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  • Chan Zuckerberg Initiative’s rBio uses virtual cells to train AI, bypassing lab work

    Chan Zuckerberg Initiative’s rBio uses virtual cells to train AI, bypassing lab work

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    The Chan Zuckerberg Initiative announced Thursday the launch of rBio, the first artificial intelligence model trained to reason about cellular biology using virtual simulations rather than requiring expensive laboratory experiments — a breakthrough that could dramatically accelerate biomedical research and drug discovery.

    The reasoning model, detailed in a research paper published on bioRxiv, demonstrates a novel approach called “soft verification” that uses predictions from virtual cell models as training signals instead of relying solely on experimental data. This paradigm shift could help researchers test biological hypotheses computationally before committing time and resources to costly laboratory work.

    “The idea is that you have these super powerful models of cells, and you can use them to simulate outcomes rather than testing them experimentally in the lab,” said Ana-Maria Istrate, senior research scientist at CZI and lead author of the research, in an interview. “The paradigm so far has been that 90% of the work in biology is tested experimentally in a lab, while 10% is computational. With virtual cell models, we want to flip that paradigm.”

    How AI finally learned to speak the language of living cells

    The announcement represents a significant milestone for CZI’s ambitious goal to “cure, prevent, and manage all disease by the end of this century.” Under the leadership of pediatrician Priscilla Chan and Meta CEO Mark Zuckerberg, the $6 billion philanthropic initiative has increasingly focused its resources on the intersection of artificial intelligence and biology.

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    rBio addresses a fundamental challenge in applying AI to biological research. While large language models like ChatGPT excel at processing text, biological foundation models typically work with complex molecular data that cannot be easily queried in natural language. Scientists have struggled to bridge this gap between powerful biological models and user-friendly interfaces.

    “Foundation models of biology — models like GREmLN and TranscriptFormer — are built on biological data modalities, which means you cannot interact with them in natural language,” Istrate explained. “You have to find complicated ways to prompt them.”

    The new model solves this problem by distilling knowledge from CZI’s TranscriptFormer — a virtual cell model trained on 112 million cells from 12 species spanning 1.5 billion years of evolution — into a conversational AI system that researchers can query in plain English.

    The ‘soft verification’ revolution: Teaching AI to think in probabilities, not absolutes

    The core innovation lies in rBio’s training methodology. Traditional reasoning models learn from questions with unambiguous answers, like mathematical equations. But biological questions involve uncertainty and probabilistic outcomes that don’t fit neatly into binary categories.

    CZI’s research team, led by Senior Director of AI Theofanis Karaletsos and Istrate, overcame this challenge by using reinforcement learning with proportional rewards. Instead of simple yes-or-no verification, the model receives rewards proportional to the likelihood that its biological predictions align with reality, as determined by virtual cell simulations.

    “We applied new methods to how LLMs are trained,” the research paper explains. “Using an off-the-shelf language model as a scaffold, the team trained rBio with reinforcement learning, a common technique in which the model is rewarded for correct answers. But instead of asking a series of yes/no questions, the researchers tuned the rewards in proportion to the likelihood that the model’s answers were correct.”

    This approach allows scientists to ask complex questions like “Would suppressing the actions of gene A result in an increase in activity of gene B?” and receive scientifically grounded responses about cellular changes, including shifts from healthy to diseased states.

    Beating the benchmarks: How rBio outperformed models trained on real lab data

    In testing against the PerturbQA benchmark — a standard dataset for evaluating gene perturbation prediction — rBio demonstrated competitive performance with models trained on experimental data. The system outperformed baseline large language models and matched performance of specialized biological models in key metrics.

    Particularly noteworthy, rBio showed strong “transfer learning” capabilities, successfully applying knowledge about gene co-expression patterns learned from TranscriptFormer to make accurate predictions about gene perturbation effects—a completely different biological task.

    “We show that on the PerturbQA dataset, models trained using soft verifiers learn to generalize on out-of-distribution cell lines, potentially bypassing the need to train on cell-line specific experimental data,” the researchers wrote.

    When enhanced with chain-of-thought prompting techniques that encourage step-by-step reasoning, rBio achieved state-of-the-art performance, surpassing the previous leading model SUMMER.

    From social justice to science: Inside CZI’s controversial pivot to pure research

    The rBio announcement comes as CZI has undergone significant organizational changes, refocusing its efforts from a broad philanthropic mission that included social justice and education reform to a more targeted emphasis on scientific research. The shift has drawn criticism from some former employees and grantees who saw the organization abandon progressive causes.

    However, for Istrate, who has worked at CZI for six years, the focus on biological AI represents a natural evolution of long-standing priorities. “My experience and work has not changed much. I have been part of the science initiative for as long as I have been at CZI,” she said.

    The concentration on virtual cell models builds on nearly a decade of foundational work. CZI has invested heavily in building cell atlases — comprehensive databases showing which genes are active in different cell types across species — and developing the computational infrastructure needed to train large biological models.

    “I’m really excited about the work that’s been happening at CZI for years now, because we’ve been building up to this moment,” Istrate noted, referring to the organization’s earlier investments in data platforms and single-cell transcriptomics.

    Building bias-free biology: How CZI curated diverse data to train fairer AI models

    One critical advantage of CZI’s approach stems from its years of careful data curation. The organization operates CZ CELLxGENE, one of the largest repositories of single-cell biological data, where information undergoes rigorous quality control processes.

    “We’ve generated some of the flagship initial data atlases for transcriptomics, and those were generated with diversity in mind to minimize bias in terms of cell types, ancestry, tissues, and donors,” Istrate explained.

    This attention to data quality becomes crucial when training AI models that could influence medical decisions. Unlike some commercial AI efforts that rely on publicly available but potentially biased datasets, CZI’s models benefit from carefully curated biological data designed to represent diverse populations and cell types.

    Open source vs. big tech: Why CZI is giving away billion-dollar AI technology for free

    CZI’s commitment to open-source development distinguishes it from commercial competitors like Google DeepMind and pharmaceutical companies developing proprietary AI tools. All CZI models, including rBio, are freely available through the organization’s Virtual Cell Platform, complete with tutorials that can run on free Google Colab notebooks.

    “I do think the open source piece is very important, because that’s a core value that we’ve had since we’ve started CZI,” Istrate said. “One of the main goals for our work is to accelerate science. So everything we do is we want to make it open source for that purpose only.”

    This strategy aims to democratize access to sophisticated biological AI tools, potentially benefiting smaller research institutions and startups that lack the resources to develop such models independently. The approach reflects CZI’s philanthropic mission while creating network effects that could accelerate scientific progress.

    The end of trial and error: How AI could slash drug discovery from decades to years

    The potential applications extend far beyond academic research. By enabling scientists to quickly test hypotheses about gene interactions and cellular responses, rBio could significantly accelerate the early stages of drug discovery — a process that typically takes decades and costs billions of dollars.

    The model’s ability to predict how gene perturbations affect cellular behavior could prove particularly valuable for understanding neurodegenerative diseases like Alzheimer’s, where researchers need to identify how specific genetic changes contribute to disease progression.

    “Answers to these questions can shape our understanding of the gene interactions contributing to neurodegenerative diseases like Alzheimer’s,” the research paper notes. “Such knowledge could lead to earlier intervention, perhaps halting these diseases altogether someday.”

    The universal cell model dream: Integrating every type of biological data into one AI brain

    rBio represents the first step in CZI’s broader vision to create “universal virtual cell models” that integrate knowledge from multiple biological domains. Currently, researchers must work with separate models for different types of biological data—transcriptomics, proteomics, imaging—without easy ways to combine insights.

    “One of our grand challenges is building these virtual cell models and understanding cells, as I mentioned over the next couple of years, is how to integrate knowledge from all of these super powerful models of biology,” Istrate said. “The main challenge is, how do you integrate all of this knowledge into one space?”

    The researchers demonstrated this integration capability by training rBio models that combine multiple verification sources — TranscriptFormer for gene expression data, specialized neural networks for perturbation prediction, and knowledge databases like Gene Ontology. These combined models significantly outperformed single-source approaches.

    The roadblocks ahead: What could stop AI from revolutionizing biology

    Despite its promising performance, rBio faces several technical challenges. The model’s current expertise focuses primarily on gene perturbation prediction, though the researchers indicate that any biological domain covered by TranscriptFormer could theoretically be incorporated.

    The team continues working on improving the user experience and implementing appropriate guardrails to prevent the model from providing answers outside its area of expertise—a common challenge in deploying large language models for specialized domains.

    “While rBio is ready for research, the model’s engineering team is continuing to improve the user experience, because the flexible problem-solving that makes reasoning models conversational also poses a number of challenges,” the research paper explains.

    The trillion-dollar question: How open source biology AI could reshape the pharmaceutical industry

    The development of rBio occurs against the backdrop of intensifying competition in AI-driven drug discovery. Major pharmaceutical companies and technology firms are investing billions in biological AI capabilities, recognizing the potential to transform how medicines are discovered and developed.

    CZI’s open-source approach could accelerate this transformation by making sophisticated tools available to the broader research community. Academic researchers, biotech startups, and even established pharmaceutical companies can now access capabilities that would otherwise require substantial internal AI development efforts.

    The timing proves significant as the Trump administration has proposed substantial cuts to the National Institutes of Health budget, potentially threatening public funding for biomedical research. CZI’s continued investment in biological AI infrastructure could help maintain research momentum during periods of reduced government support.

    A new chapter in the race against disease

    rBio’s launch marks more than just another AI breakthrough—it represents a fundamental shift in how biological research could be conducted. By demonstrating that virtual simulations can train models as effectively as expensive laboratory experiments, CZI has opened a path for researchers worldwide to accelerate their work without the traditional constraints of time, money, and physical resources.

    As CZI prepares to make rBio freely available through its Virtual Cell Platform, the organization continues expanding its biological AI capabilities with models like GREmLN for cancer detection and ongoing work on imaging technologies. The success of the soft verification approach could influence how other organizations train AI for scientific applications, potentially reducing dependence on experimental data while maintaining scientific rigor.

    For an organization that began with the audacious goal of curing all diseases by the century’s end, rBio offers something that has long eluded medical researchers: a way to ask biology’s hardest questions and get scientifically grounded answers in the time it takes to type a sentence. In a field where progress has traditionally been measured in decades, that kind of speed could make all the difference between diseases that define generations—and diseases that become distant memories.


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  • India buys palm oil cargoes from Latin America at steep discounts

    India buys palm oil cargoes from Latin America at steep discounts

    Freight to ship palm oil from the Americas is about $90 per ton, compared with $45 from Southeast Asia, said Sandeep Bajoria, chief executive of Sunvin Group, a Mumbai-based brokerage.

    Vessels will be loaded at South American ports in September to arrive at India’s Kandla port in October, said a New Delhi-based dealer.

    Latin America exports half of its five million tons of palm oil, and India’s first purchases from the region could open the door to more supplies, said Aashish Acharya, vice president at Patanjali Foods, a leading importer of edible oils.

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  • From Blocking to Locking: Rethinking How Amgen Intervenes in Disease

    From Blocking to Locking: Rethinking How Amgen Intervenes in Disease

    Summary:

    • Scientists at Amgen are creating a new class of molecules designed to stabilize natural interactions in the body, offering a novel approach to treating diseases.
    • LOCKTAC glues can precisely target disease processes by stabilizing existing cellular interactions, potentially reaching previously “undruggable” targets and minimizing side effects.
    • AMG 193, a clinical-stage LOCKTAC molecule, is designed to inhibit the enzyme PRMT5 in certain cancer cells.

    For decades, most medicines have worked the same way – by blocking something. They inhibit enzymes, shut down receptors or keep proteins from binding to one another. This approach has delivered many important therapies, but it’s not always enough. Biology isn’t just a series of simple on/off switches. Inside our cells, many vital processes rely on fast, fleeting interactions between molecules that assemble just long enough to do their job and then move on. Traditional drugs often can’t effectively target such transient interactions, and some disease drivers (like certain transcription factors that help control genes) lack a convenient place for a drug to bind.

    “At Amgen, we asked: what if we could intervene in those interactions differently?” said Ryan Potts, head of Amgen’s Induced-Proximity Platform that leverages the body’s natural mechanisms to target disease-causing molecules. “Instead of blocking a process, could we stabilize the interactions that make it work, or in some cases, lock them in a non-functional state to stop disease?”

    That question led Amgen’s discovery research team to investigate a new class of therapeutic candidates they named LOCKTACs. These molecules are designed to act as a type of molecular glue that “locks” two naturally interacting molecules and holds them in place for longer than they would bind on their own.

    The impact depends on the biology. In some cases, a LOCKTAC might enhance a beneficial interaction, making it more effective. In others, it might trap a harmful interaction in a way that shuts down a disease process. Either way, the goal is to work within the body’s natural biology, not against it.

    LOCKTACs fall within the broader category of induced proximity therapeutics, molecules that act by bringing proteins into close contact. Unlike proteolysis-targeting chimeras (PROTACs) – another induced proximity molecule that recruits a third component to degrade a protein – LOCKTACs stabilize targets by holding two molecules together to influence their interactions and function. This sets LOCKTACs apart as a unique way to modulate biological processes.

    Turning a Bold Idea into Real Science

    This isn’t just a theory. Amgen is already testing LOCKTACs in early-stage clinical trials. One example is AMG 193, an investigational medicine which is a potential first-in-class, selective inhibitor of the enzyme PRMT5 (protein arginine methyltransferase 5) for solid tumors missing a gene called MTAP (methylthioadenosine phosphorylase).

    PRMT5 is involved in tumor cell growth, particularly in MTAP-deleted cancer cells. In these cells, MTA (methylthioadenosine), a natural metabolite made by MTAP, builds up and weakly inhibits PRMT5. AMG 193 is engineered to bind to PRMT5 and MTA, stabilizing the interaction in a way that shuts the enzyme down more completely. The molecule is designed to selectively inhibit PRMT5 in MTAP-deleted tumors, with the goal of avoiding toxicity to normal cells.

    “LOCKTACs have the potential to open the door to a new kind of precision medicine,” said Potts. By building on interactions that already exist in cells, these molecules could:

    • Tune biological processes more precisely, either turning them up or down
    • Minimize side effects by acting only where they’re needed
    • Reach disease targets that have long been considered “undruggable”

    But designing a molecule that binds two partners with precise geometry and strength is challenging. For traditional bispecifics (molecules that bind two targets), it requires finding anchor points on both targets and avoiding unwanted interactions. Maintaining drug-like properties in these larger bi-functional molecules can be challenging. LOCKTACs showcase Amgen’s strength in precision chemistry and protein engineering. These molecules are designed to bind at or near two targets that are naturally present, lessening the chance of off-target effects. Finally, LOCKTAC molecular glues are compact and avoid the need for long linkers or highly engineered geometries, which could make it easier to preserve drug-like characteristics.

    Choosing which interaction to stabilize among many cellular contacts demands significant biological insight. But advances in structural biology, omics, DNA encoded libraries and computational modeling are accelerating compound discovery.

    What’s Next

    “As we continue to advance the science of induced proximity, we see LOCKTACs as a potential powerful new tool in our expanding drug discovery toolkit,” said Potts. ”Instead of always reaching for the ‘off switch’ in biology, we now have the option to press ‘pause’ or ‘hold’ on critical molecular interactions.”

    This could allow for more nuanced disease targeting – intervening where and when it counts, and doing so with specificity. By thinking differently about how to modulate biology, Amgen aims to move closer to the ultimate goal: helping patients with diseases that current medicines can’t address.

    Reference:

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  • Single-cell proteomic analysis uncovers hidden layers of blood cell formation

    Single-cell proteomic analysis uncovers hidden layers of blood cell formation

    In the past decade there has been significant interest in studying the expression of our genetic code down to the level of single cells, to identify the functions and activities of any cell through the course of health or disease.

    The identity of a cell, and the way that identity can go awry, is critical to its role in many of the biggest health challenges we face, including cancer, neurodegeneration, or genetic and developmental disorders. Zooming in on single cells allows us to tell the difference between variants which would otherwise be lost in the average of a region. This is essential for finding new medical solutions to diseases.

    Most single cell gene expression experiments make use of a technology called single cell RNA sequencing (scRNA-seq), which produces a map of exactly which genes are being copied out into short ‘transcripts’ inside the nucleus. However, scRNA-seq only gives us a window into the intermediate step between the genetic code and the proteins which take care of (almost) all the tasks inside our bodies. Scientists have known for a while that levels of mRNA don’t exactly match levels of their corresponding protein in cells. This can be influenced by many factors, including the complex ways that cells control mRNA stability and their translation into proteins, as well as how proteins are degraded, all in a context-dependent manner.

    Overcoming this challenge

    Scientists at the Finsen Laboratory at Rigshospitalet, the Biotech Research and Innovation Centre (University of Copenhagen), the Technical University of Denmark (DTU), and the Helmholtz Zentrum München, have used a new approach to analyze the complex population of proteins in individual cells, during the formation of blood cells. This single-cell proteomic analysis means bypassing the mRNA intermediates and building a map of the proteins present in cells during their differentiation from stem cells into mature blood cells.

    One of the study’s senior authors, Bo Porse, of Finsen Laboratory at Rigshospitalet and the Biotech Research and Innovation Centre (University of Copenhagen), says:

    “The process of cell differentiation is immensely complex, and we need to fully understand the nuances of what’s happening inside each cell at each stage of its life to address the cases when the process goes wrong. With this study we’ve shown the feasibility of using this technology to accurately model the exact stages of gene expression, covering both mRNA synthesis and decay, and subsequent protein synthesis and decay throughout cell differentiation.“

    This study, due to be published on 21st Aug in the journal Science, represents the first use of a technology, co-developed between DTU, Rigshospitalet and University of Copenhagen, namely single-cell proteomics by Mass Spectrometry (scp-MS) in a biologically relevant organ system – as opposed to in lab-grown cell cultures. Although it’s not yet possible to detect every protein present in each cell, the researchers were able to compare the mRNA data from the traditional (well, ok, only a decade-old) scRNA-seq method and this new single-cell protein analysis, and found that in more differentiated blood cells the two datasets correlated strongly (i.e. changes in mRNA levels correlated to changes in the levels of their corresponding proteins) however in the stem cells and more immature cells the datasets correlated poorly. This suggests that the turnover of mRNA transcripts, their rate of translation or the stability of the proteins expressed in cells early in their differentiation might change as cells become more differentiated.

    This study is the culmination of many years of intense technology development. Not long ago, the idea of measuring thousands of proteins in single human stem cells from the bone marrow felt like science fiction. We never imagined we’d be able to apply scp-MS to something as complex and dynamic as the human blood system this soon. But here we are, finally able to access layers of biology that are completely invisible to RNA-based methods alone. It’s a testament to the power of mass spectrometry, protein-level readouts, and data-driven systems biology to transform our understanding of how cells take fate decisions.”


    Erwin Schoof, Co-Senior Author, Associate Professor and Head of the Cell Diversity Lab, Department for Biotechnology and Biomedicine, Technical University of Denmark

    Findings and impact

    The researchers went on to study some of the proteins which appeared to drop in abundance during cell differentiation, despite having stable mRNA levels throughout the process. By editing the genetic code to remove (or ‘knock-out’) these genes, the scientists showed that this resulted in a reduction in stem cell numbers. This suggests that these proteins are essential to maintain a healthy population of stem cells within the system, to ensure that there’s a sufficient supply of blood cells in the body. Simply by analysing the scRNA-seq data alone, these functionally relevant proteins would never have been identified, and their roles in this important process would have remained hidden.

    “By integrating RNA and protein measurements into a dynamic model, we can capture the full life cycle of gene expression in single cells. This helps us understand not just what’s written in the genetic script, but how it’s performed in real time. I’m excited about how these cell-resolved protein readouts are increasingly opening entirely new windows into cell biology” says Fabian Theis, Director at the Computational Health Center at Helmholtz Munich, and Professor for Mathematical Modeling of Biological Systems at the Technical University of Munich.

    This work marks a turning point for single-cell biology: the ability to directly measure proteins at single-cell resolution in primary human tissue. It opens the door to discovering hidden layers of regulation in development, disease, and regeneration, layers that RNA alone could never reveal. As telescopes transform our understanding of the cosmos, single-cell proteomics is now doing the same for the inner workings of life.

    Source:

    Journal reference:

    Furtwängler, B., et al. (2025) Mapping early human blood cell differentiation using single-cell proteomics and transcriptomics. Science. doi.org/10.1126/science.adr8785.

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  • Study suggests omega-3 fatty acids might prevent nearsightedness

    Study suggests omega-3 fatty acids might prevent nearsightedness

    Omega-3 fatty acids have been shown to have a variety of potential health benefits, including a lower risk of heart disease, dementia and some forms of cancer.

    Now, new findings indicate omega-3s might help ward off the development of nearsightedness (myopia) in children, according to a reported Tuesday in the British Journal of Ophthalmology.

    People with myopia have trouble seeing distant objects clearly.

    Specifically, kids with lower omega-3 intake in their diet were more likely to develop the physical eye conditions associated with nearsightedness, including an oblong-shaped eye or a steeply curved cornea, researchers said.

    The results highlight omega-3 fatty acids “as a potential protective dietary factor against myopia development,” concluded the research team led by senior investigator Dr. Jason Yam, a professor of ophthalmology at the Chinese University of Hong Kong.

    The study also found that saturated fats from butter, palm oil and red meat might actually boost the risk of nearsightedness.

    For the study, researchers tracked the eye health of more than 1,000 Chinese 6- to 8-year-olds, randomly recruited from a larger-scale Hong Kong eye study.

    Questionnaires assessed the children’s diets, and those results were compared to results from their eye exams.

    Omega-3 fatty acids are primarily found in oily fish, but they also can be found in some seeds and nuts.

    Overall, about a quarter of the kids (28%) were nearsighted, results showed.

    Axial length — the length of the eye from the front to the back — was longest in the 25% of children with the lowest dietary intake of omega-3s, after accounting for other factors, researchers found.

    Nearsightedness (also known as shortsightedness) sometimes occurs when the shape of the eye causes incoming light rays to fall short of the retina, the wall of light-sensing cells at the back of the eye.

    The study also found that kids with the highest intake of omega-3 fatty acids had the shortest axial length, an indication that they are protected against nearsightedness.

    Similarly, measures of shortsightedness severity were highest in those kids with the lowest omega-3 fatty acids, researchers said.

    On the other hand, these indications of nearsightedness were increased among kids eating heavy amounts of saturated fats, results show.

    No other types of nutrients were associated with nearsightedness, researchers said.

    Researchers speculated that omega-3s might protect against nearsightedness by increasing blood flow to the eye, promoting healthy eye development.

    More information

    The American Academy of Ophthalmology has more on nearsightedness.

    Copyright © 2025 HealthDay. All rights reserved.

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  • Woman Recalls 1st Sign She Had Stage 4 Non-Smoking Lung Cancer: ‘I Was Floored’

    Woman Recalls 1st Sign She Had Stage 4 Non-Smoking Lung Cancer: ‘I Was Floored’

    As Tania Rodrigues drove to work one morning in January 2024, something unusual happened with her vision.

    “All of a sudden, I was looking through a kaleidoscope or perhaps like a fly’s eye,” the 66-year-old from Marin County, California, tells TODAY.com. “Everything that was in front of me on the road was now in multiples.”

    For about 20 years, Tania Rodrigues practiced taekwondo and is a second dan black belt. She took a break while busy with work and life but since being diagnosed with Stage 4 lung cancer, she started practicing again.Courtesy Tania Rodrigues

    Worried, Rodrigues visited the emergency room, where she underwent an MRI and a CT scan. Doctors soon knew what caused Rodrigues’ fractured vision.

    “He said, ‘You have Stage 4 lung cancer with two brain (metastases),” she says. “I don’t know what I was expecting to hear, but that wasn’t it. I was floored.”

    Sudden Vision Problems

    When Rodrigues, then 64, was commuting to work that day in January 2024, she felt great. She rolled the widows down and listened to music as she drove. But then her vision splintered and she saw multiples in front of her, so she pulled over for the roughly 10 seconds it lasted. After calling her brother, she decided to go to the emergency room.

    “The ER doctor asked me a bunch of questions,” she recalls. Initially, “everything that I answered didn’t seem to alarm him.”

    But then he inquired if she felt numbness, and she said she had “a little teeny bit” along her jawline. That response “concerned him,” so he sent her for the scans. Rodrigues felt surprised that when he returned, he was so certain of the diagnosis.

    “He said, ‘I know what’s going on with you,’ which I hate hearing that from doctors because that means they absolutely know what it is,” she says.

    He told her she had Stage 4 lung cancer that spread to her brain. Rodrigues felt stunned because she had no symptoms at all and had not smoked for decades.

    “I am generally in excellent health,” she says. In fact, the year before her diagnosis, she’d had a lung x-ray because of a flutter in her heart, and it didn’t detect anything in her lungs.

    The emergency room doctor admitted Rodrigues to the hospital so she could undergo more testing to determine what type of lung cancer she had. Scans revealed the cancer had spread from a nodule in her lung to her liver, the base of her spine, to two ribs and her brain, where she had 47 metastases.

    “There was an element of shock in there,” she says. “I’ve gratefully had a meditation practice for a really long time, and the very first thing that struck me when he said (my full diagnosis) was like, ‘Oh that’s what they’ve been talking about all this time, about impermanence.’”

    After a brief visual disturbance, Tania Rodrigues visited the emergency room and learned she had Stage 4 lung cancer with 47 metastases in her brain.
    After a brief visual disturbance, Tania Rodrigues visited the emergency room and learned she had Stage 4 lung cancer with 47 metastases in her brain.Courtesy Tania Rodrigues

    Doctors characterized her visual impairment as a seizure, even though she didn’t experience other symptoms, and they put her on an anti-seizure medication. Rodrigues cancer was a type that occurs more often in people who have never smoked, called EGFR-positive non-small cell lung cancer.

    Rodrigues qualified for a targeted therapy, and every day, she took a pill until it became ineffective in December 2024.

    “It worked as long as it worked and then it stopped working,” she says. “But the good news was that it got rid of almost every single brain metastases.”

    Another node on her lung has appeared, though, and the metastasis on her liver returned. Her team of doctors recommended another targeted therapy and chemotherapy, which she receives in an infusion once every three weeks.

    “This has been great,” she says. “The second node on my lung is gone. The primary node is reduced.”

    Non-Smoking Lung Cancer on the Rise

    As the number of people who smoke has decreased, so has the number of people with smoking-caused lung cancer. At the same time, experts have noticed an increase in young people, mostly women, with non-smoking lung cancers, Dr. Danny Nguyen, a medical oncologist and hematologist at City of Hope in California, tells TODAY.com.

    The causes of lung cancer in non-smokers remain unclear, and researchers are trying to understand why it occurs.

    “In terms of risk factors, I think it’s hard to really pinpoint right now,” Nguyen says. “Some of these risk factors include potentially radon (exposure), pollutants in the air.”

    Non-smokers who get lung cancer often have a mutation in a gene called the epidermal growth factor receptor (EGFR) gene, which can cause the cancer to grow.

    Since being diagnosed with Stage 4 lung cancer, Tania Rodrigues appreciates the beauty of life more.
    Since being diagnosed with Stage 4 lung cancer, Tania Rodrigues appreciates the beauty of life more.Courtesy Tania Rodrigues

    Several targeted therapies work effectively on managing Stage 4 EGFR lung cancers. A recent phase 3 clinical trial shows that a combination of two therapies, Rybrevant and Lazcluze, increased survival for patients with metastatic lung cancer, he says.

    “We definitely have those patients that are on that trial who are still alive right now because of that trial,” Nguyen says. “There are many other clinical trials for lung cancer as well.”

    Having treatments that work for patients diagnosed later remains essential as many people do not have symptoms until their cancer has progressed. Even then, the most common symptoms, such as a cough, are usually a sign of more benign conditions, and doctors often consider those before lung cancer.

    “What I’ve seen is a lot of these patients may present with a cough that just doesn’t go away,” Nguyen says. “They try antibiotics, they try inhalers and try steroids. It maybe gets better for a little bit then comes right back.”

    Current screening recommendations for lung cancer only apply to smokers.

    “A lot of times these patients don’t look like they should have lung cancer,” Nguyen says.

    Many patients are like Rodrigues and learn they have cancer when a scan for something else picks up a mass in the lungs. Doctors should consider lung cancer especially if patients present with symptoms — such as coughing up blood or a persistent cough — because it can impact anyone.

    “If you have lungs, you can get lung cancer,” Nguyen says.

    ‘My Life is Full’

    Thanks to her years of meditation, Rodrigues quickly accepted that rest of her life will always include cancer treatments. Since starting on the new therapy, she has felt better and returned to doing things she loves.

    “I trained in martial arts. I did it for years and years, almost 20,” she says. “My training slipped off … I started back at training in martial arts.”

    Having cancer has changed her perspective on life. She appreciates nature more, noticing that the “greens are brighter,” and that people are “way more interesting.”

    Tania Rodrigues feels grateful that lung cancer treatments have improved, allowing her more time to appreciate life.
    Tania Rodrigues feels grateful that lung cancer treatments have improved, allowing her more time to appreciate life.Courtesy Tania Rodrigues

    “My life is full,” she says. “I am really grateful that I get to take a spin on this globe.”

    Rodrigues also feels lucky that recent research has allowed for numerous “advancements for the treatment of cancer.”

    “If someone had gotten this news even 10 years ago, it would have been a totally different situation than it is today,” she says. “Today, I have a lot of hope.”

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  • BBC confirms Celebrity Traitors will air in October

    BBC confirms Celebrity Traitors will air in October

    The first series of the Celebrity Traitors is set to air in October, the BBC has confirmed.

    About 19 famous faces will compete in the game of deception and betrayal in the Scottish Highlands to win up to £100,000 for a charity of their choice.

    The celebrity edition will see stars including actor and broadcaster Sir Stephen Fry, Olympian Tom Daley, singer Charlotte Church and TV presenter Kate Garraway.

    The show, set in Ardross Castle, will also feature actress Celia Imrie, comedian Alan Carr, presenter Jonathan Ross, broadcaster Clare Balding and singer Paloma Faith.

    A handful of contestants, known as traitors, pick off their castmates, known as the faithful, with nightly “murders”.

    Meanwhile the faithful try to work out their identity. If any traitors remain at the end, they win the cash prize.

    The third series of The Traitors, which aired in January, attracted more than 10 million viewers.

    The BBC said the long-awaited spin-off of the hit show would be “extraordinary”.

    Speaking at the Edinburgh TV Festival, the BBC’s unscripted director Syeda Irtizaali said: “It was a real pleasure to cast this series.

    “We wanted to have a really broad range of people, but we also wanted people that were real fans of the show, that really understood it.

    “I’m not going to say it was easy. Roz, who put the cast together, did an amazing job – but we were pushing on a bit of an open door with most of them.”

    The director said she was initially worried about how the celebrities would play the game compared to members of the public who featured in the first three series.

    She added: “But we have nothing to worry about.

    “They really play the game and some of the things that you’ll see them doing is extraordinary, that’s all I’m going to say.

    “It’s well worth the wait.”

    Ms Irtizaali said that a lot of the celebrities had said they were “changed” by appearing on the show.

    Other stars joining the group at the castle are former England rugby player and podcaster Joe Marler and singer Cat Burns.

    Host Claudia Winkleman previously said: “We’re incredibly lucky these brilliant people have said yes.

    “I’d love to say we’ll take it easy on them and they’ll just wander round the castle and eat toast for a couple of weeks but that would be a lie.”

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  • Brain Neurons Key to Daily Blood Sugar Control

    Brain Neurons Key to Daily Blood Sugar Control

    The brain controls the release of glucose in a wide range of stressful circumstances, including fasting and low blood sugar levels.

    However, less attention has been paid to its role in day-to-day situations.

    In a study published in Molecular Metabolism, University of Michigan researchers have shown that a specific population of neurons in the hypothalamus help the brain maintain blood glucose levels under routine circumstances.

    Over the past five decades, researchers have shown that dysfunction of the nervous system can lead to fluctuations in blood glucose levels, especially in patients with diabetes.

    Some of these neurons are in the ventromedial nucleus of the hypothalamus, a region of the brain that controls hunger, fear, temperature regulation and sexual activity.

    “Most studies have shown that this region is involved in raising blood sugar during emergencies,” said Alison Affinati, M.D., Ph.D., assistant professor of internal medicine and member of Caswell Diabetes Institute.

    “We wanted to understand whether it is also important in controlling blood sugar during day-to-day activities because that’s when diabetes develops.”

    The group focused on VMHCckbr neurons, which contain a protein called the cholecystokinin b receptor.

    They used mouse models in which these neurons were inactivated.

    By monitoring the blood glucose levels, the researchers found that VMHCckbr neurons play an important role in maintaining glucose during normal activities, including the early part of the fasting period between the last meal of the day and waking up in the morning.

    “In the first four hours after you go to bed, these neurons ensure that you have enough glucose so that you don’t become hypoglycemic overnight,” Affinati said.

    To do so, the neurons direct the body to burn fat through a process called lipolysis.

    In the first four hours after you go to bed, these neurons ensure that you have enough glucose so that you don’t become hypoglycemic overnight.”

    -Alison Affinati, M.D., Ph.D.

    The fats are broken down to produce glycerol, which is used to make sugar.

    When the group activated the VMHCckbr neurons in mice, the animals had increased glycerol levels in their bodies.

    These findings could explain what happens in patients with prediabetes, since they show an increase in lipolysis during the night.

    The researchers believe that in these patients, the VMHCckbr neurons could be overactive, contributing to higher blood sugar.

    These nerve cells, however, only controlled lipolysis, which raises the possibility that other cells might be controlling glucose levels through different mechanisms.

    “Our studies show that the control of glucose is not an on-or-off switch as previously thought,” Affinati said.

    “Different populations of neurons work together, and everything gets turned on in an emergency. However, under routine conditions, it allows for subtle changes.”

    The team is working to understand how all the neurons in the ventromedial nucleus co-ordinate their functions to regulate sugar levels during different conditions, including fasting, feeding and stress.

    They are also interested in understanding how the brain and nervous system together affect the body’s control of sugar, especially in the liver and pancreas.

    The work was carried out by a team of U-M researchers at the Caswell Diabetes Institute who focus on the neuronal control of metabolism—the roles played by the brain and nervous system in metabolic control and disease.

    Additional authors: Jiaao Su, Abdullah Hashsham, Nandan Kodur, Carla Burton, Amanda Mancuso, Anjan Singer, Jennifer Wloszek, Abigail J. Tomlinson, Warren T. Yacawych, Jonathan N. Flak, Kenneth T. Lewis, Lily R. Oles, Hiroyuki Mori, Nadejda Bozadjieva-Kramer, Adina F. Turcu, Ormond A. MacDougald and Martin G. Myers.

    Funding/disclosures: Research support was provided by the Michigan Diabetes Research Center (NIH grant P30 DK020572), the Mouse Metabolic Phenotyping Center — Live (U2CDK135066) Physiology Phenotyping Core, the Michigan Nutrition and Obesity Center Adipose Tissue Core (P30 DK089503); Department of Veterans Affairs (IK2BX005715); the Warren Alpert Foundation; Endocrine Fellows Foundation; Marilyn H. Vincent Foundation and Novo Nordisk. This work was also supported in part by NIH grant K08 DK1297226.

    Tech transfer(s)/Conflict(s) of interest: Myers reports a relationship with AstraZeneca Pharmaceuticals LP, Eli Lilly and Company and Novo Nordisk Inc. MacDougald reports a relationship with Regeneron Pharmaceuticals Inc, CombiGene AB and Rejuvenate Biomed.

    Michigan Research Core(s): Mouse Metabolic Phenotyping Center — Live Physiology Phenotyping Core and the Michigan Nutrition and Obesity Center Adipose Tissue Core.

    Paper cited: “Control of physiologic glucose homeostasis via hypothalamic modulation of gluconeogenic substrate availability,” Molecular Metabolism. DOI: 10.1016/j.molmet.2025.102216

    /Public Release. This material from the originating organization/author(s) might be of the point-in-time nature, and edited for clarity, style and length. Mirage.News does not take institutional positions or sides, and all views, positions, and conclusions expressed herein are solely those of the author(s).View in full here.

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  • Brightest fast radio burst ever seen lets researchers pinpoint origin with unprecedented precision

    Brightest fast radio burst ever seen lets researchers pinpoint origin with unprecedented precision

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    Key takeaways

    • Fast radio bursts (FRBs) are powerful, millisecond-long flashes of radio waves from space that occur every minute or two, each putting out more energy than the sun does in an entire year. But until now, astronomers have been unable to determine the exact origin of FRBs.
    • A spectacularly bright FRB was detected in March from the direction of the Big Dipper by a transcontinental array of radio telescopes spanning North America—from British Columbia, down to Northern California, and out to West Virginia.
    • The team behind this discovery nicknamed the FRB “RBFLOAT,” short for “Radio Brightest FLash Of All Time,” and they say this approach establishes a new way of studying these cosmic enigmas.

    A team of international astronomers, including some at the University of California, Santa Cruz, have pinpointed the brightest fast radio burst (FRB) ever detected to a location in a nearby galaxy. The finding and the location surprised the team and offered new insight into FRBs, which are one of astrophysics’ biggest mysteries.

    FRBs are powerful, millisecond-long flashes of radio waves from space. Researchers suspect that they are the result of extreme cosmic events but have, so far, been unable to determine the exact origin of any of them. FRBs are notoriously difficult to study because they vanish in far less than the time it takes to blink. For the past eight years, the CHIME radio telescope in British Columbia has been casting a broad net to catch thousands of these previously rare astrophysical events. Now it can also pinpoint their origin.

    A spectacularly bright FRB, detected in March from the direction of the Big Dipper by the CHIME and formally referred to as “FRB 20250316A,” marks a significant change for researchers because it allowed for the identification of an exact point of origin using only the radio telescope. Their findings were published today in The Astrophysical Journal Letters.

    The team, led by postdoctoral researcher Amanda Cook at McGill University, has affectionately dubbed their discovery “RBFLOAT,” short for “Radio Brightest FLash Of All Time.” Collectively, UC Santa Cruz’s contributions were significant, especially relating to identifying the host galaxy for the burst and using RBFLOAT’s local environment to constrain its origins.

    Bryan Gaensler

    Study co-author and UC Santa Cruz Science Division Dean Bryan Gaensler said this establishes a new way of doing FRB science. “Before now, we were detecting lots of FRBs, but only had crude information on where they were occurring in the sky,” Gaensler said. “It was like talking to someone on the phone and not knowing what city or state they were calling from. Now we know not only their exact address, but which room of their house they’re standing in while they’re on the call.”

    ‘Like spotting a quarter from 60 miles away’

    To investigate RBFLOAT’s origin, the researchers relied on CHIME’s newly completed “outrigger” telescopes, which span North America from British Columbia, down to Northern California, and out to West Virginia. This array of vantage points gives CHIME unprecedented sharpness of vision, allowing astronomers to trace the burst to a region just 45 light years across—smaller than the average star cluster—in the outskirts of a galaxy about 130 million light-years away.

    “The precision of this localization, tens of milliarcseconds, is like spotting a quarter from 60 miles away,” said Cook, Gaensler’s Ph.D. student when he was at the University of Toronto. “That level of detail is what lets us identify the host galaxy, NGC 4141, and match the burst with a faint infrared signal captured by the James Webb Space Telescope.”

    Despite being the brightest FRB ever seen, researchers have not detected repeat bursts from the source, even in the hundreds of hours its position was observed by the CHIME survey instrument over more than six years. That goes against the prevailing idea that all FRBs eventually repeat.

    New possibilities

    The new observations are described through two studies: one is focused on the original radio discovery and localization of the burst, and the other on the James Webb Space Telescope’s near-infrared images of the exact location from which the radio burst originated. Together, these new data provide many new possibilities for studying FRBs, not just as cosmic curiosities but as tools to probe the universe.

    “This marks the beginning of a new era where we can routinely localize even single, non-repeating bursts to pinpoint accuracy. That’s a game-changer for understanding what’s behind them,” said Mawson Sammons, a postdoctoral researcher at McGill. Sammons works with McGill astrophysicist and professor Victoria Kaspi, who co-leads the CHIME/FRB research team of roughly 100 scientists and students.

    In addition to Gaensler, other UC Santa Cruz researchers who contributed to the study include Lordrick Kahinga, Lluis Mas-Ribas, and J. Xavier Prochaska.

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  • Bleecker Street Nabs Period Horror Thriller ‘Victorian Psycho’

    Bleecker Street Nabs Period Horror Thriller ‘Victorian Psycho’

    Bleecker Street has acquired the U.S. rights to the psychological horror-thriller Victorian Psycho, directed by Zachary Wigon and starring Maika Monroe, Jason Isaacs and Thomasin McKenzie.

    The film adapts the best-selling book by Virginia Feito, who also wrote the script. Set in 1858, the story centers on a governess named Winifred Notty (Monroe) who hides her psychopathic tendencies while arriving to work at a remote gothic manor.

    But as the woman takes care of her charges, staff members begin to inexplicably disappear, and the owners of the estate begin to wonder, too late mind you, if their new governess is serving up a spoonful of sugar with a little arsenic on the side.

    Bleecker Street plans a theatrical release in 2026 after production gets underway this week in Ireland. Dan Kagan is producing the feature alongside Sébastien Raybaud (Greenland: Migration, Greenland, The Night House) of Anton and Wigon, in association with Anonymous Content. Executive producer credits include Nick Shumaker, Bard Dorros, Feito, Kent Sanderson and Miranda King.

    “We are proud to partner with this incredible creative team on Victorian Psycho. Zach’s vision is thrilling, and we know every frame will be shocking, unique and for lack of a better word, cutting” Kent Sanderson, CEO at Bleecker Street, said in a statement.

    Anton is fully financing the film and is repping international rights. The U.S. distribution deal was negotiated by King and UTA Independent Film Group, CAA Media Finance and Anton on behalf of the filmmakers.

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