Scientists at Weill Cornell Medicine discovered a previously unknown link between two key pathways that regulate the immune system in mammals — a finding that impacts our understanding of chronic inflammatory bowel diseases (IBD). This family of disorders severely impacts the health and quality of life of more than 2 million people in the United States.
The immune system has many pathways to protect the body from infection, but sometimes an overactive immune response results in autoimmune diseases including IBD, psoriasis, rheumatoid arthritis and multiple sclerosis. Interleukin-23 (IL-23) is one such immune factor that fights infections but is also implicated in many of these inflammatory diseases. However, it was unknown why IL-23 is sometimes beneficial, and other times becomes a driver of chronic disease.
In the study, published June 12 in Nature, the team found that IL-23 acts on group 3 innate lymphoid cells (ILC3s), a family of immune cells that are a first line of defense in mucosal tissues such as the intestines and lungs. In response, ILC3s increase activity of CTLA-4, a key regulatory factor that prevents the immune system from attacking the body and beneficial gut microbiota. This interaction critically balances the pro-inflammatory effects IL-23 to maintain gut health, but is impaired in IBD.
The findings identify ILC3s as a critical link between potent IL-23 driven inflammatory response and checkpoints for immune regulation in the intestine. It also provides clues on how to harness this pathway to fight cancer and alleviate a serious side effect of cancer immunotherapy.
“We were surprised to uncover the unexpected connection between these two major immune pathways that control health, immunity and inflammation,” said senior author Dr. Gregory Sonnenberg, the Henry R. Erle, M.D.-Roberts Family Professor of Medicine, head of basic research in the Division of Gastroenterology & Hepatology and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine. “Until now most research on CTLA-4 focused on T cells, another type of immune cell. By uncovering that it is selectively upregulated on ILC3s by IL-23, this demonstrates that we should be thinking about these pathways more broadly to develop more selective therapeutics.”
When Inflammation is Out of Control
“IL-23 normally provides tissue protection in the gut, but something changes in chronic inflammatory diseases which makes IL-23 a key driver of tissue pathology, and that’s what we decided to investigate,” said the paper’s lead author, postdoctoral researcher Dr. Anees Ahmed.

The investigators used single-cell RNA sequencing to study the effects of IL-23 on different types of immune cells in the healthy intestine. This analysis revealed that IL-23 in the healthy gut potently turns on the CTLA-4 pathway in ILC3s. They then showed that blocking the CTLA-4 pathway in those cells led to severe intestinal inflammation.
To see if their results applied to humans, the investigators turned to the Jill Roberts Institute Live Cell Bank, which includes deidentified samples from people with IBD as well as healthy individuals. “This unique resource enabled us to quickly confirm that our findings in mice were relevant to IBD patients,” said Dr. Sonnenberg.
They then verified this finding in patients through collaboration with Dr. Robbyn Sockolow, professor of clinical pediatrics and chief of the Division of Pediatric Gastroenterology, Hepatology and Nutrition in the Department of Pediatrics at Weill Cornell Medicine and a pediatric gastroenterologist at NewYork-Presbyterian Komansky Children’s Hospital and Center for Advanced Digestive Care.
With Dr. Sockolow, they found evidence that this novel immunologic pathway exists in the healthy human intestine and becomes impaired in the inflamed intestine of IBD patients. “This may provide a new explanation of why IL-23 becomes a driver of intestinal inflammation in human IBD,” said Dr. Sockolow.
Implications for Cancer and Associated Immunotherapy
This study also suggests that this pathway may be harnessed to fight cancer and may explain why people receiving certain immunotherapy drugs often experience inflammation in the gut as a side effect. Immunotherapy drugs that block CTLA-4 are used to take the brakes off the immune system — allowing it to fight cancer. These new results suggest that CTLA-4 on ILC3 cells and other related innate or innate-like lymphocytes should be considered in fighting cancer. Further, it suggests that blocking CTLA-4 on ILC3s may lead to severe gut inflammation which can cause patients to discontinue their cancer treatment.
Much more research is needed before these findings can be applied to new treatments. Dr. Ahmed said that eventually it may be possible to develop more targeted treatments that avoid ILC3s in the gut or simultaneously block IL-23. “In the future, we may be able to find ways to selectively block CTLA-4 or IL-23 in specific immune cells,” he said. “If we could manage it, that could lead to a breakthrough in fighting cancer while protecting the gut from inflammation.”
The findings could also have long-term applications in developing new treatments for a range of autoimmune diseases known to be mediated by IL-23. Drugs that target IL-23 already exist, and potentially we could make next-generation therapies that don’t completely block IL-23 since it is still needed to fight infection but instead control the underlying mechanisms of IL-23-driven chronic inflammatory diseases, Dr. Sonnenberg said.

Women live longer than men. This isn’t unique to humans, either; we see this trend in a wide range of other animals. Biologists have theorized that the discrepancy in life expectancy between sexes might be partly related to reproduction, but how?
In a study published in Science Advances, researchers from Osaka University have discovered for the first time that germ cells, the cells that develop into eggs in females and sperm in males, drive sex-dependent lifespan differences in vertebrate animals.
The researchers examined aging in the turquoise killifish, a small, fast-growing freshwater fish with a lifespan of only a few months. As in humans, female killifish live longer than males. However, when the researchers removed the germ cells from these fish, they found that males and females had similar lifespans.
“After removing the germ cells, male killifish lived longer than usual and female lifespans became shorter,” explains lead author Kota Abe. “We wanted to understand how germ cells could affect males and females so differently. Our next step was to investigate the factors responsible.”
The team found that hormonal signaling was very different in females than in males. Female killifish without germ cells had significantly less estrogen signaling, which can shorten lifespan by increasing cardiovascular disease risk. The females also had significantly more growth factor signaling (insulin-like growth factor 1). This made the females grow larger while also suppressing signals within the body important for maintaining health and slowing aging.
In contrast, male killifish without germ cells had improved muscle, skin, and bone health. Interestingly, these fish had increased amounts of a substance that activates vitamin D, as well as evidence of vitamin D signaling in their muscles and skin.
Vitamin D can also be considered a hormone; while well known for keeping bones strong and healthy, it also seems to have wider positive effects throughout the body. The team’s results pointed to the possibility that vitamin D can improve longevity, leading them to test whether a vitamin D supplement could increase the lifespan of the fish.
“When we administered active vitamin D, we found that the lifespans of both males and females were significantly extended, suggesting that vitamin D signaling provides health benefits throughout the body,” explains senior author Tohru Ishitani. “Our work suggests that vitamin D signaling could influence the longevity of other vertebrates, including humans.”
The discovery that germ cells affect male and female longevity in opposing ways is an important clue in unravelling the mysterious interactions between reproduction, aging, and lifespan. It’s unclear exactly how vitamin D fits into this puzzle, but it could be part of future strategies to extend healthy lifespans.

In a feat aimed at understanding how cells move and creating new ways to shuttle drugs through the body, scientists at Johns Hopkins Medicine say they have built a minimal synthetic cell that follows an external chemical cue and demonstrates a governing principle of biology called “symmetry breaking.”
The findings are published June 12 in Science Advances.
A step that precedes the movement of a cell, symmetry breaking, happens when a cell’s molecules, which are initially arranged symmetrically, reorganize into an asymmetric pattern or shape, usually in response to stimuli. This is similar to how migrating birds break symmetry when they shift into a new formation in response to an environmental compass like sunlight or landmarks. On a microscopic level, immune cells sense chemical signals concentrated at an infection site and break symmetry to traverse a blood vessel wall to reach the infected tissue. As cells break symmetry, they transform into polarized and asymmetric structures that prepare them to move toward their target.
“The notion of symmetry breaking is crucial to life, impacting fields as diverse as biology, physics and cosmology,” says Shiva Razavi, Ph.D., who led the research as a graduate student at Johns Hopkins and is now a postdoctoral fellow at Massachusetts Institute of Technology. “Understanding how symmetry breaking works is key to unlocking the fundamentals of biology and discovering how to harness this information to devise therapeutics.”
Finding ways to mimic and control symmetry breaking in synthetic cells has long been considered essential for understanding how cells can survey their chemical environment and rearrange their chemical profile and shape in response.
For this study scientists created a giant vesicle with a double-layered membrane — a bare-bones, simplified synthetic cell or protocell made of phospholipids, purified proteins, salts and ATP that provides energy. With its spherical shape, the protocell is nicknamed “the bubble.” In their experiments, the scientists successfully engineered the protocell with a chemical-sensing ability that prompts the cell to break symmetry, changing from a nearly perfect sphere to an uneven shape. The system was specifically designed to mimic the first step in an immune response, able to signal for neutrophils to attack germs based on proteins they sense around them, the researchers say.
“Our study demonstrates how a cell-like entity can sense the direction of an external chemical cue, mimicking the conditions you would find in a living organism,” Razavi says. “By building a cell-like structure from scratch, we can better identify and understand the essential components required for a cell to break symmetry in its most simplified form.”
One day chemical sensing could be used for targeted drug delivery within the body, the scientists say.

“The idea is that you can package anything you want into these bubbles — protein, RNA, DNA, dyes or small molecules — tell the cell where to go using chemical sensing, and then have the cell burst near its intended target so that a drug can be released,” says senior author Takanari Inoue, Ph.D., professor of cell biology and director of the Center for Cell Dynamics at Johns Hopkins Medicine.
To activate the vesicle’s chemical-sensing ability, researchers planted two proteins that act as molecular switches — called FKBP and FRB — within the synthetic cell. The protein FKBP was placed in the center of the cell, while FRB was planted on the membrane. When the scientists introduced a chemical — rapamycin — outside of the bubble cell, FKBP moved to the membrane to bind with FRB, triggering a process called actin polymerization, or a reorganization of the synthetic cell’s skeleton.
Inside the protocell, the chemical reaction resulted in a rod-like structure made up of actin that put pressure on the cell membrane, bending it.
The researchers used a specialized type of rapid 3D imaging called confocal microscopy to record the protocell’s chemical-sensing ability; they had to record images quickly, at a rate of one frame per every 15 to 30 seconds, as the protocells responded quickly to the chemical signal.
Up next, the researchers aim to equip these synthetic cells with the ability to move toward a desired target. Ultimately, researchers hope to engineer synthetic cells that could have significant potential applications in targeted drug delivery, environmental sensing and other areas where precise movement and response to stimuli are crucial.
Other scientists who contributed to this research include Bedri Abubaker-Sharif, Hideaki T. Matsubayashi, Hideki Nakamura, Nhung Thi Hong Nguyen, Douglas N. Robinson, and Pablo A. Iglesias of Johns Hopkins; Felix Wong from Massachusetts Institute of Technology; and Baoyu Chen of Iowa State University.
Funding for this research was provided by the National Institutes of Health (5R01GM123130, R01GM136858, R35GM149329, R35GM128786, R01GM149073, R01GM66817 and S10OD016374), the Department of Defense Advanced Research Projects Agency (HR0011-16-C- 0139), the National Science Foundation and the PRESTO program of the Japan Science and Technology Agency.

For much of his childhood, Simiao Niu was troubled by psoriasis, a chronic, often painful skin condition, mostly on his arms.
Sometimes, the prescribed ointment worked and treated the inflamed, red areas produced by the disease. But he was never sure if he was using enough, whether the skin irritation was healing and when he should stop treatment.
Years later, as an engineer on the team at Apple Inc. that devised the electronics in Apple watches monitoring heart rhythm, Niu had a revelation: Could a similar wearable electronic device be developed to treat skin ailments such as psoriasis and provide patients with continuous feedback?
Now, Niu, an assistant professor of biomedical engineering in the School of Engineering at Rutgers-New Brunswick, has played a crucial role in the development of the kind of device that he dreamed of: a unique prototype of what he and his research collaborators are calling a “living bioelectronic” designed to treat psoriasis.
Describing the advance in Science magazine, Niu and collaborators, including scientists at the University of Chicago led by Bozhi Tian and Columbia University, reported developing a patch — a combination of advanced electronics, living cells and hydrogel — that is showing efficacy in experiments in mice.
The patch represents not only a potential treatment for psoriasis, but a new technology platform to deliver treatments for medical needs as diverse as wounds and, potentially, various skin cancers, Niu said.
“We were looking for a new type of device that combines sensing and treatment for managing skin inflammation diseases like psoriasis,” Niu said. “We found that by combining living bacteria, flexible electronics and adhesive skin interface materials, we were able to create a new type of device.”
The circular patch is about 1 inch in diameter and wafer thin. The patch contains electronic chips, bacterial cells and a gel made from starch and gelatin. Tests in mice conducted by the research team showed that the device could continuously monitor and improve psoriasis-like symptoms without irritating skin.

The device, Niu said, is a leap forward from conventional bioelectronics, which are generally composed of electronic components that are encased in a soft synthetic layer that reduces irritation when in contact with the body. The patches placed on a patient’s chest for an electrocardiogram are examples of conventional devices.
Niu’s invention could be seen as a “living drug,” he said, in that it incorporates living cells as part of its therapy. S. epidermidis, which lives on human skin and has been shown to reduce inflammation, is incorporated into the device’s gel casing. A thin, flexible printed circuit forms the skeleton of the device.
When the device is placed on skin, the bacteria secrete compounds that reduce inflammation, while sensors in the flexible circuits monitor the skin for signals indicating healing, such as skin impedance, temperature and humidity. The data collected by the circuits is beamed wirelessly to a computer or a cell phone, a process that would allow patients to monitor their healing process.
During his years at Apple, before he joined Rutgers faculty in 2022, Niu and other engineers were forwarded hundreds of thank-you notes that had been sent to the chief executive’s office. The customers wrote to credit their Apple watches with saving their lives, Niu said. The watches’ built-in heart rate monitors pointed to a condition — an arrhythmia known as atrial fibrillation — the customers said they didn’t know they had. Atrial fibrillation can lead to strokes if left untreated.
“When you produce the kinds of things that positively affect people’s lives, you feel very proud,” Niu said. “That is something that inspires me a lot and motivates me to do my current research.”
Clinical trials to test the device on human patients must come next, Niu said, as the first step toward commercialization. Once there is evidence of positive results with minimum side effects, the inventors would apply for FDA approval in order to bring the device to market, Niu said.
Other authors of the study from Rutgers included Fuying Dong and Chi Han, two graduate students at the Department of Biomedical Engineering in the School of Engineering.

Researchers from King’s, with doctors at King’s College Hospital NHS Foundation Trust, have successfully used a new robot system to improve treatment for debilitating eye disease.
The custom-built robot was used to treat wet neovascular age-related macular degeneration (AMD), administering a one-off, minimally invasive dose of radiation, followed by patients’ routine treatment with injections into their eye.
In the landmark trial, published today in The Lancet, it was found that patients then needed fewer injections to effectively control the disease, potentially saving around 1.8 million injections per year around the world.
Wet AMD is a debilitating eye disease, where abnormal new blood vessels grow into the macula, the light sensing-layer of cells inside the back of the eyeball. The vessels then start to leak blood and fluid, typically causing a rapid, permanent and severe loss of sight.
Globally, around 196 million people have AMD and the Royal College of Ophthalmologists estimates that the disease affects more than 700,000 people in the UK. The number of people with AMD is expected to increase 60% by 2035, due to the country’s ageing population.
Wet AMD is currently treated with regular injections into the eye. Initially, treatment substantially improves a patient’s vision. But, because the injections don’t cure the disease, fluid will eventually start to build up again in the macula, and patients will require long-term, repeated injections. Most people require an injection around every 1-3 months, and eye injections, costing between £500 and £800 per injection, have become one of the most common NHS procedures.
The new treatment can be targeted far better than existing methods, aiming three beams of highly focused radiation into the diseased eye. Scientists found that patients having robotic radiotherapy required fewer injections to control their disease compared to standard treatment.

The study found that the robotically controlled device saves the NHS £565 for each patient treated over the first two years, as it results in fewer injections.
The study lead and first author on the paper, Professor Timothy Jackson, King’s College London and Consultant Ophthalmic Surgeon at King’s College Hospital said: “Research has previously tried to find a better way to target radiotherapy to the macula, such as by repurposing devices used to treat brain tumours. But so far nothing has been sufficiently precise to target macular disease that may be less than 1 mm across.
“With this purpose-built robotic system, we can be incredibly precise, using overlapping beams of radiation to treat a very small lesion in the back of the eye.
“Patients generally accept that they need to have eye injections to help preserve their vision, but frequent hospital attendance and repeated eye injections isn’t something they enjoy. By better stabilising the disease and reducing its activity, the new treatment could reduce the number of injections people need by about a quarter. Hopefully, this discovery will reduce the burden of treatment that patients have to endure.”
Dr Helen Dakin, University Research Lecturer at the University of Oxford said: “We found that the savings from giving fewer injections are larger than the cost of robot-controlled radiotherapy. This new treatment can therefore save the NHS money that can be used to treat other patients, while controlling patients’ AMD just as well as standard care.”
The research was jointly funded by the National Institute for Health and Care Research (NIHR) and the Medical Research Council (MRC) and recruited 411 participants across 30 NHS hospitals. A Lancet-commissioned commentary that accompanied the article described it as a “landmark trial.”
This study was led by researchers from King’s College London and doctors at King’s College Hospital NHS Foundation Trust, in collaboration with the University of Oxford, the University of Bristol and Queen’s University in Belfast.

In relationships, sharing closer spaces naturally deepens the connection as bonds form and strengthen through increasing shared memories. This principle applies not only to human interactions but also to engineering. Recently, an intriguing study was published demonstrating the use of quantum dots to create metasurfaces, enabling two objects to exist in the same space.
Professor Junsuk Rho from the Department of Mechanical Engineering, the Department of Chemical Engineering, and the Department of Electrical Engineering, PhD candidates Minsu Jeong, Byoungsu Ko, and Jaekyung Kim from the Department of Mechanical Engineering, and Chunghwan Jung, a PhD candidate, from the Department of Chemical Engineering at Pohang University of Science and Technology (POSTECH) employed Nanoimprint Lithography (NIL) to fabricate metasurfaces embedded with quantum dots, enhancing their luminescence efficiency. Their research was recently published in the online edition of Nano Letters.
NIL, a process for creating optical metasurfaces, utilizes patterned stamps to quickly transfer intricate patterns at the nanometer (nm) scale. This method offers cost advantages over electron beam lithography and other processes and has the advantage of enabling the creation of metasurfaces using materials that are not available in conventional processes.
Metasurfaces have recently been the focus of extensive research for their ability to control the polarization and emission direction of light from quantum dots. Quantum dots, which are nanoscale semiconductor particles, are highly efficient light emitters capable of emitting light at precise wavelengths. This makes them widely used in applications such as QLEDs and quantum computing. However, conventional processes cannot embed quantum dots within metasurfaces. As a result, research has often involved fabricating metasurfaces and quantum dots separately and then combining them, which imposes limitations on controlling the luminescence of the quantum dots.
In this study, the researchers integrated quantum dots with titanium dioxide (TiO2), a material used in the NIL process, to create a metasurface. Unlike conventional methods, which involve separately fabricating the metasurface and quantum dots before combining them, this approach embeds the quantum dots directly within the metasurface during its creation.
The resulting metasurface enhances the proportion of photons emitted from the quantum dots that couple with the resonance mode of the metasurface. This advancement allows for more effective control over the specific direction of light emitted from the quantum dots compared to previous methods.
Experiments demonstrated that the more photons emitted from the quantum dots that were coupled to the resonant modes of the metasurface, the higher the luminescence efficiency. The team’s metasurface achieved up to 25 times greater luminescence efficiency compared to a simple coating of quantum dots.
Professor Junsuk Rho of POSTECH who led the research stated, “The use of luminescence-controlled metasurfaces will enable sharper, brighter displays and more precise, sensitive biosensing.” He added, “Further research will allow us to control luminescence more effectively, leading to advances in areas such as nano-optical sensors, optoelectronic devices, and quantum dot displays.”
The research was conducted with support from POSCO N.EX.T IMPACT, the Samsung Future Technology Incubation Program, and the Mid-Career Researcher Program of the Ministry of Science and ICT and the National Research Foundation of Korea.

Flexible piezoelectric sensors are essential to monitor the motions of both humans and humanoid robots. However, existing designs are either are costly or have limited sensitivity. In a recent study, researchers from Japan tackled these issues by developing a novel piezoelectric composite material made from electrospun polyvinylidene fluoride nanofibers combined with dopamine. Sensors made from this material showed significant performance and stability improvements at a low cost, promising advancements in medicine, healthcare, and robotics.
The world is accelerating rapidly towards the intelligent era — a stage in history marked by increased automation and interconnectivity by leveraging technologies such as artificial intelligence and robotics. As a sometimes-overlooked foundational requirement in this transformation, sensors represent an essential interface between humans, machines, and their environment.
However, now that robots are becoming more agile and wearable electronics are no longer confined to science fiction, traditional silicon-based sensors won’t make the cut in many applications. Thus, flexible sensors, which provide better comfort and higher versatility, have become a very active area of study. Piezoelectric sensors are particularly important in this regard, as they can convert mechanical stress and stretching into an electrical signal. Despite numerous promising approaches, there remains a lack of environmentally sustainable methods for mass-producing flexible, high-performance piezoelectric sensors at a low cost.
Against this backdrop, a research team from Shinshu University, Japan, decided to step up to the challenge and improve flexible piezoelectric sensor design using a well-established manufacturing technique: electrospinning. Their latest study, which was led by Distinguished Professor Ick Soo Kim in association with Junpeng Xiong, Ling Wang, Mayakrishnan Gopiraman, and Jian Shi, was published on 2 May, 2024, in the journal Nature Communications.
The proposed flexible sensor design involves the stepwise electrospinning of a composite 2D nanofiber membrane. First, polyvinylidene fluoride (PVDF) nanofibers with diameters in the order of 200 nm are spun, forming a strong uniform network that acts as the base for the piezoelectric sensor. Then, ultrafine PVDF nanofibers with diameters smaller than 35 nm are spun onto the preexisting base. These fibers become automatically interweaved between the gaps of the base network, creating a particular 2D topology.
After characterization via experiments, simulations, and theoretical analyses, the researchers found that the resulting composite PVDF network had enhanced beta crystal orientation. By enhancing this polar phase, which is responsible for the piezoelectric effect observed in PVDF materials, the piezoelectric performance of the sensors was significantly improved. To increase the stability of the material further, the researchers introduced dopamine (DA) during the electrospinning process, which created a protective core-shell structure.
“Sensor fabricated from using PVDF/DA composite membranes exhibited superb performance, including a wide response range of 1.5-40 N, high sensitivity of 7.29 V/N to weak forces in the range of 0-4 N, and excellent operational durability,” remarks Kim. These exceptional qualities were demonstrated practically using wearable sensors to measure a wide variety of human movements and actions. More specifically, the proposed sensors, when worn by a human, could produce an easily distinguishable voltage response to natural motions and physiological signals. This included finger tapping, knee and elbow bending, foot stamping, and even speaking and wrist pulses.
Given the potential low-cost mass production of these piezoelectric sensors, combined with their use of environmentally friendly organic materials instead of harmful inorganics, this study could have important technological implications not only for health monitoring and diagnostics, but also robotics. “Despite the current challenges, humanoid robots are poised to play an increasingly integral role in the very near future. For instance, the well-known Tesla robot ‘Optimus’ can already mimic human motions and walk like a human,” muses Kim, “Considering high-tech sensors are currently being used to monitor robot motions, our proposed nanofiber-based superior piezoelectric sensors hold much potential not only for monitoring human movements, but also in the field of humanoid robotics.”
To make the adoption of these sensors easier, the research team will be focusing on improving the material’s electrical output properties so that flexible electronic components can be driven without the need for an external power source. Hopefully, further progress in this area will accelerate our stride towards the intelligent era, leading to more comfortable and sustainable lives.

AI detects prostate cancer more often than radiologists. Additionally, AI triggers false alarms half as often. This is shown by an international study coordinated by Radboud university medical center and published in The Lancet Oncology. This is the first large-scale study where an international team transparently evaluates and compares AI with radiologist assessments and clinical outcomes.
Radiologists face an increasing workload as men with a higher risk of prostate cancer now routinely receive a prostate MRI. Diagnosing prostate cancer with MRI requires significant expertise, and there is a shortage of experienced radiologists. AI can assist with these challenges.
AI expert Henkjan Huisman and radiologist Maarten de Rooij, project leaders of the PI-CAI study, organized a major competition between AI teams and radiologists with an international team. Along with other centers in the Netherlands and Norway, they provided over 10,000 MRI scans. They transparently determined for each patient whether prostate cancer was present. They allowed various groups worldwide to develop AI for analyzing these images. The top five submissions were combined into a super-algorithm for analyzing MRI scans for prostate cancer. Finally, AI assessments were compared to those of a group of radiologists on four hundred prostate MRI scans.
Accurate Diagnosis
The PI-CAI community brought together over two hundred AI teams and 62 radiologists from twenty countries. They compared the findings of AI and radiologists not only with each other but also with a gold standard, as they monitored the outcomes of the men from whom the scans originated. On average, the men were followed for five years.
This first international study on AI in prostate diagnostics shows that AI detects nearly seven percent more significant prostate cancers than the group of radiologists. Additionally, AI identifies suspicious areas, later found not to be cancer, fifty percent less often. This means the number of biopsies could be halved with the use of AI. If these results are replicated in follow-up studies, it could greatly assist radiologists and patients in the future. It could reduce radiologists’ workload, provide more accurate diagnoses, and minimize unnecessary prostate biopsies. The developed AI still needs to be validated and is currently not yet available for patients in clinical settings.
Quality System
Huisman observes that society has little trust in AI. ‘This is because manufacturers sometimes build AI that isn’t good enough’, he explains. He is working on two things. The first is a public and transparent test to fairly evaluate AI. The second is a quality management system, similar to what exists in the aviation industry. ‘If planes almost collide, a safety committee will look at how to improve the system so that it doesn’t happen in the future. I want the same for AI. I want to research and develop a system that learns from every mistake so that AI is monitored and can continue to improve. That way, we can build trust in AI for healthcare. Optimal, governed AI can help make healthcare better and more efficient.’

St. Jude researchers use epigenetic clock, DNA methylation and mouse model to demonstrate that T cell proliferation can stretch past organism lifespan and acuta lymphoblastic leukemia T cells appear hundreds of years old.
While most cell types experience a functional decline after years of proliferation and replication, T cells can proliferate seemingly indefinitely and without detriment. Scientists at St. Jude Children’s Research Hospital and the University of Minnesota investigated the unique ‘epigenetic clock’ of T-cell aging, demonstrating that T cells can outlive an organism through at least four lifetimes. In addition, the researchers showed that healthy T cell age was uncoupled from the organism’s chronologic age. Furthermore, they determined that malignant T cells from pediatric patients with T-cell acute lymphoblastic leukemia (T-ALL) appeared to have aged up to 200 years. The findings were published today in Nature Aging.
As researchers explore the process of cellular aging through repeat replicative cycles of growth, some peculiar patterns have emerged regarding T cells. “The immune system by nature must mount a rapid proliferative response to a pathogen or a tumor,” said co-corresponding author Ben Youngblood, PhD, St. Jude Department of Immunology. “And in some settings, such as endemic pathogens or chronic viral infections, this happens over and over again. That’s a lot of proliferation that these T cells undergo in the lifespan of a human.” This raised the question as to why, despite these accelerated rates of proliferation, this immune response doesn’t trigger cancer development.
The answer lies in a T cell’s unique ability to defy aging.
Epigenetic markers offer more accurate metrics for age
To study this phenomenon, the researchers made use of specific biomarkers known as epigenetic markers that accumulate over time. Like counting the rings on a tree stump in a forest, this ‘epigenetic clock’ tells a retrospective story about the life cycle of a cell independent of the organism itself. The accumulation of genetic mutations, the shortening of telomeres (the protective caps on chromosomes) and methylation patterns are currently regarded as the most accurate ways to interrogate the process of aging.
The researchers saw this as an ideal way to investigate the curious case of T-cell aging. “We started asking questions about what the hallmarks of aging are, specifically the epigenetic hallmarks, and how these can be applied to long-lived T cells,” he said. “One of the big questions we had was whether these epigenetic clocks are bound by the lifespan of the organism or not.”
Model shows T cells can outlive their origin organism

Through a collaboration with co-corresponding author David Masopust, PhD, University of Minnesota, the researchers found the perfect model to address their questions. This model used the same line of T cells through several mouse life cycles. “Dr. Masopust started this model assuming the cells would eventually decline, but they didn’t, they just kept going,” explains Youngblood. “This led to his foundational 10-year mouse study which we subsequently used to address whether organismal lifespan limits constrain epigenetic clocks.”
Using this model and an epigenetic clock they developed for T cells, the researchers explored the DNA methylation patterns of T-cell lineage. They found that age is just a number, and death is not the end. “Humans don’t live forever. But in this case, we could test that concept for T cells,” Youngblood said. “Is there an end to an epigenetic clock? Does it plateau? And it didn’t for up to four lifetimes, it just kept counting, which was incredible. These cells are not bound by the reasonable limits of organism lifespan.”
Cancerous T cells appear hundreds of years old
Next, the researchers determined what happened under conditions of rapid and prolonged proliferation such as in cancer. The team interrogated the T cells of patients with pediatric T-ALL to investigate what happens to their epigenetic clock. “If epigenetic clocks were linked to the host’s chronologic age, then you would expect the T cells from pediatric T-ALL patients to appear young in age,” said co-corresponding author Caitlin Zebley, MD, PhD, St. Jude Department of Bone Marrow Transplantation & Cellular Therapy. “But our clock predicted these cells to be very old.”
From an experiential perspective, the T cells of T-ALL patients appeared to range from 100 to 200 years old. “We think this was related to the fact that they were proliferating so rapidly,” Zebley concluded. The T-ALL model offered invaluable insight into the aging process of leukemia cells. “We were able to use this as a subtraction model from all other programs in leukemia to identify ones that are associated with normal aging and proliferation versus ones that are distinct to leukemia,” Youngblood said. “We gained a better idea of which epigenetic programs are associated with leukemia and which are just normal hyperproliferation and aging.”
T-cell survival is vital to our survival
Considering how active our immune system is, T-cell survival is vital to our overall survival. “T-cells have so many opportunities to turn cancerous,” Youngblood said, “But they can’t, otherwise humanity wouldn’t exist.”

Youngblood, Zebley and Masopust are continuing to study the checks and balances that prevent T cells from undergoing malignant transformation. Through this work, potential therapies that halt, or even reverse, age-related impairments can begin to be considered.
Authors and funding
The study’s first author is Tian Mi, St. Jude. The study’s other authors are Shanta Alli, Tae Gun Kang, Anoop Babu Vasandan, Zhaoming Wang, Ilaria Iacobucci and Charles Mullighan, St. Jude; Andrew Soerens and Vaiva Vezys, University of Minnesota; Stephen Baylin, The Sidney Kimmel Comprehensive Cancer Institute at Johns Hopkins; Peter Jones, Van Andel Institute; and Christopher Hiner, April Mueller, and Harris Goldstein, Albert Einstein College of Medicine.
The study was supported by grants from the National Institutes of Health (R01AI114442, R01CA237311, U01AI144616, R01AI084913, R01AI146032, R01CA238439, R01AI172607, R01AI145024, K08CA279926), the National Comprehensive Cancer Network, Alex’s Lemonade Stand Foundation, Stand Up to Cancer, the ASSISI Foundation, the Key for a Cure Foundation and ALSAC, the fundraising and awareness organization of St. Jude.

To shield older residents from dangerous air pollution, new care homes should be built as far from heavy traffic as possible, according to a new study from the University of Surrey.
Researchers also found that trees planted between the homes and the road could significantly mitigate the impact of air pollution.
Professor Prashant Kumar, Director of Surrey’s Global Centre for Clean Air Research (GCARE), said:
“Older adults in care settings can be especially vulnerable to poor quality air. Our study confirms that building care homes next to busy roads without adequate tree planting can significantly increase their exposure to deadly fine particle pollution.
“We hope planners will be able to use our findings to make sure care homes are built in safer locations — striking the right balance between the convenience of urban living and better air quality.”
Researchers studied three care homes in the Chinese city of Nanjing. They measured fine particle pollution (PM2.5) at various locations in and around the care homes.
They found that the amount of pollution inside the care home decreased exponentially, the further it was from the road.

Huaiwen Wu, a researcher at GCARE, said:
“Our study gives so many useful insights into where to build new care homes.
“For instance, there was a significant relationship between outdoor and indoor pollution. This tells us that bedrooms should be kept on the far side of the building where possible.”
Professor Shi-Jie Cao, Visiting Professor at GCARE and Professor at the Southeast University, China, said:
“We also saw how pollution was highest during rush hour. Concentrations were higher during spells of lighter winds, and during colder seasons when more people are heating their homes.
“As such, care homes near busy roads could keep their windows closed more during those periods — then open them afterwards to mitigate the accumulation of emissions.”
The study is published in the journal Atmospheric Environment.