The study found that brief, vigorous exercise quickly changes the mix of molecules circulating in the bloodstream. These rapid shifts appear to suppress bowel cancer cell growth while also speeding up the repair of damaged DNA.

How Exercise Changes the Bloodstream

Researchers at Newcastle University discovered that exercise raises the levels of several small molecules in the blood. Many of these molecules are known to reduce inflammation, support healthy blood vessels, and improve metabolism.

When scientists exposed bowel cancer cells in the lab to blood containing these exercise-driven molecules, they observed widespread genetic changes. More than 1,300 genes shifted their activity, including genes involved in DNA repair, energy production, and cancer cell growth.

Published in the International Journal of Cancer, the findings help clarify how physical activity may lower bowel cancer risk. The research shows that exercise sends molecular signals through the bloodstream that influence genes controlling tumor growth and genetic stability.

The results add to growing evidence that staying physically active is an important part of cancer prevention.

New Possibilities for Cancer Treatment

Dr. Sam Orange, Senior Lecturer in Clinical Exercise Physiology at Newcastle University and lead author of the study, said: “What’s remarkable is that exercise doesn’t just benefit healthy tissues, it sends powerful signals through the bloodstream that can directly influence thousands of genes in cancer cells.

“It’s an exciting insight because it opens the door to find ways that mimic or augment the biological effects of exercise, potentially improving cancer treatment and, crucially, patient outcomes.

“In the future, these insights could lead to new therapies that imitate the beneficial effects of exercise on how cells repair damaged DNA and use fuel for energy.”

Slowing Cancer Growth at the Cellular Level

The research team found that exercise increased the activity of genes that support mitochondrial energy metabolism. This helps cells use oxygen more efficiently.

At the same time, genes linked to rapid cell division were turned down, which may make cancer cells less aggressive. Blood collected after exercise also boosted DNA repair, activating a key repair gene known as PNKP.

The study included 30 volunteers, both men and women between the ages of 50 and 78. All participants were overweight or obese (a risk factor of cancer) but otherwise healthy.

Each volunteer completed a short but intense cycling test that lasted about 10 minutes. Researchers then collected blood samples and examined 249 proteins. Thirteen of those proteins increased after exercise, including interleukin-6 (IL-6), which plays a role in repairing damaged DNA.

Why Even One Workout Matters

Dr. Orange, a Clinical Exercise Physiologist at The Newcastle upon Tyne Hospitals NHS Foundation Trust, said: “These results suggest that exercise doesn’t just benefit healthy tissues, it may also create a more hostile environment for cancer cells to grow.

“Even a single workout can make a difference. One bout of exercise, lasting just 10 minutes, sends powerful signals to the body.

“It’s a reminder that every step, every session, counts when it comes to doing your best to protect your health.”

Bowel Cancer Rates and Physical Activity

Bowel cancer is the 4th most common cancer in the UK, after breast, prostate and lung cancer.

In the UK, one person is diagnosed with bowel cancer every 12 minutes, adding up to nearly 44,000 cases each year. Someone dies from the disease every 30 minutes.

Researchers estimate that regular physical activity lowers bowel cancer risk by about 20%. Exercise does not have to mean gym workouts or sports. Walking or biking to work, along with everyday activities such as gardening or cleaning, can also contribute.

Looking ahead, the research team plans to examine whether repeated exercise sessions lead to long-lasting biological changes. They also aim to study how exercise-related effects interact with common cancer treatments such as chemotherapy and radiotherapy.

The study, conducted by researchers at NYU Langone Health and NYC Health + Hospitals, showed that surgery patients lost an average of 58 pounds over two years. In contrast, patients who were prescribed a GLP-1 drug for at least six months lost about 12 pounds. That translates to 24% total weight loss for surgery patients compared with 4.7% for those using medication. Even among patients who stayed on GLP-1 therapy continuously for a full year, average weight loss reached only 7%, still far below the results seen with surgery.

Real-World Results Fall Short of Clinical Trials

“Clinical trials show weight loss between 15% to 21% for GLP-1s, but this study suggests that weight loss in the real world is considerably lower even for patients who have active prescriptions for an entire year. We know as many as 70% of patients may discontinue treatment within one year,” said lead author Avery Brown, MD, a surgical resident at NYU Langone Health. “GLP-1 patients may need to adjust their expectations, adhere more closely to treatment or opt for metabolic and bariatric surgery to achieve desired results.”

The findings highlight a key gap between controlled clinical trials and everyday use, where side effects, costs, and long-term adherence can limit the effectiveness of medication-based weight loss.

How the Study Compared Surgery and GLP-1 Medications

Researchers analyzed electronic medical record data from patients treated between 2018 and 2024 within the NYU Langone Health and NYC Health + Hospitals systems. All participants had a body mass index (BMI) of at least 35 and either underwent bariatric surgery (sleeve gastrectomy or Roux en-Y gastric bypass) or received a prescription for injectable semaglutide or tirzepatide.

After adjusting for factors such as age, BMI, and co-morbidities using average treatment effect weighting, the team compared outcomes for 51,085 patients across both groups. The study was supported by NYU CTSA grant KL2 TR001446 from the National Center for Advancing Translational Sciences at the National Institutes of Health (NIH).

Future Research and Treatment Decisions

“In future studies we will aim to identify what healthcare providers can do to optimize GLP-1 outcomes, identify which patients are better treated with bariatric surgery versus GLP-1s, and determine the role out-of-pocket costs play in treatment success,” said senior author Karan R. Chhabra, MD, MSc, a bariatric surgeon and Assistant Professor of Surgery and Population Health at NYU Grossman School of Medicine.

GLP-1 drugs have gained widespread attention, with about 12% of Americans reporting they have taken one at some point and 6% saying they currently use them. However, persistence remains a major challenge. Recent research shows that 53.6% of patients with overweight or obesity stop GLP-1 therapy within one year (53.6%), and that figure rises to 72.2% by two years.

At the same time, bariatric surgery remains underused. According to the ASMBS, more than 270,000 metabolic and bariatric procedures were performed in 2023, representing only about 1% of people who meet BMI eligibility criteria.

“While both patient groups lose weight, metabolic and bariatric surgery is much more effective and durable,” said ASMBS President Ann M. Rogers, MD, FACS, FASMBS, who was not involved in the study. “Those who get insufficient weight loss with GLP-1s or have challenges complying with treatment due to side effects or costs, should consider bariatric surgery as an option or even in combination.”

Obesity Remains a Major Health Challenge

According to the U.S. Centers for Disease Control and Prevention (CDC), obesity affects 40.3% of adults in the United States, while severe obesity impacts 9.4%. Research shows obesity can impair immune function, drive chronic inflammation, and raise the risk of many serious conditions, including cardiovascular disease, stroke, type 2 diabetes, and certain cancers.

*Semaglutide is the active ingredient in Ozempic and Wegovy and tirzepatide is the active ingredient in Zepbound and Mounjaro.

• New cancer cases worldwide have more than doubled since 1990, reaching 18.5 million in 2023. Over the same period, annual cancer deaths rose by 74 percent to 10.4 million (both excluding non-melanoma skin cancers), with most cases now occurring in low- and middle-income countries.
• More than 40 percent of cancer deaths globally are linked to 44 modifiable risk factors, including tobacco use, unhealthy diets, and high blood sugar. This means a large share of cancer deaths could be prevented through proven public health measures.
• Looking ahead, researchers predict global cancer cases will increase by 61 percent over the next 25 years, reaching 30.5 million new diagnoses a year by 2050. Annual cancer deaths are forecast to rise by nearly 75 percent to 18.6 million, largely driven by population growth and aging populations.
• While age-adjusted cancer death rates have declined worldwide, this progress has not reached everyone. In several low- and middle-income countries, both cancer rates and total deaths continue to rise.
• The researchers stress that responding to this growing cancer burden will require stronger action from governments and policymakers, including expanded prevention efforts, earlier diagnosis, and better access to effective treatment at national, regional, and global levels.

A Rapid Global Rise in Cancer

The global burden of cancer has grown dramatically over the past three decades. Since 1990, the number of newly diagnosed cancer cases worldwide has more than doubled, reaching 18.5 million in 2023. Over the same period, annual cancer deaths rose by 74 percent to 10.4 million (both excluding non-melanoma skin cancers). Most of those affected now live in low- and middle-income countries.

A significant share of this burden is linked to preventable causes. More than 40 percent of cancer deaths worldwide are associated with 44 modifiable risk factors, including tobacco use, poor diet, and high blood sugar. This connection highlights major opportunities to reduce cancer deaths through prevention.

Looking ahead, researchers project that new cancer cases will climb another 61 percent over the next 25 years, reaching 30.5 million annually by 2050. Cancer deaths are forecast to rise by nearly 75 percent over the same period, reaching 18.6 million per year. These increases are largely driven by population growth and the continued aging of populations worldwide.

While age-adjusted global cancer death rates have declined overall, this progress has not been evenly shared. In several low- and middle-income countries, both the number of cancer deaths and the rates themselves are still increasing. The authors stress that meeting this growing challenge will require stronger efforts from governments and policymakers to prevent cancer, expand early diagnosis, and improve treatment access at national, regional, and global levels.

Projections Warn of a Growing Crisis

Between 1990 and 2023, global cancer cases and deaths rose sharply despite advances in treatment and expanded efforts to address cancer risk factors. Without urgent action and increased funding, researchers estimate that by 2050, 30.5 million people will receive a new cancer diagnosis each year and 18.6 million will die from the disease. More than half of new cases and nearly two-thirds of deaths are expected to occur in low- and middle-income countries (LMICs), according to a major analysis by the Global Burden of Disease Study Cancer Collaborators published in The Lancet.

Although the total number of cancer cases and deaths is projected to increase significantly between 2024 and 2050, age-adjusted incidence and mortality rates are not expected to rise globally. This suggests that most of the growth in cancer burden will be driven by demographic changes rather than worsening individual risk.

Even so, the projected improvements fall well short of the United Nations Sustainable Development Goal (SDG) to cut premature deaths from non-communicable diseases, including cancer, by one-third by 2030.

Experts Call for Greater Global Action

“Cancer remains an important contributor to disease burden globally and our study highlights how it is anticipated to grow substantially over the coming decades, with disproportionate growth in countries with limited resources,” said lead author Dr. Lisa Force from the Institute for Health Metrics and Evaluation (IHME), University of Washington, USA. “Despite the clear need for action, cancer control policies and implementation remain underprioritized in global health, and there is insufficient funding to address this challenge in many settings.”

She added, “Ensuring equitable cancer outcomes globally will require greater efforts to reduce disparities in health service delivery such as access to accurate and timely diagnosis, and quality treatment and supportive care.”

The analysis draws on data from population-based cancer registries, vital registration systems, and interviews with family members or caregivers of people who died from cancer. It provides updated global, regional, and national estimates covering 1990 to 2023 across 204 countries and territories, examining 47 cancer types or groupings and 44 attributable risk factors.^[1] The study also projects the global cancer burden through 2050 and evaluates progress toward the UN SDG target for reducing non-communicable disease deaths between 2015 and 2030.

Uneven Cancer Burden Across Countries

In 2023, global cancer deaths reached 10.4 million, while new cases climbed to 18.5 million (both excluding non-melanoma skin cancers). Compared with 1990, this represents increases of 74 percent in deaths and 105 percent in new cases.

Despite an overall 24 percent decline in age-standardized cancer death rates worldwide between 1990 and 2023, this improvement has largely occurred in high- and upper-middle-income countries. In contrast, age-standardized cancer incidence increased by 24 percent in low-income countries and by 29 percent in lower-middle-income countries, highlighting growing disparities in regions with fewer resources (see table 1 in paper).

From 1990 to 2023, Lebanon recorded the largest percentage increase in age-standardized cancer incidence and mortality rates for both sexes combined. Over the same period, the United Arab Emirates experienced the greatest decline in age-standardized incidence, while Kazakhstan saw the largest decrease in age-standardized death rates.

Breast cancer was the most commonly diagnosed cancer worldwide in 2023 for both sexes combined. Tracheal, bronchus, and lung (TBL) cancer remained the leading cause of cancer deaths globally (see table 2 in paper).

Preventable Risks Drive Millions of Deaths

The study estimates that 42 percent (4.3 million) of the 10.4 million cancer deaths in 2023 were linked to 44 modifiable risk factors, pointing to significant opportunities for prevention.

Behavioral risk factors accounted for the largest share of cancer deaths across all income levels in 2023. Tobacco use alone contributed to 21 percent of cancer deaths worldwide. Tobacco was the leading risk factor in every income group except low-income countries, where unsafe sex was the primary risk factor, linked to 12.5 percent of cancer deaths.

Men were more likely than women to die from cancers associated with modifiable risks. In 2023, 46 percent of cancer deaths in men were linked to factors such as tobacco use, unhealthy diet, high alcohol consumption, occupational risks, and air pollution. Among women, 36 percent of cancer deaths were associated with modifiable risks, with tobacco, unsafe sex, unhealthy diet, obesity, and high blood sugar playing the largest roles (see appendix 2 table 6).

“With four in 10 cancer deaths linked to established risk factors, including tobacco, poor diet, and high blood sugar, there are tremendous opportunities for countries to target these risk factors, potentially preventing cases of cancer and saving lives, alongside improving accurate and early diagnosis and treatment to support individuals who develop cancer,” said co-author Dr. Theo Vos from IHME. “Reducing the burden of cancer across countries and worldwide demands both individual action and effective population-level approaches to reduce exposure to known risks.”

Equity and Prevention as Global Priorities

The researchers emphasize that cancer prevention must be integrated into health policies in LMICs and that equitable cancer control efforts are essential to ensure timely and effective care for all patients.

“The rise of cancer in LMICs is an impending disaster,” said co-author Dr. Meghnath Dhimal from the Nepal Health Research Council. “There are cost-effective interventions for cancer in countries at all stages of development. These cancer burden estimates can help broaden the discussion around the importance of cancer and other non-communicable diseases in the global health agenda. To control the growth of non-communicable diseases including cancer in LMICs, an interdisciplinary approach for evidence generation and multi-sectoral collaboration and coordination for implementation are urgently needed.”

Dr. Force noted that the findings can help guide future policy. “These new estimates and forecasts can support governments and the global health community in developing data informed policies and actions to improve cancer control and outcomes around the world. They can also support tracking of progress towards global and regional cancer targets.”

She added, “Our analysis also highlights the need for more data from sources such as cancer and vital registries, particularly in lower resource settings. Supporting cancer surveillance systems is crucial to informing both a local and global understanding of cancer burden.”

Study Limitations and Data Gaps

The authors acknowledge several limitations. The estimates rely on the best available data but are constrained by gaps in high-quality cancer data, especially in resource-limited countries. Current Global Burden of Disease estimates do not account for several infectious diseases known to increase cancer risk in some lower-income regions, including Helicobacter Pylori and Schistosoma haematobium, which may lead to underestimation of cancer deaths linked to modifiable risks.

The projections also do not incorporate the effects of the COVID-19 pandemic, recent conflicts, or future medical breakthroughs that could significantly alter cancer trends.

In a linked Comment, Dr. Qingwei Luo and Dr. David P Smith from The University of Sydney and Cancer Council NSW, who were not involved in the study, wrote: “To ensure meaningful progress in reducing the global cancer burden, it is imperative that governments prioritize funding, strengthen health systems, reduce inequalities, and invest in robust cancer control initiatives and research on prevention, intervention, and implementation — because the future of cancer control depends on decisive, collective action today.”

Notes

1. Modifiable Risk Factors
   • Level 1: Behavioral, Environmental / Occupational, Metabolic
   • Level 2: Air pollution, Dietary risks, Drug use, High alcohol use, High body-mass index, High fasting plasma glucose, Low physical activity, Occupational risks, Other environmental risks, Tobacco, unsafe sex.
   • Level 3: Chewing tobacco, Diet high in processed meat, Diet high in red meat, Diet high in sodium, Diet low in calcium, Diet low in fibre, Diet low in fruits, Diet low in milk, Diet low in vegetables, Diet low in whole grains, Occupational carcinogens, Particulate matter pollution, Residential radon, Second-hand smoke, Smoking
   • Level 4: Ambient particulate matter pollution, Household air pollution from solid fuels, Occupational exposure to arsenic, Occupational exposure to asbestos, Occupational exposure to benzene, Occupational exposure to beryllium, Occupational exposure to cadmium, Occupational exposure to chromium, Occupational exposure to diesel engine exhaust, Occupational exposure to formaldehyde, Occupational exposure to nickel, Occupational exposure to polycyclic aromatic hydrocarbons, Occupational exposure to silica, Occupational exposure to sulfuric acid, Occupational exposure to trichloroethylene

The study was funded by the Gates Foundation, St Jude Children’s Research Hospital, and St Baldrick’s Foundation. It was conducted by the GBD 2023 Cancer Collaborators.

“Our new estimates increase the organic compound emissions from wildland fires by about 21%,” says Lyuyin Huang, the first author of the study. “The inventory provides a foundation for more detailed air-quality modeling, health-risk assessment, and climate-related policy analysis.”

Each year, wildfires burn through vast areas of vegetation, sending a complex mixture of water vapor, ash, and carbon-based chemicals into the atmosphere. Some of these chemicals are volatile organic compounds (VOCs), which readily exist as gases. Others only evaporate and become gases at warmer temperatures and are classified as intermediate- and semi-volatile organic compounds (IVOCs and SVOCs, respectively). Once in the air, these partially volatile compounds more easily form fine particles that can be harmful if breathed in, compared with VOCs.

Overlooked chemicals in wildfire smoke

Despite their importance, IVOCs and SVOCs are often missing from wildfire emission studies. Their large numbers and chemical complexity make them difficult to measure, leading many past assessments to focus mainly on VOCs. Researchers led by Shuxiao Wang aimed to include IVOCs and SVOCs alongside VOCs to better capture how wildland fires affect air quality, human health, and climate.

To do this, the team first examined a global database tracking burned land from forest, grass, and peatland wildland fires between 1997 and 2023. They then gathered information on the VOCs, IVOCs, SVOCs, and other extremely low volatility organic compounds released as different types of vegetation burn. When direct field measurements were not available, the researchers relied on laboratory experiments to estimate the chemicals produced. These data were combined to calculate yearly wildfire emissions worldwide.

Global totals and pollution hotspots

Using this approach, the researchers estimated that wildland fires released an average of 143 million tons of airborne organic compounds each year during the study period. This figure is about 21% higher than previous estimates, indicating that wildfire emissions, particularly IVOCs and SVOCs, contribute more to air pollution than scientists had recognized.

When wildfire emissions were compared with earlier estimates of pollution from human activities, the researchers found that human sources produced more airborne compounds overall. However, both sources released similar amounts of IVOCs and SVOCs. The comparison also revealed shared emission hotspots, including Equatorial Asia, Northern Hemisphere Africa, and Southeast Asia. According to the researchers, air pollution in these regions is especially complex and will require different strategies to reduce emissions from both wildfires and human activities.

The authors acknowledge funding from the National Natural Science Foundation of China, National Key R&D Program of China, the Samsung Advanced Institute of Technology, and the Center of High Performance Computing at Tsinghua University.

New research from the University of California, Riverside offers fresh insight into why this decline occurs. The study, published in the Proceedings of the National Academy of Sciences, points to malfunctioning mitochondria as a major contributor to the progressive breakdown of cerebellar neurons known as Purkinje cells. The loss of these cells appears closely tied to worsening movement problems in people with MS.

Inflammation, Myelin Loss, and Energy Failure

MS is defined by ongoing inflammation and demyelination within the central nervous system. Demyelination is the process in which the myelin sheath — a protective, insulating layer surrounding nerve fibers in the brain and spinal cord — is damaged or destroyed. Without this insulation, electrical signals struggle to travel efficiently along nerves, leading to a wide range of neurological symptoms.

Mitochondria play a different but equally critical role. These structures supply most of a cell’s energy, which is why they are often called the “powerhouses” of the cell.

“Our study, conducted by my graduate student Kelley Atkinson, proposes that inflammation and demyelination in the cerebellum disrupt mitochondrial function, contributing to nerve damage and Purkinje cell loss,” said Seema Tiwari-Woodruff, a professor of biomedical sciences in the UC Riverside School of Medicine, who led the research team. “We observed a significant loss of the mitochondrial protein COXIV in demyelinated Purkinje cells, suggesting that mitochondrial impairment contributes directly to cell death and cerebellar damage.”

Why Purkinje Cells Matter

Everyday movements such as walking, reaching, or maintaining balance rely on tight coordination between muscles, sensory organs, and multiple brain regions. The cerebellum plays a central role in this process.

“Inside the cerebellum are special cells called Purkinje neurons,” Tiwari-Woodruff said. “These large, highly active cells help coordinate smooth, precise movements — like dancing, throwing a ball, or even just walking. They’re essential for balance and fine motor skills.”

In MS and related neurological diseases, damage to the cerebellum often leads to the gradual death of Purkinje cells. As these neurons disappear, people may develop ataxia, a condition marked by poor coordination and unstable movement.

“Our research looked at brain tissue from MS patients and found major issues in these neurons: they had fewer branches, were losing myelin, and had mitochondrial problems — meaning their energy supply was failing,” Tiwari-Woodruff said. “Because Purkinje cells play such a central role in movement, their loss can cause serious mobility issues. Understanding why they’re damaged in MS could help us find better treatments to protect movement and balance in people with the disease.”

Evidence From an MS Mouse Model

To better understand how these changes unfold, the researchers also studied experimental autoimmune encephalomyelitis (EAE) — a mouse model that develops MS-like symptoms. This allowed them to track mitochondrial changes as the disease progressed.

Over time, the mice experienced a steady decline in Purkinje cells, mirroring what is seen in human MS.

“The remaining neurons don’t work as well because their mitochondria, the energy-producing parts, start to fail,” Tiwari-Woodruff said. “We also saw that the myelin breaks down early in the disease. These problems — less energy, loss of myelin, and damaged neurons — start early, but the actual death of the brain cells tends to happen later, as the disease becomes more severe. The loss of energy in brain cells seems to be a key part of what causes damage in MS.”

Although the EAE model does not replicate every feature of MS, its similarities to the human condition make it a powerful tool for studying neurodegeneration and testing new therapeutic approaches.

Targeting Mitochondria as a Treatment Strategy

“Our findings offer critical insights into the progression of cerebellar dysfunction in MS,” Tiwari-Woodruff said. “Targeting mitochondrial health may represent a promising strategy to slow or prevent neurological decline and improve quality of life for people living with MS. This research brings us a step closer to understanding the complex mechanisms of MS and developing more effective, targeted treatments for this debilitating disease.”

What Comes Next

The research team is now exploring whether mitochondrial damage extends beyond Purkinje cells to other cerebellar cell types, including oligodendrocytes, which help form white matter, and astrocytes, which support overall brain function.

“To answer this, one of our ongoing research projects is focused on studying mitochondria in specific types of brain cells in the cerebellum,” Tiwari-Woodruff said. “Such research can open the door to finding ways to protect the brain early on — like boosting energy in brain cells, helping them repair their protective myelin coating, or calming the immune system before too much damage is done. This is especially important for people with MS who struggle with balance and coordination, as these symptoms are tied to damage in the cerebellum.”

The Importance of Continued Research

Tiwari-Woodruff stressed the broader importance of sustained investment in medical research.

“Cutting funding to science only slows progress when we need it most,” she said. “Public support for research matters now more than ever.”

The study was conducted by Tiwari-Woodruff and Atkinson alongside Shane Desfor, Micah Feria, Maria T. Sekyia, Marvellous Osunde, Sandhya Sriram, Saima Noori, Wendy Rincóna, and Britany Belloa.

Researchers analyzed postmortem cerebellar tissue from individuals with secondary progressive MS and compared it with tissue from healthy donors. The samples were obtained from the National Institutes of Health’s NeuroBioBank and the Cleveland Clinic.

Funding for the study was provided by the National Multiple Sclerosis Society.

The research paper is titled “Decreased mitochondrial activity in the demyelinating cerebellum of progressive multiple sclerosis and chronic EAE contributes to Purkinje cell loss.”

A new study published in Light: Science & Applications reports a major advance in this area. Researchers from the Humboldt-Universität zu Berlin, the Leibniz Institute of Photonic Technology, and the University of Stuttgart have introduced a new type of quantum memory built from 3D-nanoprinted structures known as “light cages” filled with atomic vapor. By bringing both light and atoms together on a single chip, the team has created a platform designed for scalability and seamless integration into quantum photonic systems.

What Makes Light Cages Different

Light cages are hollow-core waveguides engineered to tightly guide light while still allowing access to the space inside. This design offers a key advantage over conventional hollow-core fibers, which can take months to fill with atomic vapor. In contrast, the open structure of light cages lets cesium atoms diffuse into the core much more quickly, cutting the filling process down to just a few days without sacrificing optical performance.

The structures are fabricated using two-photon polymerization lithography with commercial 3D printing systems. This approach allows researchers to directly print intricate hollow-core waveguides onto silicon chips with extremely high precision. To protect the devices from chemical reactions with cesium, the waveguides are coated with a protective layer. Tests showed no signs of degradation even after five years of operation, highlighting the system’s long-term stability.

“We created a guiding structure that allows quick diffusion of gases and fluids inside its core, with the versatility and reproducibility provided by the 3D-nanoprinting process. This enables true scalability of this platform, not only for intra-chip fabrication of the waveguides but also inter-chip, for producing multiple chips with the same performance,” explained the research team.

Turning Light Into Stored Quantum Information

Inside the light cages, incoming light pulses are efficiently converted into collective excitations of the surrounding atoms. After a chosen storage time, a control laser reverses this process and releases the stored light exactly when needed. In a key demonstration, the researchers successfully stored very weak light pulses containing only a few photons for several hundred nanoseconds. They believe this approach can eventually be extended to store single photons for many milliseconds.

Another major milestone was the integration of multiple light cage memories on a single chip placed inside a cesium vapor cell. Measurements showed that different light cages with the same design delivered nearly identical storage performance across two separate devices on the same chip. This level of consistency is essential for building scalable quantum systems.

The strong reproducibility comes from the precision of the 3D-nanoprinting process. Variations within a single chip were kept below 2 nanometers, while differences between chips remained under 15 nanometers. Such tight control is critical for spatial multiplexing, a technique that could dramatically increase the number of quantum memories operating together on one device.

Implications for Quantum Networks and Computing

Light cage quantum memories address several long-standing challenges in quantum technology. In quantum repeater networks, they could synchronize multiple single photons at the same time, greatly boosting the efficiency of long-distance quantum communication. In photonic quantum computing, the memories provide controlled delays that are needed for feed-forward operations in measurement-based quantum computing systems.

The platform also stands out for its practicality. Unlike many competing technologies, it operates slightly above room temperature and does not require cryogenic cooling or complex atom-trapping setups. This makes the system easier to deploy while also offering higher bandwidth per memory mode. The ability to produce many identical quantum memories on a single chip opens a clear path toward large-scale quantum photonic integration.

Thanks to its flexible fabrication process, the technology can potentially be combined with direct fiber coupling and existing photonic components. These advantages position light cage quantum memories as a strong candidate for future quantum communication infrastructure.

A Scalable Path Forward

The development of light cage quantum memories marks a significant step in quantum photonic research. By merging advanced 3D-nanoprinting with core principles of quantum optics, the researchers have created a compact, scalable system that could speed the arrival of practical quantum networks and more powerful quantum computers.

Liver fibrosis is a common but often overlooked condition that affects hundreds of millions of people worldwide. Over time, it can worsen into cirrhosis or liver cancer. Even after decades of scientific effort, there are still no antifibrotic drugs approved for clinical use.

The disease develops when repeated or long-term liver damage — caused by viral hepatitis, excessive alcohol use, metabolic disorders, toxins, or autoimmune disease — triggers an overactive healing response. A major driver of this process is the activation of hepatic stellate cells (HSCs). Under normal conditions, these cells remain inactive. When injury occurs, they switch into collagen-producing cells that build up scar tissue in the liver.

This harmful transformation is controlled by several overlapping signaling systems, including TGF-β, PDGF, and Wnt/β-catenin pathways. Because fibrosis involves many biological routes at once, drugs that target only one pathway often have limited success. This complexity has fueled growing interest in combination treatments that can block multiple drivers of disease at the same time.

A New Use for Two Familiar Drugs

A study published in Targetome on December 15, 2025 by Hong Wang’s & Haiping Hao’s team, China Pharmaceutical University, reports that a fixed-dose combination of silybin and carvedilol can strongly suppress hepatic stellate cell activation. By targeting Wnt4/β-catenin signaling, the drug pair was able to reverse liver fibrosis in experimental models, offering a promising strategy for a disease that currently lacks approved therapies.

To better understand silybin’s potential and its limitations, the researchers combined laboratory experiments, animal studies, phenotype-based drug screening, and molecular analysis. Early tests focused on liver cell injury models triggered by ActD/TNFα, tBHP, and TNFα. These experiments showed that silybin effectively protected liver cells by restoring viability, lowering harmful reactive oxygen species, and reducing inflammatory gene activity. It also showed strong antiapoptotic, antioxidative, and anti-inflammatory effects without detectable toxicity.

However, when researchers examined whether silybin could directly stop fibrosis, the results were less impressive. In human LX-2 and rat HSC-T6 stellate cells stimulated with TGFβ1, silybin only slightly lowered key fibrosis-related markers such as COL1A1, COL1A2, ACTA2, and TGFB. Similar patterns appeared in mice with liver fibrosis caused by carbon tetrachloride exposure. While silybin led to modest improvements in liver enzymes, collagen buildup, and fibrotic gene expression, its benefits appeared to come mainly from protecting liver cells rather than directly blocking stellate cell activation.

Finding the Right Partner Drug

To overcome this limitation, the research team screened 397 FDA-approved drugs using a COL1A1-luciferase reporter system to identify compounds that could enhance silybin’s antifibrotic effect. Carvedilol emerged as the strongest synergistic partner.

When used together, silybin and carvedilol sharply reduced collagen production and stellate cell activation in human and rat cell cultures, as well as in primary hepatic stellate cells. In every case, the combination outperformed either drug on its own.

Further testing in animals showed that a fixed-dose ratio of 50:1 (silybin to carvedilol) produced the most consistent and powerful results. This optimized pairing significantly reduced liver injury, inflammation, and fibrosis severity in mice. The effects increased with dose and were stronger than those seen with obeticholic acid.

How the Drug Duo Stops Liver Scarring

Mechanistic studies revealed why the combination works so well. Together, silybin and carvedilol shut down the Wnt/β-catenin signaling pathway more effectively than either drug alone. This includes suppressing the Wnt ligand Wnt4 and reducing downstream β-catenin activity. These findings provide a clear molecular explanation for the combination’s strong antifibrotic effects.

A Fast Track Toward Clinical Use

The study highlights a realistic treatment strategy based on drug repurposing and carefully designed combination therapy. Both silybin and carvedilol are already widely used in clinical practice, have established safety records, and are low in cost. As a result, their combined use could move quickly into clinical testing and help address a major unmet medical need.

Beyond liver fibrosis, the research also demonstrates how phenotype-based screening can reveal powerful and unexpected drug partnerships that may be hiding in plain sight.

Funding and Support

This work was supported by the Major State Basic Research Development Program of China (2022YFA1303800 and 2021YFA1301300); the National Natural Science Foundation of China (82373946, 82073926, 82321005, 82530122, and 81930109); Major Science and Technology Project of Jiangsu Province (BG2024045); Overseas Expertise Introduction Project for Discipline Innovation (G20582017001); the Project of State Key Laboratory of Natural Medicines, China Pharmaceutical University (SKLNMZZ202402); and the Project Program of Basic Science Research Center Base (Pharmaceutical Science) of Yantai University (P202404).