Even small asteroids lead complex lives. During its flyby of the asteroid Donaldjohanson last year, NASA’s Lucy spacecraft revealed the asteroid to be a wobbly, peanut-shaped body that has undergone a lot of activity in its relatively short history. Formed as fragments coalesced after a violent collision 155 million years ago, the asteroid was transformed by the small but inexorable force of the Sun’s radiation, all while retaining signs of the brief presence of liquid water in its distant past.

Zooming through the main asteroid belt toward one of the Jupiter Trojan asteroid groups, the Lucy spacecraft collected the first close-up images and other data at Donaldjohanson on April 20, 2025, as it passed 650 miles away from the asteroid. The data revealed that, instead of spinning simply around one axis like most other asteroids and planets, Donaldjohanson has a more complicated two-axis rotation. Scientists also saw Donaldjohanson’s peanut shape and the craters and ridges on its surface.

Lucy’s encounter with the asteroid was planned as a dress rehearsal for the spacecraft and mission team before its primary asteroid encounters, which begin with Lucy’s flyby of the Trojan asteroid Eurybates on Aug. 12, 2027. The instruments performed as expected, and, as a bonus, scientists got a rare opportunity to study a previously unexplored asteroid up close and to compare it to two asteroids with similar compositions but different histories: Bennu, the target of NASA’s OSIRIS-REx sample-return mission, and Ryugu, the site of JAXA’s (Japan Aerospace Exploration Agency) Hayabusa2 sample-return mission.

Here’s what Lucy’s science team has learned so far from Lucy’s encounter with Donaldjohanson, as reported on June 18 in the journal Science.

Wobbling rotation

With Earth-based telescopes, observers saw fluctuations in the light Donaldjohanson reflects, regular patterns of peaks and valleys, typical of an elongated object rotating once every 10.5 Earth days. But Lucy’s data revealed another pattern: Donaldjohanson appears to be rotating like a wobbly top. Paper authors reported that the asteroid rotates end-over-end once every 10.5 Earth days, and wobbles back and forth around its long axis once every 26.5 days.

Peanut shape

While the Earth-based observations hinted at Donaldjohanson’s elongated shape, the Lucy flyby revealed a “bilobate” structure: two lobes connected by a neck, like a peanut. These lobes are likely two fragments from an asteroid collision that gently came together afterward by their mutual gravity.

Donaldjohanson likely rotated at least 10 times faster when it formed, having slowed to its current rate in the last 20 to 60 million years, the team estimates. As it slowed, the balance between the centrifugal force pushing things apart and gravity pulling things together changed and loose rocky material slid down slopes creating the worn-down appearance of many craters, as the flyby images showed.

The paper’s authors say that the asteroid’s slowing rotation is likely caused by a subtle consequence of solar heating known as the YORP effect. Each part of the asteroid’s Sun-warmed surface radiates heat away as infrared light, and that radiation imparts a tiny recoil force to the surface. Because the asteroid’s shape isn’t symmetric, this results in a net torque, or twist, that can change the asteroid’s rotation. Thus, YORP can slow asteroid spins down or speed them up, as in the case of Bennu (once every four hours) and Ryugu (once about every seven hours), which both likely used to rotate much slower than they do today.

Fleeting water

As it passed by Donaldjohanson at 30,000 mph, Lucy recorded the signatures of iron-rich clay minerals on the surface. These clays must have formed in the distant past with the help of liquid water. However, the exposure must have been brief, Lucy scientists concluded, because iron in clays tends to be replaced with other elements, such as magnesium, as water lingers.

Indeed, scientists saw magnesium-rich clays at Bennu and Ryugu, which suggested prolonged water exposure, perhaps lasting millions of years, when they were still part of larger asteroids.

This difference in water exposure history, and other characteristics, may mean that the parent bodies of these asteroids formed at different times or in different regions of the solar system before relocating to the main belt.

Compare, contrast

Donaldjohanson is thought to be made from rocky remnants of a larger, carbon- and water-rich asteroid that collided with another object in the main asteroid belt. Bennu and Ryugu are thought to have formed in the same way and in the same region.

But Donaldjohanson is different. At 155 million years old, it is much younger than Bennu and Ryugu, which formed 1 to 2 billion years ago. Donaldjohanson also has remained in the asteroid belt since birth, while its wandering cousins migrated into orbits around the Sun that bring them close to Earth’s orbit about once a year (which made them perfect close targets for sample return missions).

“It’s helpful for scientists to compare Donaldjohanson with asteroids like Bennu and Ryugu, which are seemingly similar asteroids, because every subtle difference is another clue to our origin story,” said Simone Marchi, Lucy deputy principal investigator and lead author of the study at the Boulder, Colorado, office of the Southwest Research Institute.

“Once we start learning more about the Trojans, a completely different population of space rocks with very different histories, our understanding of solar system formation is destined to be challenged,” said Marchi.

Named after a fossilized skeleton of a human ancestor discovered in Ethiopia in 1974, NASA’s Lucy will be the first mission to explore Jupiter’s Trojan asteroids, a population of well-preserved space rocks that formed early in our solar system’s history and could help scientists understand how the planets formed and moved around before settling in their current configuration.

Download story graphics from NASA’s Scientific Visualization Studio.

About Lucy:

Lucy’s principal investigator is based out of the Boulder, Colorado, branch of Southwest Research Institute, headquartered in San Antonio. NASA’s Goddard Space Flight Center in Greenbelt, Maryland, provides overall mission management, systems engineering, and safety and mission assurance. Lockheed Martin Space in Littleton, Colorado, built the spacecraft. Lucy is the 13th mission in NASA’s Discovery Program. NASA’s Marshall Space Flight Center in Huntsville, Alabama, manages the Discovery Program for the agency’s Science Mission Directorate in Washington.

For more information on NASA’s Lucy mission, visit:

By Lonnie Shekhtman

NASA’s Goddard Space Flight Center, Greenbelt, Md.

and

Katherine Kretke

Southwest Research Institute, Boulder, Colo.

Media Contacts:

Karen Fox / Molly Wasser

Headquarters, Washington
240-285-5155 / 240-419-1732
karen.c.fox@nasa.gov / molly.l.wasser@nasa.gov

Sarah Frazier

NASA’s Goddard Space Flight Center, Greenbelt, Md.
202-853-7191
sarah.frazier@nasa.gov

The post NASA’s Lucy Reveals Wobbling, Peanut-Shaped Asteroid appeared first on NASA Science.

Even small asteroids lead complex lives. During its flyby of the asteroid Donaldjohanson last year, NASA’s Lucy spacecraft revealed the asteroid to be a wobbly, peanut-shaped body that has undergone a lot of activity in its relatively short history. Formed as fragments coalesced after a violent collision 155 million years ago, the asteroid was transformed by the small but inexorable force of the Sun’s radiation, all while retaining signs of the brief presence of liquid water in its distant past.

Zooming through the main asteroid belt toward one of the Jupiter Trojan asteroid groups, the Lucy spacecraft collected the first close-up images and other data at Donaldjohanson on April 20, 2025, as it passed 650 miles away from the asteroid. The data revealed that, instead of spinning simply around one axis like most other asteroids and planets, Donaldjohanson has a more complicated two-axis rotation. Scientists also saw Donaldjohanson’s peanut shape and the craters and ridges on its surface.

Lucy’s encounter with the asteroid was planned as a dress rehearsal for the spacecraft and mission team before its primary asteroid encounters, which begin with Lucy’s flyby of the Trojan asteroid Eurybates on Aug. 12, 2027. The instruments performed as expected, and, as a bonus, scientists got a rare opportunity to study a previously unexplored asteroid up close and to compare it to two asteroids with similar compositions but different histories: Bennu, the target of NASA’s OSIRIS-REx sample-return mission, and Ryugu, the site of JAXA’s (Japan Aerospace Exploration Agency) Hayabusa2 sample-return mission.

Here’s what Lucy’s science team has learned so far from Lucy’s encounter with Donaldjohanson, as reported on June 18 in the journal Science.

Wobbling rotation

With Earth-based telescopes, observers saw fluctuations in the light Donaldjohanson reflects, regular patterns of peaks and valleys, typical of an elongated object rotating once every 10.5 Earth days. But Lucy’s data revealed another pattern: Donaldjohanson appears to be rotating like a wobbly top. Paper authors reported that the asteroid rotates end-over-end once every 10.5 Earth days, and wobbles back and forth around its long axis once every 26.5 days.

Peanut shape

While the Earth-based observations hinted at Donaldjohanson’s elongated shape, the Lucy flyby revealed a “bilobate” structure: two lobes connected by a neck, like a peanut. These lobes are likely two fragments from an asteroid collision that gently came together afterward by their mutual gravity.

Donaldjohanson likely rotated at least 10 times faster when it formed, having slowed to its current rate in the last 20 to 60 million years, the team estimates. As it slowed, the balance between the centrifugal force pushing things apart and gravity pulling things together changed and loose rocky material slid down slopes creating the worn-down appearance of many craters, as the flyby images showed.

The paper’s authors say that the asteroid’s slowing rotation is likely caused by a subtle consequence of solar heating known as the YORP effect. Each part of the asteroid’s Sun-warmed surface radiates heat away as infrared light, and that radiation imparts a tiny recoil force to the surface. Because the asteroid’s shape isn’t symmetric, this results in a net torque, or twist, that can change the asteroid’s rotation. Thus, YORP can slow asteroid spins down or speed them up, as in the case of Bennu (once every four hours) and Ryugu (once about every seven hours), which both likely used to rotate much slower than they do today.

Fleeting water

As it passed by Donaldjohanson at 30,000 mph, Lucy recorded the signatures of iron-rich clay minerals on the surface. These clays must have formed in the distant past with the help of liquid water. However, the exposure must have been brief, Lucy scientists concluded, because iron in clays tends to be replaced with other elements, such as magnesium, as water lingers.

Indeed, scientists saw magnesium-rich clays at Bennu and Ryugu, which suggested prolonged water exposure, perhaps lasting millions of years, when they were still part of larger asteroids.

This difference in water exposure history, and other characteristics, may mean that the parent bodies of these asteroids formed at different times or in different regions of the solar system before relocating to the main belt.

Compare, contrast

Donaldjohanson is thought to be made from rocky remnants of a larger, carbon- and water-rich asteroid that collided with another object in the main asteroid belt. Bennu and Ryugu are thought to have formed in the same way and in the same region.

But Donaldjohanson is different. At 155 million years old, it is much younger than Bennu and Ryugu, which formed 1 to 2 billion years ago. Donaldjohanson also has remained in the asteroid belt since birth, while its wandering cousins migrated into orbits around the Sun that bring them close to Earth’s orbit about once a year (which made them perfect close targets for sample return missions).

“It’s helpful for scientists to compare Donaldjohanson with asteroids like Bennu and Ryugu, which are seemingly similar asteroids, because every subtle difference is another clue to our origin story,” said Simone Marchi, Lucy deputy principal investigator and lead author of the study at the Boulder, Colorado, office of the Southwest Research Institute.

“Once we start learning more about the Trojans, a completely different population of space rocks with very different histories, our understanding of solar system formation is destined to be challenged,” said Marchi.

Named after a fossilized skeleton of a human ancestor discovered in Ethiopia in 1974, NASA’s Lucy will be the first mission to explore Jupiter’s Trojan asteroids, a population of well-preserved space rocks that formed early in our solar system’s history and could help scientists understand how the planets formed and moved around before settling in their current configuration.

Download story graphics from NASA’s Scientific Visualization Studio.

About Lucy:

Lucy’s principal investigator is based out of the Boulder, Colorado, branch of Southwest Research Institute, headquartered in San Antonio. NASA’s Goddard Space Flight Center in Greenbelt, Maryland, provides overall mission management, systems engineering, and safety and mission assurance. Lockheed Martin Space in Littleton, Colorado, built the spacecraft. Lucy is the 13th mission in NASA’s Discovery Program. NASA’s Marshall Space Flight Center in Huntsville, Alabama, manages the Discovery Program for the agency’s Science Mission Directorate in Washington.

For more information on NASA’s Lucy mission, visit:

By Lonnie Shekhtman

NASA’s Goddard Space Flight Center, Greenbelt, Md.

and

Katherine Kretke

Southwest Research Institute, Boulder, Colo.

Media Contacts:

Karen Fox / Molly Wasser

Headquarters, Washington
240-285-5155 / 240-419-1732
karen.c.fox@nasa.gov / molly.l.wasser@nasa.gov

Sarah Frazier

NASA’s Goddard Space Flight Center, Greenbelt, Md.
202-853-7191
sarah.frazier@nasa.gov

The Expedition 74 crew explored how weightlessness affects cartilage growth and the digestive system on Thursday to protect crew health and improve patient care on Earth. The orbital residents are also gearing up for a robotics maintenance spacewalk at the end of the month on the International Space Station.

Conducting research in the microgravity environment of the orbiting laboratory provides unique insights unobtainable in Earth’s gravity. This helps scientists, doctors, and engineers develop space-influenced therapies, medicines, and products leading to advances in human health, industrial processes, spacecraft designs, and more.

Cartilage cells are growing aboard the orbital outpost that may inform new ways to treat disabilities and repair injuries. NASA flight engineers Jessica Meir and Chris Williams worked together on the biotechnology investigation using the Kibo laboratory module’s Life Science Glovebox. Williams retrieved the cartilage cell samples preserved in a science freezer then thawed them to begin scientific operations. Next, Meir nourished the cell samples inside the glovebox and stowed them inside a research incubator so they could begin growing. Manufacturing cartilage tissues in space could lead to self-repairing implants on Earth and advanced fitness techniques for astronauts on a long-term spaceflight.

Roscosmos cosmonauts Sergey Kud-Sverchkov and Sergei Mikaev joined each other after breakfast and scanned their abdominal region using an ultrasound device for a digestion study. The real-time biomedical data will give doctors insight into how microgravity affects the blood flow and shape of a crew member’s digestive organs after a meal. Results may help advance methods to monitor and improve digestive health both on Earth and in space.

Meir and flight engineer Sophie Adenot of ESA (European Space Agency) also conducted ultrasound scans using ESA’s EchoFinder-2 device to image the major blood vessels and key organs in their abdomen. The human research experiment uses augmented reality to assist with the scans and artificial intelligence to recognize organs. The lightweight, easy-to-use gear may enable independent crew health monitoring on spacecraft travelling to the Moon, Mars, and beyond.

Adenot then joined NASA flight engineer Jack Hathaway and studied procedures necessary to prepare astronauts for a spacewalk. The duo reviewed spacesuit handling techniques, Quest airlock pressurization and depressurization steps, and emergency responses. Adenot also partnered with Meir and Williams and serviced the lithium-ion batteries that power the spacesuits. NASA will soon announce the two astronauts who will exit the space station on June 30 to repair a wrist joint on the Canadarm2 robotic arm.

Roscosmos flight engineer Andrey Fedyaev had a busy day of science and maintenance beginning his shift downloading and reading data collected from a station radiation detector. Afterward, Fedyaev transferred water from the Progress 94 resupply ship into tanks inside the orbital outpost’s Roscosmos segment. Finally, the two-time cosmonaut wrapped up his shift testing artificial intelligence tools to boost crew efficiency and communications in space.

Learn more about station activities by following the space station blog, @space_stationon X, as well as the ISS Facebook and ISS Instagram accounts.

Get the latest from NASA delivered every week. Subscribe here.

The post Advanced Tech on Station Informing Space-Designed Health Treatments appeared first on NASA Science.

Alzheimer’s disease gradually steals memories, independence, and quality of life from millions of people worldwide. Despite decades of research, scientists still struggle to find treatments that can stop the disease from progressing. Most available medications provide only modest benefits and cannot fully prevent the loss of brain cells that characterizes the condition. A new study […]

The post Scientists Find a New Way to Fight Alzheimer’s After 20 Years of Research appeared first on Knowridge Science Report.

Physicians and researchers at the Netherlands Cancer Institute have unveiled a groundbreaking artificial intelligence (AI) model that fundamentally reshapes how treatment responses in pleural mesothelioma—a notoriously challenging cancer—are evaluated. This model, called ARTIMES, excels beyond traditional clinical methods, surpassing expert human judgment in accuracy and efficiency. By precisely measuring the entire tumor volume instead of relying on conventional diameter-based assessments, ARTIMES promises to revolutionize patient care and accelerate clinical research in this difficult-to-treat disease.

Pleural mesothelioma poses unique diagnostic challenges because it develops as a thin, irregular layer along the lining of the lungs rather than forming discrete masses. This morphology renders existing international standards like the RECIST (Response Evaluation Criteria in Solid Tumors) inadequate. RECIST depends primarily on simple diameter measures, which poorly represent the tumor’s true progression or regression in mesothelioma’s diffuse growth pattern. Clinicians have expressed frustration and uncertainty in evaluating treatment efficacy using these parameters, highlighting a pressing need for a more refined and reliable approach.

To address these limitations, an interdisciplinary team of AI scientists, radiologists, and pulmonologists collaborated at the Netherlands Cancer Institute. Leveraging an extensive dataset comprising over 11,000 computed tomography (CT) scans from more than 2,000 patients across 121 hospitals worldwide, they developed ARTIMES, an AI-driven volumetric response evaluation tool. Unlike humans, who face near-impossible challenges in manually delineating tumor boundaries at the pixel level on complex images, ARTIMES can effortlessly segment entire tumors and calculate their true volume with exceptional precision.

Pulmonologist Sjaak Burgers emphasizes that ARTIMES advances clinical practice by eliminating tedious and error-prone manual tumor assessments. While verifying the AI’s output remains essential, the review process is far less labor-intensive. This reduces interobserver variability and enables clinicians to obtain more consistent and objective insights into tumor dynamics. The ability to evaluate the full tumor burden rather than a single diameter mark dramatically increases sensitivity for detecting true positive or negative treatment responses.

The scientific community is witnessing a milestone with ARTIMES being the first AI model worldwide to demonstrably outperform clinicians in assessing treatment outcomes for pleural mesothelioma. Kevin Groot Lipman, lead author and technical physician, highlights that their study, published in The Lancet Oncology, cements AI’s potential to become an integral clinical decision support tool. Importantly, ARTIMES enhances rather than replaces physician judgment, interfacing smoothly into existing workflows while enabling rapid, data-driven decision-making.

Beyond measuring tumor volume, the researchers have undertaken the critical task of integrating ARTIMES measurements into actionable clinical guidelines. Since knowing the tumor size alone does not dictate specific treatment changes, these criteria empower pulmonologists to determine when to modify or cease therapies. This synergy ensures that patients receive individualized care tailored to their tumor behavior patterns, reducing exposure to ineffective treatments and unnecessary side effects while optimizing healthcare resources.

One of ARTIMES’s most transformative capabilities is its ability to detect non-response to therapy earlier than ever before. This timely recognition allows physicians to pivot treatment plans sooner, offering patients alternative therapeutic avenues or sparing them from futile and potentially harmful continuation of ineffective regimens. The combination of predictive accuracy and clinical oversight represents a major leap forward in precision oncology for pleural mesothelioma patients.

Currently, EU regulations restrict ARTIMES’s use exclusively to the Netherlands Cancer Institute under an in-house exemption, given that the model was developed internally. Nonetheless, the research team is actively pursuing regulatory approval to deploy ARTIMES globally in other hospitals. There is hopeful anticipation surrounding proposed EU frameworks aimed at streamlining the certification process for AI-enabled medical devices, which could accelerate widespread adoption and patient benefit.

The advent of ARTIMES is poised to deliver a shockwave across oncology fields by demonstrating the tangible superiority of AI over human evaluators in complex tumor assessments. To foster transparency and collaborative innovation, the Netherlands Cancer Institute has made the mesothelioma AI model publicly accessible online, enabling researchers worldwide to explore and extend its applications. This open science approach is expected to catalyze new studies and adaptations for other tumor types with challenging morphologies.

Already, the NKI team is extending their AI methodologies to address lung cancer and brain metastasis tumor evaluations. The success of ARTIMES signals the dawn of a new epoch in oncological imaging, where volumetric and morphological complexities that previously hindered precise quantification become tractable. Such breakthroughs unlock significant potential to enhance clinical trial design by furnishing robust, reproducible endpoints that more faithfully capture therapeutic impact.

Clinical trials for novel treatments stand to gain markedly from ARTIMES’s introduction. Using data from eight distinct trials, the research team validated that AI-guided volumetric criteria yield significantly improved accuracy relative to traditional RECIST assessments. This refined precision enables better evaluation of an investigational drug’s efficacy, ultimately accelerating regulatory approval timelines and facilitating faster patient access to promising therapies.

In summary, ARTIMES exemplifies how synergistic integration of AI and clinical expertise can surmount longstanding challenges in tumor measurement. By transitioning from simplistic unidimensional diameter metrics to comprehensive volumetric analysis, this technology brings unprecedented clarity and confidence to oncological decision-making. As this AI model becomes more widely disseminated and refined, it heralds a paradigm shift in cancer treatment evaluation, with rippling benefits for patients, clinicians, and research worldwide.

Subject of Research: People

Article Title: Development and validation of artificial intelligence-assisted volumetric response criteria in pleural mesothelioma (ARTIMES): a retrospective, multicohort, multicentre study

News Publication Date: 17-Jun-2026

Web References:

• The Lancet Oncology: http://dx.doi.org/10.1016/S1470-2045(26)00084-7
• Mesothelioma AI model (ARTIMES): https://huggingface.co/nki-radiology/ARTIMES
• EU Medical Devices Regulation: https://health.ec.europa.eu/medical-devices-sector/new-regulations_en

References:
Groot Lipman K, Burgers S, et al. Development and validation of artificial intelligence-assisted volumetric response criteria in pleural mesothelioma (ARTIMES): a retrospective, multicohort, multicentre study. The Lancet Oncology, 2026.

Image Credits: ©Netherlands Cancer Institute

Keywords: Cancer treatments, Artificial intelligence, Imaging analysis, Pleural mesothelioma, Tumor volumetrics, Clinical trials, Precision oncology

In an unprecedented advancement for neurodegenerative disease research, a team led by Busquets, Li, Syed, and colleagues has unveiled iSCORE-PD, an innovative isogenic stem cell repository designed explicitly to accelerate Parkinson’s disease studies. Published in Nature Communications in 2026, this comprehensive collection represents a pivotal leap toward resolving the complex pathophysiology of Parkinson’s, a condition affecting millions worldwide yet still eluding curative therapies. The iSCORE-PD platform promises to redefine experimental paradigms by providing scientists with genetically matched cellular models that mirror the intricate genetic underpinnings of Parkinson’s disease.

Parkinson’s disease is characterized primarily by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, leading to debilitating motor symptoms such as tremors, rigidity, and bradykinesia, alongside a spectrum of non-motor complications. Despite extensive research, there remains a conspicuous gap between clinical observations and mechanistic understanding at the cellular and molecular levels. Existing animal models and conventional stem cell lines often fall short in recapitulating the exact human pathology. The iSCORE-PD initiative addresses this deficiency head-on by harnessing isogenic stem cell lines, which are genetically identical except for defined Parkinson’s-relevant mutations, thus enabling unprecedented control over genetic variables.

The technical foundation of iSCORE-PD relies on advanced genome editing methodologies, most notably CRISPR/Cas9 technology. By precisely introducing or correcting mutations in key genes implicated in Parkinson’s pathogenesis such as SNCA, LRRK2, PINK1, and PARKIN, researchers have generated isogenic pairs of induced pluripotent stem cells (iPSCs). These iPSC lines can subsequently be differentiated into dopaminergic neurons or other relevant cell types, facilitating side-by-side comparisons that isolate the effects of specific genetic alterations without the confounding noise of inter-individual genetic variability.

One of the remarkable features of the iSCORE-PD collection is its extensive genomic validation pipeline. Whole genome sequencing and transcriptomic analyses are systematically employed to ensure the integrity and authenticity of the edited lines, confirming that off-target effects are minimized and that the genetic landscape conforms precisely to intended edits. This meticulous validation is crucial for downstream experiments intending to dissect subtle cellular phenotypes attributable to Parkinson’s mutations with a high degree of confidence.

The availability of these isogenic cell lines dramatically enhances the fidelity of disease modeling. Scientists can now observe, in real time and within a human cellular context, the cascade of pathological events triggered by individual mutations. For instance, iSCORE-PD lines harboring the G2019S mutation in LRRK2 have already demonstrated distinct lysosomal dysfunction and mitochondrial impairment, hallmarks of Parkinson’s-related neurodegeneration. These insights provide vital clues about the molecular mechanisms that underpin neuronal vulnerability and death.

Beyond mechanistic studies, iSCORE-PD serves as an invaluable platform for drug discovery and therapeutic screening. High-throughput assays conducted on these standardized cellular models allow for robust evaluation of candidate compounds’ efficacy and toxicity. The isogenic background ensures that drug responses can be directly attributed to genetic contributors and not extraneous genomic differences, thereby accelerating the identification of promising therapeutic leads with increased translational potential.

Moreover, the iSCORE-PD repository supports integrative omics approaches. By coupling proteomics, metabolomics, and epigenomic profiling with the genetically defined cell lines, researchers can generate comprehensive molecular atlases elucidating the multifaceted alterations engendered by Parkinson’s-associated mutations. Such data-rich resources augment our understanding of disease heterogeneity and may reveal novel biomarkers for early diagnosis and progression monitoring.

The initiative also pioneers robust methodologies for modeling non-cell autonomous effects in Parkinson’s pathology. By co-culturing isogenic dopaminergic neurons with glial cells or other brain cell types derived from similarly engineered iPSC lines, investigators can explore the cell–cell interactions and inflammatory pathways that contribute to disease propagation. These complex in vitro systems increasingly resemble the in vivo brain microenvironment, bridging translational gaps.

In addition to its scientific hinge, iSCORE-PD represents a significant step forward in reproducibility and collaborative science. By providing open-access to a rigorously characterized and genetically standardized stem cell collection, the project promotes harmonization of experimental models across laboratories worldwide. This standardization mitigates discrepancies often observed in Parkinson’s research due to genetic heterogeneity of patient-derived cells and disparate culture conditions.

Ethical considerations have been front and center in the development and dissemination of the iSCORE-PD lines. The team has implemented stringent protocols to ensure donor anonymity, informed consent, and compliance with international guidelines for stem cell research. This ethical diligence is fundamental to fostering public trust and enabling broad scientific utilization with responsibility.

The iSCORE-PD research consortium envisions future expansion of the collection to encompass additional mutations, gene variants, and epigenetic modifications implicated in Parkinson’s disease, thereby creating an ever-more comprehensive toolkit for the field. This evolving repository will facilitate the study of gene–environment interactions and provide models for the sporadic forms of Parkinson’s that constitute the majority of cases.

Importantly, the development of iSCORE-PD aligns synergistically with advances in single-cell sequencing and live-cell imaging technologies. These combined approaches empower real-time monitoring of neuronal dynamics, synaptic connectivity, and intracellular trafficking in disease-relevant contexts. Such capabilities promise to unravel the temporal progression of neuronal dysfunction in unprecedented detail.

The translational impact of iSCORE-PD extends beyond fundamental research, holding profound implications for personalized medicine. Patient-specific isogenic lines can be derived, enabling evaluation of individualized drug responses and prediction of disease progression trajectories. This precision medicine paradigm could revolutionize clinical management and therapeutic development for Parkinson’s patients.

Finally, iSCORE-PD serves as a testament to the power of interdisciplinary collaboration, integrating expertise in stem cell biology, genome editing, neuroscience, bioinformatics, and clinical neurology. This concerted effort exemplifies how cutting-edge technologies, when harnessed collectively, can illuminate complex diseases and hasten the arrival of effective treatments.

In sum, the iSCORE-PD isogenic stem cell collection stands as a groundbreaking resource that transforms the landscape of Parkinson’s disease research. By providing genetically precise, highly validated cellular models, it enables unparalleled mechanistic insights, drug discovery opportunities, and personalized medicine applications. As the Parkinson’s field grapples with its most urgent challenges, iSCORE-PD promises to be a beacon guiding innovative interventions and ultimately improving patient outcomes worldwide.

Subject of Research: Parkinson’s disease; isogenic stem cell models; neurodegeneration; genome editing; induced pluripotent stem cells.

Article Title: iSCORE-PD: an isogenic stem cell collection to research Parkinson’s disease.

Article References:

Busquets, O., Li, H., Syed, K.M. et al. iSCORE-PD: an isogenic stem cell collection to research Parkinson’s disease.
Nat Commun (2026). https://doi.org/10.1038/s41467-026-74355-8

Image Credits: AI Generated

University of Michigan Rogel Cancer Center researchers have unveiled a groundbreaking metabolic mechanism that colorectal cancer cells exploit to maintain exceptionally high iron levels, a discovery that opens promising avenues for targeted cancer therapies. Published recently in Cell Metabolism, this study provides an unprecedented insight into how tumor cells sidestep iron toxicity and evade a form of cell death known as ferroptosis, potentially revolutionizing the understanding of metal metabolism in cancer biology.

Colorectal cancer cells are known to harbor elevated iron concentrations, far surpassing those found in healthy cells. Iron is a double-edged sword in cellular physiology—essential for processes like DNA synthesis and cell proliferation but lethal in excess due to its propensity to generate harmful reactive oxygen species. Ordinarily, cells with excessive iron succumb to ferroptosis, a specialized form of oxidative cell death driven by iron-mediated lipid peroxidation. Tumor cells subvert this natural safeguard, sustaining iron overload without triggering their own demise, but how they achieve this has remained elusive—until now.

The investigative team led by Dr. Yatrik Shah, Horace W. Davenport Collegiate Professor of Physiology at Michigan Medicine, employed a metabolism-directed CRISPR screening approach to systematically dissect the pathways protecting colorectal cancer cells from iron-induced oxidative damage. Surprisingly, canonical ferroptotic enzymes, previously presumed central to this resistance, were found non-essential for tumor survival. This redirected focus led the scientists to explore mitochondrial metabolism more profoundly.

Their research unveiled that the mitochondrial enzyme complex II plays a pivotal role in safeguarding cancer cells from iron-induced toxicity. Complex II regulates coenzyme Q (CoQ) within mitochondria, a key antioxidant molecule that quells oxidative stress. By fine-tuning CoQ’s redox state, complex II effectively buffers the destructive potential of accumulated iron, preventing ferroptosis and enabling cancer cell proliferation. When researchers knocked out complex II in colorectal cancer models, iron toxicity became unmanageable for the tumor cells, leading to widespread cell death and marked tumor growth inhibition.

Crucially, complex II’s protective mechanism appears specific to the high-iron environment of cancer cells. In mouse models, disruption of complex II elicited negligible adverse effects on normal tissues, underscoring the therapeutic potential of selectively targeting this mitochondrial axis in colorectal cancer. This specificity addresses a significant hurdle in oncology: minimizing treatment toxicity while maximizing antitumor efficacy.

Further intricacies emerged as the study revealed a feedback loop wherein iron itself modulates complex II activity, suggesting a sophisticated regulatory axis that maintains iron homeostasis within tumors. This bidirectional interaction offers additional molecular targets for disrupting iron tolerance in cancer cells and deepening our understanding of tumor metabolism.

These findings represent a paradigm shift from earlier hypotheses centered on canonical ferroptosis regulators, highlighting the necessity of focusing on mitochondrial metabolism in cancer research. By leveraging sophisticated genome-editing tools and bioenergetic profiling, the Rogel Cancer Center team charted a novel course for drug discovery efforts aimed at crippling iron addiction—a hallmark of not only colorectal but potentially many other malignancies.

The next phase of this research endeavors to identify and develop potent inhibitors of complex II or its associated metabolic pathways. Given that dysregulated iron metabolism is a common vulnerability across diverse cancer types, these interventions could herald a new era of broad-spectrum anticancer strategies. Moreover, detailed characterization of iron complex II interplay might uncover additional metabolic dependencies exploitable for therapeutic gains.

This transformative research underscores the intricate metabolic adaptations that empower colorectal cancers to circumvent intrinsic iron toxicity constraints. By illuminating the heme-complex II axis as a linchpin in maintaining oxidative balance amid iron overload, it offers a highly selective target for the design of next-generation anticancer agents.

Researchers anticipate that combining complex II inhibition with other therapies may amplify treatment responses and overcome resistance mechanisms. As the quest to outsmart cancer evolves, this study reinforces the vital role of mitochondrial metabolism understanding in crafting innovative clinical interventions.

In sum, the University of Michigan team’s discovery of complex II’s role in buffering iron toxicity not only deciphers a long-standing biological enigma but also charts a compelling translational pathway. It epitomizes how fundamental metabolic insights can accelerate the development of precision treatments conferring hope to millions affected by colorectal cancer worldwide.

Subject of Research: Cells
Article Title: Iron addicted colorectal cancers exploit heme-complex II axis to resist oxidative cell death
News Publication Date: June 17, 2026
Web References: http://dx.doi.org/10.1016/j.cmet.2026.04.020
References: “Iron addicted colorectal cancers exploit heme-complex II axis to resist oxidative cell death,” Cell Metabolism, DOI: 10.1016/j.cmet.2026.04.020
Image Credits: Shah Lab, Rogel Cancer Center
Keywords: Colorectal cancer, iron metabolism, ferroptosis, complex II, coenzyme Q, mitochondrial metabolism, oxidative cell death, tumor metabolism, cancer therapy

Microplastics: Unseen Threats to Liver Health Revealed Through Cutting-Edge Spatial Transcriptomics

In recent years, microplastics have emerged as pervasive environmental contaminants, infiltrating virtually every corner of the globe. These minuscule plastic particles, derived from the breakdown of larger plastic debris, have invaded air, water, and soil, exposing humans to continuous contact via inhalation, ingestion, and dermal absorption. Despite the ubiquity of microplastics, understanding their direct impact on biological systems has remained a formidable challenge within the scientific community. A groundbreaking study by researchers at the University of Oklahoma, recently published in the journal Science Advances, delves into this critical area by examining how microplastics particularly affect liver health under dietary stress conditions.

Tae Gyu Oh, Ph.D., an assistant professor of oncology science at the University of Oklahoma College of Medicine and lead author of the study, highlights the pressing concern: “Exposure to microplastics is inevitable. Their presence in human tissues has been confirmed across multiple studies. However, we wanted to investigate how microplastic exposure interacts with a high-fat, high-cholesterol diet, known to independently induce liver damage.” The study offers compelling evidence that the combination of a typical Western diet and microplastic exposure exacerbates liver injury, potentially accelerating the progression of metabolic liver diseases.

Central to the study is the focus on polyethylene, the most prevalent plastic polymer globally, commonly found in everyday items such as plastic bags and milk containers. The research team administered polyethylene microplastics to mice over eight weeks, with one cohort receiving a standard diet and another subjected to a diet mimicking metabolic dysfunction-associated steatohepatitis (MASH). This severe form of fatty liver disease is characterized by inflammation and liver cell damage, often culminating in cirrhosis and liver failure if untreated.

The findings were striking: mice consuming the high-fat diet alongside microplastic exposure exhibited blood markers indicating liver injury more than twice as elevated as those on a standard diet experiencing similar exposure. This synergistic effect underscores the intricate interplay between environmental pollutants and diet-induced metabolic stressors, intensifying hepatic damage beyond what each factor causes independently.

To unravel the molecular and cellular underpinnings of this phenomenon, the research employed an array of sophisticated analytical techniques, culminating in the use of spatial transcriptomics. Unlike conventional bulk transcriptomic approaches, which average gene expression across millions of cells and can obscure localized responses, spatial transcriptomics enables researchers to map transcriptional activity within intact tissue sections at near single-cell resolution. This technique revealed precise “hot spots” of inflammation and tissue injury within the liver, a breakthrough insight unattainable by earlier methodologies.

Analysis of gene regulatory networks through spatial transcriptomics indicated a pivotal role for PPAR-alpha (peroxisome proliferator-activated receptor-alpha), a nuclear receptor that orchestrates fat metabolism and energy homeostasis in liver cells. PPAR-alpha appears to engage in cross-talk with Anxa2, a gene implicated in tissue repair and membrane dynamics. The altered activity of this axis in microplastic-exposed livers suggests that microplastics may disrupt the liver’s natural defense and regenerative processes, impairing its capacity to recover from metabolic insults.

This discovery has profound implications for understanding the mechanistic pathways by which environmental contaminants like microplastics contribute to liver pathology. The perturbation of PPAR-alpha and Anxa2 signaling potentially links microplastic exposure with the dysregulation of lipid metabolism and compromised repair, exacerbating the severity of conditions such as nonalcoholic fatty liver disease (NAFLD) and MASH.

While these findings were generated in a murine model, they establish an essential framework that informs potential human health risks. Given the parallels between murine and human liver physiology, it is plausible that microplastic exposure combined with high-fat diets could similarly predispose humans to aggravated liver damage. However, the researchers caution that further studies are necessary to confirm this translation and to elucidate the long-term implications for populations worldwide.

Dr. Oh emphasizes the broader relevance of this research: “Microplastics are now inextricably linked to daily life, yet their biological impact is only beginning to be understood. Through advanced spatial transcriptomic mapping, we have visualized the precise loci of hepatic damage induced by microplastics, revealing a novel environmental dimension to liver disease pathogenesis.” This nuanced comprehension paves the way for future investigations targeting environmental and dietary risk factors in liver health.

Moreover, these insights open avenues for therapeutic targeting. Modulating the PPAR-alpha-Anxa2 pathway could become a strategy to mitigate microplastic-induced liver injury or fortify the liver’s resilience against environmental toxins. Understanding such molecular crosstalk also facilitates improved diagnostic markers sensitive to environmental damage, allowing for earlier intervention in vulnerable populations.

This pioneering study exemplifies the intersection of environmental health, genomics, and hepatology, demonstrating how innovative technologies can elucidate complex biological interactions. It underscores the urgent need to address microplastic pollution not only as an ecological crisis but as a public health priority, particularly in societies where high-fat diets are prevalent.

As humanity grapples with escalating plastic waste and its fragmentary descent into invisible pollutants, research such as this serves as a clarion call for comprehensive strategies. Reducing plastic production, enhancing waste management, and fostering healthier dietary practices collectively form the cornerstone of mitigating hidden dangers to liver health and overall well-being.

The University of Oklahoma study, titled “Spatial Transcriptome Mapping Identifies Ppara-Anxa2 Crosstalk in Microplastic-Induced Hepatotoxicity,” stands as a seminal contribution offering unprecedented mechanistic clarity. Through employing spatial transcriptomics, the researchers have achieved a level of resolution that redefines how environmental toxicology and metabolic disease research can coalesce to confront emergent health threats posed by our plastic-saturated environment.

Subject of Research: Animals
Article Title: Spatial transcriptome mapping identifies Ppara-Anxa2 cross-talk in microplastic-induced hepatotoxicity
News Publication Date: 17-Jun-2026
Web References: https://doi.org/10.1126/sciadv.aec8681
References: Oh, T.G., Jung, W., Joshi, A.D., et al. Spatial Transcriptome Mapping Identifies Ppara-Anxa2 Crosstalk in Microplastic-Induced Hepatotoxicity. Science Advances, 2026.
Image Credits: University of Oklahoma
Keywords: Microplastics, Liver Disease, Fatty Liver Disease, Polyethylene, High-Fat Diets, Spatial Transcriptomics, PPAR-alpha, Anxa2, Hepatotoxicity, Environmental Health, Metabolic Dysfunction, Inflammation

Across the expansive military installations of the United States, where substantial tracts of restricted-access natural lands persist, an evolving challenge has taken shape: how to effectively conserve endangered species amid overlapping and often conflicting recovery plans. These lands, which serve dual purposes of defense readiness and environmental stewardship, present a unique ecological puzzle. Amid this complexity, researchers at Virginia Tech’s College of Natural Resources and Environment have embarked on pioneering projects funded by two $2 million grants, aiming to redefine conservation strategies on military properties by emphasizing ecosystem-wide management rather than isolated species-specific interventions.

Historically, wildlife management on military bases has heavily relied on individual species’ recovery plans, a methodology that becomes problematic when multiple endangered species inhabit the same territory. Each species’ plan often prescribes distinct conservation actions, potentially leading to redundant efforts, increased management complexity, and sometimes conflicting directives. Recognizing these inefficiencies, the Virginia Tech research initiative seeks to develop integrated strategies that optimize land management actions to benefit diverse species assemblages simultaneously. This integrative approach has the potential not only to streamline operational practices on military lands but also to serve as a scalable model for ecosystems worldwide grappling with multifaceted conservation demands.

One cornerstone of this research is led by Assistant Professor Elizabeth Hunter, who operates within the U.S. Geological Survey’s Virginia Cooperative Fish and Wildlife Research Unit. Hunter’s project area in southeastern Georgia—including large military bases characterized by fire-managed ecosystems—examines the application of prescribed burning as a habitat management tool. Prescribed fire has traditionally been tailored around a handful of focal species, such as the red-cockaded woodpecker, leaving many other species with differing ecological needs inadequately addressed. Hunter’s work challenges this paradigm by employing cutting-edge monitoring technologies to survey a wide spectrum of taxa, from avian and mammalian species to amphibians, reptiles, insects, and crucial pollinators, aiming to capture a comprehensive biological response to various fire regimes.

By integrating extensive biodiversity data into a sophisticated multi-objective optimization framework, Hunter’s team can evaluate how different prescribed burning strategies affect numerous species simultaneously. This analytical tool allows for the assessment of trade-offs and synergies in conservation outcomes, addressing complex ecological interactions. The methodology asks crucial questions such as whether it is possible to adjust burn frequency, intensity, and spatial patterns to enhance habitats for multiple species concurrently. Such questions are vital for military land managers, who must balance ecosystem health with operational imperatives. Collaborations with organizations like the Orianne Society and the National Council for Air and Stream Improvement anchor this work in both academic and applied conservation contexts.

Parallel to Hunter’s fire ecology focus, Associate Professor Haldre Rogers directs research tackling the inefficiencies inherent in the current species-by-species recovery plan framework under the U.S. Endangered Species Act. Rogers’ project, focused on the Marianas Islands, explores whether ecosystem-wide habitat management can serve as an effective surrogate for the management of multiple individually listed species. Given that military lands often harbor dozens of endangered species with overlapping but separate recovery plans, the question arises: can habitat proxies be identified that allow for effective ecosystem-level conservation without the cumbersome requirement of separate interventions and monitoring for each species?

Rogers utilizes innovative ecosystem hypergraph modeling to encapsulate the intricate web of species interactions, habitat connectivity, and life-history traits, thereby identifying clusters of species that might respond similarly to shared management actions. This approach strives to uncover ecological congruencies and potential conflicts, aiming to inform management choices that maximize conservation benefits while minimizing inadvertent harm to co-occurring species. The project acknowledges inevitable ecological trade-offs but aspires to equip land managers with a landscape-scale understanding that promotes more efficient and informed decision-making.

The ecological importance of military installations in the United States cannot be overstated. Many contain well-preserved habitats that have been safeguarded from urban development, offering refugia for imperiled species. Activities such as prescribed burning and restricted access have inadvertently preserved biodiversity hotspots. At the same time, these installations must fulfill critical defense and training missions, underscoring the need for a delicate balance between operational readiness and environmental stewardship. The innovations proposed by Hunter, Rogers, and their teams promise a new frontier in reconciling these dual mandates through science-driven, scalable conservation models.

Their research partnership traverses multiple disciplines and institutions, spanning Virginia Tech’s Department of Fish and Wildlife Conservation and Statistics, collaborations with Rice University, Brown University, MIT, and contributions from postdoctoral scholars. This transdisciplinary approach enriches the projects with a fusion of ecological expertise, advanced computational modeling, and applied management perspectives. By leveraging emerging technologies and sophisticated analytical tools, these projects are poised to generate transformative insights relevant to conservation practitioners, policymakers, and military land managers alike.

In essence, these Virginia Tech-led studies embody a paradigm shift: transitioning from fragmented, species-specific management plans to holistic ecosystem-based strategies is both a necessity and an opportunity. This shift acknowledges the complex interdependencies among species and their habitats, calling for innovative methodologies that embrace ecological complexity rather than oversimplify it. For military lands, where the intersection of conservation and operational use is most pronounced, such research can catalyze both more effective biodiversity protection and enhanced land-use efficiency.

By integrating large-scale biological monitoring with computational optimization and ecosystem modeling, this research presents a robust framework for addressing the mounting challenges of endangered species management amid competing land uses. The implications extend far beyond military properties, offering a strategic blueprint adaptable to diverse ecosystems facing overlapping conservation mandates. The collective efforts spearheaded by Hunter and Rogers represent a significant leap forward in safeguarding the nation’s biological heritage through science-guided stewardship, setting the stage for broader applications in the global conservation community.

As endangered species faces continue to escalate globally, the insights arising from military installation ecosystems can inform best practices worldwide. The integration of multi-species data into management decisions, the recognition of ecosystem processes over isolated species needs, and the embracing of technological and analytical innovation underscore the future of conservation science. In a world of finite conservation resources and competing priorities, finding operationally feasible yet ecologically sound approaches is paramount.

These projects, supported by the Strategic Environmental Research and Development Program, exemplify such an approach, bridging theoretical science and practical land management. Their success will not only enhance the resilience of endangered species populations on military lands but also serve as a clarion call to redefine conservation paradigms universally. Ultimately, their work invites a transformative dialogue around how humanity navigates the complex stewardship of nature amid modern societal demands.

Subject of Research:
Endangered species management on military lands through ecosystem-based strategies and multi-species conservation optimization.

Article Title:
Rethinking Conservation: Integrated Ecosystem Management for Endangered Species on Military Installations

News Publication Date:
Not provided

Web References:

• Virginia Tech College of Natural Resources and Environment: https://cnre.vt.edu/
• Department of Fish and Wildlife Conservation: https://fishwild.vt.edu/
• Orianne Society: https://www.oriannesociety.org/
• National Council for Air and Stream Improvement: https://ncasi.org/

Image Credits:
Photo courtesy of Elizabeth Hunter.

Keywords:
Endangered species, Extinction, Wildlife management, Conservation biology, Ecosystem management, Prescribed fire, Habitat connectivity, Multi-species optimization, Military land conservation, Ecosystem hypergraphs.

In a groundbreaking study led by The University of Texas MD Anderson Cancer Center, researchers have unveiled compelling insights into how radiation therapy can profoundly influence the immune landscape of brain metastases, opening new avenues for combinational immunotherapeutic strategies. Brain metastases, secondary tumors that originate from cancers elsewhere in the body and colonize the brain, represent one of the most formidable clinical challenges in oncology. Their treatment has been notoriously difficult due to the highly immunosuppressive nature of the brain tumor microenvironment and the protective blood-brain barrier, which together blunt the effectiveness of conventional immunotherapies.

Despite the advances in immune checkpoint inhibitors and cellular therapies that have revolutionized treatment for many cancers, these modalities have shown limited success in brain metastases. The prevailing concept attributes this resistance largely to the “cold” immune microenvironment within the brain, characterized by suppressed immune activation and poor T cell infiltration. Radiation therapy, traditionally employed for its cytotoxic effects on cancerous cells, has garnered interest as a potential immunomodulatory agent. However, the precise mechanisms by which radiation alters immune dynamics within brain metastases remained elusive until now.

Leveraging an integrative approach encompassing RNA sequencing and T cell receptor (TCR) profiling on samples from over 300 patients harboring brain metastases sourced predominantly from breast and lung primaries, the research team decoded the complex interplay between radiation and immune activation. Their findings, recently published in Clinical Cancer Research, reveal that pre-operative radiation not only directly damages tumor DNA but also reshapes the tumor microenvironment through enhanced recruitment and activation of cytotoxic T lymphocytes. This dual impact fundamentally transforms the previously immunologically inert metastatic lesions into immunologically responsive entities.

Mechanistically, radiation induces the release of tumor-associated antigens and danger signals, which act as potent stimulators for antigen-presenting cells and infiltrating lymphocytes. This cascade prompts an upregulation of inflammatory cytokines and immune checkpoints, effectively increasing tumor visibility to the immune system. Interestingly, radiation also modulates tumor vasculature, facilitating enhanced permeability and immune cell trafficking into the tumor bed. Concurrently, suppressive myeloid populations within the microenvironment are either depleted or reprogrammed, further alleviating immunosuppression.

One of the study’s pivotal revelations centers on T cell receptor diversity as a prognostic biomarker. Enhanced TCR diversity corresponds with better immunotherapeutic outcomes, suggesting that radiation-induced augmentation of this diversity might predict patient responsiveness. Such biomarkers hold immense clinical promise, enabling personalized treatment algorithms that optimize radiation-immunotherapy combinations tailored to individual tumor immune profiles.

Dr. Jason Huse, M.D., Ph.D., a leading pathologist at MD Anderson and co-senior author, emphasizes the transformative nature of these findings. “Our results demonstrate that instead of merely bypassing the blood-brain barrier, we should recalibrate our therapeutic focus toward the tumor microenvironment itself. Radiation effectively ‘primes’ these metastases, enabling robust immune engagement that was previously unattainable. This paradigm shift paves the way for clinical trials harnessing synergistic radiation and immunotherapy regimens.”

This shift is particularly significant given the limitations of systemic therapies in penetrating brain lesions. By directly modifying the local immune milieu, radiation circumvents longstanding pharmacologic barriers and leverages the body’s own immune arsenal for tumor eradication. The implications extend beyond localized control; emerging evidence hints at the potential for abscopal effects where immunity induced in the irradiated site mediates systemic antitumor responses.

The research incorporated tissue specimens from a contemporaneous clinical trial spearheaded by Dr. Debra Nana Yeboa, which contrasted pre-operative and postoperative radiation regimens. This comparative analysis reinforced the immunomodulatory superiority of pre-operative radiation, highlighting its capacity to bolster immune infiltration and activation before surgical tumor resection.

While the experimental findings are preliminary and retrospective, the investigators are actively validating these observations in larger, prospective clinical cohorts. The overarching goal is to delineate optimized therapeutic windows and dosing sequences that exploit radiation’s immunogenic potential in concert with checkpoint inhibitors, vaccines, or adoptive cell therapies.

In summary, this study delineates a critical and previously underappreciated function of radiation therapy in rendering brain metastases immunologically “hot.” By integrating radiation with immunotherapeutic modalities, there is a tangible prospect of overcoming the entrenched resistances posed by the brain’s unique protective and suppressive environment. This work marks a pivotal step toward improved survival rates and quality of life for patients afflicted with metastatic brain tumors.

As the oncology community eagerly anticipates forthcoming clinical trials, this research provides an urgent biological rationale for a comprehensive therapeutic strategy that targets both tumor cells and their microenvironment. The convergence of radiation biology and immunotherapy represents a new frontier with the capacity to redefine standard-of-care paradigms for brain metastases.

Subject of Research: The immunomodulatory effects of radiation therapy on brain metastases and the tumor immune microenvironment.

Article Title: Ionizing Radiation Enhances Prognostically Relevant Immune Signatures in Brain Metastases, Paving the Way for Combined Radiation-Immunotherapy Approaches.

News Publication Date: June 17, 2026

Web References:

• MD Anderson Cancer Center
• Clinical Cancer Research Journal

Image Credits: The University of Texas MD Anderson Cancer Center

Keywords: Brain metastases, Tumor microenvironment, Radiation therapy, Immunotherapy, T cell receptor diversity, Immune modulation, Blood-brain barrier, Cytotoxic T cells, Immune checkpoints, Biomarkers, Clinical oncology, Cancer treatment

Ebola Virus Finds Sanctuary in the Brain: Breaking Ground with Human Cerebral Organoids

In a landmark study published in Nature Microbiology, researchers from the Icahn School of Medicine at Mount Sinai and the Bernhard Nocht Institute for Tropical Medicine (BNITM) have uncovered how the deadly Ebola virus can persist and replicate stealthily within the human central nervous system. By leveraging cutting-edge cerebral organoid models—three-dimensional brain-like structures derived from human pluripotent stem cells—the team has shed light on the viral mechanisms that allow long-term survival, raising critical implications for treatment and prevention strategies of Ebola virus disease (EVD).

It has long been a harrowing clinical observation that survivors of acute Ebola infections sometimes suffer relapses or develop inflammatory syndromes months or even years after recovery. This enduring threat is attributed to the virus’s ability to hide out in “immune-privileged” regions of the body—such as the central nervous system (CNS)—where the immune surveillance is deliberately restrained to protect vulnerable tissue from damaging inflammation. This latest research elucidates the ways Ebola virus exploits this sanctuary and endures prison-like conditions inside cerebral tissue without fully succumbing to immune clearance.

The team engineered cerebral organoids by coaxing human induced pluripotent stem cells (iPSCs) into forming spherical, differentiated structures composed of multiple neural cell types: neurons, astrocytes, and microglia alike. These organoids mimic the cellular environment of the human brain closely enough to serve as a viable model to explore viral persistence with unprecedented resolution and relevance. Unlike traditional animal models, these human-derived organoids enable direct examination of host-virus interactions in a context that recapitulates human neuroanatomy and immunology.

Longitudinal infection experiments revealed that Ebola virus and related filoviruses—including Sudan, Reston, and Marburg viruses—could sustain active replication within these cerebral organoids for up to 120 days. More intriguingly, Ebola virus infected not just neurons but also astrocytes and microglia, the brain’s resident immune cells. The virus exhibited two spreading modalities: direct cell-to-cell contact transmission as well as classical budding from host cells. This productive persistence clearly places the virus in an infectious, replicative state rather than a latent or inactive one.

Despite the robust production of pro-inflammatory cytokines by infected organoids, the innate immune responses orchestrated within this model failed to clear the infection entirely. The study observed an upregulation of immune and inflammatory markers at later stages, mirroring clinical presentations seen in Ebola virus disease survivors who develop delayed meningoencephalitis and other inflammatory sequelae. The data affirm that persistent filovirus infection in immune-privileged tissues contributes to localized inflammation, fostering neurological disease conditions even after primary viremia subsides.

At the molecular level, whole-genome sequencing of viral populations recovered from persistently infected organoids uncovered the presence of defective viral genomes (DVGs) and a spectrum of mutations emerging during chronic replication. DVGs are truncated or mutated forms of viral genomes known to modulate replication dynamics and immune evasion in other viral families. These defective genomes may allow the Ebola virus to dampen replication while maintaining a foothold inside host tissue, facilitating long-term survival without triggering overwhelming immune destruction.

Several mutations identified in the viral sequences corresponded to variants previously reported to attenuate replication in natural infections, while others were novel and uncharacterized. This emerging mutational landscape hints at an ongoing evolutionary arms race as the virus adapts to the CNS environment and immune pressures. Such adaptations could be critical determinants in the capacity of Ebola virus to establish persistent reservoirs and cause relapses.

This cerebral organoid model’s faithful recapitulation of human Ebola virus infection patterns underscores its utility as a powerful platform for mechanistic studies of viral persistence. Unlike animal models, which often fail to mimic intricate human neural immunology adequately, organoids offer a nearer-to-human experimental system. This breakthrough has potential ramifications for testing and optimizing targeted antiviral therapies aimed specifically at reservoirs residing in immune-privileged compartments.

Moreover, cerebral organoids provide an ethically favorable and scalable alternative to animal experiments, fostering more humane and potentially faster progress in infectious disease research. This innovation aligns with global efforts to reduce animal use in biomedical studies and to increase translational fidelity to human conditions.

Looking ahead, the research team emphasizes expanding their investigations to include other lesser-studied filoviruses such as Taï Forest, Bombali, and Bundibugyo viruses. Comprehensive deciphering of host–virus dynamics in such a model may unravel universal persistence mechanisms across filovirus species, informing cross-cutting therapeutic strategies. Crucially, this work also lays groundwork for exploring how viral persistence in the CNS intersects with immune modulation, neuroinflammation, and long-term neurological sequelae in EVD survivors.

Persistent Ebola infection in the brain highlights a formidable challenge for public health, given the potential for virus reactivation or even transmission from immune-privileged sanctuaries. This study delivers a compelling window into that hidden battleground, leveraging state-of-the-art human cellular models to confront a deadly pathogen’s stealth strategies. Unlocking the biology of Ebola’s cerebral persistence may ultimately pave the way for interventions that not only save lives during acute infection but also circumvent post-recovery complications and community outbreaks.

As our understanding deepens, harnessing cerebral organoids as investigative tools promises to revolutionize the study of neurotropic viral infections. The Mount Sinai and BNITM collaboration exemplifies how multidisciplinary, translational research can illuminate the dark corners of viral pathogenesis and guide clinical innovation for diseases once deemed intractable.

Subject of Research: Animals (via human-derived cerebral organoids)

Article Title: Host–virus determinants of Ebola virus persistence in a human cerebral organoid model

News Publication Date: 12-Jun-2026

Web References:
https://www.nature.com/articles/s41564-026-02388-2
http://dx.doi.org/10.1038/s41564-026-02388-2

Keywords: Ebola virus, cerebral organoids, central nervous system, viral persistence, filoviruses, neuroinflammation, antiviral therapy, immune evasion, defective viral genomes, virus-host interaction

In recent years, the coastal waters of Vancouver have witnessed an unprecedented resurgence of whale activity, captivating marine biologists and local observers alike. This renewed presence, not merely anecdotal, stems from a culmination of seasonal patterns, thriving ecosystems, and impactful conservation measures. A comprehensive study led by researchers at the University of British Columbia’s Institute for the Oceans and Fisheries (IOF) has quantitatively confirmed that transient killer whales now inhabit the Salish Sea for more than two-thirds of the year. Alongside these apex predators, humpback and grey whales are increasingly frequenting these waters, signaling a dynamic shift in regional marine biodiversity.

Transient killer whales, known for their elusive nature and specialized diet of marine mammals, particularly seals and sea lions, are now commonly sighted along Vancouver’s shoreline and within the surrounding straits and harbors. Data collected from 2016 to 2023 underscores not only their presence but also their routine exploitation of these rich feeding grounds. This expanded usage correlates strongly with the rebound of pinniped populations, themselves benefiting from decades-old protections that halted their severe culling. The recovery has thus created a robust trophic cascade, enabling transient killer whales to establish a near year-round residency within the inside waters of Vancouver Island.

Humpback whales represent another remarkable comeback story in this region. Historically decimated by intense commercial whaling in the early 20th century, these baleen giants were completely extirpated from British Columbia waters by 1910. Without older generations to transmit migratory and feeding knowledge, their return to ancestral feeding grounds was lost for nearly a century. However, conservation efforts since the 1960s, including international bans on whaling and improved fisheries management, have facilitated a population recovery that now sees substantial numbers of humpbacks returning each summer to feast on abundant krill, herring, and other prey.

The presence of grey whales in areas around Vancouver is comparatively anomalous but increasingly documented. These whales typically forage offshore near Alaska, subsisting on amphipods—small crustaceans dependent on nutrient-rich algae associated with Arctic sea ice. The drastic loss of sea ice due to climate change directly undermines this fundamental food source, causing nutritional stress especially among pregnant and lactating females who must meet extraordinarily high energetic demands during migration and calf-rearing periods. Consequently, some grey whales are observed making unscheduled stops in the Salish Sea, an adaptation that reflects their deteriorating foraging options rather than traditional migratory behavior.

Studies estimate that pregnant grey whales require a daily intake of approximately 1,600 to 1,900 kilograms of prey to sustain both fetal development and energy reserves critical for postnatal care during their long migrations. Following calving, lactating females continue to consume between 1,300 and 1,600 kilograms of prey daily to nourish their calves for several months. Disruptions in prey availability, driven by climate-induced changes in sea ice and associated ecosystem dynamics, are thus placing immense physiological strain on these populations. The unfortunate consequence has been an observed increase in mortality rates, with malnourished grey whales occasionally stranding along the coastline.

This resurgence of whale activity near Vancouver not only highlights the success of targeted conservation policies but also underscores emerging challenges. Increased interactions between humans and whales necessitate rigorous adherence to safe viewing practices. Researchers advocate for maintaining substantial distances from whales—minimum thresholds are typically 200 meters for most killer whales and extend to 1,000 meters for the endangered southern resident killer whales. The regulations also stipulate 100 meters for other cetaceans, increasing to 200 meters when whales are resting or accompanied by calves. These guidelines are critical in minimizing disturbances and preventing collisions, which pose significant risks to these vulnerable animals.

Furthermore, the role of public awareness and responsible recreational boating cannot be overstated. Boaters, kayakers, and paddleboarders are urged to stay vigilant and reduce speeds when whale blowholes are sighted. The unpredictability of whale movements demands a precautionary approach to navigation within whale habitats. Educational initiatives, such as free online whale-safe boating courses offered by organizations like the Marine Education & Research Society (MERS), have proven effective tools in promoting safer human-wildlife coexistence in marine environments.

The broader implications of these findings extend into the realm of ecosystem health and global climate resilience. Whales function as keystone species, their feeding and migratory behaviors facilitating nutrient transport and productivity within marine systems. The return of diverse whale populations to coastal waters symbolizes not just ecological recovery but offers hope for restoring complex marine food webs fractured by human exploitation. Yet, the acute vulnerability of species such as grey whales to climate-driven habitat changes serves as a stark reminder of ongoing environmental threats.

Simultaneously, the study’s revelations about transient killer whales reveal a nuanced predator-prey dynamic finely attuned to regional ecosystem changes over recent decades. The resurgence of pinniped populations has provided these cetaceans with ample sustenance, allowing for sustained presence in traditionally seasonal zones. This trophic realignment invites further studies into the long-term evolutionary and behavioral adaptations of marine mammals in a rapidly changing oceanic milieu.

Whale conservation is, thus, at a critical juncture. While success stories abound, exemplified by humpback recovery, emerging stressors including climate change, ship traffic, and underwater noise pollution complicate the ecological narrative. The scientific community and policymakers must continue fostering adaptive management strategies that address these multifaceted challenges while engaging public participation for effective stewardship.

In conclusion, the intensifying presence of transient killer whales, humpbacks, and grey whales in Vancouver’s coastal waters offers a vivid testament to both nature’s resilience and the pressing need for sustained conservation vigilance. These marine mammals, emblematic of wider ocean health, depend on intact habitats, thoughtful human behaviors, and responsive environmental policies. As our understanding deepens through ongoing research, so too must our commitment to coexistence with these ocean giants, ensuring their survival amidst an era of rapid ecological transformation.

Subject of Research: Marine mammal population dynamics and conservation in Pacific Northwest coastal waters.

Article Title: Rebounding Giants: The Return of Whales to Vancouver’s Coastal Waters

News Publication Date: Not specified in the provided content.

Web References:

• https://onlinelibrary.wiley.com/doi/epdf/10.1111/mms.70205
• https://onlinelibrary.wiley.com/doi/10.1111/mms.70119
• https://courses.mersociety.org/courses/whale-safe-boating

References:

• Taryn Scarff et al., “Transient killer whales in the Salish Sea,” Marine Mammal Science
• Grey whale energetics and climate impact study, Marine Mammal Science

Image Credits: Julia Adelsheim

Keywords: Whales, Cetaceans, Marine mammals, Transient killer whales, Humpback whales, Grey whales, Conservation, Climate change effects, Salish Sea, Marine ecology, Pinnipeds, Fisheries management

In a groundbreaking advancement for artificial intelligence in healthcare, researchers at Mass General Brigham have unveiled BRIDGE, a comprehensive multilingual benchmark designed to critically assess how effectively large language models (LLMs) comprehend and interpret clinical patient-care text. Unlike existing AI evaluation metrics that rely primarily on structured and standardized medical exam questions, BRIDGE is engineered to engage with the multifaceted and complex language found in real-world clinical communications, including electronic health records (EHRs), case reports, and patient-doctor consultations, across nine different languages. This innovation represents a transformative step toward making AI tools more reliable and contextually aware in actual healthcare settings.

The existing paradigm in medical AI evaluation has predominantly centered on licensing exam questions composed in a controlled, formalized medical lexicon. These assessments, while rigorous, often fall short of reflecting the nuanced, variable, and sometimes ambiguous language used in actual clinical environments. The BRIDGE benchmark circumvents this limitation by employing authentic clinical texts, which capture the complexities and heterogeneity inherent to patient care dialogues, medical documentation, and clinical decision-making processes. This shift brings essential granularity and relevance to model performance metrics, providing clinicians and developers with more actionable insights.

The creators of BRIDGE demonstrated the stark contrast in performance between conventional exam-based evaluations and real-world clinical comprehension. For instance, the highest-performing LLM evaluated scored impressively on standard medical exams, achieving up to 92%. However, when subjected to BRIDGE’s rigorous clinical text test, the same model’s proficiency plummeted to only 44.8%. This significant disparity exposes considerable gaps in the AI’s ability to grasp the subtle clinical context, implicit meanings, and domain-specific language patterns prevalent in healthcare communications.

To validate the robustness and breadth of BRIDGE, the research team conducted a systematic performance evaluation of 95 distinct LLMs sourced from 59 different clinical AI initiatives. These models were subjected to a comprehensive battery of real-world clinical tasks encompassing the entire patient care continuum, ranging across 14 medical specialties. The tasks included patient triage, extraction of critical information from records, diagnostic reasoning, prognostic forecasting, and administrative functions such as billing code assignment. This extensive benchmarking provides a panoramic view of LLM capabilities and limitations in diverse clinical scenarios.

One of the more innovative features of BRIDGE is its public and continuously updated leaderboard hosted on the Hugging Face platform. This dynamic leaderboard catalogs the performance metrics of over 100 LLMs, enabling stakeholders including clinicians, health administrators, and AI developers to track comparative model efficacy in near real-time. The leaderboard thus fosters transparency and spurs iterative improvements by highlighting strengths and vulnerabilities within specific clinical tasks or language domains.

Another salient discovery made possible by BRIDGE is the identification of variability in AI performance across different medical specialties. Given that the benchmark corpus includes nine languages, the tool also illuminates disparities in model effectiveness when dealing with non-English clinical texts. This multilingual adaptability is particularly crucial as healthcare becomes more globally interconnected, underscoring the urgent need to develop culturally and linguistically sensitive AI applications that avoid exacerbating health inequities.

The scientific rigor of BRIDGE is underscored by its deep collaboration among experts spanning pharmacoepidemiology, pharmacoeconomics, clinical medicine, and computational modeling. The team includes senior authors such as Jie Yang, PhD, and Joshua Lin, MD, along with co-first authors Jiageng Wu and Bowen Gu, whose collective expertise was critical in ensuring the benchmark’s relevance and accuracy. Such interdisciplinary engagement is vital for bridging the gap between AI innovation and clinical applicability.

BRIDGE’s architecture and methodology leverage advanced computational simulation and modeling techniques, facilitating nuanced task designs that mimic real clinical workflows. This approach allows the benchmark to capture the dynamic and context-rich nature of clinical text interactions, incorporating elements like colloquial doctor-patient exchanges, complex diagnostic narratives, and procedural documentation. Consequently, BRIDGE functions as a high-fidelity proxy for real healthcare communication scenarios, offering a much-needed calibration tool for medical LLMs.

Funding generously provided by the Patient-Centered Outcomes Research Institute, the National Institutes of Health, and institutional scholarships reflects the strategic priority placed on refining AI’s role in healthcare delivery. Moreover, the rigorous conflict of interest disclosures and adherence to institutional compliance underscore the study’s commitment to transparency and ethical research standards. These factors enhance the credibility of BRIDGE as a benchmark tool destined to influence clinical AI development profoundly.

Importantly, BRIDGE is more than a passive evaluation tool—it is a catalyst for elevated AI design tailored to the clinical domain. By exposing the blind spots and differential performance across specialties and languages, it empowers AI developers to iterate more purposefully, embedding clinical nuance and real-world complexity into model training. This iterative feedback loop has the potential to accelerate the maturation of AI models from theoretical capabilities to practical clinical decision-support systems.

The release of BRIDGE is poised to address one of the persistent challenges in clinical AI—trust. Reliable understanding of patient-care language is paramount to fostering clinician confidence in AI-assisted diagnoses, prognoses, and patient management recommendations. The benchmark’s capacity to expose and rectify shortcomings before clinical deployment mitigates risks of errors caused by misinterpretation of nuanced clinical text, thereby safeguarding patient safety and improving care outcomes.

In closing, BRIDGE exemplifies a paradigm shift that acknowledges the inherent complexities of clinical language and seeks to elevate the fidelity of AI’s interpretative functions accordingly. As healthcare continues its digital transformation, integrating intelligent systems into everyday practice demands benchmarks as sophisticated and reflective as the environments they serve. BRIDGE sets a new gold standard in this endeavor, bridging the divide between cutting-edge AI performance and meaningful clinical utility.

Subject of Research: People

Article Title: BRIDGE: benchmarking large language models for understanding real-world clinical practice texts

News Publication Date: 17-Jun-2026

Web References:

• Mass General Brigham
• Nature Biomedical Engineering Article
• BRIDGE Medical Leaderboard

References: Wu, J. et al. “BRIDGE: Benchmarking Large Language Models for Understanding Real-world Clinical Practice Text” Nature Biomedical Engineering DOI: 10.1038/s41551-026-01719-2

Keywords: Artificial intelligence, machine learning, clinical medicine, large language models, electronic health records, multilingual AI, clinical text comprehension, medical AI benchmarking, healthcare AI, patient care AI

Physical therapy for stroke survivors has long relied on the physical presence and hands-on expertise of therapists walking alongside their patients. Now, a remarkable technological leap is reshaping this dynamic. Researchers at Northwestern University in collaboration with Shirley Ryan AbilityLab have unveiled a revolutionary rehabilitation system that forges a direct, real-time link between therapists and patients via robotic exoskeletons. This novel system, known as Therapist-Exoskeleton-Patient Interaction (TEPI), ushers in a new era of highly adaptive, personalized post-stroke gait therapy.

At the heart of TEPI lies a pair of lower-limb exoskeletons worn by the therapist and the stroke survivor, virtually coupled at the hips and knees through a sophisticated control interface. The virtual connection mimics the behavior of springs and shock absorbers, dynamically transmitting forces and movements between the two exoskeletons. This bidirectional, compliant coupling enables therapists to intuitively influence patient gait patterns in real time, offering a level of interaction that is vastly more nuanced than conventional robotic or manual therapies.

Traditional stroke rehabilitation often involves therapists physically assisting patients through limited aspects of movement, constrained by human strength and availability. In contrast, TEPI leverages robotics to augment the therapist’s capacity, delivering whole-body gait training that adjusts fluidly to the patient’s evolving performance. The hands-on adaptability of therapists is thus preserved but enhanced with robotic precision and scalability, facilitating more comprehensive, sustained walking practice without requiring multiple caregivers.

The core engineering breakthrough enabling TEPI is a control framework that models the mechanical interaction between therapist and patient exoskeletons as a coupled spring-damper system. This design imparts compliance and responsiveness, harmonizing the biomechanical inputs from both participants while preventing unnatural or jarring forces. By embedding this interactive virtual linkage, TEPI provides continuous haptic feedback to therapists, allowing them to modulate support, resistance, and corrective assistance in tune with patient movement intentions.

In a recent clinical evaluation published in Science Robotics, TEPI demonstrated superior outcomes compared to conventional therapist-guided treadmill training. Stroke survivors using the system achieved significantly greater joint range of motion, executed longer and higher stepping patterns, and maintained muscle activation at levels comparable to or exceeding standard therapy regimes. Importantly, patient motivation and enjoyment remained consistently high, underlining the system’s potential to foster engagement and adherence during demanding rehabilitation processes.

The TEPI platform addresses prominent limitations of current rehabilitation exoskeletons, many of which rely on rigid, preprogrammed gait cycles that lack real-time adaptability. By contrast, TEPI integrates therapist expertise directly into the robotic control loop, enabling instantaneous behavioral adjustments that match the patient’s unique recovery trajectory. This synergy of human judgment and machine assistance embodies a new paradigm in rehabilitation robotics, where technology serves to amplify, not replace, therapeutic skill.

José L. Pons, the project’s visionary leader and a professor at Northwestern, emphasizes that TEPI’s promise lies in its ability to unify the therapeutic closeness of manual training with the replicability and intensity of robotic interventions. Such hybrid systems are poised to transform stroke recovery protocols by bridging gaps between efficacy, accessibility, and individualized care. They not only alleviate therapist physical burden but also enhance the precision and personalization of rehabilitation exercises.

The development team included multidisciplinary experts spanning mechanical engineering, physical medicine, biomedical engineering, and robotics, fostering innovation at the interface of human-machine interaction and clinical practice. This collaboration ensured that TEPI’s control algorithms and mechanical design were continuously refined based on real-world clinical feedback, resulting in a system deeply attuned to both biomechanical and therapeutic demands.

Looking ahead, the research group plans to expand TEPI’s application beyond treadmill walking, exploring its integration into functionally critical daily activities such as overground ambulation, stair climbing, and sit-to-stand transitions. Longitudinal studies are also underway to assess the benefits of repeated therapy sessions over extended recovery periods. Additionally, efforts are progressing to miniaturize and streamline the technology for potential deployment in home environments, promising scalable remote rehabilitation solutions that can transcend geographic and logistical barriers.

TEPI’s pioneering approach was made possible by funding from the U.S. National Science Foundation’s National Robotics Initiative, reflecting the strategic importance of robotics in advancing healthcare outcomes. By embedding robotic exoskeletons within a responsive therapeutic framework, the system exemplifies how cutting-edge engineering can catalyze transformative changes in the treatment of neurological impairments.

This breakthrough not only advances rehabilitation science but also redefines the human role in therapy. TEPI empowers therapists to become active collaborators with their patients through enhanced, augmented physical connection, promoting a more effective and responsive recovery journey for stroke survivors. It stands as a shining example of innovation that is as empathetic as it is technological — a true step forward in restoring mobility and quality of life.

Subject of Research:
Robotic exoskeleton-assisted gait therapy for stroke rehabilitation through therapist-patient real-time interaction.

Article Title:
Therapist-exoskeleton-patient interaction for gait therapy

News Publication Date:
17-Jun-2026

Web References:
http://dx.doi.org/10.1126/scirobotics.adz9628

Image Credits:
Shirley Ryan AbilityLab

Keywords

Robotic exoskeletons, Robotics, Robotic gaits, Robotic walking, Physical therapy, Physical rehabilitation, Brain damage, Brain injuries, Brain ischemia, Neuromuscular diseases, Neurological disorders

St. Jude Children’s Research Hospital has reaffirmed its pivotal role in the global fight against pediatric cancer with its recent redesignation as a World Health Organization (WHO) Collaborating Centre for Childhood Cancer. This prestigious status not only honors St. Jude’s deep-rooted commitment to advancing pediatric oncology but also solidifies its unique position as the sole WHO Collaborating Centre exclusively dedicated to childhood cancer worldwide. The designation reflects the hospital’s substantial contributions in providing strategic, scientific, and technical expertise to WHO’s mission, thereby accelerating progress in improving survival rates and care quality for children afflicted by cancer internationally.

At the heart of this collaboration lies a fundamental conviction championed by St. Jude: a child’s geographic location must never dictate their likelihood of surviving cancer. Under the leadership of Dr. James R. Downing, St. Jude’s President and CEO, the institution actively partners with global health bodies, governments, academic institutions, and clinical providers to broaden access to comprehensive cancer care. These alliances are designed to fortify health infrastructures and knowledge exchange systems, ensuring equitable delivery of lifesaving therapies and supportive services for pediatric patients, irrespective of their origin.

St. Jude’s designation is not isolated but part of a sophisticated network of over 800 WHO collaborating centers distributed across more than 80 nations. Uniquely, St. Jude is dedicated exclusively to pediatric malignancies, making it an unparalleled resource in formulating childhood cancer policies and disseminating best practices. Since its inception as a WHO Collaborating Centre in 2018, St. Jude has leveraged its expertise to influence national health policies, boost technical capacity, and nurture multisectoral collaborations. These endeavors have collectively enhanced the global capacity to prevent, diagnose, and treat childhood cancers, shaping a more coordinated and effective response to pediatric oncology challenges.

The influence of St. Jude’s WHO Collaborating Centre extends significantly through the St. Jude Global Alliance, which encompasses over 400 institutions and foundations in more than 90 countries. This expansive network forms a robust implementation infrastructure that translates scientific discoveries into real-world improvements in pediatric cancer outcomes. As described by Dr. Catherine Lam, the Centre’s Director and a faculty clinician-scientist, this alliance fortifies the hospital’s academic and clinical expertise on an international scale, fostering innovation and knowledge transfer essential for tackling global disparities in pediatric oncology.

One of the landmark achievements stemming from this collaboration was the establishment of the WHO Global Initiative for Childhood Cancer (GICC) in 2018. This ambitious program targets a doubling of survival rates globally, aiming for at least 60% survival for childhood cancers by 2030. Complementing this, the 2025 launch of the Global Platform for Access to Childhood Cancer Medicines underscores a coordinated approach to overcoming barriers in medication availability and affordability—critical hurdles in low- and middle-income countries where cure rates have historically lagged behind.

The expanded remit of the WHO Collaborating Centre now includes not only oncology but also the management of catastrophic pediatric diseases such as sickle cell disease, representing an integrated strategy that acknowledges the complex medical and supportive care needs of these patient populations. This progression enhances the Centre’s potential to impact child health comprehensively, integrating palliative care and systems strengthening into its core objectives.

Driving the Centre’s evolving agenda, Dr. Carlos Rodriguez-Galindo, Executive Vice President and Chair of the Department of Global Pediatric Medicine, emphasizes the aim to ameliorate survival rates in regions where it has remained below 30%. Expanding the scope of pediatric care to encompass palliative services and holistic disease management initiatives ensures that children everywhere receive not only curative treatments but also dignified, comprehensive care throughout their disease trajectory.

The WHO recognizes the critical role of collaborating centers such as St. Jude in facilitating technical support, knowledge dissemination, and health system strengthening at the country level. According to Dr. Roberta Ortiz, medical officer at WHO Headquarters and focal point for the GICC, these centers bring invaluable expertise and tools that underpin successful implementation of global childhood cancer strategies. This partnership model is instrumental in translating high-level policy into practical actions that directly benefit pediatric populations.

St. Jude’s profound impact on national cancer control planning ensures that pediatric oncology is meaningfully integrated into broader health systems and governance frameworks. By embedding child-specific needs within policy platforms, the hospital advances a child-centered approach to cancer care that elevates research-driven innovations and frontline clinical breakthroughs. This comprehensive strategy enhances survivorship and quality of life for pediatric patients on a global scale.

In addition to its leadership in pediatric oncology, St. Jude also maintains a longstanding designation as a WHO Collaborating Centre for Influenza, a role it has fulfilled since 1975. This dual recognition highlights the institution’s diverse expertise and sustained contributions to global health, reaffirming its status as a vanguard institution whose research and clinical programs catalyze transformative progress across multiple domains of pediatric medicine.

St. Jude Children’s Research Hospital’s redesignation as the exclusive WHO Collaborating Centre dedicated to childhood cancer embodies the epitome of global health collaboration. Anchored in robust scientific inquiry, innovative care models, and strategic partnerships, this status propels forward a shared vision of equitable cancer care access and improved outcomes for all children—irrespective of geography. As the global pediatric oncology landscape evolves, St. Jude’s leadership and expansive alliance ensure that the journey toward eradicating childhood cancer is both scientifically rigorous and compassionately inclusive.

Subject of Research: Pediatric cancer, childhood oncology, global health collaboration

Article Title: St. Jude Reaffirmed as WHO Collaborating Centre Driving Global Pediatric Cancer Progress

News Publication Date: June 17, 2026

Web References:

• https://www.stjude.org/research/departments/global-medicine/who-collaborating-centre-for-childhood-cancer.html
• https://www.stjude.org/global/collaborating-to-cure/global-initiative.html
• https://global.stjude.org/en-us/featured/global-platform-for-access-to-childhood-cancer-medicines.html

Image Credits: St. Jude Children’s Research Hospital

Keywords: Pediatric cancer, Childhood cancer survival, WHO Collaborating Centre, Global pediatric oncology, St. Jude Global Alliance, Childhood cancer treatment access, Global Initiative for Childhood Cancer, Pediatric oncology research

In a groundbreaking study that redefines our understanding of how language is encoded in the human brain, researchers have mapped the diverse landscape of neurons distributed across frontal and temporal cortical regions, revealing a complex yet lateralized neural architecture for human language processing. By leveraging advanced single-neuron recording techniques alongside sophisticated language models, the team has identified not just the locations but the nuanced encoding properties of neurons implicated in various linguistic computations. This work illuminates how language, a uniquely human faculty, is instantiated at the neuronal level with precision and regional specificity.

The study’s comprehensive neuronal recordings spanned key brain areas historically associated with language, including the frontal cortex, anterior temporal cortex, and posterior temporal cortex. These regions were chosen given their established roles in speech production and linguistic comprehension, as well as their demonstrated selective responses in prior localized brain imaging studies. Importantly, the neurons examined were broadly distributed across both hemispheres and these cortical regions, showcasing the widespread neural substrate involved in language tasks.

One of the seminal findings was that roughly half of the neurons, 289 out of 579, exhibited selective responsiveness to one or more linguistic features. Intriguingly, this selectivity was evenly distributed across the three cortical sites — frontal, anterior temporal, and posterior temporal — and did not significantly differ between the left and right hemispheres. This suggests a foundational neural scaffold where language-related computations recruit a multitude of neurons across large-scale networks rather than isolated hotspots, emphasizing distributed processing over modular localization.

However, beyond this broad distribution, the study uncovered striking lateralization and regional differentiation in the strength and informational content of neural modulation. Neurons within the left hemisphere exhibited significantly stronger modulation—quantified by their z-scored activity changes—in response to linguistic features compared to their right hemisphere counterparts. This enhanced sensitivity encompassed a range of linguistic elements, including lower-order features like pitch, underscoring the superior role of the left hemisphere in detailed linguistic encoding.

Further dissecting these lateralized effects across cortical regions revealed that the posterior temporal cortex showed the most pronounced difference in left-right modulation strength, significantly outperforming other areas. This aligns well with the notion that posterior temporal areas are central to decoding complex linguistic dependencies and syntactic structures, functions critical for fluent language comprehension and production.

Conversely, the prefrontal cortex displayed the strongest overall neuronal modulation to these language features, both in the left and right hemispheres, compared to temporal regions. This finding suggests a hierarchical and possibly integrative role for the frontal cortex in orchestrating language processing, perhaps linked to higher-order syntactic planning, working memory, or executive control mechanisms required for natural speech.

The neural predictivity analysis, leveraging embeddings from cutting-edge contextual language models, further corroborated the lateralized and regionalized pattern. Neural activity in the left anterior temporal cortex was most accurately predicted by these language model features, highlighting this region’s role in abstract linguistic representation and semantic integration during language tasks.

Methodologically, the study capitalized on the precise temporal resolution of single-neuron recording combined with sophisticated statistical analyses, including permutation and rank-sum tests, to quantify neuronal response selectivity and modulation. This rigorous approach afforded a fine-grained characterization of how individual neurons adapt their firing patterns to various syntactic and prosodic elements of language in real-time.

Collectively, these data challenge conventional notions that neural language processing is confined to narrowly defined “language centers.” Instead, the findings advocate for a model of language representation as a widely distributed but regionally specialized system with marked hemispheric dominance. This has profound implications for understanding the neural basis of language disorders, suggesting that therapeutic interventions might need to consider both distributed network integrity and hemispheric targeting.

Moreover, the study’s integration of naturalistic language models with neurophysiological data marks a pioneering step in computational neuroscience, bridging theoretical frameworks of language with tangible neural mechanisms. By showing how models trained solely on linguistic input can approximate neuronal responses, this research points toward a future where artificial intelligence and neuroscience synergistically unravel human cognition.

Importantly, the results underscore the unique neural architecture supporting language that has evolved in humans, outstripping earlier simplistic models focused on gross anatomical mapping. These advances set the stage for future investigations that might explore how these neuronal populations interact dynamically during complex language tasks such as conversation, narrative comprehension, or bilingual processing.

In conclusion, this landmark research paints a detailed, high-resolution portrait of the neuronal building blocks underpinning human language. It reveals an exquisitely lateralized and regionally differentiated system whereby distributed neurons collectively encode the multifaceted features of speech. Such insights not only deepen fundamental neuroscience but also hold promise for novel clinical interventions and computational linguistic advancements.

Subject of Research: Neuronal encoding of human language features across frontal and temporal cortical regions; lateralization and regional differentiation of linguistic processing in the brain.

Article Title: Mapping the neuronal building blocks of human language with language models.

Article References:
Cai, J., Kfir, Y., Jamali, M. et al. Mapping the neuronal building blocks of human language with language models. Nature (2026). https://doi.org/10.1038/s41586-026-10691-5

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41586-026-10691-5

Biomedical tests using augmented and virtual reality tools to advance space health dominated the research schedule aboard the International Space Station on Wednesday. The Expedition 74 crew is also turning its attention to a spacewalk at the end of the month following the departure of a U.S. cargo spacecraft.

NASA flight engineers Jessica Meir and Jack Hathaway began their shift in the Columbus laboratory module conducting vein scans with guidance from doctors on the ground. The duo took turns scanning each other with the EchoFinder-2 ultrasound device that collects health data using augmented reality and artificial intelligence tools. The medical hardware provided by ESA (European Space Agency) provides a screen using augmented reality to guide the operator’s probe motion and artificial intelligence software to detect the subject’s organs. The lightweight, easy-to-use gear may enable independent crew health monitoring on spacecraft travelling to the Moon, Mars, and beyond.

Afterward, Hathaway moved to the Harmony module and loaded bacteria samples into a portable DNA sequencer to read their genetic code. Scientists will use the knowledge to understand bacterial resistance to antibiotics in the space environment potentially affecting an astronaut’s ability to fight an infection.  

Meir assisted NASA flight engineer Chris Williams who wore virtual reality goggles for a test measuring his ability to detect balance, movement, orientation in microgravity. The goggles recorded Williams’s eye movements as he responded to visual stimuli generated by computer software operated by Meir. The vestibular system investigation, just one part of the CIPHER suite of 14 human research experiments, is studying how astronauts neurologically adapt to weightlessness to improve crew training and safety.

ESA flight engineer Sophie Adenot helped her crewmates with the digital health science on Wednesday first setting up the EchoFinder-2 hardware, connecting it to a computer tablet, and installing a camera to track the vein study. Next, Adenot configured Harmony’s maintenance work area and retrieved a mini-cold bag to house the bacteria samples for the antibiotics study. Finally, she took pictures of the Moon to observe Earth’s light reflecting off the lunar surface.

All four astronauts gathered together at the end of their shift for a conference call with spacewalk experts on the ground. The quartet and the engineers discussed the tools and procedures necessary to repair a wrist joint on the Canadarm2 robotic arm during a spacewalk planned for June 30. NASA will soon announce the spacewalkers and provide a live televised briefing for more details before the end of the month.

Roscosmos flight engineer Andrey Fedyaev conducted another neurological study while wearing a virtual reality headset and responded to computerized stimuli as electrodes measured brain activity and tracked eye movement, testing his sense of direction, movement, and position. Station commander Sergey Kud-Sverchkov and flight engineer Sergei Mikaev, both from Roscosmos, started their shift in the Nauka science module checking the operation of components supporting the Elektron oxygen generator. Kud-Sverchkov then tested communications gear inside the Soyuz MS-28 crew spacecraft. Mikaev took a computer quiz documenting his mental state before terminating a 24-hour heart and blood pressure monitoring session.

A SpaceX Dragon cargo spacecraft is back on Earth following its undocking from the orbital outpost on Tuesday and splashdown in the Pacific Ocean at 5:11 a.m. PDT/8:11 a.m. EDT on Wednesday. Dragon returned sensitive scientific samples from investigations studying stem cell manufacturing, cartilage tissue printing, and more to treat a range of conditions from blood diseases, cancers, and cartilage injuries.

Learn more about station activities by following the space station blog, @space_stationon X, as well as the ISS Facebook and ISS Instagram accounts.

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The post Advanced Health Research on Station Using Augmented, Virtual Reality Tools appeared first on NASA Science.

Researchers at Washington University School of Medicine in St. Louis have made a groundbreaking discovery that could revolutionize the prevention of diarrheal diseases caused by enterotoxigenic Escherichia coli (ETEC) and Shigella. These two bacterial pathogens are responsible for hundreds of millions of infections annually and are leading causes of diarrheal mortality worldwide, particularly among young children. Despite decades of efforts, vaccine development has encountered significant obstacles, primarily due to the extensive strain variability that hampers the identification of universal vaccine targets.

In a recent study published in the Proceedings of the National Academy of Sciences, the WashU team, collaborating with scientists at the University of Missouri and the International Centre for Diarrhoeal Disease Research in Bangladesh, identified a shared vulnerability within these pathogens that could open the door for a combined vaccine platform. This innovative approach hinges on targeting homologous enzymes that these bacteria use to degrade the mucus lining in the human gut, a critical step in establishing infection.

For bacterial pathogens like ETEC and Shigella to cause illness, they first need to overcome the intestinal mucus barrier. This thick layer of mucus serves as a physical and biochemical shield protecting the gut epithelium and regulating the microenvironment by keeping pathogenic entities at bay while preserving the beneficial microbiota. The ability to breach this barrier is a hallmark of pathogenicity, allowing bacteria to access the underlying tissues and deploy additional virulence factors, including enterotoxins that induce diarrhea.

The study’s focal point is a family of mucin-degrading enzymes that facilitate this breaching process. The researchers detail three closely related enzymes—EatA, SepA, and Pic—that are expressed by ETEC, Shigella, and other diarrheal pathogens. EatA, an acronym for “eat away,” is produced by ETEC and was previously identified by Fleckenstein’s laboratory as a critical mucinase targeting the primary structural protein within mucus. SepA and Pic, related enzymes produced by Shigella and some other bacteria, perform analogous roles. Their enzymatic activity effectively dismantles the mucosal barrier, clearing a path for bacterial invasion.

Intriguingly, the antibodies that the team isolated from individuals infected with ETEC or experimentally exposed to the bacteria displayed a functional cross-reactivity. The antibodies not only neutralized EatA but also inhibited SepA and Pic, indicating a conserved epitope region among these mucinases. This neutralization prevents the enzymes from degrading intestinal mucus, thereby blocking the pathogens’ entry into host tissues. The concept of a single antibody interfering with multiple bacterial targets underscores a significant breakthrough in vaccine strategy.

To unravel the structural mechanics behind this immune neutralization, the researchers leveraged cryo-electron microscopy—a state-of-the-art imaging method that preserves biomolecules in near-native states by flash-freezing samples. This technique enabled detailed visualization at atomic resolution, revealing the precise binding site of the neutralizing antibodies. Remarkably, the site of interaction was a structurally conserved region across EatA, SepA, and Pic, providing a rational basis for the design of vaccine antigens that elicit broadly neutralizing antibodies.

“The identification of this shared Achilles’ heel among diverse diarrhea-causing bacteria signifies a paradigm shift in vaccine development,” explains James M. Fleckenstein, MD, co-senior author of the study and professor of medicine at WashU. “It suggests we can target a common mechanism of gut colonization rather than chasing highly variable surface molecules, which has been the stumbling block in the field for so long.”

Further bolstering the translational potential of these findings, epidemiological data from children in Dhaka, Bangladesh, indicate that naturally acquired antibodies against EatA correlate with protection from diarrheal illness. This natural immunity validates EatA as a viable immunological target and encourages the pursuit of vaccines that induce similar protective responses.

The implications extend beyond the developing world, as enterotoxigenic E. coli has been implicated in recent foodborne outbreaks in industrialized countries such as the United States. The difficulty in distinguishing pathogenic ETEC from non-pathogenic strains in clinical settings further complicates diagnosis and containment. Moreover, reliance on antibiotics to treat infections caused by these bacteria accelerates the evolution of antibiotic resistance, posing a global public health threat.

Zachary Berndsen, PhD, assistant professor of biochemistry at the University of Missouri and co-senior author, emphasizes the rational approach to vaccine design enabled by these insights. “By pinpointing enzyme domains targeted by neutralizing antibodies, we provide a template for crafting precise immunogens that can stimulate protective immunity across multiple pathogens. This can streamline the production of vaccines that are both effective and broad-spectrum,” Berndsen says.

Development of such a vaccine could not only reduce the global burden of diarrheal diseases but also mitigate the spread of antibiotic resistance by decreasing the frequency of bacterial infections requiring treatment. Additionally, preserving the gut microbiota through targeted disruption of pathogenic mechanisms may alleviate some adverse consequences associated with broad-spectrum antibiotic use.

Going forward, the research team is focused on translating their molecular discoveries into practical vaccine candidates. This involves preclinical testing of immunogens incorporating the conserved epitopes identified, assessing their immunogenicity and protective efficacy in animal models, and progressing toward human clinical trials.

“In our ongoing battle with enteric pathogens that have coevolved with humans for millennia, blocking the enzymatic opening of the mucus gate represents a promising strategy,” Fleckenstein concludes. “If successful, this vaccine would preempt infection at its earliest and most vulnerable stage, changing the trajectory of diarrheal disease worldwide.”

The study was supported by grants from the National Institute of Allergy and Infectious Diseases and the Department of Veterans Affairs. The multidisciplinary collaboration brings together expertise in infectious diseases, structural biology, immunology, and clinical research, underscoring the necessity of integrated approaches to tackle complex global health challenges.

Subject of Research: Human tissue samples

Article Title: Human enterotoxigenic Escherichia coli (ETEC) infections elicit antibodies that broadly neutralize mucinases of pathogenic Escherichia coli and Shigella

News Publication Date: 15-Jun-2026

References:
Buckley DP, Akhtar M, Thapa M, Schmitz A, Turner J, Vickers TJ, Khatoon N, Kaisar MH, Coggin JA, Ganguli D, Sheikh A, Laird RM, Poly F, Porter CK, Ruiz-Perez F, Miller MJ, Chowdhury F, Bhuiyan TR, Qadri F, Trillo-Muyo S, Dolan B, van der Post S, Ellebedy A, Berndsen ZT, Fleckenstein JM. Human enterotoxigenic Escherichia coli (ETEC) infections elicit antibodies that broadly neutralize mucinases of pathogenic Escherichia coli and Shigella. PNAS. June 15, 2026.

Image Credits: David Hasty

Keywords: Infectious diseases, Microbial infections, Diarrhea

Each year, nearly 800,000 Americans survive a stroke, embarking on a challenging journey toward recovery marked by relearning foundational motor skills such as walking. The aftermath of a stroke often results in muscle weakness, impaired coordination, and compromised leg control, making even the simplest of movements daunting. Traditional rehabilitation protocols heavily depend on intensive, therapist-led sessions where patients progressively regain mobility, independence, and confidence. However, the physical demands on therapists and the limitations of conventional methods necessitate innovative approaches that can enhance therapy effectiveness while mitigating therapist fatigue.

A groundbreaking study led by researchers from Shirley Ryan AbilityLab and Northwestern University introduces a novel paradigm that integrates lower-limb exoskeletons to enhance therapist-patient interaction during functional gait training. Published in the prestigious journal Science Robotics, the study unveils a transformative approach termed Therapist-Exoskeleton-Patient Interaction (TEPI). This system connects a therapist and a stroke survivor physically via complementary lower-limb exoskeletons, linked through virtual spring-damper elements at the hips and knees. This design facilitates real-time bidirectional physical interaction, where the therapist’s movements dynamically guide and respond to the patient’s gait by modulating forces through the exoskeleton interface.

Conventional physical therapy for gait rehabilitation involves therapists providing hands-on corrective assistance to patients, focusing typically on isolated aspects of walking mechanics due to their ability to assist only a limited number of joints or movements simultaneously. Complex, whole-body retraining often demands multiple therapists, posing logistical and physical constraints. While robotic rehabilitation devices can increase therapy intensity by enabling prolonged walking practice, most systems operate on preprogrammed, fixed movement trajectories that lack the flexibility to adapt instantaneously to patient performance or allow meaningful therapist input. This gap limits personalized care and the nuanced adaptability essential in neurorehabilitation.

TEPI fundamentally redefines this intervention landscape by leveraging the dexterous control capabilities of therapists in conjunction with robotic consistency and scalability. Through the exoskeleton-mediated connection, therapists can impose finely tuned guidance, resistance, or assistance, tailored in real time to the patient’s biomechanical status and response patterns. This synergy allows the therapy to encompass intricate whole-body dynamics within a single therapeutic session, eliminating the need for multiple practitioners in many cases. Moreover, the system’s responsiveness facilitates continuous adjustment throughout the gait cycle, enhancing motor learning through immediate feedback.

During the pilot evaluation involving eight stroke survivors, TEPI was contrasted with conventional therapist-guided treadmill walking sessions. Quantitative motion analysis revealed that TEPI training elicited significantly greater joint range of motion, augmented step length, and increased step height compared to standard therapy. Electromyographic assessments indicated comparable muscle activation patterns between the two modalities, affirming that TEPI does not compromise neuromuscular engagement while augmenting kinematic outcomes. Subjective evaluations reflected high patient motivation and enjoyment, underscoring the system’s potential to enhance adherence and therapeutic enthusiasm.

The TEPI framework also addresses a critical occupational health issue: therapist fatigue and injury risk associated with manual gait rehabilitation. By externalizing some physical effort to the exoskeleton-mediated interaction, therapists can guide patient movements more sustainably and ergonomically. This innovative method not only preserves the expertise of hands-on care but also reduces the biomechanical strain on providers, potentially extending the longevity and well-being of rehabilitation professionals.

From an engineering perspective, the system employs a sophisticated control architecture that harmonizes the exoskeleton’s stiffness and damping properties with the therapist’s voluntary movements. The virtual spring-damper coupling dynamically modulates mechanical impedance at key lower-limb joints, enabling a naturalistic yet controlled interaction paradigm. This technical advancement permits the system to act almost like an intelligent mechanical extension of the therapist’s own legs, enabling seamless transfer of movement intent and corrective forces.

Looking ahead, the researchers plan to expand the TEPI model beyond treadmill walking to include overground ambulation, stair navigation, and sit-to-stand transitions—functional tasks that more holistically represent daily living activities. The capacity to apply this approach across varied locomotor challenges promises to broaden its clinical applicability and deepen its therapeutic impact. Furthermore, scaling the technology into more accessible and user-friendly configurations could facilitate home-based rehabilitation, supporting remote care delivery and extending therapeutic supervision beyond clinical settings.

Such remote rehabilitation capability aligns with emerging trends in teletherapy and digital health, addressing barriers to access and continuity of care, especially for patients in underserved regions or with mobility limitations. By integrating sensor networks, adaptive control algorithms, and connectivity protocols, future iterations of TEPI could enable therapists to remotely guide patients through personalized gait training regimens with real-time haptic feedback and data monitoring.

This pioneering work symbolizes a major step forward in merging human expertise and robotic technology to optimize post-stroke rehabilitation. By synergizing the adaptability and intuitive understanding of therapists with the precision and endurance of robotic exoskeletons, TEPI opens a new frontier for restoring functional mobility—ultimately enhancing quality of life for millions of stroke survivors.

The collaborative research team behind this innovative study includes José L. Pons, PhD, scientific chair at Shirley Ryan AbilityLab and professor at Northwestern University; postdoctoral researchers Lorenzo Vianello, PhD, and Matthew R. Short, PhD; and co-first author Emek Barış Küçüktabak, PhD. Their collective expertise spans neurorehabilitation, robotics, and biomechanical engineering, driving the development of this cutting-edge, translational technology.

As the field advances, the TEPI approach may serve as a blueprint for next-generation rehabilitation robotics, where human-robot collaboration is optimized to support recovery from complex neurological impairments. The blend of immersive therapist control, real-time adaptability, and patient-centered design embodied by TEPI heralds a new era in rehabilitation science—one poised to transform care standards and patient outcomes.

Subject of Research: People
Article Title: Therapist-exoskeleton-patient interaction for gait therapy
News Publication Date: 17-Jun-2026
Web References: DOI link
Image Credits: Shirley Ryan AbilityLab
Keywords: Health care, Diseases and disorders, Biomedical engineering