bioinnovationbeacon.com

Author: admin

  • China’s surging biotech sector represents both competition and lifeline for the US

    China’s surging biotech sector represents both competition and lifeline for the US

    Emerging from stealth earlier this month, Boston-based Solstice Oncology highlighted its origins in a trans-Pacific exchange that’s grown commonplace. The startup licensed its lead asset, colon cancer candidate porustobart, from Chinese biotech Harbour BioMed in February in a deal worth more than $100 million upfront and potentially upwards of $1 billion. Such deals are helping to fuel the rapid growth of Chinese biotech, which is also the beneficiary of decades of focused support by its government.

    There’s ample reason to believe that trend will continue: Last week, the Chinese government released a new five-year plan that lays out a goal of $521.8 billion in combined revenue for its domestic biotech industry by 2030. It also aims to originate at least 25% of first-in-class drugs on the global market by that date.

    Meanwhile, out-licensing from Chinese biotechs has surged since the start of the COVID-19 pandemic, from 35 such deals worth a total of $989 million in 2019 to 186 deals worth $137.7 billion in 2025, according to data from PharmCube. Evaluate has predicted that Chinese assets will make up more than two-thirds of total deal value this year, up from less than 5% five years ago.

    “The number of licensing deals have radically accelerated, wherein large pharmaceutical companies are increasingly turning their business development to China,” Jeremy Levin, executive chairman of Ovid Therapeutics, told BioSpace. “The shift of pharmaceutical licensing activity toward China-originated assets is now an established fact, and two years ago it was far less pronounced.”

    Such licensing deals may be a boon to companies like Solstice Oncology, but the rise of Chinese biotech has prompted considerable handwringing about U.S. competitiveness.

    “We have to start thinking about what it means if we so erode our innovation base here in the U.S. that we are dependent on a potential adversary for life-sustaining medications,” Caitlin Frazer, executive director of the National Security Commission on Emerging Biotechnology (NSCEB), told BioSpace last month.

    How China gained momentum

    The Chinese government’s prioritization of biotech traces back to a 2006 mention of related terms in a medium- and long-term planning document, said Alexander Brown, a senior analyst at the Mercator Institute for China Studies (MERICS). The sector has continued to crop up in government planning documents in the two decades since. While experts say it’s difficult to quantify how much the Chinese government puts into its domestic biotech sector, Brown and a MERICS co-author estimated the investment was at least 20 billion renminbi (about $3 billion) in 2023.

    One difficulty in quantifying the government’s support is that it goes beyond direct investment in startups, Cyriac Roeding, CEO of the cancer therapeutics firm Earli, said in an interview. “The Chinese government does a lot of things in many different ways, not just direct investments, but also purchases, like getting into the game as a customer, or cheaper supplies,” he explained.

    Levin said the Chinese government’s biotech strategy has taken decades to execute. First, it established the ability to manufacture medications. Next came domestic contract research organizations (CROs). “That gave them the ability to make a molecule and then to test it,” Levin said. “As they did that, they studied very carefully how we approved drugs. And so they established and continually refined their drug approval process in China.”

    In step three, China launched clinical trials “in a way that complemented their testing of drugs in the CRO-like environment,” Levin said. “They established a highway which was high speed for the development of so-called lookalikes or bio-betters,” medications based on the mechanism of action of existing drugs developed elsewhere. In step four, the government launched programs aimed at attracting researchers who’d gained valuable training and experience abroad to return and put their skills to work domestically. These programs cover a range of science and engineering fields in addition to biotech.

    Some commenters have used the specter of Chinese competition to argue for more streamlined regulation of clinical trials in the U.S. On the flip side of the same coin, two lawmakers called for increased FDA oversight of Chinese study sites and scrutiny of data collected there after several clinical trial deaths in the country. But none of the experts who spoke with BioSpace cited a superior regulatory process as a factor in the rise of the Chinese biotech industry.

    “Yes, [regarding the] FDA, there’s a lot of things that can be done better. No question,” Roeding said. But that’s not going to reorient the trajectories of the U.S. and Chinese biotech sectors. Rather, he argued, you have to follow the money.

    A funding double-bind

    Roeding pointed out that the billions poured into licensing deals with Chinese companies represent money not going to innovative early-stage research happening stateside. That compounds what he sees as the major factor holding U.S. biotech back as China rises: a lack of consistent funding.

    While he conceded that boom and bust cycles have always characterized private investment in U.S. biotech, he said funding for early-stage, innovative research is far worse than in the past because of a prolonged post-COVID bust and because AI ventures are now attracting the vast majority of venture capital investment, leaving little leftover for biotech. And while currently the “XBI looks great,” Roeding said, most investment that does reach biotech goes to clinical-stage companies rather than earlier-stage work.

    “This industry is deeply suffering from the lack of consistency. That’s our biggest problem,” Roeding said. “Consistent funding for innovation that has long cycles of time, much longer than others, is critical.”

    To accomplish that, he argues for the creation of a publicly funded sovereign wealth fund. Its investments should be concentrated in bust cycles and in bridging the “valley of death” between early, NIH-funded research and clinical validation, he said. “And now you can start flattening the [boom-and-bust investment] curve and you can be internationally competitive.”

    Moreover, Roeding added, “the beautiful thing about it is if it’s done right. . . . It’s actually going to pay itself back and more. Society is going to make money off this.”

    Levin has a different take. A lack of appreciation for biotech and a failure to differentiate it from pharma mean that the former sector suffers from price-control policies such as the IRA and Most Favored Nation, as well as a health insurance industry that often pushes the cost of drugs onto patients, he said.

    Then to add insult to injury, Levin continued, the FDA substantially reduced its workforce last year, laying off about 20% of employees. That loss of institutional knowledge caused what he called “structural damage” that risks widening an already established competitive gap as China moves rapidly in biotechnology.

    That said, Chinese biotech faces barriers of its own, Levin noted, especially in their capability to scale, to fully develop drugs on their own and to reach overseas markets. “And that’s why we’re seeing a huge takeoff, also, of out-licensing deals in recent years,” Levin told BioSpace.

    “So it’s not all rosy for the Chinese biotech sector,” he continued, “but certainly this long-term government backing and just the fact that they’re able to do research and do certain processes in China at a higher scale, at a cheaper cost, at a faster speed than in other countries is really a core reason why they’re rising so quickly.”

    The new five-year plan, he said, demonstrates that “China has moved well beyond trying to become faster and better at drug development. It now wants to discover important new medicines in China, develop them there and build companies that sell them around the world. That represents a fundamental change in China’s ambition for its pharmaceutical industry.” Even if it falls short of its “extraordinarily ambitious” 25% first-in-class target by 2030, “What matters is what China will have built along the way.”

    “When China decides to make something a priority, it follows through with strategy, planning and investment,” Roeding said.

    A geopolitical lever?

    Levin postulated that the Chinese government plan for the rise of biotech culminates with a fifth step in which a Chinese company develops a groundbreaking medication—he gives the example of a cure for Alzheimer’s—but withholds it from the U.S. if relations between the two countries are tense at the time. In other words, China could use life-sustaining medicines as a bargaining chip, just as it has with magnets, solar technology and rare earth metals.

    Roeding warned that Chinese dominance could become an issue even when there is no competitive intent involved, namely if supplying a drug domestically needs to be prioritized. He pointed to the COVID pandemic, when each country prioritized its own supply of vaccines. Becoming dependent on a drug sourced from China would make the U.S. vulnerable to supply chain issues.

    Brown agreed it’s a possibility the Chinese government could use a crucial drug as a strategic lever. In his view, that’s more likely to work after a Chinese drug is already established in the U.S. or another market, rather than with a newly launched medication. But he said there are ways to mitigate that risk, such as stockpiling drugs and encouraging Chinese companies to set up manufacturing facilities within the country where their drugs will be sold.

    Brown noted it’s still the case that companies in the U.S. and other Western countries have a “huge advantage” over their Chinese counterparts: the market size of their home countries. And accessing U.S. and European markets has been key to some of the Chinese industry’s biggest success stories.

    “That places a question mark on [Chinese companies’] development going forward: whether or not access to those markets will remain open, or whether or not China itself will take measures to expand its own market,” Brown said.

    “[T]he wrong American response is to try to hold China back,” Levin said. “We need to look at what we are doing at home.”

  • MIT’s tiny flying robot gets 450% faster with AI

    MIT’s tiny flying robot gets 450% faster with AI

    Tiny flying robots may one day help rescuers search for people trapped beneath collapsed buildings after earthquakes. Because of their small size, these robotic insects could potentially move through narrow spaces that larger drones cannot enter while avoiding walls, debris, and falling objects.

    Until recently, however, aerial microrobots have been far less nimble than the insects that inspired them. They typically moved slowly and followed relatively simple flight paths.

    Researchers at MIT have now demonstrated a new approach that gives an insect-scale flying robot much greater speed and agility. The team developed an AI-based controller that allows the robotic bug to perform demanding aerial maneuvers, including repeated body flips.

    Using a two-part control system designed to balance performance with computational efficiency, the researchers increased the robot’s speed by about 450 percent and its acceleration by about 250 percent compared with their previous best results.

    The robot was agile enough to complete 10 consecutive somersaults in 11 seconds, even while wind disturbances tried to knock it away from its intended path.

    “We want to be able to use these robots in scenarios that more traditional quadcopter robots would have trouble flying into, but that insects could navigate. Now, with our bioinspired control framework, the flight performance of our robot is comparable to insects in terms of speed, acceleration, and the pitching angle. This is quite an exciting step toward that future goal,” says Kevin Chen, an associate professor in the Department of Electrical Engineering and Computer Science (EECS), head of the Soft and Micro Robotics Laboratory within the Research Laboratory of Electronics (RLE), and co-senior author of a paper on the robot.

    Chen is joined on the paper by co-lead authors Yi-Hsuan Hsiao, an EECS MIT graduate student; Andrea Tagliabue PhD ’24; and Owen Matteson, a graduate student in the Department of Aeronautics and Astronautics (AeroAstro); as well as EECS graduate student Suhan Kim; Tong Zhao MEng ’23; and co-senior author Jonathan P. How, the Ford Professor of Engineering in the Department of Aeronautics and Astronautics and a principal investigator in the Laboratory for Information and Decision Systems (LIDS). The research was published in Science Advances.

    AI Gives the Robot a Smarter Flight Controller

    Chen’s group has spent more than five years developing robotic insects.

    The team recently created a more durable version of their tiny robot, which is about the size of a microcassette and weighs less than a paperclip. This newer design has larger flapping wings that support more agile flight. The wings are driven by soft artificial muscles that contract rapidly enough to produce extremely fast wingbeats.

    The physical design had improved, but the robot’s controller remained a major limitation. This controller acts as the robot’s “brain,” determining where the robot is and deciding how it should move. In earlier versions, a human had to tune the controller by hand.

    For the robot to fly with the speed and aggressiveness of a real insect, the researchers needed a system that could handle uncertainty while rapidly solving complex control problems.

    A controller powerful enough to do that would normally demand too much computation to operate in real time, especially because the aerodynamics of such a lightweight flying machine are highly complex.

    To solve this problem, Chen’s group collaborated with How’s team to develop a two-step AI-driven control system. The design combines the robustness needed for difficult, high-speed maneuvers with enough computational efficiency to work in real time.

    “The hardware advances pushed the controller so there was more we could do on the software side, but at the same time, as the controller developed, there was more they could do with the hardware. As Kevin’s team demonstrates new capabilities, we demonstrate that we can utilize them,” How says.

    Teaching a Tiny Robot to Plan Difficult Maneuvers

    The first part of the system uses what is known as a model-predictive controller. This type of controller relies on a dynamic mathematical model to predict how the robot will behave and determine the best sequence of actions for safely following a desired flight path.

    Although this method requires substantial computing power, it can plan difficult movements such as aerial flips, sharp turns, and aggressive changes in body angle. The planner also takes into account limits on the amount of force and torque the robot can produce, helping it avoid movements that could lead to a crash.

    Repeated flips are particularly challenging. To perform one somersault after another, the robot must slow down in exactly the right way so that it begins each new flip under the proper conditions.

    “If small errors creep in, and you try to repeat that flip 10 times with those small errors, the robot will just crash. We need to have robust flight control,” How says.

    The researchers then used this expert planner to train a “policy” built on a deep-learning model through a process called imitation learning. The policy serves as the robot’s real-time decision-making system, determining how and where it should fly.

    In effect, imitation learning allows the team to capture the behavior of the more computationally demanding controller in a faster AI model that can operate quickly enough for real-time flight.

    A major part of the challenge was generating enough useful training data to teach the policy how to handle aggressive maneuvers without creating an unnecessarily large data set.

    “The robust training method is the secret sauce of this technique,” How explains.

    During flight, the AI-based policy receives information about the robot’s position and converts it into real-time commands controlling factors such as thrust force and torques.

    Insect-Like Speed and Agility

    Experiments showed that the two-step control system dramatically improved the robot’s performance. The insect-scale machine flew 447 percent faster and achieved a 255 percent increase in acceleration.

    It also completed 10 somersaults in only 11 seconds while remaining within about 4 or 5 centimeters of its planned flight path.

    “This work demonstrates that soft and microrobots, traditionally limited in speed, can now leverage advanced control algorithms to achieve agility approaching that of natural insects and larger robots, opening up new opportunities for multimodal locomotion,” says Hsiao.

    The team also demonstrated a movement known as a saccade. In insects, this involves pitching the body sharply, rapidly moving to a new position, and then pitching in the opposite direction to stop. This quick acceleration and braking can help insects determine their position and maintain clear vision.

    “This bio-mimicking flight behavior could help us in the future when we start putting cameras and sensors on board the robot,” Chen says.

    Toward Autonomous Flying Microrobots

    One major goal for future research is to equip the microrobots with onboard cameras and sensors. That could eventually allow them to fly outdoors without depending on a sophisticated external motion capture system.

    The team also plans to investigate whether onboard sensing could help groups of the robots avoid crashing into one another and coordinate their movements while navigating.

    “For the micro-robotics community, I hope this paper signals a paradigm shift by showing that we can develop a new control architecture that is high-performing and efficient at the same time,” says Chen.

    This research is funded, in part, by the National Science Foundation (NSF), the Office of Naval Research, Air Force Office of Scientific Research, MathWorks, and the Zakhartchenko Fellowship.

  • Stopping Ozempic may raise heart attack and stroke risk

    Stopping Ozempic may raise heart attack and stroke risk

    GLP-1 drugs such as semaglutide (Ozempic and Wegovy) and tirzepatide (Mounjaro and Zepbound) have surged in popularity for treating diabetes and helping people lose weight. About one in eight U.S. adults now use these medications, which are also known to provide cardiovascular benefits. But new research suggests that those heart benefits may fade quickly when treatment is stopped.

    Researchers at Washington University School of Medicine in St. Louis tracked more than 333,000 U.S. veterans with type 2 diabetes for three years. They found that interrupting or stopping GLP-1 treatment for as little as six months was associated with a meaningful increase in the risk of major cardiovascular events compared with remaining on the medication.

    The longer patients stayed off treatment, the greater the increase in risk. After two years without GLP-1 therapy, the risk of heart attack, stroke and death was up to 22% higher than among people who continued treatment, largely wiping out the cardiovascular protection gained while taking the drugs.

    The findings, published in BMJ Medicine, suggest that stopping GLP-1 medications may have consequences that extend well beyond weight regain. They also point to the importance of uninterrupted treatment for maintaining heart protection.

    “There is enormous exuberance about starting GLP-1 drugs, but not nearly enough attention to what happens when people stop,” said senior author Ziyad Al-Aly, MD, a WashU Medicine clinical epidemiologist and chief of the Research and Development Service at the VA Saint Louis Health Care System. “Many quit after a few months because of cost, side effects or shortages. When they stop, it’s not just weight that comes back; they experience a resurgence in inflammation, blood pressure, and cholesterol. Weight regain is visible; the metabolic reversal is not.”

    “Our data suggest this metabolic whiplash is detrimental to heart health,” Al-Aly added. “Restarting the medication helped restore some protection, but only partially, showing that discontinuation leaves a lasting scar.”

    Heart protection depends on continued GLP-1 use

    GLP-1 medications include the semaglutide drugs Ozempic and Wegovy and the tirzepatide drugs Mounjaro and Zepbound. After observing that about half of users stop taking GLP-1 drugs not long after beginning treatment, Al-Aly set out to examine what happens to cardiovascular health after therapy is discontinued.

    The study focused on major adverse cardiovascular events, including heart attack, stroke and death. Researchers analyzed data from 333,687 veterans with type 2 diabetes. Of those, 132,551 had been prescribed GLP-1 drugs, while 201,136 had been prescribed sulfonylureas, another class of diabetes medications.

    Sulfonylureas include glipizide (Glucotrol), glimepiride (Amaryl), and glyburide (Diabeta and others). Participants were followed for up to three years.

    Researchers reassessed GLP-1 treatment status every six months. During the study, 26% of GLP-1 users stopped taking the medication altogether. Another roughly 23% experienced a treatment gap lasting at least six months before eventually restarting therapy.

    Continuous treatment produced the greatest benefit

    The clearest cardiovascular benefit appeared among people who remained on GLP-1 medications throughout the full three-year study period.

    Compared with participants taking sulfonylureas, those who consistently stayed on GLP-1 therapy had an 18% lower risk of major cardiovascular events. That translated to about four fewer major cardiovascular events for every 100 people over three years.

    Participants who stayed on GLP-1 treatment for two years or two-and-a-half years before stopping for the rest of the study also saw meaningful reductions in risk, at 7% and 15%, respectively.

    By contrast, people who discontinued GLP-1 therapy before reaching 18 months showed no significant reduction in cardiovascular risk compared with those taking sulfonylureas by the end of the study.

    Treatment gaps weakened heart protection

    Interrupting treatment and then restarting it also appeared to reduce the cardiovascular benefit.

    People who remained on GLP-1 drugs continuously for three years had an 18% reduction in risk, while those who stopped temporarily and later resumed treatment saw an average reduction of 12%.

    Even a six-month interruption before restarting therapy was enough to weaken the benefit. Compared with continuous use, those treatment gaps were associated with a 4% to 8% increase in cardiovascular risk.

    Longer periods off the drugs were linked to even greater losses of protection. People who stopped GLP-1 treatment for one year without restarting had a 14% higher risk of cardiovascular events compared with continuous users. After two years off treatment, that increase reached 22%.

    The pattern suggests that cardiovascular benefits accumulated during GLP-1 treatment can be lost relatively quickly once the medication is discontinued.

    Restarting may not fully restore lost benefits

    The findings reinforce the importance of continuous treatment if patients and clinicians want to preserve the cardiovascular effects of GLP-1 therapy. They also suggest that reducing treatment interruptions could help maximize the drugs’ protective effects on the heart.

    “Clinicians should treat adherence to GLP-1 treatment as an important outcome in its own right — not an afterthought,” Al-Aly said. “Health systems need plans in place to help people continue their medication indefinitely, recognizing that GLP-1s treat chronic conditions. That includes proactive management of side effects, candid conversations about the long-term nature of treatment, infrastructure to identify and support patients at risk of stopping and addressing the cost barriers that make GLP-1 therapy unsustainable for many.”

    Al-Aly noted that this is especially important because cardiovascular protection from GLP-1 treatment appears to accumulate gradually but disappear much more quickly.

    For study participants, spending only one year off the medication was enough to lose benefits that had taken years of continuous treatment to build. Restarting the drug restored some of that protection, but not all of it.

    The research was funded by the United States Department of Veterans Affairs. The funders had no role in considering the study design or in the collection, analysis, interpretation of data, writing of the report, or decision to submit the article for publication. The contents do not represent the views of the US Department of Veterans Affairs or the US Government.

  • Chronic stress may be quietly reshaping your heart

    Chronic stress may be quietly reshaping your heart

    Chronic stress linked to everyday life may leave a lasting physical mark on the heart, potentially damaging cardiovascular health and shortening lifespan.

    That conclusion comes from a study of nearly half a million adults in the UK, led by researchers at the MRC Laboratory of Medical Sciences (LMS) and Imperial College London. The researchers believe it is the largest study of its kind.

    Their findings suggest that chronic inflammation, which is associated with lifestyle and socioeconomic circumstances, may contribute to harmful changes in the heart’s structure. It was also linked to a greater risk of heart attack and stroke.

    Importantly, these changes may begin years before a person notices any cardiovascular symptoms, allowing the damage to build silently over time.

    Hidden Inflammation May Change the Heart

    Professor Declan O’Regan, British Heart Foundation Chair of Cardiovascular AI at Imperial College London and Head of the Computational Cardiac Imaging Group at the LMS, said: “Our study, which is the largest of its kind, suggests that millions of people could be living with hidden inflammation, which is slowly changing their heart and causing long-term damage – increasing the risk of heart attack and stroke. Chronic inflammation is complicated, but we know it’s tied to our health and driven by a range of lifestyle and economic factors – meaning people may be at more risk just because of their surroundings, their economic status, their family’s health and their lifestyle.”

    “But while tackling health inequalities remains an issue, there are things that we can do about inflammation, including reducing risk factors like smoking and obesity.”

    Chronic inflammation occurs when the immune system remains mildly activated for long periods rather than switching off after an immediate threat has passed. This persistent, low-level immune activity has been associated with several diseases, including cancer and diabetes, and researchers increasingly suspect that it may also play an important role in heart disease.

    For the new study, the team examined UK Biobank data from nearly 480,000 adults in the UK. They assessed inflammation using a blood marker called glycoprotein acetyls (GlycA) and combined those measurements with heart imaging and genetic information.

    A 43% Higher Risk of Heart Attack and Stroke

    People with the highest inflammation levels (the top 20%) had a 43% higher risk of heart attack and stroke than participants with the lowest levels (the bottom 20%).

    The researchers also found signs that inflammation was associated with physical remodeling of the heart. People with higher inflammation tended to have thicker heart walls, smaller heart chambers and poorer heart filling – all changes which may develop quietly for years before progressing to heart failure.

    Inflammation was also strongly associated with socioeconomic disadvantage and psychological distress. More familiar cardiovascular risk factors, including smoking and excess body fat, were linked to higher inflammation as well.

    People whose inflammation remained elevated over time had a 43% greater risk of heart attack and stroke, even when they had no previously existing heart disease.

    The findings suggest that inflammation may provide one biological route through which pressures from everyday life, including poverty and mental health problems, can affect the body and increase cardiovascular risk.

    Social Factors, Mental Health, and Genetics

    Professor Declan O’Regan added, “The surprising thing was how much social factors and mental health are linked to inflammation and damage to the heart — as well as more well-known risk factors like smoking and inactivity. There was also a strong genetic factor, with some people being naturally more resilient or susceptible to the inflammatory damage that comes from different lifestyles.”

    The researchers emphasize, however, that genetic susceptibility or difficult life circumstances do not make heart disease inevitable. There are still opportunities to reduce persistent inflammation and lower cardiovascular risk.

    The analysis also highlighted inflammatory proteins in the interleukin-1 and TNF families as possible contributors to the observed heart damage.

    Several of these proteins are already being targeted by drugs being tested in clinical trials. That raises the possibility that anti-inflammatory therapies could eventually help prevent cardiovascular disease before symptoms begin.

    Blood Tests Could Help Identify People at Risk

    The researchers also suggest that inflammation blood tests could potentially be combined with genetic risk scores to identify people who may benefit most from early intervention.

    Professor Bryan Williams, Chief Scientific and Medical Officer at the British Heart Foundation, said: “Inflammation is part of the body’s healing process, but there is also a darker side to it. This large-scale study found people with higher levels of inflammation experienced silent changes to the structure of their hearts and had a higher risk of major cardiac events including heart attacks and strokes.”

    “The research provides valuable insights into how our genes and lifestyle factors, such as smoking, poor mental health and socioeconomic status, can converge to trigger inflammation. It also identifies several inflammatory proteins that appear to play a key role in the heart changes linked to chronic inflammation, and it is to be hoped that anti-inflammatory medicines could become an important tool in preventing cardiovascular disease.

    “These findings reinforce the importance of tackling the causes of inflammation and poor cardiovascular health, while also supporting people to make lifestyle changes that can help protect their hearts.”

    The study was funded by the Medical Research Council and British Heart Foundation.

    The work was also supported by the NIHR Imperial Biomedical Research Centre, a translational research partnership between Imperial College Healthcare NHS Trust and Imperial College London.

  • Scientists find that “perfect” systems may be surprisingly fragile

    Scientists find that “perfect” systems may be surprisingly fragile

    Perfection may not always be the best recipe for stability, especially in complex systems such as electrical grids, ecosystems, and advanced materials.

    For years, researchers often worked from the assumption that networks should perform more reliably when their individual parts behave as similarly as possible. Real systems, however, rarely look that tidy. Power generators operate differently from one another, neurons vary in form and behavior, species occupy different roles in ecosystems, and the components inside engineered materials are not always perfectly uniform.

    Physicists at Northwestern University now say those differences may sometimes be an advantage rather than a defect.

    Why Disorder Can Improve Stability

    In a new study, the researchers created a mathematical framework designed to determine when variation, which scientists often describe as disorder, can actually make a network more stable. Their results suggest that many physical, engineered, and biological systems can become more resilient when their components, or the connections between them, are not identical.

    That finding challenges the idea that uniformity should always be the goal. Instead, carefully introducing differences into a system could help engineers design more resilient power grids, architected materials and other interconnected technologies. The work also may help explain why irregularity is so common in natural systems, including neural, biological and ecological networks.

    The study was published Sept. 17 in the journal Science. The researchers also developed a website that allows users to explore the framework visually. By adjusting different parameters, users can watch network components interact, synchronize and form organized patterns.

    “Previous studies found a growing number of cases in which disorder (also called heterogeneity, irregularity or asymmetry) across a network’s nodes can actually improve stability and desirable behavior,” said Northwestern’s Adilson Motter, who led the work. “We have seen this in important real-world systems, including power grids, metamaterials and brain computation. But we didn’t know how widespread this effect was or which kinds of systems could benefit from it. Our new study answers those questions, explains why these differences can improve stability and even reveals why scientists overlooked this effect for so long.”

    Motter is the Charles E. and Emma H. Morrison Professor of Physics and Astronomy at Northwestern’s Weinberg College of Arts and Sciences and director of the Center for Network Dynamics. Northwestern postdoctoral researcher Arthur Montanari and graduate student Pietro Zanin, both members of the Motter group, are the study’s co-first authors.

    Why Older Network Models Missed the Effect

    Many interconnected systems survive only if they can recover from disturbances. A strong gust can break apart a flock. A sudden spike in electricity demand can strain a power grid. An impact can deform a material.

    Scientists often represent these systems as networks made up of individual components, called nodes, that are connected by links. In an electrical grid, generators act as the nodes and transmission lines form the links between them. In an ecological network, species are the nodes while their relationships (competition, cooperation, and predation) form the links.

    Traditionally, researchers have focused heavily on how those nodes are connected. Many studies also rely on simplified mathematical models, including the widely used Kuramoto model, that represent each node with only a single variable.

    Those simplified approaches have produced valuable insights, but they can leave out important behavior found in real-world systems, where individual components and their interactions can be far more complicated.

    “Real systems are rarely uniform,” Montanari said. “Birds differ in personalities, neurons vary in shape, and even our social relationships can be asymmetric. These differences might appear random, but they can profoundly affect how the whole system behaves.”

    Earlier research had already suggested that such differences could sometimes be beneficial. In a 2020 Nature Physics study, Motter’s team showed that electrical generators could synchronize more successfully when they operated somewhat differently from one another. A 2025 Nature Communications study led by Montanari found comparable effects in models involving flocking behavior and drone swarms.

    What remained unclear was whether these examples represented rare exceptions or pointed to a much broader rule.

    “Disorder can stabilize networks, but only when the node dynamics are rich enough,” Motter said. “Simplified models can inadvertently strip away the very stabilizing effect we want to capture.”

    Finding the Right Amount of Disorder

    To investigate the question more broadly, the researchers developed a mathematical framework that could account for more realistic network behavior.

    They first examined systems close to a stable condition. Next, they calculated what happened after small disturbances were introduced. If those disturbances gradually disappeared, the system returned to stability. If they grew larger, the system moved toward instability.

    The team then compared networks whose components were identical with networks containing differences among their components or connections. This allowed the researchers to identify the general circumstances in which heterogeneity can outperform uniformity.

    Motter and his colleagues tested the framework using models of power grids, neurons, flocks, architected materials and ecological networks.

    They found that disorder can improve stability in two main ways. Differences can exist among the nodes themselves, or they can appear in the links connecting those nodes. The effect also depends on both the location and the amount of variation.

    A moderate level of disorder might make a network more stable, while excessive variation could eventually push that same system in the opposite direction.

    “If you make the system more homogeneous, you lose stability,” Montanari said. “But if you increase disorder too much, you also lose stability. Our framework can help pinpoint the level of disorder that helps the system achieve optimal stability.”

    Random Variation Can Sometimes Be Enough

    The researchers also discovered that beneficial differences do not always need to be carefully designed in advance.

    In many of their models, randomly introduced variation produced greater stability than the best completely uniform configuration. That means simply allowing some degree of diversity within a system can sometimes provide an advantage.

    There was an important exception when the variation occurred in the links connecting nodes rather than within the nodes themselves. In those cases, even networks with relatively simple node dynamics could gain stability from disorder.

    Why Nature May Favor Imperfect Networks

    The findings could help researchers better understand existing complex systems, particularly ecological networks, while also providing engineers with new strategies for designing systems from the ground up.

    One longstanding ecological puzzle is that older mathematical models predicted large, complicated ecosystems should be inherently unstable. Nature, however, contains many ecosystems that are both highly diverse and persistent.

    “Since the 1970s, mathematical models have predicted that large, complex ecosystems should destabilize and collapse,” Montanari said. “Yet very large and highly diverse ecosystems persist in nature. Our findings suggest that variation among mutually beneficial interactions, such as those between pollinators and flowers, could help explain this paradox.”

    The same principle could eventually influence the design of advanced materials.

    Architected materials are often built from repeating, nearly identical units. The new findings suggest engineers might be able to create different or improved behaviors by deliberately varying the shapes, sizes, orientations, and physical properties of those units.

    To do that effectively, researchers would need to treat these materials as mechanical networks and use models detailed enough to preserve the system’s true dynamics. Computational techniques could then be used to search for combinations of variation that provide the greatest benefit.

    “When disorder enhances stability, the next challenge is figuring out how best to design it,” Motter said.

    The study, “Disorder-promoted stability,” was supported by the Army Research Office (grant number W911NF-22-2-0109) and the National Science Foundation (grant number DMS-2308341). The study also acknowledges the stimulating research environment provided by the NSF-Simons National Institute for Theory and Mathematics in Biology (NSF grant number DMS-2235451 and Simons Foundation grant number MP-TMPS-00005320).

  • Scientists solve a 50-year mystery and discover a new human blood group

    Scientists solve a 50-year mystery and discover a new human blood group

    More than half a century after scientists first encountered a mysterious marker on human red blood cells, researchers finally traced it to its genetic source. The breakthrough established MAL as a human blood group system and gave doctors a new way to identify the exceptionally rare people whose blood lacks the AnWj antigen.

    The work was led by scientists at NHS Blood and Transplant in Bristol, including researchers from the International Blood Group Reference Laboratory (IBGRL), together with colleagues at the University of Bristol. Their findings solved a puzzle dating back to 1972 and could help prevent dangerous transfusion reactions in a small number of patients.

    Although most people are familiar with the ABO and Rh blood groups, those are only part of a much larger biological system. Red blood cells carry hundreds of different molecules on their surfaces. Many of these molecules act as antigens, markers that the immune system can recognize.

    For most transfusions, ABO and Rh compatibility receive the most attention. But in patients with unusual antibodies or rare blood types, matching some of these lesser-known antigens can become crucial.

    A Blood Marker Found in More Than 99.9% of People

    The AnWj antigen was discovered in 1972, but for decades scientists did not know which gene produced it or which protein carried it on red blood cells.[1]

    More than 99.9% of people are AnWj positive. For the tiny minority who are AnWj negative, however, the distinction can matter enormously.

    If an AnWj negative person develops antibodies against AnWj and then receives AnWj positive blood, those antibodies can attack the transfused red blood cells. In some circumstances, that can trigger a potentially serious transfusion reaction.

    There are also two very different reasons someone can lack the antigen. In most cases, AnWj expression appears to be suppressed because of an underlying hematological disorder or certain cancers.[2] Much more rarely, a person is born without the antigen because of an inherited genetic change.

    Only a handful of people with this inherited form had ever been identified, making the mystery especially difficult to investigate.

    The Genetic Clue Was Hidden in MAL

    To find the source, the researchers turned to whole exome sequencing. This technique examines the portions of DNA that contain instructions for making proteins, allowing scientists to search across thousands of genes for unusual variants shared by affected individuals.

    The analysis pointed unexpectedly to the MAL gene.

    The researchers found that people with the inherited AnWj negative phenotype carried homozygous deletions affecting MAL. Homozygous means that the relevant change was present in both copies of the gene, one inherited from each parent.

    The MAL gene produces a small membrane protein called Mal. When the team examined red blood cells, people who were AnWj positive produced the full-length Mal protein on their cells, while it was missing from AnWj negative cells.

    Five genetically AnWj negative individuals were included in the investigation, including members of an Arab Israeli family.[3] The samples also included blood donated in 2015 by the woman who had been the first AnWj negative person identified in the 1970s.

    The researchers did not stop at finding a genetic association. They needed to demonstrate that Mal really was responsible for the antigen.

    When scientists introduced the normal MAL gene into laboratory cells, the cells became reactive with AnWj antibodies. Introducing the altered form did not produce the same response. Additional experiments showed that Mal was both necessary and sufficient for expression of the AnWj antigen.

    MAL Becomes an Official Blood Group System

    Those results provided the evidence needed to establish MAL as a distinct blood group system, with AnWj as its defining antigen.

    The International Society of Blood Transfusion later formally reported MAL as ISBT 047. MAL was one of four blood group systems ratified during the period covered by the organization’s 2026 terminology report, alongside ER, CD36 and ATP11C.

    That designation is more significant than simply adding another name to a list. For something to qualify as a blood group system, researchers must connect an antigen to a defined genetic and molecular basis.

    MAL was the 47th officially recognized blood group system at the time. The field has continued to move quickly since then. In September 2026, the International Society of Blood Transfusion announced JAMA as the 49th blood group system, illustrating how the genetic map of human blood is still being expanded.

    Why the Discovery Matters for Transfusions

    Knowing the gene behind AnWj gives blood specialists something they did not previously have: a direct genetic way to search for people who inherit AnWj-negative blood.

    Genotyping tests can now be designed to identify rare patients and donors carrying the relevant MAL changes. These tests can potentially be incorporated into existing blood group genotyping systems.

    That matters because finding compatible blood for someone with an antibody against a marker present in more than 99.9% of people can be extraordinarily difficult.

    The need is not merely theoretical. Earlier clinical reports have shown that anti-AnWj antibodies can cause hemolytic transfusion reactions, in which transfused red blood cells are destroyed by the recipient’s immune system.

    More recent cases have underscored just how complicated the situation can become.

    In 2026, researchers reported a 75-year-old man with severe anemia and an anti-AnWj autoantibody. Compatible blood was unavailable, so physicians ultimately transfused unmatched red blood cells after weighing the risks. Genetic testing showed that his MAL gene was normal, supporting the conclusion that his antibody was acquired rather than caused by the rare inherited MAL deficiency. He did not experience a hemolytic transfusion reaction in that case.

    Another 2026 case involved a patient with high-grade B-cell lymphoma and a complement-binding anti-ANWj autoantibody. After incompatible transfusions were followed by signs of red blood cell destruction, clinicians used sutimlimab, a drug that blocks part of the immune complement pathway. The patient’s laboratory measurements improved, although the researchers stressed that the complicated case and short treatment period prevent firm conclusions about the treatment’s effectiveness. It was reported as the first use of sutimlimab for this particular type of anti-AnWj-associated hemolysis.

    Together, these cases highlight an important distinction. Some people are AnWj negative because of inherited MAL changes, while others can lose AnWj expression because of disease and develop an antibody against a marker their cells previously carried.

    A Mystery That Took Decades to Crack

    Louise Tilley, Senior Research Scientist, IBGRL Red Cell Reference at NHS Blood and Transplant, said: “The genetic background of AnWj has been a mystery for more than 50 years, and one which I personally have been trying to resolve for almost 20 years of my career. It represents a huge achievement, and the culmination of a long team effort, to finally establish this new blood group system and be able to offer the best care to rare, but important, patients.

    “The work was difficult because the genetic cases are very rare. We would not have achieved this without exome sequencing, as the gene we identified wasn’t an obvious candidate and little is known about Mal protein in red cells. Proving our findings was challenging, and we appreciate the help of all our collaborators, and the patients, without whom we would not have got to this point.”

    One reason the mystery endured for so long was simply the rarity of inherited AnWj negative blood. With so few known cases, researchers had very little genetic material from affected people to compare.

    The Mal protein itself also offered few obvious clues. It is a very small protein embedded in cell membranes and has been associated with processes involving membrane organization and cellular transport. Nothing immediately pointed to it as the carrier of a long mysterious red blood cell antigen.

    Gene Editing Helped Confirm the Answer

    Ash Toye, Professor of Cell Biology in the School of Biochemistry and Director of the NIHR Blood and Transplant Research Unit in red cell products at the University of Bristol, said: “It’s really exciting we were able use our ability to manipulate gene expression in the developing blood cells to help confirm the identity of the AnWj blood group, which has been an outstanding puzzle for half a century. This development will help identify these rare donors and help patients in the future.”

    Manipulating gene expression allowed the researchers to test cause and effect rather than simply observe that a genetic variant happened to occur in AnWj negative people. By changing which genes cells expressed and then testing whether AnWj appeared, the scientists could build a much stronger case that MAL was the missing piece.

    Nicole Thornton, Head of IBGRL Red Cell Reference at NHS Blood and Transplant, said: “Resolving the genetic basis for AnWj has been one of our most challenging projects.

    “There is so much work that goes into proving that a gene does actually encode a blood group antigen, but it is what we are passionate about, making these discoveries for the benefit of rare patients around the world.

    “Now genotyping tests can be designed to identify genetically AnWj-negative patients and donors. Such tests can be added to the existing genotyping platforms.”

    The official ISBT blood group database now lists the reference MAL allele along with the null allele associated with the AnWj negative phenotype, turning what was once an unexplained serological curiosity into a genetically defined blood group system.

    Human Blood Is Far More Complicated Than ABO

    The MAL story also illustrates how much complexity is hidden behind the familiar letters A, B, AB and O.

    Blood groups are defined by inherited differences in molecules on red blood cells. These differences often have little noticeable effect in everyday life. They become important when the immune system encounters red blood cells carrying an antigen it recognizes as foreign, particularly during transfusion or pregnancy.

    That is why rare blood group research can have an outsized clinical impact despite involving very few people. If a patient has an antibody against an antigen carried by nearly everyone else, locating compatible donor blood can require specialized laboratories, rare donor registries and sometimes international cooperation.

    Dr. Tim Satchwell, Senior Lecturer at UWE Bristol, who contributed to the study whilst a Research Fellow at the University of Bristol, said: “Mal is a very small protein with some interesting properties which made it difficult to identify and meant we needed to pursue multiple lines of investigation to accumulate the proof we needed to establish this blood group system. Being able to combine our expertise to finally achieve this has brought the whole team a lot of satisfaction.”

    For more than 50 years, AnWj was a blood antigen without a known genetic home. The identification of MAL changed that, giving researchers a molecular explanation, clinicians a path toward better genetic testing, and rare patients a better chance of being identified before a difficult transfusion becomes an emergency.

    Notes

    • Blood groups are complex. The two best known blood group systems are ABO and Rh. Within each blood group, red cells can carry surface markers called antigens. For example, within the ABO blood group system, there are the A and B antigens – people with A have the A antigen, people with B have the B antigen, people with AB blood have both and people with O have neither. There are now 47 recognized blood group systems together containing more than 360 recognized blood antigens.
    • AnWj is named after the first people who made the antibody (Anton and Wj).
    • The disorders suppress Mal and make patients AnWj-negative, unless they have the rare inherited form (MAL deletion). The inherited AnWj-negative people are healthy.
  • These blood thinners may have an unexpected benefit for Alzheimer’s patients

    These blood thinners may have an unexpected benefit for Alzheimer’s patients

    People who have both atrial fibrillation and Alzheimer’s disease may experience slower cognitive decline when treated with newer NOAC blood thinners, according to research from Karolinska Institutet published in the European Heart Journal.

    Atrial fibrillation is a common heart rhythm condition in older adults and also affects many people living with Alzheimer’s disease. Doctors often prescribe blood thinners to these patients to reduce the chance of blood clots and stroke. Earlier research has suggested that anticoagulant treatment may lower the risk of developing dementia, but far less is known about whether these drugs influence cognitive decline after Alzheimer’s disease has already been diagnosed.

    “There are reasons to believe that the treatment could have a positive effect on cognition, for example by improving blood flow and reducing small-scale damage in the brain,” says Maria Eriksdotter, professor at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, and senior consultant in geriatric medicine at Karolinska University Hospital, who led the study.

    Comparing Newer and Older Blood Thinners

    Researchers analyzed information from SveDem (Swedish Register for Cognitive Disorders/Dementia), a national quality registry, and included 7,308 people diagnosed with both atrial fibrillation and Alzheimer’s disease.

    Participants were placed into three matched groups. One group received newer anticoagulants known as NOACs, another was treated with the older blood thinner warfarin (Waran), and the third did not receive any anticoagulant medication.

    To track changes in thinking and memory over time, researchers used the standardized Mini-Mental State Examination (MMSE).

    Slower Cognitive Decline With NOACs

    People taking NOACs showed a significantly slower decline in cognitive function than those treated with warfarin or those who received no anticoagulant medication.

    The difference amounted to slightly more than 0.2 MMSE points per year. While that change is relatively small over a single year, the researchers say it could become more meaningful if it continues over a longer period.

    “The difference is modest for an individual patient from one year to the next, but over a longer period even such an effect could influence how cognitive function develops. Our findings suggest that NOAC treatment may also be significant for cognition in this patient group,” says Nanbo Zhu, researcher at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet.

    Lower Risks of Stroke and Other Complications

    The potential benefits were not limited to cognition. Compared with people who did not receive anticoagulants, those treated with NOACs also had lower risks of death, stroke, blood clots and fractures.

    Warfarin was also associated with lower risks of death, stroke, and blood clots. However, people taking warfarin had a higher risk of major bleeding.

    Why the Findings Need Caution

    The researchers emphasize that the study has important limitations. Because it was observational, the results cannot prove that NOACs directly caused the slower cognitive decline or the other health benefits seen in the data.

    Some factors that could affect both which treatment a patient received and how their health changed over time could not be fully evaluated. The researchers also note that some participants may have switched from one medication to another during the follow-up period.

    The study was funded by, amongst others, the Swedish Research Council, the Swedish Brain Foundation, CIMED, ALF project funding and Karolinska Institutet funds. Maria Eriksdotter has participated as a consultant in one-off meetings with BioArctic AB, Roche, Eli Lilly, Biogen/Eisai and Novo Nordisk, and has given lectures at symposia sponsored by Roche and BioArctic/Eisai. No other conflicts of interest are reported.

  • New mesothelioma drug turns cancer’s own defenses against it

    New mesothelioma drug turns cancer’s own defenses against it

    Mesothelioma is a rare and aggressive cancer that is most often linked to asbestos exposure. When asbestos fibers are inhaled, they can become trapped in the lungs, where they trigger chronic inflammation that may eventually lead to cancer decades later.

    About 30,000 people worldwide are diagnosed with mesothelioma every year. Treatment options remain limited. Immunotherapy and chemotherapy can help some patients, but the disease is still extremely difficult to control. Patients, many of whom are men who previously worked in industries such as shipbuilding, oil refining, and asbestos manufacturing, have a median survival of about 12 months. The five year survival rate is approximately 10 percent.

    “It’s a disease of a significant unmet medical need,” says Brian Cunniff, a professor at the University of Vermont.

    Now, research published in Nature Communications by Cunniff, UVM research scientist Victoria Gibson, and an international team of collaborators describes an unusual strategy that could offer a new way to treat mesothelioma and potentially other forms of cancer.

    In a phase one clinical trial sponsored by RS Oncology, LLC, patients with relapsed mesothelioma received an experimental drug that controlled disease progression in 67% of participants. Tumors also shrank in some patients. The drug was generally well tolerated, and the critically ill patients in the trial lived longer than patients receiving standard treatments.

    Turning Cancer’s Protective System Into a Weakness

    Mesothelioma cells, like many cancer cells, produce unusually high levels of “reactive oxygen species,” unstable molecules that can damage cells. These molecules are generated in part because tumor cells have highly active metabolisms.

    To survive that stressful environment, cancer cells increase production of antioxidant enzymes that help neutralize the damaging molecules. One of those enzymes is peroxiredoxin 3, or PRX3, which operates inside mitochondria, the structures that produce much of a cell’s energy.

    The UVM researchers decided to reverse the usual logic behind antioxidant-based cancer strategies.

    For years, scientists tested whether increasing antioxidants could help fight cancer by reducing reactive oxygen species. Many of those clinical trials failed, and some research suggested that boosting antioxidants could actually help tumors grow.

    The UVM team instead asked what would happen if cancer cells were deprived of one of their most important antioxidant defenses.

    Their approach focuses on blocking PRX3. Without this protective enzyme, oxidative stress builds inside tumor cells until the damage becomes overwhelming.

    An Antibiotic That Overloads Tumor Cells

    The experimental treatment developed by RS Oncology grew out of discoveries made at UVM. It uses thiostrepton, a naturally occurring antibiotic, to disable PRX3.

    Blocking the enzyme causes hydrogen peroxide to accumulate inside the mitochondria of tumor cells, eventually triggering cell death.

    Cancer cells may be particularly vulnerable to this strategy because they already produce more reactive oxygen species than normal cells. PRX3 also turns over more rapidly in tumor cells, potentially allowing the treatment to target cancer more selectively while having less effect on healthy tissue.

    Laboratory experiments provided further evidence that PRX3 is important for mesothelioma survival.

    When researchers completely deleted PRX3 from mesothelioma tumor cell lines, mitochondrial function declined, cell growth slowed sharply, and the cancer cells could no longer form tumors in animal experiments.

    Other research groups have also shown that eliminating PRX3 in healthy mice does not produce adverse effects. That finding is important because mitochondria perform essential functions in nearly every cell, leading some scientists to question whether they can be safely targeted.

    “People will come up to us at conferences and state that you can’t target the mitochondria because they’re too important,” said Gibson. “The evidence — that you can knock out PRX3 in mice and there’s no adverse phenotype — supports our approach.”

    In other words, researchers have shown that mice can develop and function normally even when the genes responsible for producing PRX3 are removed.

    From a UVM Laboratory to Human Patients

    The scientific groundwork for the treatment began at UVM’s Cancer Center around 2015.

    After early experiments with thiostrepton produced encouraging results, researchers helped establish RS Oncology, a private pharmaceutical company created to move the UVM discoveries toward clinical testing. Brian Cunniff, an associate professor in the Department of Pathology and Laboratory Medicine at the university’s Larner College of Medicine, serves as the company’s chief science officer.

    The team eventually transformed thiostrepton into a clinical formulation called RSO-021.

    Between 2022 and 2023, researchers tested RSO-021 in a phase one clinical trial in the United Kingdom. The study was conducted under the oversight of the MHRA, the UK equivalent of the FDA.

    The treatment is delivered directly into the chest through a catheter that many mesothelioma patients already have in place because of “pleural effusions,” a buildup of fluid in the space between the lung and chest wall.

    Approximately 90 percent of mesothelioma patients develop pleural effusions.

    Delivering the drug locally allows doctors to concentrate it near the tumor while reducing the amount of medication circulating throughout the rest of the body.

    Early Trial Shows Encouraging Survival Results

    The phase one study met its safety and tolerability goals at a dose of 90 milligrams, and no patient deaths were attributed to the drug.

    Researchers also found evidence in patient tissue that RSO-021 was hitting its intended biological target. That result confirmed that the mechanism previously observed in cells and mice was also occurring in human tumors.

    Average progression-free survival was 4.2 months, roughly comparable to existing treatments.

    The researchers were more encouraged by overall survival. Among the 15 patients in the cohort, survival was better than what is typically seen with currently available therapies. Cunniff described the finding as a potential “game changer.”

    “Our overall survival data is very promising and will hopefully persist with additional patients,” Cunniff said.

    The findings also suggest that RSO-021 may do more than directly kill cancer cells. It may also alter the immune environment around the tumor in a way that helps the immune system attack or restrain the cancer.

    “Our drug has both cytotoxic activity, it can kill the tumor cells, but it also has immunomodulatory capacity where it can modulate the immune system to now manage the tumor,” said Cunniff.

    Phase two of the clinical trial has now been completed. The researchers expect to present the results at a global oncology meeting this year.

    Expanding the Strategy Beyond Mesothelioma

    The research is now moving in several directions.

    Scientists from UVM and RS Oncology, working with the University of Leicester and other institutions in the UK, are developing second-generation PRX3 inhibitors with improved solubility.

    Future versions could potentially be taken as an oral tablet, which could make the treatment easier to administer and potentially broaden its use beyond mesothelioma.

    At UVM, Gibson, the lead author of the new study, is continuing the work as a postdoctoral researcher. She is helping launch research investigating thiostrepton in peritoneal malignancies, including mesothelioma, gastric cancer, and other gastrointestinal cancers.

    That work is being conducted in collaboration with Conor O’Neill, a surgical oncologist at the UVM Cancer Center and UVM Health.

    “We believe this mechanism could be applicable to other cancers,” Cunniff said.

    For Gibson, seeing the research move from laboratory experiments into human trials has given the project a deeply personal dimension.

    “I’ve always just had a desire to help people because I feel like everyone has experienced cancer in their life, whether it’s them, friends, or family members,” she said.

    Even so, she was surprised when a family member contacted the laboratory hoping to enroll her dying father in the clinical trial.

    “We just work in a lab all day working with cells,” she recalled, “and the fact that we’re making an impact on people, that they’re wanting to be on this clinical trial, just was amazing to me.”

  • The shape behind the Einstein problem just revealed strange new physics

    The shape behind the Einstein problem just revealed strange new physics

    A mathematical shape that drew global attention for solving a decades-old puzzle is now revealing an unexpected connection to physics. Researchers have found that structures based on the shape can make light form unusual chiral patterns, pointing to new ways of exploring how geometry can influence optical behavior.

    In a study published in Nature Communications, researchers from the Institute of Industrial Science, The University of Tokyo, and collaborating institutions built optical structures inspired by the “Smith hat.” This unusual shape is known for solving the so-called Einstein problem in mathematics. When the team illuminated the structures with laser light, they observed diffraction effects unlike those seen in conventional quasicrystals.

    The Shape That Solved the Einstein Problem

    The Einstein problem asks whether a single tile shape, known as a “monotile,” can cover an entire surface without creating a repeating pattern.

    Familiar tilings such as checkerboards and honeycombs repeat in a regular way. An aperiodic monotile, by contrast, can fill a surface without ever settling into a repeating arrangement.

    In 2023, researchers discovered the first such monotile, the Smith hat. The finding attracted widespread attention because it provided a long-sought solution to the mathematical problem.

    “What is especially fascinating about the hat tile is that, although the resulting pattern appears irregular at first glance, it is actually constructed from the honeycomb lattice,” says lead author Yuto Moritake. “We wanted to see whether this unique shape could also produce any unexpected physical phenomena.”

    Turning a Mathematical Pattern Into an Optical Structure

    To test that possibility, the researchers created nanoscale versions of the pattern on silicon nitride films using electron beam lithography.

    When laser light was directed at the structures, the resulting diffraction patterns formed distinctive pinwheel-like shapes. These patterns directly revealed the chiral character of the aperiodic structure.

    Chirality refers to a form of handedness in which a structure and its mirror image cannot be perfectly matched. In this case, the unusual arrangement of the monotile pattern caused the light itself to display a chiral response.

    “We found that the diffraction patterns themselves become chiral because the structure lacks mirror symmetry,” explains senior author Masaya Notomi. “This kind of optical response is fundamentally different from that observed in conventional quasicrystalline materials.”

    Light Responds to Direction and Polarization

    The researchers also found that the diffraction pattern changed depending on both the direction and polarization of the incoming light.

    When the physical structures were mirrored, their optical behavior reversed as well. This showed that the response of the light was directly tied to the symmetry of the underlying pattern, revealing a new type of symmetry-controlled optical behavior.

    “These results open a new direction of research on the fusion of quasiperiodic order and chirality,” remarks Moritake. “Monotile patterns provide a platform for exploring optical phenomena that emerge from the interplay of symmetry, chirality, and aperiodicity.”

    From Abstract Mathematics to New Optical Physics

    The researchers say structures inspired by monotiles could eventually contribute to technologies designed to manipulate light, control polarization, and support advanced optical devices.

    More broadly, the findings show how a discovery that began as an abstract mathematical puzzle can lead to unexpected physical effects. The Smith hat was first celebrated for solving a question about how shapes can cover a surface. Now, its unusual geometry may also help researchers uncover new ways to control and study light.

  • Scientists find a hidden cause of high blood pressure that routine tests can miss

    Scientists find a hidden cause of high blood pressure that routine tests can miss

    A common and frequently missed cause of high blood pressure may be easier to detect with help from a wearable device that tracks hormone changes throughout the day and night.

    New research published in Science Translational Medicine focuses on primary aldosteronism, a hormone disorder that may affect up to one in five people with high blood pressure. The condition is associated with an increased risk of heart disease, stroke, diabetes, and other serious health problems.

    Researchers from the University of Bristol and the University of Manchester in the UK, the University of Bergen in Norway, and collaborators in Stockholm and Athens found that people with primary aldosteronism can experience bursts of hormone production both during the day and while asleep at night. Those nighttime surges are especially important because routine blood tests are rarely performed during sleep.

    A Wearable Device Tracks Hormones Around the Clock

    To capture these hidden changes, the research team used a portable device developed at the University of Bristol that allowed patients to have their hormone levels monitored continuously while living normally at home rather than staying in a hospital or research facility.

    This type of continuous monitoring could reveal abnormalities that may be missed by conventional testing, potentially helping doctors identify hormone-related conditions earlier.

    Study co-lead author Dr. Thomas Upton, Clinical Research Fellow in Automated Sampling Clinical Fellow at the University of Bristol, and Senior Clinical Fellow at Bristol Hospitals NHS Foundation Trust said: “Primary aldosteronism is an important cause of high blood pressure and the most common cause of secondary hypertension we see in our blood pressure clinic. It could be affecting millions of people in the UK. However, due to the way hormones change during the day and the current complexity of the diagnostic process, diagnosis is often delayed or never made at all.

    “In our study, patients were monitored at home during normal activity, and this allowed us to see how hormones changed over time in realistic settings. This approach could potentially revolutionize how we diagnose hypertension and ultimately reduce cardiovascular disease – particularly heart disease and strokes – that could have been prevented.”

    Measuring Hormones Every 20 Minutes

    The proof-of-concept study followed 60 patients in Bristol, Bergen, Stockholm, and Athens over a 24-hour period. Hormone levels were measured every 20 minutes using a lightweight wearable device about the size of a mobile phone that attaches at the waist.

    Because the device samples hormones from the skin, participants were able to continue with their usual activities, including sleeping at night, while researchers collected detailed hormone data.

    The technology, known as U-RHYTHM, was adopted and further developed by the spinout company Dynamic Therapeutics in 2023.

    Study senior author Dr. Eder Zavala, UKRI Future Leader Fellow at the University of Manchester, said: “By continuously monitoring hormones over 24 hours, we were able to reveal a previously hidden pattern of nocturnal hormone bursts. This gives us a much clearer understanding of the disease and could ultimately help doctors detect it earlier and treat patients more effectively.

    “A more detailed mathematical and computational analysis of daily hormonal profiles could eventually also help uncover earlier and more subtle forms of the disease, opening new opportunities to improve outcomes for patients living with high blood pressure.”

    Why Standard Blood Tests May Miss the Disorder

    Researchers used computational analysis to study changes in aldosterone, a hormone that helps control salt and water balance in the body. They also tracked two closely related hormones, 18-hydroxycortisol and 18-oxocortisol.

    The results suggest that current diagnostic approaches may miss some patients because aldosterone does not remain consistently elevated.

    Even in some of the most severe cases, hormone levels sometimes dropped below the minimum thresholds typically used to diagnose primary aldosteronism. A single blood test taken at one moment could therefore capture a period when hormone levels appear relatively normal.

    Instead of remaining constantly high, aldosterone showed repeated bursts of secretion at night while the overall day-night rhythm of hormone activity remained intact.

    Nighttime Hormone Bursts Offer a New Clue

    The hormone spikes came from the adrenal glands and were especially pronounced in patients whose primary aldosteronism was caused by a problem affecting only one adrenal gland rather than both.

    Importantly, the unusual hormone patterns disappeared after the affected adrenal gland was surgically removed. That finding provided additional evidence that the bursts were directly associated with the disease.

    Study co-author Prof Stafford Lightman, Professor of Medicine at the University of Bristol and inventor of the U-RHYTHM technology, added: “The findings suggest that clinicians may need to rethink how they look for the disorder, which the Endocrine Society clinical practice guidelines now recommend should be considered for all people with hypertension, also known as high blood pressure.

    “Future diagnosis could move away from single time point blood tests and towards tracking the body’s hormone rhythms over time, particularly the overnight patterns that appear to hold crucial clues to disease. Further research is needed to define the best clinical pathways, using dynamic hormone measurement, to ensure early diagnosis of this common and potentially curable cause of high blood pressure.”

    Toward Earlier Detection of High Blood Pressure Causes

    The findings raise the possibility that future testing for primary aldosteronism could rely less on a single blood sample and more on monitoring how hormones change over time.

    Because the disorder can be treated and, in some cases, potentially cured, detecting it earlier could help reduce the risk of preventable cardiovascular complications.

    The research was funded by EU Horizon 2020, the Trond Mohn Foundation, the UKRI Biotechnology and Biological Sciences Research Council (BBSRC), Medical Research Council, University Hospitals Bristol and Weston NHS Foundation, the Swedish Medical Research Council and Knut and Alice Wallenberg Foundation.

    The findings support the University of Bristol’s research ‘Grand Challenge’ focus on Understanding and Preventing Cardiovascular Disease and builds on NIHR-funded initiatives aimed at earlier identification of people with hypertension and other cardiovascular risk factors.