Avocado Trial showed that adding a daily avocado did not reduce body weight or waist circumference in people with obesity. However, it appeared to lower LDL cholesterol levels.

Daily Avocados Lowered LDL Particle Levels

For the current study, researchers compared blood samples collected at the beginning and end of the six-month trial.

Among participants assigned to eat one avocado per day, LDL particle concentrations fell by 49 nanomoles per liter. According to the researchers, that change corresponds to an estimated 4% reduction in heart disease risk.

"Four percent is a modest reduction compared with the 14-29% lower heart disease risk associated with improving the overall diet," Damani said. "However, it is a step in the right direction."

The improvement in LDL particle levels was consistent across participants. Sex, race, ethnicity, age and body mass index did not significantly affect the likelihood of experiencing the benefit.

The findings suggest that adults with obesity from a wide range of backgrounds could potentially benefit from including avocados in their diets. However, the researchers advised people to speak with a registered dietitian nutritionist or physician for personalized guidance before making dietary changes.

A Benefit Seen in Real World Diets

Previous Penn State research also found that avocado consumption could lower LDL cholesterol and LDL particle levels. In that earlier experiment, however, researchers closely controlled everything the participants ate.

"Penn State researchers demonstrated several years ago that avocado consumption could reduce LDL cholesterol and levels of LDL particles," said Kristina Petersen, associate professor of nutritional sciences and senior author of this study. "But in that study, the researchers controlled participants' entire diets throughout the experiment. This study demonstrated benefits in the real world, where people's diets are much less predictable. In the course of people's normal lives, avocado consumption still contributes to a healthier diet."

The latest findings indicate that a single, manageable change may improve one measure of cardiovascular health even when the rest of a person's diet remains largely unchanged. The benefit was modest and did not lead to weight loss, but the researchers said it could still represent progress toward better heart health.

Penny Kris Etherton, retired Evan Pugh University Professor of Nutritional Sciences at Penn State, also contributed to the research.

Other co-authors include Nirupa Matthan of the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University; Zhaoping Li of the David Geffen School of Medicine at University of California, Los Angeles; Joan Sabaté of the School of Public Health at Loma Linda University; and David Reboussin of the Wake Forest University School of Medicine.

The Avocado Nutrition Center supported this research.

Reporting from ScienceDaily contributed to this story.

High blood pressure, also known as hypertension, affects more than 1.28 billion adults around the world. It is also a major risk factor for cardiovascular disease. Current public health recommendations generally emphasize reducing sodium as the primary dietary step for lowering blood pressure and protecting heart health.

Looking Beyond Sodium Reduction

The physicians and health experts behind the report argue that lowering sodium may have a greater effect when it is paired with increased potassium intake. Potassium can also be used as a substitute for some of the sodium in salt.

According to the researchers, growing evidence about potassium's role in blood pressure regulation supports a major change in public health guidance. Rather than considering sodium and potassium separately, recommendations should address how the two nutrients work together.

"It is time to view dietary interventions holistically because food components interact and physiology is integrative across systems" said Naomi Fukagawa, M.D. Ph.D, professor of medicine emerita at the Robert Larner, M.D. College of Medicine at the University of Vermont and first author on the report. "Growing evidence shows that increasing dietary potassium as well as reducing sodium intake work together to better manage hypertension."

A New Framework for Hypertension Guidance

The peer-reviewed report was published in the American Journal of Clinical Nutrition and was supported by the IAFNS Sodium in Food and Health Implications Committee.

It reviews the evidence behind current sodium and potassium intake recommendations, possible methods for reducing sodium and increasing potassium, obstacles to putting those strategies into practice, and future research and policy priorities that could improve public health.

Too much sodium and too little potassium are both major dietary factors that can be changed to help reduce elevated blood pressure. Average sodium consumption continues to exceed recommended levels, while potassium intake is frequently "far below optimal levels in both developed and developing nations," according to the authors.

Foods That Supply More Potassium

Fruits, vegetables, legumes and dairy products are among the main dietary sources of potassium.

Food manufacturers can also replace some sodium with potassium salts, but there are practical limits. When too much potassium salt is added, foods can develop a metallic taste. Manufacturers therefore have to carefully balance sodium reduction with potassium enhancement when reformulating products.

The authors conclude that "dietary sodium reduction is a foundational strategy for hypertension prevention and management. However, new evidence supports a broadening of the current approach that focuses solely on sodium reduction and provides equal emphasis on increasing potassium intake."

Reporting from ScienceDaily contributed to this story.

The study, published in Science Advances, found that TRF2 does much more than shield chromosomes. Within muscle stem cells, it helps preserve the genetic instructions that define the cells and allow them to regenerate muscle after damage.

"For years, TRF2 has been viewed as a protein whose primary job is protecting the ends of chromosomes from damage or corruption," said senior author Foteini Mourkioti, PhD, an associate professor of Orthopedic Surgery at Penn Medicine. "But rather than simply protecting DNA, TRF2 seems to be key to regenerating muscle throughout life."

TRF2 Has an Unexpected Role in Muscle Repair

Scientists have long known that TRF2 mainly operates at telomeres, the protective DNA caps located at the tips of chromosomes. Telomeres help keep chromosomes from deteriorating or being incorrectly identified by cells as broken pieces of DNA.

Muscle stem cells normally remain inactive until tissue is injured. They then become active, multiply, rebuild the damaged area, and produce replacement stem cells that return to a dormant state.

Laboratory experiments showed that TRF2 levels change in a carefully timed pattern as muscle stem cells move through these different stages. The amount of the protein rises and falls as the cells shift between rest, tissue repair, and self-renewal, suggesting that TRF2 helps organize the regeneration process.

Muscle Stem Cells Lost Their Identity

To determine what happens without the protein, the researchers removed TRF2 from muscle stem cells in laboratory mice. The animals' muscles initially looked normal, but their supply of muscle stem cells gradually decreased.

The cells did not die, which was unexpected based on the effects of TRF2 loss in other tissues. Instead, they lost the molecular characteristics that allowed them to function as muscle stem cells.

This loss of identity had serious consequences after injury. Rather than rebuilding healthy muscle, the damaged areas accumulated fat and scar tissue.

"This completely changes how we think about TRF2's role in these cells," said Mourkioti. "The loss of identity has severe implications for whether recovery from injury is even possible."

Duchenne Muscular Dystrophy Progressed Faster

The team also examined TRF2 in a mouse model of Duchenne muscular dystrophy. When the protein was removed from muscle stem cells, the disease advanced much more rapidly. Muscle deterioration became more severe, and the mice had shorter lifespans.

Further investigation revealed how TRF2 produces these effects. The protein does not operate exclusively at chromosome ends. It also attaches to regulatory regions throughout the genome that control genes needed to preserve muscle stem cell identity.

Many of those genomic regions contain secondary DNA formations known as G-quadruplexes, which are also being studied as potential targets for cancer therapies.

"We found that TRF2 works through these secondary DNA structures to preserve the identity of muscle stem cells and keep them capable of repairing damaged muscle," Mourkioti said. "That was completely unexpected."

A Possible Connection Between Regeneration and Cancer

The findings reveal a biological mechanism that allows muscle stem cells to retain their regenerative abilities. They also show that this mechanism can affect the progression of Duchenne muscular dystrophy in mice.

The discovery may help scientists investigate a longstanding puzzle. Skeletal muscle has an exceptional ability to regenerate, yet cancers that begin in muscle tissue are relatively uncommon.

Determining how muscle stem cells use TRF2 differently from cells in other tissues could eventually help researchers stimulate tissue repair without also raising the risk of cancer.

Mourkioti and her colleagues are now studying whether this unusual use of TRF2 could lead to new therapeutic approaches for muscular dystrophy. They also hope it will provide insight into cancer biology in tissues that are more vulnerable to the disease.

The research was supported by grants from the National Institutes of Health/ National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 DK123356, R01s CA174904, GM101149, and FDN-143330).

Reporting from ScienceDaily contributed to this story.

Cancer cells are often able to repair the damage and continue growing. However, repeated cycles of breaking and repair can introduce errors, allowing mutations to accumulate in these highly active regions. The same biological machinery that helps tumors grow rapidly may therefore make their DNA increasingly unstable, potentially enabling cancers to change, adapt, and become more aggressive.

Cancer Growth Places DNA Under Stress

To multiply rapidly, cancer cells activate certain genes far more strongly than healthy cells normally would. Many of these genes help tumors divide, survive, and maintain the cellular programs required for continued growth.

A study published in Science Advances now indicates that this unusually intense gene activity has a physical consequence. As cancer cells push important genes to work at full capacity, the DNA in those regions can become damaged.

The research was led by PhD student Osama Hidmi under the guidance of Prof. Rami Aqeilan of the Hebrew University of Jerusalem. Their findings identify a previously overlooked contributor to genetic instability in cancer cells.

The researchers discovered that DNA breaks often appear in the same locations where cancer cells are driving growth-related genes most aggressively. Their investigation centered on super-enhancers, sections of DNA that function as powerful control panels. These regions strongly increase the activity of nearby genes and help keep cancer-promoting programs operating at very high levels.

Mapping Serious Breaks Across the Cancer Genome

Using a sensitive genome-mapping method, the team created detailed maps showing where double-strand breaks occur. These are among the most severe forms of DNA damage because both strands of the DNA molecule are severed.

The damage did not appear randomly throughout the genome. Instead, the breaks clustered inside genes controlled by super-enhancers. This pattern suggests that forcing certain genes to remain continuously active can place enough pressure on the DNA to cause it to snap.

The researchers also followed a natural cellular "alarm" signal that marks damaged DNA and attracts the machinery needed to repair it. Their results showed that cancer cells repeatedly damage and restore DNA within these intensely active regions.

Repairing these breaks allows tumor cells to survive. Yet every repair creates an opportunity for small errors. Over time, those mistakes may make the affected regions more likely to collect additional mutations.

A Cycle That Could Help Tumors Evolve

"Cancer cells rely on super-enhancers to keep growth genes running at high speed," said Prof. Rami Aqeilan. "What we found is that this same high-output activity can put real strain on the DNA, creating break hotspots that the cell has to repair again and again. That cycle may help tumors survive in the short term, but it also increases the risk of mutations that can fuel cancer's evolution."

The findings suggest that genetic instability may not simply be a side effect of cancer. In some cases, it could emerge directly from the intense gene activity tumors require to keep growing.

As mutations build up, cancer cells can develop new traits. Some of these changes may help tumors spread, withstand stressful conditions, or become less responsive to treatment.

Turning Cancer's Dependence Into a Weakness

"What is especially exciting," added Osama Hidmi, the PhD student who led the study, "Because cancer cells depend on these high-stress DNA regions to keep growing, they may also be more vulnerable there. This opens the door to treatments that target the very processes tumors rely on to survive."

That vulnerability could give researchers a new direction for cancer treatment. Therapies might eventually be designed to disrupt the intense gene activity driven by super-enhancers or prevent tumor cells from repairing the resulting DNA damage.

Because cancer cells depend so heavily on these processes, interfering with them could make it more difficult for tumors to survive and continue evolving.

Why DNA Damage Matters in Cancer

DNA damage and repair play major roles in how cancers grow, change, and resist treatment. The new study offers an explanation for where some of that damage occurs and what may be causing it.

Cancer's strongest gene control regions also appear to be locations of repeated DNA strain. These areas could represent weak points that are especially sensitive to treatments that reduce runaway gene activity or interfere with the repair of broken DNA.

A better understanding of this process may help scientists develop strategies that limit a tumor's ability to adapt. By exposing the connection between rapid growth and genetic instability, the research provides another piece of the puzzle behind cancer's aggressive behavior.

The findings also raise the possibility that one of cancer's greatest strengths may eventually be used against it. The drive to keep growing places constant pressure on the tumor's own DNA, creating damage that could reveal new opportunities for treatment.

Reporting from ScienceDaily contributed to this story.

Published July 31 in the Cell Press journal Cell Press Blue, the review examines how reducing protein may influence aging. The researchers conclude that protein restriction can improve metabolism, alter the way cells react to nutrients, limit cellular damage, and help cells maintain normal function.

"It's absolutely crystal clear that there are benefits of protein to muscle growth and exercise response of active individuals," says Dudley Lamming, the paper's corresponding author, of the University of Wisconsin-Madison. "But because most people are relatively sedentary, many people are likely consuming more protein than they actually need, which probably has negative health consequences."

An Alternative to Calorie Restriction

Scientists have long known that reducing calorie intake can lengthen lifespan in many organisms and lower the risk of age-related illnesses such as cancer. In practice, however, following a calorie-restricted diet over the long term is extremely difficult for most people.

Protein restriction may offer another route. Earlier studies found that flies and rodents lived longer when they consumed less protein, even when their overall calorie intake did not decline.

Recent human clinical trials have also produced promising results. People who lowered their protein intake lost weight and body fat and showed improvements in fasting blood sugar, despite often consuming more total calories.

Why More Protein Can Still Be Beneficial

The evidence is not one-sided. Other studies indicate that higher protein intake can support weight loss and help older adults preserve muscle, particularly when combined with exercise.

Those findings contributed to updated US dietary guidance this year. The new recommendations call for daily protein consumption of 1.2-1.6 grams per kilogram of body weight (0.5-0.7 grams per pound), nearly twice the previous amount.

As Americans consume more protein than ever and older adults are increasingly advised to raise their intake, Lamming and his colleague reviewed decades of evidence to better understand the relationship between protein, metabolism, and aging.

Their analysis of more than 350 papers identified several recurring biological mechanisms that could explain why protein restriction may improve health and promote longevity. Across the research, lower protein intake was linked to better metabolic function, altered nutrient signaling, reduced cellular damage, and improved maintenance of healthy cells.

A Hormone Linked to Longevity

One important factor is fibroblast growth factor 21 (FGF21), a hormone that increases when protein intake falls. FGF21 can raise energy expenditure, improve blood sugar regulation, and reduce inflammation.

Mouse studies have shown that animals with elevated levels of FGF21 lived longer than typical mice. The effect was stronger in male mice than in female mice. Lower protein intake also increases FGF21 levels in humans.

Certain Amino Acids May Drive Aging

The review also focuses on several amino acids, which are the individual building blocks of protein. Methionine, isoleucine, and valine appear to play especially important roles.

Research suggests that excessive intake of these amino acids may activate biological pathways that encourage growth. When those pathways remain highly active, they may increase the risk of obesity, inflammation, and other conditions associated with aging.

"These studies show that the amount of protein sedentary people are eating today may have negative health consequences, at least at the population level," Lamming says.

Protein Needs Vary From Person to Person

Some groups clearly require more protein. Pregnant women and certain older adults, for example, may have higher nutritional needs. For many sedentary adults, however, protein-fortified foods may not offer the health advantages they expect.

Athletes often consume large quantities of protein without developing metabolic disease. Lamming suspects that regular physical activity may offer protection by directing protein toward the development and maintenance of strong, healthy muscle.

"Recent recommendations have encouraged people to eat more protein, but they've also encouraged people to exercise more," Lamming says. "We probably need to personalize protein recommendations based not just on age, but also on how physically active people are."

The findings suggest that protein guidance may be most effective when it takes both age and activity level into account, rather than applying the same recommendation to everyone.

This work was supported by the National Institute on Aging, the Wisconsin Partnership Program, and the University of Wisconsin-Madison.

Reporting from ScienceDaily contributed to this story.

The work focused on wolfsbane and larkspur and brought together scientists from Michigan State University and the Czech Academy of Sciences. The findings were published in the journal Molecular Plant.

"These plants have been used in different forms of medicine throughout the world for thousands of years," said MSU alum Garret Miller, co-first author of the paper and now an assistant professor of biotechnology at the University of Michigan-Flint.

"We know they interact with our bodies in so many ways, and understanding how to create them can help provide totally new routes of testing."

The Powerful Chemistry of Poisonous Plants

Despite major advances in modern science, plants remain unmatched in their ability to produce intricate natural chemicals.

"Plants are the best chemists around, upgrading their arsenal of natural compounds over millions of years to help them survive," said Björn Hamberger, study author and the James K. Billman Endowed Professor in MSU's Department of Biochemistry and Molecular Biology.

"Humans have found countless uses for these molecules in everyday life," added Lana Mutabdžija, a graduate student at the Czech Academy of Sciences and co-first author of the latest paper.

"These include caffeine, capsaicin, menthol and vanillin, not to mention the fact that many of the medicines we use today either come directly from plants or are inspired by plant chemistry."

The Hamberger Lab at MSU studies these natural substances, known as specialized metabolites, and explores how they might be put to practical use.

In recent years, the group turned its attention to larkspur, which is also called delphinium because of its dolphin-shaped flowers. The researchers wanted to determine how the plant produces diterpenoid alkaloids, a group of chemicals that are highly toxic but may also have useful medical properties.

A Long-Standing Chemical Puzzle

Unraveling this process presented a major challenge.

Diterpenoid alkaloids combine features from two of the planet's oldest and largest groups of plant chemicals. Their structures are so complicated that scientists have struggled for decades to understand exactly how plants construct them.

Aconitine, one of the most familiar compounds in this family, was isolated nearly 200 years ago. Even so, researchers have still not successfully synthesized it in a laboratory.

The project gained momentum through an unexpected partnership.

At a scientific conference in Barcelona, Hamberger met researchers from Tomáš Pluskal's laboratory at the Czech Academy of Sciences. The Pluskal Group, including Mutabdžija, was studying the same difficult family of diterpenoid alkaloids in wolfsbane, a famously poisonous relative of larkspur that is also known as monkshood.

"When this happens, we can either go our own ways, or come together, and it's joining up that always leads to the best science," said Hamberger.

Tracing the Plants' Chemical Assembly Line

After joining forces, the international team set out to identify the precise sequence of biochemical steps used by wolfsbane and larkspur to make diterpenoid alkaloids.

The search resembled a molecular scavenger hunt. Researchers examined several species of both plants and tracked thousands of genes, looking for those that became "switched on" in the right tissues at the right moment.

"You can imagine a biosynthetic pathway almost as an assembly line," said Miller, who earned his Ph.D. in the Hamberger Lab. "If you have ten steps in a row needed to build a finished product, and suddenly one quits, the next steps can't happen."

Plants generally make specialized metabolites in very small quantities and at a slow pace. Identifying the biochemical pathways behind them is therefore essential for producing these compounds on a larger scale and applying them to real-world problems.

Once researchers solve a pathway, they can transfer the genetic instructions for building a compound into an engineered host, such as yeast.

This form of biohacking can turn the host into a biological production system, allowing it to manufacture larger amounts of the desired chemical for further study and development.

"In an ideal scenario, this could eventually help create new drugs inspired by these natural products," said Mutabdžija.

Tobacco Plants Become Living Biofactories

After identifying a promising collection of genes from wolfsbane and larkspur, the researchers transferred those genetic instructions into tobacco plants. The tobacco served as a convenient living factory for testing whether the genes could reproduce the plants' chemical process.

Analysis showed that the modified tobacco plants had assembled the pathway the team was seeking. Six distinct enzymes worked together to produce atisinium, a diterpenoid alkaloid.

The enzymes helped shape the molecule into its complicated final structure. They also enabled the addition of an essential source of nitrogen that the researchers had not expected.

By identifying the first biochemical steps required to make atisinium, the team has gained an important starting point for studying the broader diterpenoid alkaloid family and its potentially useful medicinal properties.

"Our vision is to provide green, sustainable tools that will allow us to harness these plants' natural power," Hamberger said.

Reporting from ScienceDaily contributed to this story.

Sohail Tavazoie, who leads Rockefeller University's Elizabeth and Vincent Meyer Laboratory of Systems Cancer Biology, has spent years studying this connection. In 2023, his team reported that depriving colon cancer cells of arginine caused them to accumulate more mutations.

Their latest research shows that arginine deficiency may also weaken the immune system. When arginine is scarce, cells struggle to produce MHC-1, a protein that helps alert the immune system to threats such as mutated cells and invading viruses.

Arginine May Restore a Key Immune Signal

The researchers also found that a moderate amount of arginine, roughly equivalent to the quantity in a couple of over-the-counter tablets, could potentially restore expression of the genes involved in MHC-1 production. The findings were published in Cell.

"Our work reveals how a lack of arginine interferes with the immune system, and suggests that upping arginine intake could prove beneficial," says first author Qiushuang Wu, a postdoc in the lab. "Perhaps that means it could be used in combination with other therapies to treat both cancer and viral infections."

"Arginine supplementation could be readily tested in patients receiving immunotherapies or given to high-risk populations exposed to viral pathogens," Tavazoie suggests. "Considering that arginine is inexpensive and readily available, we hope that therapeutic and preventative studies could be undertaken soon."

How Codons Guide Protein Production

Amino acids are commonly described as the building blocks of proteins. Their production is directed by codons, groups of three DNA bases that provide cellular instructions for making individual amino acids. Six different codons encode arginine, highlighting its broad importance in protein production.

Scientists already know that changes in amino acid availability can affect cellular metabolism and signaling. Far less is understood about whether those changes can directly influence gene expression.

For the new study, Wu examined whether shifts in arginine levels caused by diet or disease could alter gene expression. The work was supported in part by the Stavros Niarchos Foundation (SNF) Institute for Global Infectious Disease Research at The Rockefeller University and the Weill Cancer East Hub.

The researchers studied several disease models, including colon cancer, influenza, and SARS-CoV-2. Each of these conditions has previously been associated with unusual levels of different amino acids.

"One of the most dramatic patterns to emerge was that arginine was the most depleted amino acid in all of these diseases," she says.

Low Arginine Disrupts Immune Recognition

Wu used cell cultures to identify genes and proteins affected by declining arginine levels. She found that 414 proteins were present at unusually low levels. Most were produced by genes connected to arginine's established molecular functions.

A more unexpected result involved three HLA genes responsible for producing MHC-1 (major histocompatibility complex class I) proteins. MHC-1 proteins appear on the surfaces of cells throughout the body. They display foreign or abnormal proteins to T cells, which then recruit other immune cells to respond to the threat.

MHC-1 contains many sites where arginine must be incorporated during production, so the researchers suspected that arginine scarcity was interfering with the process. Further experiments revealed exactly where production broke down.

When cells were deprived of arginine, ribosomes, the cellular machines that assemble proteins, stalled while trying to produce MHC-1. Without enough arginine, they could not complete the protein. As a result, cells displayed fewer signals capable of alerting T cells to cancer-related or viral proteins. This allowed potentially dangerous cells to escape immune detection more easily.

"These findings are exciting because they reveal that consumption of a specific amino acid can directly regulate gene expression in an organism by increasing production of a protein enriched in that amino acid," Tavazoie says. "We believe that such selective translational tuning of gene expression through dietary manipulation likely extends to many other proteins and amino acids."

Fewer Colon Tumors in Mice

Wu next tested how different amounts of dietary arginine affected mice. Animals fed a diet low in arginine developed more colon cancer tumors. Mice that received more arginine developed fewer colon tumors.

Working with Heinz-Heinrich Hoffman, a research assistant professor in Charles Rice's Laboratory of Virology and Infectious Disease, Wu repeated the dietary studies using mouse models of influenza and SARS-CoV-2. The results followed a similar pattern and produced another surprising finding.

"Not only did mice with an arginine-rich diet have milder symptoms from viral infections, giving the mice arginine after influenza infection improved their outcomes too," Wu notes. "That was very surprising. From our genetic models, we knew manipulating arginine levels had a strong effect on gene expression, but we didn't expect the dietary manipulation to be equally impactful."

Possible Implications for Aging and Disease

The findings suggest that falling arginine levels may help explain why poor nutrition and aging are associated with greater vulnerability to certain cancers and viral infections. Arginine levels naturally decrease with age, potentially weakening the immune system's ability to recognize abnormal or infected cells.

"Qiushuang's findings illuminate how poor diet and aging -- during which arginine levels naturally decline -- could create the perfect storm for the initiation of colon cancer. Similarly, age-related arginine loss could partially contribute to the greater mortality caused by respiratory viruses," Tavazoie says. "We're also investigating whether making dietary changes in other amino acids has beneficial effects in a variety of disease contexts. There are no doubt more discoveries to come."

Reporting from ScienceDaily contributed to this story.

The findings support once weekly brisk interval walking as a practical therapeutic option for adults with central obesity, especially those who have difficulty fitting several workouts into their schedules. The study was published in Nature Communications.

A More Practical Approach to Reducing Body Fat

Obesity is a chronic health condition involving an unhealthy buildup of body fat. Fat that accumulates around the abdomen is especially concerning because it is associated with cardiovascular disease, metabolic disorders, and a higher risk of premature death.

Exercise plays an important role in managing obesity and offers a wide range of health benefits. Even so, many people, particularly those living with obesity, struggle to maintain regular physical activity over time.

Interval training alternates between more vigorous periods of exercise and lower-intensity periods of active recovery. Research has shown that it can be a time-efficient way to reduce overall body fat and visceral fat compared with continuous exercise performed at a moderate intensity.

Most exercise recommendations call for interval training three days each week. That schedule may be difficult for people with demanding jobs, family responsibilities, limited time, or restricted access to exercise facilities.

Previous research has suggested that a "weekend warrior" pattern, in which most weekly exercise is completed over one or two days, can still produce health benefits. However, there has been relatively little evidence showing whether interval training remains effective when concentrated into a single weekly session.

Professor Parco Siu Ming-fai, Professor and Head of Division of Kinesiology at the School of Public Health, HKUMed, said it was important to determine whether once weekly interval training could match the results of a traditional three-session schedule and provide a more accessible alternative.

One Session Versus Three

From September 2021 to September 2024, the HKUMed team carried out a randomized trial in Hong Kong involving 315 Chinese adults aged 18 or older. All participants were overweight and had central obesity.

Participants were assigned to one of three groups. One group completed interval training once each week, another completed interval training three times each week, and the third served as a control group.

The control group took part in a 2.5-hour health education session every two weeks for four months. Both exercise groups completed a total of 75 minutes of interval training each week. One group performed the full amount in a single session, while the other divided it across three sessions.

Researchers measured body fat using dual-energy X-ray absorptiometry at three stages: before the program began (baseline), after 16 weeks (post-intervention), and at 32 weeks (four-month post-intervention follow-up).

Similar Fat Loss and Fitness Benefits

At the 16-week assessment, both interval training groups showed similar improvements. Participants who exercised once per week and those who exercised three times per week reduced total body fat mass, body fat percentage, and waist circumference. Both groups also improved their cardiorespiratory fitness compared with the control group.

"While thrice-weekly interval training remains a commonly recommended approach for the therapeutic management of excess adiposity, our findings show that once-weekly interval training offers similar benefits and represents a practical exercise strategy," said Professor Siu. "For many adults with central obesity who struggle to balance work, study, family and other commitments, time constraints are a primary barrier to exercising multiple days per week."

"Instead of relying solely on high-frequency exercise prescriptions, once-weekly interval training can be considered a feasible and effective alternative," added Professor Siu.

The study was led by Professor Parco Siu Ming-fai, Professor and Head of Division of Kinesiology at the School of Public Health, HKUMed. The co-first authors were Dr. Leung Chit-kay and Mr. Joshua Bernal, both from the same School.

The research was supported by the General Research Fund of the Research Grants Council, the University Grants Committee of Hong Kong, China, and the Seed Fund for Basic Research, HKU.

Reporting from ScienceDaily contributed to this story.

Scientists have now identified a protein pathway that may help connect aging with the harmful protein buildup seen in disorders such as Huntington's disease and amyotrophic lateral sclerosis (ALS).

Searching for the Link Between Aging and Brain Disease

A research team led by Professor Dr. David Vilchez at the CECAD Cluster of Excellence for Aging Research investigated this connection using the small nematode worm Caenorhabditis elegans. The researchers examined a signaling pathway that becomes increasingly active with age and contributes to the accumulation of abnormal proteins.

Their study, titled "The aging factor EPS8 induces disease-related protein aggregation through RAC signaling hyperactivation," was published in Nature Aging.

The team concentrated on EPS8, an aging-associated protein, and the signaling pathways it controls. Previous research showed that EPS8 accumulates as worms grow older and activates damaging stress responses that shorten their lifespan.

EPS8 Drives Toxic Protein Buildup

The researchers found that higher EPS8 levels and increased activity in its signaling pathways promote pathological protein aggregation and neurodegeneration. Both are defining features of age-associated neurodegenerative conditions, including Huntington's disease and ALS.

When the scientists reduced EPS8 activity, toxic protein aggregates no longer accumulated as readily. The treatment also helped preserve neuronal function in worm models of both diseases.

"We are delighted to uncover a molecular mechanism that could shed light on to how aging contributes to diseases like ALS and Huntington's," says first author Dr. Seda Koyuncu. "For years, we've known that age is the major common risk factor for different neurodegenerative diseases. However, how exactly age-related changes contribute to these diseases remains largely unknown. This study may contribute to filling in a part of that puzzle."

Similar Results in Human Cells

EPS8 and the signaling molecules associated with it have been preserved throughout evolution and are also found in human cells. This allowed the researchers to determine whether the mechanism they observed in worms might also be relevant to human disease.

Reducing EPS8 levels in human cell models of Huntington's disease and ALS produced results similar to those seen in C. elegans. The intervention prevented the accumulation of toxic protein aggregates in the cells.

"It's incredibly exciting that the mechanisms we uncovered in C. elegans are also conserved in human cell models," says Professor Dr. David Vilchez, highlighting how the use of simpler model organisms like the nematode worm can prove extremely useful to uncover disease mechanisms relevant to humans.

A Potential Target for Future Treatments

Scientists still do not know precisely how increased EPS8 activity causes toxic proteins to aggregate. Even so, the results address an important gap in neurodegenerative disease research by identifying a direct molecular connection between aging and neurodegeneration.

The findings also point to EPS8 and its signaling partners as possible targets for future therapies. Treatments aimed at this pathway could potentially slow or prevent the progression of ALS, Huntington's disease, and other brain disorders associated with aging.

Reporting from ScienceDaily contributed to this story.

The researchers found that fructose serves as one of the chemical messages released by these treatment-surviving cells. The discovery reveals a previously unknown way that cancer cells left behind after therapy may contribute to metastasis.

"Some cancer cells that survive chemotherapy aren't dividing anymore, but they're still biologically active," said Aidan Cole, Ph.D., a postdoctoral fellow in the lab of Katherine Aird, Ph.D., at The Wistar Institute and first author on the study. "Instead, they continue to release molecules that send signals to nearby cells. Our study is among the first to show that a nutrient -- in this case, fructose -- can act as one of those signals."

Why Ovarian Cancer Often Returns

Nearly all ovarian cancer patients receive platinum-based chemotherapy, and the initial response is often strong. Even so, the cancer returns in most cases and typically spreads throughout the abdominal cavity. This process, known as metastasis, is responsible for roughly 90% of deaths from the disease.

Previous studies have indicated that cancer cells surviving chemotherapy may help drive recurrence by releasing a complicated mixture of signaling molecules. To investigate this possibility, Cole and his colleagues developed an experiment that separated the surviving cells from the substances they released.

The team collected molecules produced by chemotherapy-surviving cells and exposed other cancer cells to them. Those released substances alone were enough to significantly increase the cancer cells' ability to spread.

"As far as we know, this is the first time anyone has shown, in a preclinical model rather than just a dish, that it's the molecules these cells release -- not the cells themselves -- that drive the cancer's spread," said Cole.

Fructose Acts as a Signal for Cancer Spread

The researchers then set out to determine which released substance was causing this effect. Their analysis showed that the surviving cancer cells produced fructose and used it as a signal that encouraged neighboring cells to spread.

The team also found that high amounts of dietary fructose, comparable to the levels present in sugary drinks, could encourage cancer spread even when chemotherapy had not been given. This result raises the possibility that dietary habits may influence how cancer progresses.

That possibility is especially notable because fructose is widely consumed in the United States. In some people, high fructose corn syrup accounts for ~8-20% of daily calorie intake. Unlike many risk factors that patients cannot change, fructose intake can be reduced through dietary choices.

Researchers have not yet tested whether lowering fructose consumption improves outcomes in patients. Still, the findings suggest that nutrition may affect cancer progression in ways that were previously overlooked.

How Fructose Helps Cancer Cells Escape

The team next investigated how fructose makes cancer cells more likely to spread. Using several large-scale analytical methods, including a CRISPR screen, they discovered that fructose lowers cholesterol production inside neighboring cancer cells.

Cholesterol helps cells remain attached to one another, functioning like a form of biological glue. When cholesterol levels fall, those cellular bonds weaken, allowing cancer cells to separate more easily and move into other areas.

This mechanism offers a possible explanation for how a common nutrient can alter the physical behavior of tumor cells and increase their ability to escape.

Questions About Statins and Chemotherapy

The discovery that reduced cholesterol production may encourage cancer spread also has potential clinical significance. Statins, which are used by 39 million people in the United States, work by lowering cholesterol production.

In the study, statins alone weakened the connections between cancer cells and made it easier for them to escape. The researchers are now investigating whether these drugs could interfere with the effects of chemotherapy.

However, the team emphasizes that the findings are not a reason for patients to stop taking statins or any other prescribed medication.

"We haven't tested this effect in patients yet, but it raises questions about combining cholesterol-lowering drugs with chemotherapy, especially since ovarian cancer is most common in postmenopausal women who are often already on statins," said Katherine Aird, Ph.D., professor and co-leader of the Molecular and Cellular Oncogenesis Program in the Ellen and Ronald Caplan Cancer Center at The Wistar Institute, and senior author of the study.

The Mechanism May Affect Other Cancers

The researchers are also studying whether the same fructose-related pathway could play a role in cancers beyond ovarian cancer.

"We think other cancers that spread within the torso -- pancreatic, colon, liver -- could behave similarly. We can't call it universal yet, but we think the effects are not just limited to ovarian cancer," said Aird.

Aird and Cole have already begun planning follow-up studies to determine whether the results can be reproduced in several other types of cancer.

Co-authors: Raquel Buj, Apoorva Uboveja, Alexander Tom, Amandine Amalric, Baixue Yang, Miho Naruse, Frederick Keeney, Andrew Kossenkov, and Qin Liu from The Wistar Institute; Evan Levasseur, Hui Wang, Katarzyna M. Kedziora, Naveen Kumar Tangudu, Jeff Danielson, Callen T. Wallace, Esther Elishaev, Lauren Borho, Huda Atiya, Lan G. Coffman, Steffi Oesterreich, Aditi U. Gurkar, Francesmary Modugno, and Simon C. Watkins from University of Pittsburgh School of Medicine; Amal Elhaw, Sierra White, Danyang Li, Dorota E. Jazwinska, Matthew S. Laird, George Tseng, Francisco J. Schopfer, Ioannis K. Zervantonakis, Wayne Stallaert, and Nadine Hempel from University of Pittsburgh; Adam Chatoff, Andrea Andress Huacachino, Mariola M. Marcinkiewicz, and Nathaniel W. Snyder from Lewis Katz School of Medicine at Temple University; Felicia Lazure and Ana P. Gomes from H. Lee Moffitt Cancer Center & Research Institute; Hope A. Townsend, Robin D. Dowell, and Aaron Clauset from University of Colorado Boulder; Denarda Dangaj from Ludwig Institute for Cancer Research, University of Lausanne (UNIL); and Benjamin G. Bitler from University of Colorado Anschutz Medical Campus.

Work supported by: National Institutes of Health grants R37 CA240625, R01 CA259111, R01 CA298386, P50 CA272218, T32 GM133332, R01 CA242021, R21 CA267050, R21 CA291905, and U01 AG077923; American Cancer Society grant RSG-19-113-01-CCG; Ovarian Cancer Research Alliance grant MIG-2023-2-1018; Congressionally Directed Medical Research Program grants HT9425-23-1-0436, W81XWH2110338, OC210139, and OC230324; HERA Ovarian Cancer Foundation; Melanoma Research Foundation; Janet Burroughs Ovarian Cancer Foundation; Silicon Valley Community Foundation Chan Zuckerberg Initiative DAF grant 2023-329680; UPMC Hillman Cancer Center; and The Wistar Institute.

Reporting from ScienceDaily contributed to this story.

"Alzheimer's is a condition that remains recalcitrant to the scientific community's attempts at developing a cure or preventative treatment," said Daniel Schultz, a former postdoctoral fellow in the Vanderbilt University Warren Center for Neuroscience Drug Discovery.

Gaps in Alzheimer's Biology

One major obstacle to developing better therapies is that researchers still do not fully understand the biology behind Alzheimer's disease. The same problem affects research into many other neurological diseases and neurodevelopmental disorders.

Scientists have identified genes and proteins that may contribute to these conditions, but studying them can be extremely difficult when researchers lack a reliable way to change how those biological targets behave.

One approach involves using tool compounds. These chemicals interact with particular proteins and either raise or reduce their activity. Although many tool compounds are unsuitable for use as medicines because they may affect unintended targets or cause toxicity, they are still highly valuable for investigating what a protein does. That knowledge can become an important early step toward developing new treatments.

Targeting the TAOK1 Protein

In a study published in ACS Chemical Neuroscience, Schultz and co-first author Lauren Parr, a Ph.D. student in the Department of Pharmacology, developed a compound that selectively inhibits TAOK-1. The protein has been linked to Alzheimer's disease, but it has remained poorly understood partly because researchers have lacked suitable compounds for studying it.

Most of the work was carried out at the WCNDD under the leadership of Executive Director Craig Lindsley. The WCNDD is a clinical-stage biotech start-up within Vanderbilt. Its drug discovery pipeline currently includes five compounds in phase I clinical trials.

The center is also a founding pillar of the new Vanderbilt Institute for Therapeutic Advances, a next-generation drug discovery institute that is also led by Lindsley.

To find useful compounds, Schultz, Parr, and other WCNDD researchers created a large collection of related molecules. Each one had a slightly different structure. The team then evaluated how the compounds affected TAOK-1 and assessed whether they had properties considered desirable in potential drugs.

"This project showcased the strength of the WCNDD's drug discovery infrastructure," Schultz said.

The First Selective TAOK1 Inhibitor

The collaboration led to the discovery of VU6083859, the first selective inhibitor of TAOK-1. The compound could provide a starting point for research aimed at developing future Alzheimer's disease treatments.

Another molecule produced an unexpected result. The compound, named VU6080195, activated all three proteins in the TAOK family rather than inhibiting them.

"Our understanding of TAOK proteins largely centers around their inhibition, so we are excited at the prospect of studying the neurological effects of increasing their activity," Schultz said. "As scientists, we can get lost in planning our projects to the last detail and expecting things to go a certain way, so it was quite fun to see this unexpected result."

Schultz hopes the two compounds will encourage more researchers to investigate the TAOK protein family. So far, these proteins have received relatively little attention in in vivo models.

New Tools for Alzheimer's Research

A deeper understanding of disease biology can improve the chances of finding effective treatments. With these two compounds now available, neuroscientists can examine how the TAOK protein family functions and explore its links to Alzheimer's and other neurological diseases.

The findings could eventually help researchers identify new treatment strategies and perhaps contribute to the long-term search for a cure.

The paper "Discovery of VU6083859, a TAOK1 Selective Inhibitor, and VU6080195, a pan-TAOK Activator" was published in ACS Chemical Neuroscience.

The research used funding from the William K. Warren Foundation and received support from the Zenobia and Mark Godschalk Alzheimer's Research Endowment, the Helen H. and Morris D. Hartman, MD 1910, Neurological Research Fund, the Warren Center for Neuroscience Drug Discovery, and the Vanderbilt Institute for Therapeutic Advances.

Reporting from ScienceDaily contributed to this story.

Available medications often provide limited relief from trauma-related nightmares. Researchers at Charité -- Universitätsmedizin Berlin therefore examined whether a prescription drug containing THC, one of the active compounds found in cannabis, could help. The findings, published in Nature Medicine, showed that more than half of the participants responded to the treatment. More than one-third said their nightmares disappeared completely.

Why PTSD Nightmares Are So Difficult to Treat

The effects of a terrifying or life-threatening experience can continue long after the immediate danger has passed. In post-traumatic stress disorder (PTSD), the brain has difficulty processing overwhelming events. The memories may be stored in a way that makes them return involuntarily and without conscious control.

This can happen during the day and at night. While sleeping, people with PTSD may repeatedly relive the trauma until they wake in panic. Antidepressants and medications that lower blood pressure are among the treatments sometimes used, but their effectiveness is limited. They also often do little to relieve the nightmares themselves. Germany has not yet approved a medication specifically for trauma-related nightmares.

Prof. Stefan Röpke studies trauma-related disorders at the Department of Psychiatry and Neurosciences on the Benjamin Franklin Campus of Charité. While exploring possible new treatments, he and his team, working with additional research partners, turned their attention to tetrahydrocannabinol, commonly known as THC. It is the primary psychoactive compound in cannabis.

THC interacts with the body's endocannabinoid system, which helps regulate sleep, stress, and the way emotional memories are processed. Stefan Röpke explains: "There is evidence suggesting that during REM sleep -- the intense dream phases in which the brain processes experiences and regulates emotions -- THC reduces dream activity and thereby alleviates nocturnal stress responses."

Testing Dronabinol for PTSD Nightmares

Cannabis-based medicines are already used in pain treatment, especially when standard therapies do not work well enough or cause intolerable side effects. In Germany, access became easier after the so-called "Cannabis for medical purposes" law went into effect in 2017. The legislation expanded the medical and scientific use of cannabinoids derived from plants or produced synthetically.

For the study, the researchers used Dronabinol, a prescription medication containing THC obtained directly from the cannabis plant and administered as drops. They wanted to find out whether the drug could safely reduce nightmares linked to PTSD.

More than 170 people with post-traumatic stress disorder and frequent, severe nightmares took part. For ten weeks, participants received either Dronabinol or a cannabis-flavored placebo that looked identical. They took the drops each evening before going to bed.

Neither the participants nor the healthcare professionals knew who received the medication and who received the placebo. This double-blind, placebo-controlled design is considered the gold standard for testing medical treatments.

Nightmares Declined More With THC Treatment

At the end of the ten weeks, nightmare severity had fallen significantly more in the Dronabinol group than in the placebo group. On a scale ranging from zero to eight, the average nightmare burden dropped by 3.7 points among participants taking Dronabinol. The placebo group experienced an average decrease of 2.2 points. For the people affected, the difference was clearly noticeable.

"More than a third of the patients treated with Dronabinol reported that they no longer experienced any nightmares after ten weeks. Another 21 percent reported that their nightmare burden had been at least halved," as Stefan Röpke stated. "And about five out of six patients in the dronabinol group felt their health had markedly improved."

No Severe Side Effects or Signs of Dependence

The cannabinoid appeared to act specifically on nightmares and sleep rather than on every aspect of PTSD. The researchers could not conclusively show that it reduced the overall severity of post-traumatic stress disorder or any accompanying depression.

Even so, most participants experienced meaningful relief. By interrupting the repeated nighttime reliving of trauma, the treatment allowed many of them to sleep more peacefully.

No severe side effects were reported. Mild and moderate effects, including dizziness, headaches, and increased appetite, occurred more frequently among those receiving Dronabinol. The researchers also found no withdrawal symptoms after participants stopped taking the evening doses at the end of the study.

Future studies will examine whether the treatment remains safe and effective when used for longer periods. Researchers also want to determine whether patients may gradually develop tolerance to the drug.

Charité initiated and led the research. Scientists from the Psychiatric University Clinic of the Charité at St. Hedwig Hospital, the University Medical Center Hamburg-Eppendorf, and the Central Institute for Mental Health in Mannheim also participated. The company Bionorica SE supported the work.

Reporting from ScienceDaily contributed to this story.

The effects were relatively small and were observed under controlled conditions. Still, the findings offer new evidence that physical position can influence mood and behavior, said Jorge Armony, a professor in the Departments of Psychiatry and Psychology at McGill and the study's senior author.

Researchers Changed Posture Without Revealing the Study's Goal

Armony worked with graduate student Soren Wainio-Theberge, who developed the original idea for the research and coauthored the paper. The team recruited nearly 200 people from the McGill community.

Participants first completed tests using a computer monitor. They were then asked to perform another task on a tablet while being told that the researchers were evaluating a mobile application.

The tablet setup was designed to subtly influence how each person sat. In one group, the device was placed on a stand supported by an adjustable table, encouraging participants to remain upright. In another group, the tablet lay flat on a desk set at a lower height, which encouraged participants to lean forward and hunch over.

Upright Participants Took More Effective Risks

The participants next completed a risk-taking game involving a virtual balloon. Players could earn larger rewards by continuing to inflate the balloon, but they could lose everything from that round if it burst.

People in the upright group generally took greater risks and earned larger rewards over the course of the game. The researchers concluded that these participants were not simply behaving more recklessly.

"This suggests they were not acting more impulsively but rather were engaging in more effective risk-taking," explained Armony.

Responses to a questionnaire also showed that participants in the upright group reported significantly stronger feelings of pride, an emotion associated with a more positive mood.

A New Test of the Posture and Mood Connection

Scientists have long debated whether body posture can meaningfully affect thoughts, emotions, and behavior. The McGill researchers designed the experiment to address several concerns raised by earlier studies.

Rather than directly instructing participants to sit in a particular way, the team altered the environment so that posture changed without the participants knowing why. This approach helped address a major criticism of earlier "power pose" research: that participants may have behaved differently because they understood what the researchers expected.

During interviews conducted after the experiment, most participants said they had not realized that their posture was being manipulated.

The team also used video software to measure each participant's neck angle and verify whether the physical setup produced the intended posture. Earlier studies had not often included this type of objective measurement.

Desk Design May Subtly Influence Behavior

Armony cautioned that simply changing posture is unlikely to produce a dramatic transformation in someone's life. However, the results raise questions about whether ordinary environmental features, including workplace ergonomics, may have small but measurable effects on emotions and decision making.

"Manipulating posture implicitly through environmental constraints influences mood and risk-taking behaviour," by Soren Wainio-Theberge and Jorge Armony, was published in the British Journal of Psychology.

The research received support from the Natural Sciences and Engineering Research Council of Canada and the Social Sciences and Humanities Research Council of Canada.

Reporting from ScienceDaily contributed to this story.

Published in the Annals of the Rheumatic Diseases (ARD), The EULAR Journal, by Elsevier, the findings suggest that air quality may be an important consideration for both healthcare professionals treating rheumatoid arthritis and policymakers working to protect public health.

Environmental Factors in Rheumatoid Arthritis

Rheumatoid arthritis, commonly known as RA, is a chronic autoimmune condition that causes inflammation and damage in the joints. It can also produce widespread symptoms that affect other areas of the body.

The disease affects an estimated 0.5% to 1% of adults worldwide. Its development is influenced by a combination of genetics, changes in immune function, and environmental exposures. Some of these environmental influences may contribute not only to the initial development of RA, but also to worsening symptoms after the disease has been diagnosed.

Importantly, several environmental risk factors can potentially be modified. Smoking is already recognized as a major risk factor. Researchers have also examined the possible effects of temperature, humidity, silica, and other pollutants.

Earlier population studies found that exposure to polluted air was associated with a greater likelihood of developing RA. Researchers in South Korea wanted to determine whether air pollution could also affect disease activity and trigger flares in people who already had the condition. They also investigated the biological processes that might explain such a connection.

In an accompanying editorial Jeffrey A. Sparks, MD, MMSc, Division of Rheumatology, Inflammation, and Immunity, Mass General Brigham / Brigham and Women's Hospital, and Harvard Medical School, comments, "This is one of the largest studies to use robust methods to link air pollutants with RA disease activity. Considering rising levels of air pollutants, these results have significant clinical, biologic, and public health implications. They also further reinforce that inhalants may have broad implications for risk and progression of RA and perhaps other autoimmune diseases. From a clinical perspective, this may offer avenues to lower the risk of RA flares by avoiding air with poor quality and provide some potential explanation for otherwise idiosyncratic RA flares."

Tracking Air Pollution and Arthritis Flares

The prospective cohort study followed 1,070 people with RA at a major medical center in South Korea. Over four years (2021-2024), the researchers collected information from 12,583 outpatient visits conducted under real-world clinical conditions.

To estimate each patient's exposure, the team examined monthly levels of six common air pollutants (sulfur dioxide, SO2; nitrogen dioxide, NO2; ozone, O3; carbon monoxide, CO; particulate matter with a diameter of 10 µm, PM10; and particulate matter with a diameter of 2.5 µm, PM2.5). These measurements were then compared with disease activity and flare outcomes recorded during each visit.

The analysis accounted for a wide range of factors that could influence the results. These included patient demographics, serologic status (the presence of specific antibodies typical for RA in the blood), medication use, socioeconomic conditions, and weather-related variables.

The researchers also performed a sensitivity analysis designed to reduce the influence of factors that remained constant over time and to limit the possibility that disease activity itself affected the pollution measurements used in the monthly analysis. For this part of the research, they used a case crossover design based on daily pollutant concentrations before each appointment. Conditional logistic regression allowed them to compare changes within individual patients.

PM2.5 Emerges as the Strongest Factor

"Our study found that higher PM2.5 concentration was associated with increased disease activity and flare risk, notably prolonged exposure to elevated PM2.5 over more than two weeks," explains lead investigator Eun Bong Lee, MD, PhD, Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, and Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, Republic of Korea.

Among the pollutants studied, PM2.5 appeared to be the main contributor associated with increased RA activity.

These particles are extremely small, even smaller than red blood cells. After being inhaled, they can pass from the lungs into the bloodstream and travel to organs throughout the body.

Researchers say the particles may stimulate excessive production of reactive oxygen species, which are harmful molecules that can place cells under stress. This process may damage DNA and activate inflammatory responses in different organs, potentially contributing to greater RA activity and more frequent flares.

Air Quality Could Affect RA Management

Dr. Lee concludes, "Our study has important implications for public health policy making. While further studies are warranted to determine whether improving air quality can reduce disease activity in RA patients, we would recommend these patients avoid prolonged exposure to poor air quality, particularly high PM2.5 levels."

The researchers emphasized that additional studies are needed to determine whether reducing pollution exposure or improving air quality can directly lower disease activity in people with RA. Even so, the results suggest that limiting prolonged exposure during periods of poor air quality may be a practical precaution.

ARD Editor-in-Chief Josef Smolen, MD, from the Medical University of Vienna, adds: "As always, this paper underwent thorough peer review, and it was nice to learn that all reviewers agreed on the importance and interest of these findings. Nevertheless, we should be aware that the observations pertain to the studied Korean population, with a specific genetic background and under specific environmental circumstances. Whether these data hold true in other regions of the world should be a focus of future investigations. However, it is an excellent starting point for our better understanding of factors that may play a role in influencing disease activity and therapeutic responses of patients with RA. And: it is an important wake-up call: the environment is likely an essential contributor to pain and inflammation in the patients for whom we care."

Reporting from ScienceDaily contributed to this story.

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Radio 4,·04 Aug 2026,·27 mins

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More than six years since the start of the Covid pandemic, it might feel like we're pretty over it, yet that's simply not the case for the millions of people who suffer from long Covid. But could there be hope on the horizon? A new clinical trial led by University College London and University College London Hospitals found that over-the-counter antihistamines and a prescription anti-inflammatory drug called colchicine offered a small reduction in fatigue for people with long Covid. But it's still not a cure. Professor Danny Altmann, an immunologist at Imperial College London, joins us to discuss this new research and the problems with understanding long Covid. He also tells us about some of the upcoming studies that might help us better get a handle on the condition. Also this week, did you know that around one in 335 people in the UK are living with a stoma? Yet according to Colostomy UK, more than 60 per cent of those with a stoma say a lack of suitable toilet facilities affects their daily lives. Thanks to a campaign that started in Bristol, B&Q has now made the disabled toilets across its stores stoma-friendly. We pay a visit to B&Q with The Traitors' Mollie Pearce, who has been living with a stoma since she was 18, and colorectal surgeon Ms Caroline Burt from Bristol Foundation Trust to find out more. Finally, many of us have been guzzling ice cream to cool off during the hot weather. But have you seen the social media claims that the frozen treat can reduce your risk of developing type 2 diabetes? We asked nutritional scientist Dr Sarah Berry from King's College London to give us the scoop on the 'ice cream paradox'. Presenter: James Gallagher Producer: Alice Lipscombe-Southwell Production coordinator: Stu Laws Editor: Ilan Goodman

Reporting from BBC contributed to this story.

Whether associated with the deadly reputation of the Black Widow or the fictional bite that transformed Spider-Man, fangs have become one of the most recognizable features of spiders. Their evolutionary story, however, began long before modern spiders appeared.

A new study published in Nature traces the origins of this powerful hunting tool to Urokodia, a small marine creature that lived during the early Cambrian Period.

The Ancient Origins of Spider Fangs

Spiders belong to a large group of invertebrates called chelicerates, which also includes scorpions and ticks. More than 100,000 chelicerate species have been described.

These animals have jointed limbs and hard external skeletons. Their defining feature is a pair of specialized appendages called chelicerae, located near the front of the body. Depending on the species, chelicerae can function as pincers or fangs that grip, pierce, or stab prey.

Urokodia fossils were discovered at the renowned Chengjiang fossil site in Yunnan Province in southern China. The study was published on the 42nd anniversary of the site's discovery.

The creature measured only around 2-3 cm in length. It had large eyes extending from stalks at the front of its body, along with a segmented skeleton and jointed limbs attached beneath its narrow frame. Its appearance bears little obvious resemblance to the spiders and scorpions that descended from its broader evolutionary lineage.

X-Rays Reveal Preserved Soft Anatomy

Researchers from Yunnan University, China, and the University of Leicester used X-ray technology to examine the rock surrounding the fossil. The scans revealed that much of the animal's soft anatomy had remained preserved in a mummified state for hundreds of millions of years.

Most importantly, the researchers identified two pincer-like appendages positioned just behind the creature's eyes. These structures represent an early form of chelicerae and provide evidence of the evolutionary beginnings of the pincers and fangs seen in chelicerates today.

The fossil also preserves features on Urokodia's legs that may have served as book gills, allowing the animal to breathe underwater. Similar respiratory structures are still found in aquatic chelicerates such as horseshoe crabs.

A Successful Lineage of Hunters

Chelicerates have become one of the most successful animal groups in both marine and terrestrial environments. Those that moved onto land developed into highly effective predators, and fossils show that their ancestors had already been hunting for hundreds of millions of years.

Despite the frightening image of spiders presented in movies such as Arachnophobia, most species pose no danger to people. Their venom and bites evolved to subdue prey that is far smaller than a human.

The research was led by Professor Yu Liu of Yunnan University, who is also a Visiting Professor at the University of Leicester.

Professor Liu said: "We were using X-ray tomography analysis of these fossils to reveal their soft anatomy buried in the rocks for hundreds of millions of years, when suddenly we noticed the pincer-like limbs at the front of the animal. We knew immediately that this was a very exciting fossil and indeed a distant ancestor of living chelicerates like scorpions and spiders."

A Window Into the Dawn of Animal Life

Urokodia lived within a rich marine ecosystem during a crucial period in the history of animal evolution. The Chengjiang fossils preserve evidence of more than 200 types of animals that inhabited the oceans over 500 million years ago.

Co-author Professor Mark Williams from the University of Leicester School of Geography, Geology and the Environment said: "Urokodia was part of an ancient ecosystem of over 200 different types of animals living in the seas over 500 million years ago. These spectacularly preserved fossils provide real insights into how life was evolving on our planet at the very dawn of animals."

This study was supported by a grant from the Department of Science and Technology of Yunnan Province (202401BC070012) to Professor Yu Liu, who is further funded by the Yunnan Revitalization Talent Support Program.

Reporting from ScienceDaily contributed to this story.

More on that in a moment. But first, let’s go back a few hundred thousand years to examine our early human ancestors. Because we can blame a lot of the difficulty we have with weight loss today on our predecessors of the past – maybe the ultimate case of blame the parents.

For our early ancestors, body fat was a lifeline: too little could mean starvation, too much could slow you down. Over time, the human body became remarkably good at guarding its energy reserves through complex biological defenses wired into the brain. But in a world where food is everywhere and movement is optional, those same systems that once helped us survive uncertainty now make it difficult to lose weight.

When someone loses weight, the body reacts as if it were a threat to survival. Hunger hormones surge, food cravings intensify and energy expenditure drops. These adaptations evolved to optimize energy storage and usage in environments with fluctuating food availability. But today, with our easy access to cheap, calorie-dense junk food and sedentary routines, those same adaptations that once helped us to survive can cause us a few issues.

As we found in our recent research, our brains also have powerful mechanisms for defending body weight – and can sort of “remember” what that weight used to be. For our ancient ancestors, this meant that if weight was lost in hard times, their bodies would be able to “get back” to their usual weight during better times.

But for us modern humans, it means that our brains and bodies remember any excess weight gain as though our survival and lives depend upon it. So in effect, once the body has been heavier, the brain comes to treat that higher weight as the new normal – a level it feels compelled to defend.

The fact that our bodies have this capacity to “remember” our previous heavier weight helps to explain why so many people regain weight after dieting. But as the science shows, this weight regain is not due to a lack of discipline; rather, our biology is doing exactly what it evolved to do: defend against weight loss.

Hacking biology

This is where weight-loss medications such as Wegovy and Mounjaro have offered fresh hope. They work by mimicking gut hormones that tell the brain to curb appetite.

But not everyone responds well to such drugs. For some, the side effects can make them difficult to stick with, and for others, the drugs don’t seem to lead to weight loss at all. It’s also often the case that once treatment stops, biology reasserts itself – and the lost weight returns.

Advances in obesity and metabolism research may mean that it’s possible for future therapies to be able to turn down these signals that drive the body back to its original weight, even beyond the treatment period.

Research is also showing that good health isn’t the same thing as “a good weight.” As in, exercise, good sleep, balanced nutrition, and mental well-being can all improve heart and metabolic health, even if the number on the scales barely moves.

A whole society approach

Of course, obesity isn’t just an individual problem – it takes a society-wide approach to truly tackle the root causes. And research suggests that a number of preventative measures might make a difference – things such as investing in healthier school meals, reducing the marketing of junk food to children, designing neighborhoods where walking and cycling are prioritized over cars, and restaurants having standardised food portions.

Scientists are also paying close attention to key early-life stages – from pregnancy to around the age of seven – when a child’s weight regulation system is particularly malleable.

Indeed, research has found that things like what parents eat, how infants are fed, and early lifestyle habits can all shape how the brain controls appetite and fat storage for years to come.

If you’re looking to lose weight, there are still things you can do – mainly by focusing less on crash diets and more on sustainable habits that support overall well-being. Prioritising sleep helps regulate appetite, for example, while regular activity – even walking – can improve your blood sugar levels and heart health.

The bottom line though is that obesity is not a personal failure, but rather a biological condition shaped by our brains, our genes, and the environments we live in. The good news is that advances in neuroscience and pharmacology are offering new opportunities in terms of treatments, while prevention strategies can shift the landscape for future generations.

So if you’ve struggled to lose weight and keep it off, know that you’re not alone, and it’s not your fault. The brain is a formidable opponent. But with science, medicine and smarter policies, we’re beginning to change the rules of the game.

Reporting from ScienceDaily contributed to this story.

Some jumping genes can also remove themselves from RNA with the help of an RNA enzyme. These elements, known as ribozymes or self-splicing introns, represent a distinctive group of mobile genes.

Moving within a single cell is one thing. Crossing into another cell or even another species is far more difficult. Genetic family tree studies show that such transfers have occurred, but scientists have generally assumed that jumping genes traveled as passengers inside plasmids or viruses.

Jens Harder and his colleagues have now observed something unexpected that points to another possible route.

A Methane-Producing Microbial Community

The researchers studied a slowly growing enrichment of bacteria and archaea that produces methane (biogas). The community contained an unusual dominant organism, a very small predatory bacterium.

Candidatus Velamenicoccus archaeovorus feeds on microorganisms that convert limonene, the compound responsible for the scent of oranges, into methane and carbon dioxide. Within filaments of Methanothrix soehngenii, the most important methane producer on Earth, the researchers noticed that individual cells were dead.

They suspected that Ca. Velamenicoccus archaeovorus might be responsible. To test that possibility, they needed to find molecules from the predator inside the dead cells.

Searching for a Mobile Intron

While examining the genome of Ca. Velamenicoccus archaeovorus, Jens Harder identified an intron that functions as a jumping gene. Intron RNA had never been detected outside a cell, which made the researchers especially interested in looking for it inside the bacterium's prey.

Scientists at the Max Planck Institute for Marine Microbiology had developed methods sensitive enough to detect very small amounts of RNA in bacterial cells. Using specially designed nucleic acid probes, the team produced microscopic images showing intron RNA in living cells of Ca. Velamenicoccus archaeovorus and in dead cells of Methanothrix soehngenii.

The researchers had effectively caught the intron while it was trying to replicate. However, Ca. Velamenicoccus archaeovorus had already killed the new host. The gene's attempted transfer therefore ended as a jump into an empty cell.

Why the RNA Survived

Ribonucleic acids act as messengers in living cells. These long-chain molecules carry instructions from the genetic material to the cell's protein factories. They are normally broken down quickly, beginning at their exposed ends.

For that reason, dead cells usually do not contain ribonucleic acids.

The intron RNA survived because it forms a circular molecule with no open ends. This ring-shaped structure protects it from enzymes that would otherwise break it apart.

"The stability of intron RNA in its ring form is a distinctive feature. In humans, circular RNA molecules influence many metabolic processes, and their role in tumor development is currently the subject of intensive research. Applications in RNA vaccines, for example against the Covid virus and certain forms of cancer, are also in the pipeline. Our study has shown that in microorganisms jumping genes can be transferred to other species via their circular RNA," says Jens Harder.

Reporting from ScienceDaily contributed to this story.

The discovery was made in planarian flatworms, small aquatic animals known for their extraordinary ability to regenerate. Even when cut into pieces, these worms can rebuild missing tissues and, in some cases, produce complete new organisms. Studying how their immune systems have survived and adapted over hundreds of millions of years could offer useful clues for modern medicine.

In a study published in Cell, the researchers named the newly discovered cells "ruptoblasts" because of the dramatic way they respond to a specific hormone.

"We never expected that a cell could just explode like a bomb and kill the cells surrounding it," said senior author Bo Wang, associate professor of bioengineering in the schools of Engineering and Medicine.

Flatworms Reject Foreign Tissue

Chew Chai, a postdoctoral researcher in Wang's laboratory, first noticed the unusual cells while investigating a long-standing question in flatworm biology. Scientists wanted to know whether flatworms can distinguish their own tissues from those belonging to another individual.

To test this, Chai sliced worms lengthwise and fused each one with part of a different worm. Flatworms are highly effective at rebuilding their own bodies, but these fused "Frankenstein" worms rejected tissue from unrelated individuals. The reaction resembled the way a human immune system may reject a transplanted organ.

The cellular response, however, was very different from anything normally seen in humans.

"It's this huge inflammatory response. Like there's a fire and an alarm goes off, and the cells just blow up," said Chai, who is lead author of the paper.

Activin Triggers Severe Inflammation

Previous research into flatworm regeneration has shown that the hormone activin plays an important role in their survival. Elevated activin levels can weaken a worm's ability to regenerate, while low levels interfere with its ability to reproduce with other worms.

As the fused worms began rejecting foreign tissue, Chai detected a rise in activin followed by chronic inflammation. The animals did not die immediately, but they perished within several days. She also found that injecting activin into healthy, nonfused flatworms produced a similar inflammatory response.

To examine what was happening inside individual cells, Chai used live cell microscopy and flow cytometry, a technique that uses lasers to analyze and separate cells. She marked the cells with different fluorescent dyes and then isolated those that reacted to activin.

A small group of cells suddenly burst open, released substances that killed nearby cells, and disappeared within five minutes. Chai and Wang named this explosive process "ruptosis."

Cell Death in Seconds

The speed and completeness of ruptoblast self-destruction distinguish ruptosis from other known forms of cell death.

"Some mammalian cells and bacteria may also do an explosive sort of cell death, but the timescale is really long. They are exploding, but it's more like pores that slowly leak things out over the course of several hours," said Chai. "Ruptosis happens within seconds to minutes."

This rapid destruction appears to turn each ruptoblast into a highly localized weapon. Instead of slowly releasing harmful material, the cell unloads its contents almost instantly.

Explosive Cells Destroy Multiple Targets

Researchers tested ruptoblasts against E. coli bacteria, human kidney cells, and mouse blood cells. The ruptoblasts destroyed all three types of targets.

The damage remained limited to cells located close to the explosion. It did not spread through a chain reaction or leave behind persistent toxicity. According to Wang, this ability to deliver a powerful but tightly contained attack could have implications for future treatments targeting bacterial infections or tumors.

Ruptoblasts also differ from familiar immune cells such as T cells and neutrophils. Those cells are hematopoietic cells, meaning they are blood cells produced in bone marrow. Ruptoblasts are glandular cells.

The researchers believe ruptoblasts intensify their normal secretion systems so they can release toxic substances suddenly and violently after encountering activin. A rapid surge of calcium from the endoplasmic reticulum inside the cell helps drive ruptosis.

An Ancient Immune Strategy

When Chai searched for similar cells in other species, she found them only in basal bilaterians such as flatworms. Their restricted distribution suggests that ruptoblasts originated early in animal evolution.

Chai proposed that vertebrates may have lost this defense because they cannot easily repair the surrounding damage caused by ruptosis. Flatworms, by contrast, contain abundant stem cells and can replace damaged tissues with remarkable efficiency.

"It demonstrates there's lots of different immune mechanisms out there. There's all these animals that live in an environment where there's lots of bacteria, lots of viruses, and we know so little about their immune mechanisms," said Wang.

The findings show how much scientists may learn by examining animals that are rarely used as traditional research models. Although flatworms may appear simple, their unusual biology could reveal immune strategies that are absent from humans and other vertebrates.

Wang said that investigating a wider range of organisms may inspire new approaches to some of medicine's most challenging problems.

Acknowledgements

Additional Stanford co-authors include postdoctoral scholar Souradeep Sarkar; former Undergraduate Visiting Research Program scholar Lihan Zhong; Dania Nanes Sarfati, PhD '24; Christine Jacobs-Wagner, the Dennis Cunningham Professor and professor of biology in the School of Humanities and Sciences and of microbiology and immunology in the School of Medicine; and Hawa Racine Thiam, assistant professor of bioengineering in the schools of Engineering and Medicine and of microbiology and immunology in the School of Medicine. Additional co-authors, including co-senior author Benyamin Rosental, are from Ben Gurion University of the Negev.

Jacobs-Wagner is also a member of Stanford Bio-X and an institute scholar at Sarafan ChEM-H. Thiam is also a member of Bio-X and the Maternal & Child Health Research Institute (MCHRI), and an institute scholar at Sarafan ChEM-H. Wang is also a member of Bio-X and the Wu Tsai Neurosciences Institute.

This research was funded by a National Science Foundation Graduate Research Fellowship, a Stanford Graduate Fellowship, a Stanford DARE fellowship, a Human Frontier Science Program grant, a National Institutes of Health grant, and the European Research Council.

Reporting from ScienceDaily contributed to this story.

The research team was led by Henry Daniell of the School of Dental Medicine at the University of Pennsylvania. The findings were published in Scientific Reports and could support the development of more accessible and affordable treatments.

A Need for Better Head and Neck Cancer Therapies

Head and neck squamous cell carcinoma (HNSCC) is a common form of cancer that begins in the tissues lining the mouth and throat. The disease can be particularly aggressive, and outcomes are often poor when it is discovered at a later stage.

Daniell says that many recently approved cancer medications have not produced major improvements in patients' quality of life or five-year survival. That limited progress highlights the need for new approaches that can work alongside existing treatments.

Targeting HPV and Harmful Oral Bacteria

The new study builds on earlier research involving chewing gum made from lablab beans (bean gum). The gum contains FRIL, a naturally occurring antiviral protein.

Daniell and his colleagues used oral samples from patients with HNSCC to study three microbes associated with cancer. These included human papillomavirus, or HPV, along with two bacterial species, Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn).

"The global increase in oropharyngeal cancer is linked to HPV infection," says Daniell. "And Pg and Fn infections worsen survival rates of untreated recurrent or metastatic oral cancer, even after surgery and risk-adjusted adjuvant, or supplemental, therapies."

Gum Extracts Sharply Reduce Microbe Levels

Tests showed that extracts from the bean gum lowered HPV levels by 93% in saliva samples. HPV levels also fell by 80% in oral rinse samples.

The researchers then engineered the bean gum to contain protegrin, an antimicrobial peptide capable of killing harmful bacteria. A single dose brought levels of Pg and Fn down to almost zero.

Importantly, the treatment did not appear to harm the beneficial bacteria that normally live in the mouth. Radiation therapy can have a different effect, reducing helpful bacteria while encouraging the growth of disease-causing yeast (Candida albicans).

A Potential Addition to Cancer Treatment

The ability to target dangerous microbes while preserving the healthy oral microbiome could make the gum useful in several ways. Researchers believe it may eventually serve as an additional therapy alongside current cancer treatments or as a preventive measure against infection and transmission.

"Lip and oral cavity cancer was the seventh leading cancer type in cancer incidence and mortality rate worldwide in adolescents, young adults, and middle-aged adults in 2022," says Daniell. "Our findings support the value of advancing these therapies to clinical trials as adjuvants with current treatments or as prophylaxis to prevent infection and transmission."

Henry Daniell is the W.D. Miller Professor in the Department of Basic & Translational Sciences at the School of Dental Medicine at the University of Pennsylvania.

Other authors include Geetanjali Wakade, Rahul Singh, and Smruti Nair of Penn Dental Medicine; Andrés M. Bur and Sufi M. Thomas of the University of Kansas Medical Center; Eri S. Srivatsan and Marilene B. Wang of the University of California at Los Angeles; and Saroj K. Basak of the Veterans Administration Greater Los Angeles Healthcare System.

The research received support from NIH (grant 5-R01-HL 107904-13 awarded to Henry Daniell), the Academic Senate Grant of the David Geffen School of Medicine at UCLA (the Surgical Education Research program), and the National Cancer Institute Cancer Center (Support Grant P30 CA168524).

Reporting from ScienceDaily contributed to this story.

A person's dementia risk is shaped partly by factors that cannot be altered, including age, gender and genetics. Other influences may be modifiable, such as smoking, cardiovascular disease, high blood lipids, physical activity, alcohol consumption, hearing loss and high blood pressure.

Dementia is not a single disease. It is a collection of symptoms that can result from several different disorders, which means the risks may vary depending on the underlying cause. Researchers at Lund University examined how individual risk factors are connected to brain changes associated with Alzheimer's disease and vascular dementia.

"Much of the research available on the risk factors that we ourselves can influence does not take into account the different causes of dementia. This means that we have had limited knowledge of how individual risk factors affect the underlying disease mechanisms in the brain," explains Sebastian Palmqvist, senior lecturer in neurology at Lund University and senior physician at the Memory Clinic at Skåne University Hospital.

Researchers Tracked Brain Changes for Four Years

The study involved almost 500 participants who had an average age of 65 and showed no signs of cognitive impairment. Researchers followed them for four years, measuring changes in the brain's white matter, the nerve fibers that are often damaged in vascular dementia.

The team also monitored levels of amyloid β and tau, two proteins associated with Alzheimer's disease. Their goal was to determine how both modifiable and nonmodifiable risk factors were related to changes in the brain over time.

Vascular Risks Were Linked to White Matter Damage

Most of the modifiable factors examined, including smoking, cardiovascular disease, high blood lipids and high blood pressure, were associated with damage to blood vessels in the brain. They were also linked to a more rapid buildup of changes in white matter.

"We saw that most modifiable risk factors -- smoking, cardiovascular disease, high blood lipids and high blood pressure, among others -- were linked to damage to the brain's blood vessels and a faster accumulation of so-called white matter changes. This damage impairs the function of the blood vessels and leads to vascular brain damage - and can ultimately lead to vascular dementia," says Isabelle Glans, doctoral student at Lund University and resident in neurology at Skåne University Hospital.

The researchers also identified possible connections between certain risk factors and the proteins involved in Alzheimer's disease.

"Diabetes was associated with increased accumulation of amyloid β, while people with lower BMI had faster accumulation of tau. However, these findings need to be investigated further and validated in future studies," continues Isabelle Glans.

Healthy Habits May Reduce Multiple Forms of Damage

Adopting healthier habits and addressing modifiable risks may help delay the appearance of Alzheimer's symptoms. This may be especially important because many people with dementia have more than one type of disease process occurring in the brain, including both vascular damage and Alzheimer's related changes.

Palmqvist said that improving vascular and metabolic health may therefore remain valuable even for people at risk of Alzheimer's disease.

"Focusing on vascular and metabolic risk factors can still help reduce the combined effects of several brain changes that occur simultaneously," he concludes.

Reporting from ScienceDaily contributed to this story.

Some specimens appear to be about 567 million years old. Their age suggests that animal movement and sexual reproduction began 5-10 million years earlier than previous evidence indicated. The study, led by scientists at the American Museum of Natural History and Dartmouth, was published in Science Advances.

"For 3 billion years, life on Earth was dominated by microbes. Then, all the sudden, we get these strange-looking marine animals big enough to see and capable of behaviors we would find familiar today," said the study's lead author Scott Evans, assistant curator of invertebrate paleontology at the American Museum of Natural History. "If we want to understand this transition, when life first became large, complex and unmistakably animal, this new site has tremendous potential."

A Rare Window Into the First Animals

Ediacaran organisms came in many unfamiliar forms, including flat discs, leafy shapes, and ribbed ovals. Their fossils provide the earliest direct record of multicellular animal life.

Some Ediacaran species have been connected to animal groups that still exist, including mollusks, nematodes, comb jellies, and cnidarians (a group that spans jellyfish and corals). Other species resemble nothing alive today. Even so, they include the oldest known animals capable of moving to find food or reproducing sexually.

Most of these organisms lived before animals commonly developed shells, bones, or other hard body parts. Their soft bodies rarely fossilized, meaning that only exceptional environmental conditions could preserve them.

Ediacaran fossils have been found on every continent except Antarctica, but sites with more than 10 species are extremely uncommon. As a result, scientists have had only limited evidence from this crucial period, which lasted roughly 40 million years.

A White Sea Community Found in North America

Researchers divide Ediacaran organisms into three major groups, known as assemblages, based on where they fall in the geologic record. These are the Avalon assemblage (575-559 million years ago), the White Sea assemblage (559-550 million years ago), and the Nama assemblage (550-538 million years ago).

Before this discovery, White Sea fossils had been documented in Europe, Asia, and Australia, but not in North America. The new fossils were found in ancient rock layers in Canada's Mackenzie Mountains.

The site is located on the traditional lands of the Sahtú Dene and Métis. Members of those communities gave the researchers guidance and permission to enter and study the area.

The work builds on previous geological research in the region, but the scale and diversity of the discovery mark a major advance. Scientists identified more than 100 fossils, including six groups that had never previously been recorded in North America.

Even more surprising was their age. Some specimens date to approximately 567 million years ago, making them 5-10 million years older than other known White Sea fossils. That places them within the same broad time period as the older Avalon assemblage.

The fossil-bearing layers are also covered by hundreds of feet of rock that may contain additional specimens, suggesting that much more remains to be discovered.

"Not only is this new site highly diverse, but also it is from a part of the rock succession where we have previously lacked fossil remains," said study co-author Justin Strauss, an associate professor of Earth and Planetary Sciences from Dartmouth, who has been exploring this area for about 15 years. "This is really exciting. Given our understanding of the regional geology in northwestern Canada, there is great potential here to revisit our understanding of Ediacaran Earth history."

Strange Creatures From an Ancient Seafloor

Several of the fossils represent organisms never before found in North America.

Dickinsonia was a flat animal that traveled across the seafloor. It had no mouth and apparently obtained nutrients by absorbing bacteria and algae through its entire lower surface. Evans compared its divided circular body to a "bathmat" or "pancake."

Funisia was a stationary, tube-shaped organism that lived in clusters of similarly sized individuals. It provides the oldest known fossil evidence of sexual reproduction. Like modern corals, it may have reproduced through a coordinated release of sperm and eggs into the surrounding water.

Kimberella moved with the help of a muscular foot and scraped food from the seafloor. Scientists commonly interpret it as an early relative of mollusks. The newly discovered specimens may also make it the oldest known fossil bilaterian, the group of animals with distinct front, back, top, and bottom with symmetric left and right sides that makes up more than 99% of all known animals.

The site also preserved Eoandromeda, a possible comb jelly with eight arms arranged in a spiral.

Did Animal Innovation Begin in Deep Water?

The fossils indicate that these organisms lived in deeper water than scientists had previously associated with the White Sea assemblage.

This supports a developing idea that early animals may have first appeared in offshore, deep marine environments before gradually spreading into shallower coastal waters. That pattern is the reverse of what became more common in later animal evolution.

"These results suggest a pattern where evolutionary innovation begins in deeper environments and later spreads toward the coast," Evans said. "We think of the deep ocean as a dark, inhospitable place, but it is also relatively stable, with few fluctuations in things like temperature and oxygen essential to most animal life. This stability may have provided key opportunities to support early animal life."

The stable conditions of the deep ocean may therefore have offered a favorable setting for the earliest stages of animal diversification.

Preserving Canada's Fossil Record

The fossils will eventually become part of the permanent collection at the Prince of Wales Northern Heritage Centre in Yellowknife, Northwest Territories.

Other coauthors on the study include Erik Sperling, Stanford University; and Kimberly Lau, The Pennsylvania State University.

This work was supported by a NASA Exobiology grant (# 80NSSC25K7024); a U.S. National Science Foundation (NSF) grant (# EAR-20 2143164); and NSF Frontier Research in Earth Science grants (# EAR-2021324 EAR-2021176).

Reporting from ScienceDaily contributed to this story.

Loss of motivation is common in conditions such as depression, addiction, and ADHD. Even so, scientists still do not fully understand the brain processes that contribute to these motivational difficulties.

Orexin Neurons and Motivation

The research was led by Hiroyuki Mizoguchi, associate professor, and Kiyofumi Yamada, professor emeritus, at Nagoya University's Graduate School of Medicine. Their team focused on orexin neurons, which help control vital functions including sleep, appetite and energy expenditure.

Previous research has suggested that these neurons may also affect motivation, but their specific contribution has remained uncertain.

To investigate, the scientists studied how changes in orexin neuron activity affected rats seeking food rewards. Earlier studies in this area have generally used mice, but rats have stronger learning abilities and are often better suited to complicated behavioral tasks. Research involving specific neuron types in rats has been more difficult because those cells are harder to target precisely.

The team overcame this obstacle by creating genetically modified "orexin-Cre" rats. This new model allowed the researchers to selectively target and manipulate neurons that produce orexin.

Measuring How Hard Rats Would Work

The researchers first used chemogenetics to activate orexin neurons. They then placed the rats in a progressive ratio test, in which the animals had to make an increasing number of touches to receive each food reward.

The point at which an animal stopped trying (the breakpoint) was used as a measure of motivational strength. Rats whose orexin neurons had been activated reached higher breakpoints, showing that they were willing to perform more work for the reward.

The opposite pattern appeared in rats whose orexin neurons had been selectively degenerated. These animals reached lower breakpoints, indicating that their motivation had weakened.

Brain Activity Rose With Effort

The team next used fiber photometry to monitor orexin neuron activity in real time while the rats waited for and received food.

Activity increased as the animals anticipated the reward, then fell after the food was delivered. When an expected reward did not appear, however, orexin neuron activity remained high.

The response also became stronger as the amount of work required increased. According to the researchers, this pattern may show how the brain connects the expectation of a reward with the effort needed to obtain it.

Suppressing Orexin Reduced Motivation

To determine whether orexin neurons directly influenced behavior, the scientists used optogenetics to control the neurons at the moment the rats expected a reward.

When the researchers suppressed orexin neuron activity using an inhibitory protein, the animals showed less motivated behavior. They took longer to finish tasks that required effort, and their breakpoints decreased.

The team also tried increasing orexin neuron activity at the same moment using an excitatory protein. Although the stimulation successfully activated the cells, it did not cause the rats to work harder or show any further rise in motivation.

These results suggest that orexin neurons are required to maintain motivated behavior, but increasing their activity beyond normal levels may not be enough to produce additional motivation. More research will be needed to determine why the effects are uneven and whether factors such as the duration or pattern of activity influence the outcome.

Mizoguchi concluded, "Our study demonstrated significant changes in orexin neuron activity depending on expected rewards and the effort required, suggesting a potential mechanism for translating expectations into sustained action."

Understanding Loss of Motivation

Future studies will examine the brain circuits that send information to orexin neurons and receive signals from them. A clearer understanding of how these neurons function could eventually contribute to new ways of addressing motivational deficits, including loss of motivation and difficulty maintaining goal-directed behavior.

This work was supported by Grant-in-Aid for Scientific Research [22K19749; 23K27360; and 23H02669 (2023)]; SENSHIN Medical Research Foundation; Naito Foundation, Japan; Takeda Science Foundation, Japan; SRF, Japan; Asahi Glass Foundation, Japan; Mishima Kaiun Memorial Foundation, Japan; Kao Health Science Foundation, Japan; and AMED, Japan (JP21wm0425014).

Reporting from ScienceDaily contributed to this story.

For many years, the debate centered on two main possibilities. Some scientists proposed that snakes first became elongated and limbless while adapting to underground life, while others argued that the body plan emerged in aquatic environments. New research published in Nature suggests the answer was more complicated. Instead of following a single ecological route, early snakes appear to have occupied several habitats and developed different sensory adaptations.

"Our findings show that early snakes had already achieved remarkable ecological and morphological diversity by the Late Cretaceous, around 80 million years ago," says lead author Tiago Simões, Assistant Professor at Princeton University.

An Exceptionally Preserved Ancient Snake

The researchers examined a newly identified snake species from Late Cretaceous deposits in southeastern Brazil dating to around 80 million years ago. Named Tametara mirim, the species is represented by one of the most complete fossil snake skeletons ever discovered.

Using computed tomography and cinematic 3D rendering, the team created a detailed digital reconstruction of the specimen. The scans revealed features of the skull, vertebrae, and brain endocast that would have been difficult to study from the exposed bones alone.

Postdoctoral researcher Simone Macrì and Research Director Nicolas Di-Poï, both at the University of Helsinki's HiLIFE Helsinki Institute of Life Science, directed the reconstruction and comparative study of the brain anatomy. Their work connected the neuroanatomy of early snakes with their sensory abilities, habitats and evolutionary history.

Fossil Brains Reveal Different Lifestyles

The team compared Tametara with Dinilysia patagonica, another fossil snake discovered in Argentina. The comparison showed that the two species had very different brain structures, suggesting they were adapted to distinct ways of life.

"The two had strikingly different brain shapes, both from each other and from most other snakes studied. Brain shape and bone microstructure pointed to the same conclusion: Tametara was adapted to burrowing, Dinilysia to life on the ground. Together with evidence from marine sediments, the findings reveal several shifts between burrowing, terrestrial and marine lifestyles in early snake evolution. Different lineages explored different habitats much earlier than previously thought," concludes Research Director Nicolas Di-Poï.

The findings indicate that early snake evolution involved repeated movement between underground, terrestrial and marine environments. Rather than progressing toward one standard body form or sensory system, separate snake lineages developed adaptations suited to different ecological settings.

"The brain tells a much richer story than the skeleton alone. By combining computed tomography-based brain reconstructions with data from living snakes, we could show that early snakes were not simply progressing toward one modern condition but experimenting with different sensory and ecological strategies. This means that early snakes did not follow a single evolutionary pathway," says Researcher Simone Macrì.

A Broader View of Snake Evolution

The study was led by Tiago Simões of Princeton University, with senior authors Nicolas Di-Poï of the University of Helsinki and Annie Hsiou of the University of São Paulo, together with an international team of collaborators.

Reporting from ScienceDaily contributed to this story.

The researchers examined arthropods, the enormous group of animals that includes insects, spiders, crabs and centipedes. They investigated examples from across evolutionary history in which arthropod sperm joined into organized groups or structures that may help them reach and fertilize an egg. Known as sperm conjugation, this coordinated behavior is changing how scientists view both reproduction and evolution.

How Sperm Cooperation Works

Sperm conjugation can be compared to a rowing team moving in a coordinated way. Scientists first documented the phenomenon more than 100 years ago, but it was generally considered uncommon. The new study, published in Nature Communications, indicates that sperm cooperation occurs widely among arthropods and has evolved many separate times.

"Fertilization is often viewed as a competition among individual sperm, but in many species we see cells working together in ways that can influence reproductive success," says Steve Dorus, professor of biology at Syracuse University's College of Arts and Sciences (A&S) and co-author of the study.

In many species, this cooperation involves sperm-associated material (SAM). This membrane-enclosed substance can attach sperm to one another or create structures around them that arrange the cells into groups. The researchers suggest that SAM may have helped sperm conjugation emerge, possibly beginning as a mechanism for packaging or protecting sperm.

A single sperm cell must travel through a difficult and highly complex female reproductive tract. By moving or functioning in groups, sperm may gain advantages in mobility, organization or overall performance. In these cases, fertilization becomes a coordinated effort rather than a contest involving isolated cells.

This finding calls into question long-established assumptions about fertility. Scientists may need to look beyond the abilities of individual sperm and pay greater attention to how group behavior affects reproductive outcomes.

An Evolutionary Pattern of Gain and Loss

The repeated appearance and disappearance of sperm conjugation is one of the study's most notable findings. The strategy originated hundreds of millions of years ago, but different species have gained and lost it many times. The analysis also concluded that the common ancestor of all insects possessed conjugated sperm.

To trace this history, the team carried out a broad comparison of sperm structures across arthropods using decades of previously published research. They examined sperm characteristics from hundreds of species and placed those traits onto an evolutionary family tree. This allowed the scientists to estimate when various forms of sperm cooperation appeared and how frequently they vanished or returned.

The resulting timeline tracks sperm conjugation and sperm-associated material (SAM) across major animal lineages over the past 600 million years. It reveals a recurring pattern in which evolutionary innovations appeared, disappeared, and later emerged again.

"Evolution has effectively run the same experiment over and over again across different groups of arthropods," says R. Antonio Gomez, postdoctoral scholar in A&S' Department of Biology and lead author of the study. "That allows us to see not only when sperm cooperation emerges, but also when it disappears and reappears under different evolutionary conditions."

According to the researchers, this recurring pattern illustrates the experimental nature of evolution.

"Sperm are the most rapidly evolving cell type," says Scott Pitnick, Weeden Professor of Biology in A&S and senior author of the study. "They are shaped by the unique challenge of operating outside the body in the complex environment of the female reproductive tract."

Possible Implications for Fertility

Although the study centers on evolutionary biology, its findings could influence several other areas of research. One possibility is a broader understanding of fertility throughout the animal kingdom.

Pitnick describes fertilization as an obstacle course rather than a straightforward race. Sperm must navigate a complicated environment and interact with the female reproductive tract in many ways. Learning how sperm cooperate or depend on shared biological structures may eventually point scientists toward new ways of studying human reproductive difficulties.

A New Target for Pest Control

The research may also support new methods for controlling destructive pests. Scientists are investigating whether sperm conjugation or SAM could be disrupted to interfere with reproduction in harmful species. One potential target is the invasive spotted lanternfly, which has become an increasing agricultural concern in New York and other eastern states.

Spotted lanternfly sperm differ from the cooperative sperm found in many other arthropods. They do not join into coordinated groups. Instead, every sperm cell is surrounded by a thick layer of SAM.

"Their sperm are highly unusual," Pitnick says. "They do not have conjugation, but each individual sperm is completely embedded in this material, and we do not even know how they are motile."

Scientists still do not understand how these sperm move and function. That mystery could also create an opportunity. If SAM is essential for lanternfly reproduction, interfering with the material might offer a highly specific way to control the species.

Why Does Sperm Cooperation Evolve?

A central question remains unresolved: Why does sperm cooperation develop at all?

One possibility is that working together improves movement through the reproductive tract. Another is that grouped sperm help transport important molecules to particular locations. Confirming these ideas is difficult because sperm observed on glass slides often behave differently from sperm moving inside the much more complicated environment of the female body.

Future studies will attempt to observe sperm groups within actual reproductive systems. Researchers also hope to determine the specific benefits and possible costs associated with this cooperative behavior.

Cooperation and Competition Work Together

The findings point to a broader lesson about biology. Cooperation and competition are not necessarily opposing forces. They can operate together, and even microscopic cells may depend on a balance between the two.

"What makes this pattern so fascinating is that evolution keeps arriving at similar cooperative solutions in very different groups and across vast expanses of time," says Dorus. "These examples remind us that cooperation can be just as important as competition in shaping biological success."

By studying how sperm cells coordinate to overcome reproductive challenges, scientists are uncovering new details about evolution, fertility and the biological strategies that support life. The work also helps address a major gap in understanding how elaborate reproductive traits have emerged and changed over hundreds of millions of years.

Reporting from ScienceDaily contributed to this story.

Happily, they can also be rediscovered, as a new study shows, with the vertebrae of the legendary predatory shark known to the world under its old name of Megalodon (now properly Otodus megalodon) turning up on a museum shelf decades after they were seemingly lost.

The new paper takes another look at the size and growth of this giant shark that lived between 15 and 3.5 million years ago. The study confirms previous estimates that these animals might have been longer than 24 meters (79 feet). To put that in context, even the most unnaturally exaggerated sharks in the Jaws franchise topped out at 10.5 meters (34 feet). These were seriously big fish.

The work is based on an analysis of several 11-million-year-old vertebrae from one animal, found in Denmark. Apart from the jaws and teeth, shark skeletons are mostly cartilage, so vertebrae are rare and important. Compared to a tooth, they give a much better indication of the size of the owner and here these are the largest known of any O megalodon (23 cm / 9 inches in diameter).

These important specimens were thought to have been destroyed in a move from the Geological Museum of Copenhagen (now part of the Natural History Museum of Denmark) to the Museum of Southern Jutland in 1989. The scientific records of them were limited to old photos and descriptions. A couple of these vertebrae have now turned up, having apparently sat on a shelf unrecognized for decades. This allowed for the new study, which also estimated that a newborn O megalodon might be 3.6 meters (12 feet) long and live for nearly a century.

How can museums and paleontologists lose valuable fossils?

All manner of unlikely and unfortunate actions can lead to the loss of fossils from museums.

Most obviously this can happen during times of conflict. The second world war saw the loss of dinosaur fossils on both sides of the conflict. The original specimens of the sail-backed dinosaur Spinosaurus were destroyed in Munich by an allied bombing raid in 1944. Earlier, a number of specimens, including parts of the early dinosaur Thecodontosaurus, were destroyed in Bristol after an Axis raid in 1940.

These were not even the first losses from enemy action in international wars. In 1916, the Canadian ship SS Mount Temple was sunk by a German ship. Although it was mostly carrying wheat, it also had a cargo of dinosaur fossils from Alberta that were being moved to the UK. The cargo lists are vague so we don’t even know what dinosaurs were on board.

Indirect action could be problematic too. In 1941, the Chinese attempted to move as many as 40 specimens of “Peking man” (Homo erectus), the first of our relatives to have human-like proportions, to the US to try to save valuable early hominid fossils from the invading Japanese forces. They never arrived, and might have been lost at sea after the ship they were on was sunk. Although it’s possible they never even made it on board the vessel.

Things can also be simply lost or fall apart. An apparent giant sauropod dinosaur similar to Diplodocuswas named by the US paleontologist Ed Cope in 1877 as Amphicoelias fragillimus. He described it from a single, incomplete, fragile, but giant, vertebra.

Cope gave differing measurements of the vertebra at various times, making it unclear quite how large it actually was. When he died, his collection was sold to the American Museum of Natural History, but they were never able to find this specimen. Given how fragile it was, it may simply have disintegrated on the shelf and been overlooked or thrown away.

Museums are not immune to losses either. If you have an enormous number of specimens (the Natural History Museum in London has an estimated 80 million objects in its collection), it is inevitable that one or two may simply get lost.

I’ve been an eyewitness to lost specimens turning up in a museum when a colleague spotted a dinosaur skull and pterosaur skeleton sitting on the wrong shelf like misplaced library books. Then there’s the more nefarious activities – I’ve heard of researchers deliberately moving specimens to make them hard to find so other researchers cannot examine them, and occasionally things are stolen from collections.

On top of this, natural disasters and accidents can wipe out history. The Fukushima earthquake and tsunami of 2011 in Japan caused major damage to the nearby Iwaki museum with damage to some of the fossils in their collections. And in 2018, one wing of the Nation Museum of Brazil in Rio de Janeiro burned down with the loss of many fossil specimens that were on display.

For all the examples raised here, museums are inherently safe places for specimens. There are millions and millions of fossils that have been held in institutions around the world for decades and even centuries. It is inevitable that accidents will happen, and that bad actors will cause occasional losses. Fortunately, at least on occasion these do reappear and give us some exciting new research opportunities.

Reporting from ScienceDaily contributed to this story.

A study using zebrafish found that altered gene activity can cause minerals to accumulate within the spine. This process resembles bone forming where it should not, eventually making spinal tissue unusually hard.

Researchers say the results reveal several biological processes that could become targets for future back pain treatments. The work also indicates that zebrafish may provide a useful model for testing potential therapies.

Why Spinal Discs Break Down

Most people experience back pain at some point. A major cause is the progressive deterioration of the discs that cushion the bones of the spine, a condition called intervertebral disc degeneration (IVDD).

Although IVDD is widespread and places a considerable burden on patients and health care systems, no medications can currently halt or reverse its progression. Surgery is still the only available long-term treatment.

Inherited factors are known to influence a person's risk of developing IVDD. Previous research has repeatedly connected early disc problems to a gene associated with collagen IX, a protein that helps bind together the structural fibers inside spinal discs.

To investigate how defects in this gene might cause disc disease, researchers from the Universities of Edinburgh and Bristol studied zebrafish bred without a functioning copy of it.

Zebrafish Developed Human-Like Spinal Damage

As the zebrafish grew older, they developed spinal abnormalities that closely resembled disc disease in people. Their vertebrae fused, while mineral deposits caused the tissue between the bones to become abnormally hard.

The researchers discovered that this mineralization did not begin immediately. First, a supportive scaffold layer within the developing spine started to deteriorate. Mineral deposits appeared only after this early structural damage had occurred.

The team then examined patterns of gene activity in the fish to determine which genes had become more or less active.

Their analysis revealed problems with fat processing and with mTOR, a pathway that regulates growth. They also found changes involving phosphate control and vitamin A signaling. Each of these processes has been associated with abnormal mineral accumulation.

Existing Osteoporosis Drug Reduced Mineral Buildup

The researchers also identified several approaches that reduced the spinal damage.

A bisphosphonate, a type of bone-protecting medication already used to treat osteoporosis, prevented minerals from accumulating. Spinal fusion was also reduced when the fish received less food or were treated with drugs that suppressed fat metabolism.

According to the researchers, the results highlight phosphate regulation and fat metabolism as especially promising areas for the development of future medicines.

The study was funded by Arthritis UK and BBSRC and published in the journal Communications Biology.

New Possibilities Beyond Surgery

Study lead, Dr. Erika Kague, from the University of Edinburgh's Institute of Genetics and Cancer, said: "For decades, surgery has been the only real answer for disc disease. By understanding the biology that drives the spine to harden, our zebrafish studies point to several ways of slowing it down, including a drug already used safely in patients. There's more work to do, but for a condition that's affected people for generations without a treatment in sight, this is super exciting."

Dr. Caroline Aylott, Head of Research Delivery at Arthritis UK, said: "For the 9.5 million people across the UK living with back pain, this research brings fresh hope that potential new therapeutic approaches are on the horizon.

"We are proud to fund research that is unlocking the science behind the processes leading to spinal disc degeneration. Back pain is one of the UK's most common conditions that has blighted millions over generations. Dr. Erika Kague and her team at the University of Edinburgh have uncovered important genetic evidence that could pave the way for new treatments, bringing us one step closer to a future where fewer people have to live with the daily pain and challenges that back pain can bring."

Dr. Jef Grainger, Executive Director of Bioscience Advancing Knowledge at BBSRC, said: "This research shows how publicly funded discovery bioscience can generate the knowledge needed to address major health challenges. By revealing new knowledge of how healthy biological processes break down in aging-related spinal disc degeneration, the study opens up promising avenues for future treatment development. It's a great example of how BBSRC-supported research helps turn scientific discovery into knowledge and innovations that have the potential to improve people's lives."

Reporting from ScienceDaily contributed to this story.

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Radio 4,·30 Jul 2026,·28 mins

Available for 21 days

Scientists have long referred to the Goldilocks zone – the region around a star where conditions are not too hot and not too cold but “just right” for life. Joined by a live audience at the Cheltenham Science Festival in the UK, Tom Whipple asks what are the true limitations of alien life? How do we spot it? And have we been looking too narrowly? Planetary scientist at MIT Sara Seagar discusses her team’s mission to Venus where, on the surface, temperatures can reach 500 degrees Celsius and it rains sulphuric acid. Above the rain, up in the clouds, Sara Seagar tells us how there could be life. And Lewis Dartnell, Professor of astrobiology at the University of Westminster, describes how he looks for extremophiles. These are organisms on earth that are found in places we once thought impossibly hostile to life. Plus, the missions to find life on Mars.... Presenter: Tom Whipple Producer: Dan Welsh Editor: Ilan Goodman & Martin Smith Production Coordinator: Jana Bennett-Holesworth

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Radio 4,·06 Aug 2026,·28 mins

Available for 28 days

Large parts of Europe are in the grip of drought. According to the UK Meteorological Office, last week was the UK's driest July on record. Katie Field, professor of plant-soil processes at Sheffield University, joins us to discuss the state of our struggling substrate. Next week, a dramatic solar eclipse will be sweeping down the Atlantic. In the past, eclipses have been vital to astronomers exploring the outer reaches of the Sun. Now though, they can make their own on demand. Esther Bastida-Pertegaz, project engineer at the European Space Agency, discusses the flying formation Proba-3 mission. A highly pathogenic bird flu has arrived in Australia, threatening local wildlife. Every continent in the world is now affected, and the harm that could be done to bird populations and mammals could be devastating. Thijs Kuiken, virologist at Erasmus University Medical Center in Rotterdam, brings us up to date with the situation. And Lizzie Gibney of Nature Magazine joins us to discuss this week’s science news. Presenter: Roland Pease Producer: Clare Salisbury, Tabitha Taylor-Buck, Keiran Manetta-Jones Editor: Martin Smith Production Co-ordinator: Jana Bennett-Holesworth

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Tech Now - Rainforests: Can Tech Help to Protect Trees?

Yasmin Morgan-Griffiths finds out how new technologies are being used to measure the world's forests in more detail than ever before. Suranjana Tewari takes us inside a robotics factory in Beijing. 

• Duration24 mins
• First shown1:30pm 1 Aug 2026
• Available for 11 months

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World Service,·04 Aug 2026,·26 mins

Available for over a year

The transition from petrol to electric cars is well underway. But why are most aircraft in the skies still burning jet fuel? We look at new developments in electric aviation. Also this week: keeping children safe online - a leading international child charity talks to Tech Life. Presenter: Shiona McCallum Producer: Tom Quinn (Photo: An all-electric CX300 aircraft from BETA Technologies takes part in a demonstration flight in Scotland. It is a small white aircraft, flying at low altitude. The propeller can be seen at the rear of the fuselage. Credit: Loganair/BETA Technologies)

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Researchers from the University of Toronto, L'École Normale Supérieure in Paris and Lehigh University in Pennsylvania reached the finding by studying ultracold potassium atoms cooled to nearly absolute zero. As the scientists increased the frequency of collisions between the atoms, resistance initially rose. Beyond a certain point, however, it stopped climbing.

The result offers a more detailed view of how resistivity develops at the microscopic level.

Why Electrical Resistance Matters

"Electron-on-electron collisions are known to increase resistivity in some pure materials," explains Professor Joseph Thywissen in the Department of Physics and the Centre for Quantum Information and Quantum Control in the Faculty of Arts & Science at the University of Toronto, senior author of a study published in Physical Review Letters. "The energy produced by electrical resistance shows up as heat. Transmission lines, for instance, lose up to eight per cent of generated electrical power. Resistivity is also interesting to study because it can be a signature of new physics in materials."

To investigate these collisions under tightly controlled conditions, the team used an optical lattice. This grid of light traps atoms and allows them to mimic the behavior of electrons moving through a solid.

The setup made it possible to recreate extreme conditions that ordinary solid materials cannot reach while isolating the effects of particle collisions.

Ultracold Atoms Mimic Electrons

"We observed that the atoms, which are only a few nanometers in size, bump into each other as if they were much larger," says Thywissen. "This quantum enhancement of the effective atom size makes collisions on a given lattice site much more likely, increasing the resistivity of the system."

As the interactions grew stronger, collision-driven resistivity eventually leveled off instead of continuing to rise. The researchers say this saturation suggests that electron collisions in a metal may also face a similar upper limit.

A New Window Into Quantum Materials

The findings provide a clearer microscopic explanation for how resistance behaves in low-density metals. They may also help guide future research into strongly correlated atomic systems and quantum materials, where particles interact in unusually complex ways.

"Our results provide a clear microscopic understanding of how resistivity works in low-density metals and open the door to new studies of strongly correlated atomic systems and quantum materials," says Thywissen.

Reporting from ScienceDaily contributed to this story.

The findings, published in Nature in the study "Magnetic Character of the Low-Energy Enhancement in 70Zn," resolve a long-standing question in nuclear physics and could improve scientific models of how heavy elements are created in space.

The international collaboration brought together researchers from 25 institutions across the United States, Canada, Italy, Germany, Norway and South Korea.

A Surprising Gamma-Ray Signal

Gamma rays belong to the same broad family of electromagnetic radiation as visible light and radio waves. When an excited atomic nucleus moves to a lower and more stable energy state, it can release energy in the form of gamma rays.

Scientists measure how often nuclei emit gamma rays at different energies using a quantity known as the gamma-ray strength function.

Transitions between nuclear energy states are described as either electric or magnetic. Each type reflects a different way that protons and neutrons reorganize inside a nucleus before releasing gamma rays.

For decades, scientists have detected an unexplained rise in the number of low-energy gamma rays emitted by certain nuclei. Known as the low-energy enhancement, or LEE, this feature appears in the gamma-ray strength function, but researchers had not been able to determine what produced it.

The experiment included staff scientists from several national laboratories, including Lawrence Livermore National Laboratory (LLNL) and Los Alamos National Laboratory (both National Nuclear Security Administration, or NNSA, laboratories); Lawrence Berkeley National Laboratory; and Pacific Northwest National Laboratory.

The work also reflects FRIB's larger partnership with national laboratories, which encourages the exchange of knowledge between fundamental research and national security applications. At the same time, the program gives students and early-career scientists practical training that supports the future nuclear workforce.

"This low-energy enhancement wasn't predicted by theory, so it was kind of a shock to the community when it was first observed," said Eleanor Ronning, lead author of the study and former FRIB graduate student who is now a postdoctoral research fellow at the National Institute for Nuclear Physics in Padova, Italy. "It is difficult to predict where LEE occurs -- we don't know which nuclei will exhibit it."

The new measurements provide strong evidence that magnetic transitions within the nucleus are responsible for the enhancement.

"This is a key step forward," said Andrea Richard, co-lead of the study and assistant professor and interim director of the Edwards Accelerator Laboratory at Ohio University. "We now have a consistent explanation that connects experimental observations with theory."

Why the Discovery Matters for Astrophysics

Explaining LEE is important for understanding the internal structure of nuclei, but its significance extends far beyond nuclear physics.

The enhancement can increase the frequency of neutron-capture reactions beyond what scientists would normally predict. These reactions play a central role in producing heavy elements during extreme cosmic events, including supernovae and neutron star mergers.

Across many different nuclei, the combined effects of LEE can substantially change calculated reaction rates. Those changes can affect models of nuclear activity inside stars, nuclear energy systems, and NNSA national security applications.

Measuring a Faint and Elusive Effect

LEE has been exceptionally difficult to study because scientists cannot easily predict where it will appear. Its signal is also weak and can be obscured by background noise, making highly precise equipment and advanced analysis methods essential.

"Our collaboration has been searching for ways to identify the nature of this low-energy enhancement in gamma-ray emission for over a decade," said Artemis Spyrou, professor of physics at FRIB and in Michigan State University's Department of Physics and Astronomy. "This result only became possible thanks to the development of new experimental capabilities and new analysis techniques that did not exist when we began."

Sean Liddick, professor of chemistry at FRIB, interim chairperson of MSU's Department of Chemistry, and Ronning's graduate advisor, said the study depended on experimental resources available only at FRIB.

"We used a novel experimental technique that combines specialized instruments in a way that effectively used the entire facility," Liddick said. "It is exciting to see that effort lead to such a clear result."

Two Paths Into Zinc-70

The researchers focused on zinc-70, a nucleus believed to show the low-energy enhancement and one whose arrangement of energy levels is already well understood. Instead of studying zinc-70 directly, they examined the beta decay of two separate states of its parent nucleus, copper-70.

The team isolated copper-70 in two forms: its ground state and an excited, or isomeric, state. These two states provided separate pathways into zinc-70.

Each pathway filled a different combination of energy levels within zinc-70, allowing researchers to observe its nuclear structure from two complementary perspectives.

Producing the two pathways required exceptionally pure beams of both copper-70 states. The researchers created them with FRIB's Low Energy Beam and Ion Trap, or LEBIT, a high-precision mass spectrometer.

"We used LEBIT in this way for the first time," said Ryan Ringle, associate professor of physics at FRIB and LEBIT group leader. "It was an interesting challenge to work on, which provided additional training opportunities for our group's graduate students. This new technique for isomer separation opens the door to study many more nuclei and motivates technical developments to expand our capabilities in this area."

Magnetic Transitions Reveal the Answer

The gamma rays released by zinc-70 were recorded with the Summing NaI, or SuN, detector. Researchers then used two analytical approaches, the beta-Oslo method and the Shape method, to determine the gamma-ray strength function associated with each initial state.

Comparing the two strength functions allowed the team to determine conclusively that magnetic transitions inside the nucleus produce the low-energy enhancement.

The result gives nuclear theorists a new experimental benchmark and provides a strategy for investigating the phenomenon in additional nuclei.

"We look forward to applying this separated-isomers technique to more nuclei," Liddick said. "Knowing which nuclei should exhibit this low-energy enhancement is key to designing experiments to investigate them at facilities like FRIB and to improve models of how elements are created in astrophysical environments."

Training Future Nuclear Scientists

The project also demonstrates the value of collaboration among institutions, established researchers, students and postdoctoral scholars.

Ronning and Richard helped write the experimental proposal during FRIB's second call for proposals by its Program Advisory Committee. Both were early in their careers at the time. Ronning was a graduate student at FRIB, while Richard was a postdoctoral scholar at LLNL.

After completing her first postdoctoral position at MSU, where she worked in nuclear astrophysics and national security, Richard pursued opportunities that connected fundamental science with NNSA mission objectives. That path led to another postdoctoral position at LLNL.

Now based at Ohio University, she continues to contribute to both basic research and national security efforts.

"The combined expertise of our research teams is what really made it all possible," Richard said. "It was a privilege to work with the various teams across institutions over the years. It was a formative experience as an early-career researcher."

For Ronning, the publication marked the completion of a project she had helped guide from its earliest stages.

"Working on the entire process -- from writing the proposal and running the experiment to publishing the paper in Nature -- has been a rewarding experience," Ronning said.

This research is based upon work supported by the U.S. Department of Energy Office, the U.S. National Science Foundation, the National Nuclear Security Administration, the U.S. Nuclear Data Program, the Research Council of Norway, the Norwegian Nuclear Research Center, the Natural Sciences and Engineering Research Council of Canada and the Canada Foundation for Innovation.

Reporting from ScienceDaily contributed to this story.

Primordial black holes (PBH) are hypothetical remnants of the universe's earliest moments. Scientists think they may have formed during cosmic inflation, when rapid expansion amplified small fluctuations in the distribution of matter.

These black holes have been proposed as possible candidates for dark matter, the invisible material thought to account for about 90% of all matter in the Universe by mass. Although dark matter cannot be seen directly, its gravitational effects can be detected throughout galaxies and across the wider cosmos.

Primordial black holes could travel through stars as they move across the universe. Earlier research suggested that if one passed through a white dwarf, its gravity could create powerful tidal forces inside the star. Those forces might destabilize the white dwarf and cause it to explode as a Type Ia supernova (SNe Ia).

A white dwarf is the dense stellar remnant left behind after a low-mass star runs out of fuel. Type Ia supernovae are extremely bright explosions that are generally believed to occur when a white dwarf becomes unstable and undergoes a runaway thermonuclear reaction.

Testing a New Path to Type Ia Supernovae

The research was led by Shing-Chi Leung, an assistant professor at SUNY Polytechnic Institute and a visiting associate scientist at The University of Tokyo Kavli Institute for the Physics and Mathematics of the Universe (Kavli IPMU). The team also included Kavli IPMU Visiting Senior Scientist Ken'ichi Nomoto and Kavli IPMU Senior Fellow Alexander Kusenko.

The scientists investigated the motion, brightness, and chemical properties of supernovae produced through this proposed PBH-triggered explosion channel.

In an earlier paper published in 2025, the team showed that PBH-triggered explosions could produce SNe Ia with properties that closely resemble those generated by standard Type Ia supernova models.

Comparing Models With Real Supernovae

For the new study, the researchers compared their models with several well known supernova remnants (Tycho, Kepler, 3C 397), nearby supernovae (e.g., SN 2011fe, SN 2012cg) and the chemical abundances of Milky Way stars.

Their results showed that PBH-triggered SNe Ia could reproduce several characteristics observed in these supernovae and their remnants.

The researchers examined radioactive isotopes such as Ni-56, Ni-57, and stable elements such as Mn and Ni. These chemical signatures allowed them to estimate the masses and metallicities of the stars that produced the explosions.

Metallicity (the amount of metal when the star is formed, which probes when the star is born in the cosmic age) can provide clues about when a star formed and the chemical conditions that existed at that point in the history of the universe. In astronomy, metals are elements heavier than hydrogen and helium.

Primordial Black Holes May Shape Galactic Chemistry

The team also used supernova models to explore how this explosion mechanism could contribute to galactic chemical enrichment. Supernovae release newly formed elements into space, where those materials can later become part of new stars and planets.

The analysis indicated that a non-zero fraction of PBH-triggered SN Ia may be needed to explain the chemical abundance trend observed in stars across the Milky Way. This suggests that primordial black holes may have influenced the chemical evolution of our galaxy through the stellar explosions they triggered.

"Our work suggests that some supernova that we observe in the sky could be a result of the PBHs. Therefore, even though we cannot directly observe these evasive entities, they leave many interesting clues in nature for us to probe their properties," Leung said.

The researchers plan to broaden their investigation by studying how PBH-triggered explosions might affect the overall population of conventional supernovae and the combined rates of these brief but powerful cosmic events.

Reporting from ScienceDaily contributed to this story.