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New vitamin B12 therapy shows promise against deadly brain cancer
Researchers have identified a vitamin B12–based compound that can cross the blood-brain barrier and home in on glioblastoma tumors. In animal studies, the compound accumulated preferentially in tumor tissue and delivered sustained nitric oxide directly to cancer cells. It also worked synergistically with existing glioblastoma treatments, significantly enhancing their tumor-fighting effects.
Scientists Intrigued by Chunk of Flesh That Refuses to Die After Several Years
An amputated sea cucumber tissue survived for years in a natural environment, leading researchers to declare it immortal.
Scientists shrank mice's brains and replaced the missing tissue with human 'organoids'
Scientists have devised a new way to incorporate human brain tissue into living mice, opening the door to new research.
Experimental compound helps burn fat without muscle loss
A decades-old compound may point to a new way of treating obesity by making the body burn more energy rather than simply reducing appetite. In mice, TOFA increased energy use by as much as 18%, reduced body fat without significant muscle loss, and improved blood sugar, triglycerides, and fatty liver disease. It also produced stronger results when combined with GLP-1 drugs such as Ozempic, Wegovy, Mounjaro, and Zepbound.
'Winning the lottery': Preserved fossil tissue reveals shocking cause of death for largest T. Rex ever found
It got Tyrannosaurus wrecked.
The Science of “Ramping Up”: Why Aaron Glenn Playing Starters is a Calculated Risk Worth Taking
For years, the conventional wisdom in NFL training camps was simple: wrap the starters in bubble wrap, hold them out of preseason games, save them for Week 1. And every September, like clockwork, the league watches soft-tissue injuries pile up anyway – hamstrings, calves, Achilles, all the non contact stuff that has nothing to do […]
Making Our Own Luck
We are cross-posting a piece that former NIH official Kris Willis wrote for Macroscience. Kris is now the President and Founder of the Woodley Park Institute, for which I’m a board member. Picking winners or hedging bets? Federal science agencies have long wrestled with the question of how to ensure their billions of dollars of grants and contracts result in maximum benefits for Americans. On the surface, it might seem that a goal-oriented, interventionist style of management would be the best policy: prioritize our most pressing problems and distribute funding accordingly.This top-down strategy creates a unique hazard, though: bad choices can send resources in the wrong direction, resulting in slow progress that impedes the delivery of tangible benefits to citizens. Moreover, if decision makers pursue an applied advance when the underlying scientific principles remain poorly understood, they risk costly failures and a loss of support for the research enterprise at large. Examples include Nixon’s 1971 War on Cancer, undertaken on the premise that a cure could be achieved in less than a decade, the drive to build an operational commercial fusion plant by the mid-1990s, and the National Plan to Address Alzheimer’s Disease, which failed to produce the effective treatments and prevention strategies promised by 2025. The contrasting laissez-faire approach is to hedge your bets. If the path to an advance is impossible to predict, then the wisest choice might be to distribute funding to as widely as possible. The main risk of this strategy is that spreading funding thinly may limit the resources available to the most promising research, resulting in the same negative outcomes as the interventionist approach: limited support for the most promising topics, slow progress, and delayed returns. In reality, at science agencies like the National Science Foundation and National Institutes of Health, program managers navigate between these two extremes, setting some funds aside to target high-priority areas and using the rest to cover the widest possible range of meritorious proposals. This middle path seems like the most rational way to proceed, but it still requires making choices. How much should be set aside for high priority topics? What should those topics be? How should we define merit? Expert opinion can provide a helpful guide, but leading experts can have remarkably different opinions about what matters and what should be prioritized. Moreover, experts and administrators alike can be risk averse, giving an edge to high-profile, well-established concepts. What’s really needed is a data-driven framework to help guide decision-making, one that doesn’t simply repackage prestige or incumbency. Recognizing breakthroughs years in advance Many breakthroughs fail to attract funding or recognition at the earliest stages of development. Katalin Karikó, for example, spent years struggling to win grants for work on mRNA that would eventually win her and Drew Weissman a Nobel Prize. Similar stories can be told about Jim Allison’s groundbreaking studies leading to the development of cancer immunotherapy, Stan Pruisner’s demonstration that prions can self-replicate without DNA, or Robin Warren and Barry Marshall’s proof that Helicobacter pylori, not stress, causes ulcers. Yet at some point, the scientific community recognizes and responds to transformative breakthroughs like these. How does that change happen? And what if science funders could identify the areas that are on the cusp of a breakthrough? Those questions led my collaborators and me to study how scientists responded to past breakthroughs. Based on patterns in that data, we developed a means of predicting future breakthroughs, using biomedicine as a proof of concept. It’s worth taking a moment to describe how our approach works. Briefly, our prediction process begins by grouping the 18 million or so peer-reviewed papers in PubMed, the authoritative database of biomedical research, into roughly 50,000 unique topics. A small subset of these topics are so widely acclaimed as breakthroughs that they have been recognized with a major prize like a Nobel or a Lasker Award. We theorized that studying the development of these outliers over time, especially before they gained acclaim, was the key to identifying future instances of them. After defining topics, we chose 21 representative breakthroughs and asked what they looked like before they won prestigious prizes. To answer that question, we re-ran our topic-mapping algorithm repeatedly, winding back the clock one year each time, stringing together the years to follow the progress of each field as it grew and advanced. We found that in each case, the years leading up to a discovery followed a pattern: a burst of papers on a new, rapidly evolving topic, many of which quickly became influential. These characteristics—the percent of papers that are new, the percentage of papers that are brought in from other topics, and the influence of each individual paper—can all be measured separately for any given topic. Together, they act as a predictive signal that is detectable an average of five years before a transformative discovery is made, and up to thirty years before the discovery receives a major prize. Scanning the current research landscape for topics that display this signal allows us to predict what work will likely produce a future breakthrough. Each year we analyzed includes four or five signals, a number that appears to have remained constant across a twenty year time frame. In their classic work on the sociology of science, Bruno Latour and Steve Woolgar established that the desire to participate in a major discovery is an important motivator for scientists as they consider whether they should take up (or abandon) a research problem. Although further work is needed, the simplest explanation for our results is that this behavior is widespread enough to detect at scale. A foundational advance, or something like it, draws the attention of scientists and causes them to change the direction of their research. They vote with their feet, staking their own reputation and careers by publishing on and citing the new idea. That upswell of interest is the foundation of our breakthrough signal. What kind of research does our model identify as a breakthrough? After building a model based on the patterns in our 21 preselected breakthroughs, we tested it by identifying all early signals of discovery from 1994 through 1997. Of the 18 signals we found in that time period, 17 can be traced forward in time to a breakthrough. Examples include super-resolution fluorescence microscopy (see the image above), the directed evolution of proteins and enzymes (Chemistry Nobel, 2018), and sequencing the human genome (National Medal of Science, 2008). The discovery of the role of leptin signaling in obesity is a particularly interesting case study. Around 1950, scientists noticed the existence of a type of lab mouse that suffered from a unique inherited form of obesity. When given the freedom to choose their own diet, these mice ate more than normal and preferred food that was high in fat. Researchers had few clues as to why the animals overate; early experiments pointed to the existence of a soluble ob factor found circulating in the bloodstream that regulated appetite, but its identity was unknown. In 1994, Jeffrey Friedman and colleagues identified and sequenced the ob gene, noting that the protein it encoded appeared to fit the profile of a circulating factor. A year later, a trio of high-profile publications demonstrated that ob was a hormone that regulated body weight and fat deposition by regulating appetite. One of these was co-authored by Friedman, who christened it leptin from the ancient Greek word for thin. Using our model, the data from 1996 make it clear this advance would become a breakthrough. Scientists had flocked to study the biology of the new hormone, generating the flurry of new papers and citations required to produce a signal. One of these demonstrated that serum leptin concentrations reflected the amount of adipose tissue in the human body, providing clinical validation of the earlier mouse studies. Before the identification of leptin, scientists were unable to point to a specific molecule that controlled appetite and adiposity, so that it was impossible to rule out non-physiological causes of obesity; its characterization fundamentally changed our concept of weight gain. In 2010, Friedman and fellow pioneer Douglas Coleman were awarded a Lasker for the discovery. Our work also identifies breakthroughs in clinical practice and behavioral and social sciences, even though these areas are less likely to draw the attention of major prize committees. One example that falls into this category is the introduction of endovascular aneurysm repair, a minimally invasive surgical procedure for the treatment of abdominal aortic aneurysm, a leading cause of death among Americans over the age of 65. Relative to the previous standard of care, it reduces in-hospital mortality by almost four-fold. In 2017, Timothy Chuter received the American College of Surgeons’ prestigious Jacobsen Innovation award for his multiple refinements to the technique. Another under-recognized breakthrough identified by our model is the development of standardized survey instruments to assess the quality of life for HIV+ patients. The antiretroviral cocktails introduced in the mid-1990s reduced AIDS mortality, but treatment came with serious side effects. The new evaluations showed that patients whose disease progressed had worse physical functioning than Americans with other chronic diseases, while those who were asymptomatic maintained a health-related quality of life on par with the overall US population. This evidence made it possible for patients and activists to argue that even in the absence of a total cure, and in spite of the side effects, alleviation of symptoms was a worthwhile priority for clinicians. My colleagues and I have failed to identify any significant recognition for the physicians and health policy experts who pioneered this advance, although in 2016, researchers called for the World Health Organization to set targets for good health-related quality of life as part of its framework to end the AIDS pandemic. From forecasting to funding How should science funders use our predictions? Any serious discussion of what we should do with this new capability needs to begin with an understanding of its limitations. We can’t (and shouldn’t) invest all of our resources in the small number of topics predicted to produce breakthroughs. Innovative new fields are born from existing ones; they rarely arise de novo. If funders don’t maintain a diverse portfolio, the breakthroughs of tomorrow will have no antecedents. Think of this as eating the seed corn, or killing the goose that lays the golden egg. There are also multiple goals of funding beyond basic scientific discovery, including translating discoveries into clinical practice, developing new technologies, supporting economic development, and training new scientists. The investments needed to accomplish these goals are likely different from those required to support emerging breakthroughs. Finally, we must be aware that we may not capture every instance of a breakthrough. The concept is fuzzy, and not every significant discovery is recognized with a major award. Further, breakthroughs are rare, meaning that our dataset is, by necessity, small. This makes formal estimates of accuracy challenging. Although our overall success rate appears to be high, any one signal may turn out to be a false positive. We found one apparent example: the development of the third generation COX-2 inhibitors, Vioxx and Celebrex, which were much celebrated in the early 2000s as effective but non-addictive pain relievers, meets all the algorithmic criteria of a breakthrough. Five years after it received FDA approval, researchers demonstrated that Vioxx was associated with serious cardiovascular complications, and the manufacturer voluntarily pulled the drug from the market. Celebrex remains available, although like other NSAIDs, it carries an FDA warning for increased cardiovascular risk. Decision makers who were overly focused on the breakthrough potential of this research might have wasted substantial resources nurturing an area that ultimately proved to be a failure—but so would those who relied on expert opinion at the time. That said, the potential benefits of funding the next mRNA vaccine or cancer immunotherapy years earlier than we might have are large. When we can’t assume the outcome of an action, it’s worth conducting an experiment. Can targeted support for areas that are poised to produce a breakthrough increase the return on scientific investment without cannibalizing future advances? With the necessary administrative infrastructure in place, conducting this experiment would be straightforward. First, identify all the breakthrough signals between 2018 and 2023, select half at random, and commit to a decade of investment. For biomedicine, a six year window should yield about 30 topics with the potential to produce a breakthrough. Providing strong support to half of these might be accomplished for $300 million a year. That’s roughly half of the recent annual budget of the NIH Common Fund or around 20% of the fiscal year 2025 budget for ARPA-H. After five years, then again at ten, compare to see which group — the one that was actively managed, or the control — produced more breakthroughs, and on what timescale. Although we used biomedicine as an example, the same experiment could just as well be run for physics, materials science, or any other discipline. Any attempt to undertake such an experiment should keep three points top of mind. First, we can predict the topic of future breakthroughs, but the people and vision for how to move the work forward are still important. In practice, this means success requires active program managers with the expertise to develop the science and the authority to do so, including by recruiting investigators. Second, we would be wise to learn from the failures of past attempts to fund transformative research. High among these are funding modestly repackaged work, confusing the genuinely novel with the merely unfamiliar, and relying too much on incumbent investigators. All of these risks can be mitigated by thoroughly and intelligently integrating high quality data into portfolio management. Finally, we need to have patience. Even with strong funding support, producing a breakthrough takes time. If supporting breakthroughs is the best way to nurture the birth of new fields, we also need to accurately describe and properly manage the other two stages, so that we invest wisely throughout the productive lifetime of ideas and divest once they reach the point of diminishing returns. We would benefit from more study of all of these phases, especially the transition from one to another. More research could answer questions like: When does a breakthrough become an established field? How do the availability of funding, the size and characteristics of the available workforce, and the accumulation of evidence that disagrees with prevailing models affect a field’s decline? Exactly how do old ideas give birth to new ones, and can we speed up the process? The more we understand about the dynamics of scientific progress, the better we can maximize the odds that our curiosity leads to results. I’d call that finding a way to make our own luck.
Science on Target: Q2 Research Cores Update
Use the below jump links to navigate to each Research Core update. Postmortem Tissue (PMT) Core Longitudinal Biofluid Core Data Engine Stem Cell Core Postmortem Tissue (PMT) Core The Target ALS Postmortem Core has now collected 650 cases, making it the most comprehensive ALS tissue repository worldwide that is accessible with no-strings-attached to the global […]
MIT scientists discover amino acid that helps the gut heal itself
MIT scientists have identified cysteine — an amino acid found in foods like meat, dairy, beans, and nuts — as a potent trigger for intestinal repair. In mice, a cysteine-rich diet activated immune cells that released healing signals, helping stem cells rebuild damaged intestinal tissue after radiation exposure. Researchers say the discovery could eventually lead to new dietary therapies for cancer patients suffering from treatment-related gut damage.
One flash of red light could check health of bioprinted tissue and implants
Using 3D printers to create complex structures from biocompatible materials that can include living cells has the potential to revolutionize medicine. This process—3D bioprinting—has powered breakthroughs ...
Michael Polansky is training an AI model on skin that’s still alive
Michael Polansky — better known publicly as Lady Gaga's partner and a former top deputy to Sean Parker — has quietly spent years building an AI-driven startup that keeps living human skin tissue alive for weeks outside the body to discover new skincare compounds, and is only now going public about it.
UK fish fossil sat sealed since the Carboniferous, and its brain tissue is still helping science
The specimen also followed an unusual path into the scientific record.
Rapid weight loss on popular drugs could ‘starve’ the brain, expert warns
Dr. Tommy Wood warns GLP-1 drugs like Ozempic and Wegovy can shrink brain tissue when caloric restriction cuts off vital energy the brain needs.
Polystyrene nanoplastics may threaten reproductive health and offspring development
Plastic pollution is increasingly being recognized as more than an environmental problem. Tiny plastic particles can enter living organisms, circulate through biological systems, and potentially reach reproductive tissues.
This ultrasound treatment may help stop arthritis before it starts
A simple, non-invasive ultrasound treatment could one day help injured joints heal instead of remaining trapped in a cycle of damaging inflammation. Researchers at The University of Alabama in Huntsville found that continuous low-intensity ultrasound encouraged key immune cells called macrophages to shift from an inflammatory state toward one that supports tissue repair.
Why cancer spreads more in middle age than in old age
Melanoma may not become steadily more dangerous with age as scientists once assumed. In a surprising discovery, researchers found that cancer spread was lowest in young mice, surged in middle-aged mice, and then dropped again in very old mice. The key appears to be a special type of immune cell that helps keep cancer dormant and prevents it from spreading.
New MatterChat Model Helps AI to ‘See’ the Language of Science
From writing emails to generating computer code, much of the artificial intelligence prevalent in our daily lives has succeeded by mastering one domain: text. However, this leaves a major blind spot in the physical sciences, where models depend on the high-resolution, three-dimensional data of the physical world, like the intricate lattice of atoms in a crystal. Delivering on the promise of using AI for science requires teaching these data-driven text models to seamlessly “talk to” physics-based models. Now, a new AI framework from Lawrence Berkeley National Laboratory (Berkeley Lab), called MatterChat, solves this problem by creating a specialized “bridge.” It connects the conversational power of a Large Language Model (LLM) with a physics-based AI that models “interatomic potentials”: the complex physical forces between atoms. The resulting system already significantly outperforms general-purpose AI tools like GPT-4 at predicting material properties, and the team hopes it can accelerate scientific discovery by serving as a robust research partner that provides grounded insights and generates step-by-step instructions for synthesizing novel materials. A paper describing this work was recently published in Nature Machine Intelligence. “Traditional simulations can provide the physical rigor required for materials science, yet their computational cost remains prohibitive for high-throughput screening. Conversely, while LLMs excel at rapid knowledge synthesis, they inherently lack the ‘structural vision’ to interpret materials directly from their underlying atomic coordinates,” said Yingheng Tang, a postdoctoral researcher in Berkeley Lab’s Applied Math and Computational Research Division (AMCR) and lead author on the paper. “MatterChat was built to solve this dilemma, empowering LLMs with a structural ‘vision’ that allows researchers to leverage their full potential for solving complex, real-world materials challenges.” Empowering language models to solve complex challenges in materials science To build MatterChat, the Berkeley Lab team drew inspiration from technologies like Vision Question Answering (VQA) and Text-to-Image (T2I) generation. In these tasks, AI must translate high-level text concepts into visual images, or vice versa. Doing so requires developers to build tools that “bridge” two fundamentally different forms of data. The researchers adapted this concept to the physical sciences. With MatterChat, they created a “bridge model” that successfully connects an LLM’s general knowledge with the deep understanding of the atomic-scale world encoded in scientific interatomic potentials. Until now, researchers using LLMs to solve materials problems usually had to feed them raw data files as if they were just strings of text. It’s like asking an AI to understand a complex 3D engine based only on a parts list: the LLM can read the names, but it can’t “see” how the atoms fit together in space. MatterChat solves this by training a specialized AI bridge model, pre-trained on millions of crystal structures and an LLM, to align the LLM’s representation of the world with the interatomic potential’s representation of the world. The bridge model can translate physical insights into a format the LLM can actually understand. By giving the LLM these “scientific eyes”— a scientific “inductive bias” in the terminology of AI — the Berkeley Lab team has transformed it into a robust research tool capable of providing grounded scientific insights into complex materials challenges, such as predicting thermal stability or analyzing electronic band gaps. “We think of atoms as living in a physical space, but from a machine learning perspective, they are just vectors living in some very non-trivially structured manifold in a high-dimensional Euclidean space; and, of course, the same is true for the sentences and paragraphs that we use to express our ideas about those atoms,” said co-author Michael Mahoney, Berkeley Lab’s Scientific Data Division (SDD) AI Initiative Research Lead. “The bridge model basically gets those two structures to ‘talk with’ each other.” As a proof-of-concept of this general approach, the team trained their bridge model on a dataset curated by pairing nearly 143,000 stable atomic structures from the Materials Project with their corresponding physical properties. This training data was automatically assembled using the Materials Project’s API and deliberately enriched with properties fundamental to microelectronics design — like formation energy and bandgap — allowing MatterChat to learn the complex patterns connecting a material’s atomic blueprint to its functional performance. To validate their model, the researchers benchmarked MatterChat against a suite of other AI systems, from general-purpose LLMs to other specialized scientific AI methods. The results show that MatterChat consistently outperformed its competitors across a range of tasks. The model was more accurate in classifying material types and demonstrated superior precision in predicting numerical properties. For example, it excelled at predicting a material’s bandgap, a property critical for designing new electronics from high-capacity energy storage to next-generation computer chips. “Our design is significantly more efficient because we don’t have to build a massive AI model from the ground up,” said co-author Zhi (Jackie) Yao, a research scientist in Berkeley Lab’s AMCR. “Instead, we take two powerful, pre-trained models — a structural encoder for materials physics and an open-source LLM — and use them off-the-shelf. The only component we actually train is the lightweight ‘bridge model’ that translates between them. It’s the difference between building an entire car factory and simply designing a smart adapter that connects a world-class engine to a world-class navigation system. This approach is not only computationally efficient, but also makes the system modular, so we can easily upgrade components or adapt the bridge for other scientific domains in the future.” Crucially, this modular design highlights exactly how institutions like Berkeley Lab and the Department of Energy are carving out a highly valuable niche in the booming AI landscape. Rather than competing with Silicon Valley tech giants to build ever-larger language models from scratch, the lab is focusing on the specialized connective tissue that makes commercial AI useful for hardcore science. Because the bridge model approach underlying MatterChat is forward-compatible, it is perfectly positioned to leverage these parallel tracks of innovation. As Mahoney pointed out, “We expect that industry will continue to develop improved LLMs, and we expect domain scientists and facilities will continue to generate new data. An important part of scientific machine learning is not simply to solve problems on today’s data, but instead to develop general methods that will be forward-compatible with orders of magnitude more data, whether from scientific domains or from LLMs.” According to Yao, the MatterChat project, which was initially developed and enhanced with funding from a Berkeley Lab Laboratory Directed Research & Development (LDRD) Program, will now expand its capabilities. In a collaboration with Fermilab, MatterChat is already contributing to a U.S. Department of Energy Genesis Mission project — called Accelerating eXtreme Environment Specs-to-Silicon (AXESS) — that aims to speed up the development of next-generation, high-speed, radiation-hardened detectors for challenging particle physics experiments by using advanced 3D integrated circuits (chiplets) and AI-driven data analysis. In addition to the LDRD support, the team also credits supercomputing resources at the National Energy Research Scientific Computing Center (NERSC), located at Berkeley Lab, with MatterChat’s success. “We are incredibly grateful to NERSC; this research simply would not have happened without access to the Perlmutter supercomputer through their AI for Science program,” said Tang. Wenbin Xu, a NERSC postdoctoral fellow at the time, was also a major co-author of the work, as was Benjamin Erichson, a research scientist in Berkeley Lab’s SDD, highlighting the benefits of AMCR-SDD collaboration on AI for science. ### Lawrence Berkeley National Laboratory (Berkeley Lab) is committed to groundbreaking research focused on discovery science and solutions for abundant and reliable energy supplies. The lab’s expertise spans materials, chemistry, physics, biology, earth and environmental science, mathematics, and computing. Researchers from around the world rely on the lab’s world-class scientific facilities for their own pioneering research. Founded in 1931 on the belief that the biggest problems are best addressed by teams, Berkeley Lab and its scientists have been recognized with 17 Nobel Prizes. Berkeley Lab is a multiprogram national laboratory managed by the University of California for the U.S. Department of Energy’s Office of Science. DOE’s Office of Science is the single largest supporter of basic research in the physical sciences in the United States, and is working to address some of the most pressing challenges of our time. For more information, please visit energy.gov/science.
These mice have human (nerve cells) on the brain
Scientists have grown human brain tissue to fill most of a mouse’s cortex, creating a new model for studying brain disease and neural circuits.
This diet may slow brain aging by 2.5 years
People who followed the MIND diet more closely showed slower brain shrinkage and less grey matter loss over time, with the strongest differences equivalent to about 2.5 years of delayed brain aging. Berries and poultry were linked with healthier brain changes, while sweets and fried fast foods were associated with greater tissue loss.
Childhood Chemotherapy Leaves Lasting DNA Damage in Healthy Tissues
Certain chemotherapy drugs can age children’s healthy cells to levels comparable to those found in adult tissues.
Biological aging offers clues to long-term health after Fontan surgery
Our birthdays tell us how long we have lived, but not necessarily how our bodies are aging. Biological age reflects the condition and function of our cells and tissues, shaped by genetics, lifestyle, ...
Our Fat Tissue May 'Remember' Obesity, Even After We've Lost Weight
Another potential reason your diet isn't working.
New adenomyosis atlas reveals lesion-specific signals that may spare healthy uterine tissue
Researchers at the University of Liverpool have identified distinctive biological characteristics within adenomyosis lesions that could help pave the way for more targeted, less invasive treatments. The ...
These fat-filled brain cells may be making multiple sclerosis worse
Scientists have uncovered a surprising clue that may help explain why multiple sclerosis (MS) progresses rapidly in some people but not others. In brain tissue from patients with severe MS, researchers found large numbers of “foamy” immune cells packed with fat droplets after absorbing damaged myelin. These overloaded cells appear to switch from helping repair the brain to fueling ongoing damage and inflammation.
Biodegradable implant can deliver targeted cancer immunotherapy while protecting healthy tissue
Scientists at Houston Methodist Research Institute have developed a biodegradable implant designed to deliver cancer-fighting immunotherapy drugs directly into tumors over an extended period, a strategy ...
Scientists Discover Ultrasound May Stop Arthritis Before It Starts
A new study suggests low-intensity ultrasound can influence immune cell behavior in ways that may reduce chronic inflammation and encourage tissue repair after joint injury.
FDA-approved drug may finally help immunotherapy defeat rare liver cancer
Researchers found that a rare liver cancer evades immunotherapy by luring immune T cells away from the tumor and trapping them in nearby fibrous tissue. An FDA-approved drug called AMD3100 freed those T cells to attack the cancer, significantly improving the effectiveness of immunotherapy in tumor samples.
Butterfly lilies wing their way to Science
Many animals and plants show left-right differences in how their bodies or organs are arranged, but we still know little about how such asymmetries evolve or how genes control them in natural populations. Mirror-image flowers, in which female and male sex organs are deflected to opposite sides in left- and right-handed forms, provide a notable example of such asymmetry. Here, we studied South African butterfly lilies, where individual plants produce only left- or right-handed flowers. Their mirror-image flowers promote outcrossing by depositing pollen from each floral form onto a specific region of a pollinator’s body that matches the stigma position of the opposite form. This suggests that selection for efficient pollen transfer between forms maintains this natural polymorphism. Our work uncovers a hemizygous supergene that coordinates the left-right orientation of female and male sex organs in mirror-image flowers by linking two independently acting genes for style and stamen handedness in a single, nonrecombining genomic segment. This architecture ensures the coinheritance of a matched pair of organ orientations that is essential for efficient cross-pollination between floral forms. At the developmental level, we show that floral handedness emerges from the interaction between an intrinsic tissue chirality and a gravitropic response that orients the style and median stamen relative to gravity. Together, these findings reveal how a supergene, hormone and microRNA signaling, tissue chirality, and an external physical cue combine to produce and maintain a stable left-right polymorphism in natural plant populations.
What’s Next for Artemis II AVATARs
Organ chips from Artemis II's AVATAR investigation have arrived at the laboratory at Emulate, Inc. in Boston, Massachusetts for analysis. The AVATAR (A Virtual Astronaut Tissue Analog Response) investigation uses personalized organ chips made from each astronaut's own cells to study the impacts of space radiation and microgravity on human health.
Offworld Space Biology: Setting Up The Life Science Glovebox
Bioengineering cartilage tissues and manufacturing advanced materials kicked off the week aboard the International Space Station
Time matters: circadian genetics and the molecular logic of human health and disease
Nature Reviews Genetics - The circadian clock controls transcriptional and signalling networks across tissues to maintain homeostasis, with pathological consequences to its disruption. Kuo et al....
Scientists find breast cancer cells hiding behind protective “shields”
Researchers have mapped breast tumors in striking detail and uncovered hidden pockets of dormant cancer cells that may help explain why cancer can return after treatment. Unlike rapidly dividing cells, these quiet cells can essentially hibernate, allowing them to evade chemotherapy and reactivate later. The team found that they are often surrounded by immune cells and connective tissue cells that may act like a protective shield.
Lunit and Discovery Life Sciences Collaborate to Expand AI-Powered Tissue Analysis for Biopharma Research
/PRNewswire/ -- Lunit (KRX: 328130), a leading provider of AI for cancer diagnostics and precision oncology, today announced a strategic collaboration with...
What happened when scientists grew human brain tissue inside mice - Futura-Sciences
Without native tissue in the way, the transplanted human cells multiplied to five times their initial size, grew their own blood vessels, and connected directly to the mice’s spinal cords. Led by first author Kelley Kaganovsky and senior author Sergiu Pașca, the team published the findings in Nature on September...
Scientists Grew Human Brain Tissue Inside Mice and It Actually Worked
The transplanted cells formed circuits, reached the spinal cord and responded to injury.
'Everyone on Earth is exposed': Scientists map microplastics deep inside living tissue
It does show that researchers are developing better tools to study exposure.
Netflix’s #1 Movie Has Viewers Ugly Crying
Netflix’s #1 movie is leaving viewers reaching for the tissues. Find out more here.
Immune Cells’ Role as Quality Control Boosts Tissue Health
Macrophages maintain the function of certain organs by eliminating waste products. Studying this process could lead to clues for healthier aging.
Stanford Grows Human Brain Tissue Inside Mice in Science Breakthrough
Stanford grew human brain tissue inside mice, creating living neural models that could transform drug testing for epilepsy, autism, and schizophrenia.
Meet the scientists 3D printing corneas to restore people's vision, potentially filling a worldwide shortage of transplantable tissue
Corneal blindness affects millions of people globally, but donor tissue for transplants is in short supply. These researchers believe that 3D bioprinting can help close that gap.
Stanford scientists transplanted human brain tissue into mice missing most of their cortex; within months, it grew to occupy more than 90% of the space
Stanford scientists have created a new model for studying human brain development by transplanting lab-grown human brain tissue into mice that were engineered to lack most of their cerebral cortex. Within months, the human tissue not only survived but expanded to occupy more than 90 percent of the cortical space, forming working connections with the mouse brain and spinal cord.
A vitamin A discovery is changing what scientists know about vision
A surprising discovery is reshaping scientists' understanding of how humans develop sharp central vision before birth. Instead of blue cone cells migrating away from the retina's center, the study found they transform into red and green cones under the influence of vitamin A-related signals and thyroid hormones. The findings could improve lab-grown retinal tissue and lay the groundwork for future cell therapies to restore vision lost to age-related eye diseases.
‘A mouse can’t tell us what works’: UK scientists to grow miniature human organs for drug testing
Organoids and tissues grown from human cells promise more accurate results, with £20m Cambridge project to create standardised models
Virginia Tech leads multimillion-dollar project for women's health
A team of researchers from across the country will investigate the connection between hormones and vaginal tissue health in a project funded by the National Institutes of Health.
A common sugar may help cancer cells break free and spread
Chemotherapy-surviving ovarian cancer cells may release fructose to help neighboring tumor cells loosen, escape, and spread. The discovery suggests that sugary diets and cholesterol-lowering drugs could influence cancer progression, though the effects have not yet been confirmed in patients.
Scientists spur growth of implanted liver tissue
Researchers developed a way to control the growth of lab-grown liver tissue after it was implanted into mice.
Insurance Coverage Lags as Cancer Science, Treatment Move Forward
“Brain cancer” or “H4 G34-mutant”? As knowledge about genetics advances, some doctors say cancers should be defined by their mutations, not the tissues where they manifest.
Science on Target: Q3 Research We Enable
Read on for updates across the Research we Enable Postmortem Tissue (PMT) Core The Target ALS Postmortem Core has now collected brain and spinal cord tissue from over 650 cases, making it the largest and most comprehensive ALS tissue repository worldwide that is accessible with no-strings-attached to the global research community. This robust and expanding […]
Science Vs on the 49ers Substation: Anatomy of a Hatchet Job
In August, Pablo Torre Finds Out and Science Vs released an episode about my theory that electromagnetic fields from the electrical substation beside the 49ers facility may be contributing to the team’s run of soft-tissue injuries. As the originator of the theory, I was also a subject of the episode. I sat was interviewed by Wendy Zukerman and Rose Rimler of Sciene Vs. I sent them research, connected them with scientists, and spent hours digging through the City of Santa Clara’s and Silicon Valley Power’s records to help clarify critical details. Both Wendy and Rose came off as affable and professional, showing curiosity during the interviews, with Wendy going out of her way to question the “conspiracy theory” framing itself. Then they titled the episode We Solve the 49ers Viral Conspiracy Theory. I was familiar enough with their catalog that I never expected them to agree with my theory, but I did expect them to give it a fair hearing and to deliver their findings honestly. On both counts they came up short. They were not directly dishonest in anything they said, but rather in what they left out, in how what remained was cut, and in the picture painted by those two things in combination. They asked me to recorded the interview on my phone for better audio quality, and I held on to my copy for reference later. That turned out to be a fortuitous decision. Here is the raw audio of my first interview, unedited*. Only my side was recorded, so their questions aren’t on it, but you can generally infer them from the answers, and every claim I make below about what I said can be checked against my statements in this clip. (Note: Wendy had connection trouble at the beginning of the interview and was cutting in and out, which accounts for the false starts.) 0:00 -1:19:13 Audio playback is not supported on your browser. Please upgrade. Science Vs is a fun show. It is pitched at roughly a high-school understanding of science, for an audience that is skeptical, Snopes-oriented, and worried about misinformation. Take a claim circulating online, interview a supporter of the claim, interview consensus scientists, and then tell people which side of the line it lands on. I have listened to their episodes on raw milk, seed oils, 5G and other contested issues in the wellness space. I have problems with all of them, but each at least made an honest attempt to represent the actual range of scientific opinion by talking to credentialed scientists with differing perspectives. Dissenting researchers were heard from, answered, and often given a chance to respond. This episode did not do that. This article is not a relitigation of the science. I have written extensively about that already. This post is for the record. It is simply an accounting of what was wrong with their episode. Contents Is there a power plant next to the 49ers practice facility? — the clearest single example of getting something objectively wrong For the record — a high-level overview of all of the problems with their investigation Draw your own conclusions — why they had to make this episode at all What they left out about childhood leukemia — the exposure threshold, and playing games with statistics to minimize sick children What they left out about the mechanism — the body of literature they refused to cover, and evidence for the mechanism used against it The scientists Science Vs interviewed and did not air — four credential scientists who support myhe theory, recorded and cut, or not even called How they misrepresented me and my case — an answer severed from its question, and three telling edits How you would actually study the injuries — it doesn’t actually matter which team is the most injured, overall The theory: magnetic fields, oxidative stress, and collagen Since the episode never states my theory, here it is below. Those who are familiar with my work can skip this section. Electrical equipment produces magnetic fields, and those fields induce faint electrical currents in anything that passes through them, including people. My argument goes further than induced current. Mitochondria — the structures that generate a cell’s energy — run on continuous flows of electrons and protons, and those flows carry faint electromagnetic fields of their own. Maxwell’s principle of superposition shows that when two fields share the same space, they add together. An external field does not need to be strong to alter an internal field, it only needs to be present. The electron transport chain inside the mitochondria leaks a small fraction of its electrons by design, and those become reactive oxygen species — free radicals, which healthy cells use as signals. External magnetic fields cause the rate of leakage to change, increasing free radicals. When free radicals accumulate faster than the cell’s antioxidant systems can clear them, the result is oxidative stress. Oxidative stress is a recognized driver of chronic illness, including cardiovascular disease, neurodegeneration, diabetes and cancer, and it is in every medical school curriculum. One of its ordinary effects in connective tissue is that it switches on matrix metalloproteinases — MMPs, the enzymes that break collagen apart — while suppressing new collagen synthesis. Tendons are made of collagen. An athlete loading his soft tissue heavily six days a week is already creating oxidative stress in the tendons, so the addition of magnetic field exposure compounds the damage and inhibits repair, making him more susceptible to injury when enormous force lands on a tendon in a fraction of a second. That is the theory. We know that EMF causes oxidative stress, and we know that oxidative stress degrades collagen. The only thing missing is a study showing that direct connection. I have never claimed certainty that the substation is contributing to the elevated injury rate. I do believe it is likely, and I believe it warrants caution, and that a revenue machine like a major NFL team can easily afford to remove the exposure out of precaution. Is there a power plant next to the 49ers practice facility? Here is the clearest single instance of the problem with this episode. It requires no knowledge of electromagnetic fields at all. This story first came to me through Jon Feliciano, a former 49er, in an interview on Willard & Dibs on 95.7 The Game. Asked about why the 49ers are always injured, he said players used to joke that it was the power plant behind the practice fields. Wendy Zukerman corrects him on air. “It’s important to say that it’s not a power plant near the 49ers site.” Torre then asks her to explain the difference between a substation and a power plant. Her answer: a power plant generates electricity and transmits it to a substation, which converts the voltage into something your house can use and sends it on to your home or your business. There are two problems with that. The first is that there is a power plant on that site. The Gianera Generating Station is a natural-gas-fired peaker plant owned by Silicon Valley Power, and it has been there since 1986. I have published aerial photographs of the location from 1987 in which the gas plant is the only thing standing, before the practice facility was even there. I even mentioned the gas plant in my first interview. (Feliciano has since gone on record about this issue, and it is clear he had the substation in mind rather than the gas plant.) The second is that her definition describes a distribution substation, and the facility beside the 49ers is not that. It is the Northern Receiving Station, which takes in bulk power from outside the city’s grid and delivers it to distribution substations. Silicon Valley Power’s own map distinguishes receiving stations from substations, and Rose Rimler even reads the label out loud in the episode when she walks through that map on air. A few minutes before the map segment, Zukerman tells Torre: “like I said, we fact check everything.” Well, maybe not everything. I made a mistake On the morning of July 6th, at 10:20, I sent Rose and Wendy two studies. During the interview I had been asked which human studies show oxidative stress from electromagnetic fields, and I had not been able to name one on the spot. Rose emailed asking for the studies, I quickly searched for a couple, and I wrote that I thought these were the most relevant from that search. Unfortunately, I was busy and did not read either one closely at first. I picked them because they were topically relevant — one on substation workers, one on power plant workers. Neither were great studies, and their problems go past the ones raised in the episode. That was careless on my part. There is context that did not make the episode, though. Before that email I had been on a Zoom call with Rose talking about EMF and oxidative stress, and I pointed her to Dr. Henry Lai at the University of Washington, who has spent years aggregating the literature on this question. His tallies show that roughly 90% of studies since the late 1990s find oxidative effects from electromagnetic field exposure — hundreds of studies, systematically counted. Rose told me she was already aware of his work. So when she asked for studies, I understood her to have the aggregate view already and that she would report anything within that context. Not reading those two carefully was still a mistake, but the larger mistake was assuming the episode would be based on a thorough review of the actual body of literature, rather than on whatever I happened to send that morning. The second email At 1:49 that same afternoon — three hours and twenty-nine minutes after the first — I sent them a second email that I had been preparing for a while. It was a structured document in six numbered sections, written in response to a request they had made two weeks earlier, laying out my entire argument with citations attached to every link in the chain. The episode aired on August 13th, five weeks later, and not a single item from the second email is in it. Here is how it opens: The full email is included at the bottom of this post in Appendix B. Nearly 1,500 words in total. It contains two named mechanisms with the physics behind them. Occupational studies in humans. The literature on oxidative stress and collagen. A section addressing the strongest counter-evidence against my own theory, which I raised myself. And a closing section stating plainly what the theory cannot yet show. My entire argument, in writing, with detailed citations for every claim, provided to them five weeks before broadcast, and none of it made it into the episode. That is the single largest omission, but it is not an isolated one. The whole episode is riddled with similar problems, and the conclusion they came to is not merely a difference of opinion about the scientific evidence. Through omission and through strategic editing, Science Vs misinformed its audience — about what the evidence shows, about what I argued, and about who they spoke to. That is a notable outcome for a show whose stated purpose is correcting misinformation. For the record I am not going to tell you that Science Vs set out to discredit me, or that they had come to their conclusion before they reported the story, or that they used misleading editing to make me look like a man retreating from his own theory. I cannot know what was in anyone’s head, and I am not going to pretend otherwise, either. What I can tell you is what is on the record. They asked me for evidence and aired the weakest thing I sent. They interviewed three scientists who supported my theory and aired none of them. They discussed childhood leukemia without ever saying the exposure level at which it appears. And they took an answer I gave weeks before Ken Karipidis, the one EMF scientist who was put on air, was interviewed, and placed it directly after his critique, where it comes off as a major concession. A friend of mine who has worked as a journalist for thirty years read that last one and called it sleazy. I agree with her. Those are just the four issues that are impossible to defend as pure editorial decision, but they are not the only issues. The most glaring issues stem from what they left out: The exposure level at which the childhood leukemia association actually appears — three to four milligauss, a number the episode never states despite it being much lower than what I measured. The mechanism itself: The episode gets as far as “oxidative stress could weaken collagen,” which leaves it sounding like speculation, rather than a known pathway. The second email, and all the studies in it. Dr. Paul Héroux at McGill, whose work my proposed mechanism rests on, whose contact details I supplied, and who was never called. Dr. Beatrice Golomb at UC San Diego, who runs a research group on oxidative stress and mitochondrial function and has specific expdertice in collagen, interviewed and not aired. Dr. David Carpenter at Albany, the most prominent academic voice on the harm from magnetic field exposure, interviewed and not aired. Dr. Joel Moskowitz at Berkeley, interviewed and not even credited. The specific, testable condition I put in writing that would make me abandon the theory. My own unprompted statement of the theory’s evidentiary gap. My caveats about my own measurements. My ranking of EMF as one factor among several rather than the only one. The new equipment installed at those facilities between 2010 and 2014, and the sharp rise in system load from 2013 onward. But that is not all. What they kept, they selectively edited to serve a narrative that was not served by the raw transcripts of the interviews. A description of thousands of commercial routers in a workplace, reduced to the Wi-Fi in your house. My own acknowledgment, multiple times, that "I'm not a scientist" clipped in an episode that spends considerable energy pointing out that I am not a scientist. And a qualification I volunteered about my own measurements, cut from my answer and delivered later by their EMF expert as a correction. Together their edit produce a portrait of a wellness guy with Wi-Fi phobia and two bad studies, backing away from his theory the moment a “real” scientist looked at it. A practice facility where nothing changed because no new substation was built. Injuries written off as random because the 49ers were not quite the single most injured team in the league over the period in question. That portrait is false even though almost no individual statement made in the episode is. Draw your own conclusions At the top of the episode, Pablo Torre says his show had been flooded with requests to investigate the substation — that it was the thing they were asked to look into over and over again. Neither show went hunting for this story. It arrived from their own audience, in volume, and it could not be waved off. A thread I posted on X reached twenty-two million people. A guy with a gaussmeter and a brand-new Substack obligated a Pultizer prize winning program to spend an hour on a question about player health, that is considered fringe enough that most media operations won’t touch it. Pablo Torre Finds Out could not ignore it. So Science Vs came in and ran a “debunking” operation instead of an investigation. Everything below is what had to be left on the cutting room floor to deliver the “debunking”. They could not ignore it. So they tried debunked it instead. The demand was strong enough to force an episode, and since the episodes release the 49ers have sustained more injuries, including season ending ones, and interest has only grown. Demand from fans and playets is strong enough to force a better investigation from someone else. An omission is not a lie until you find out what was omitted. What follows is the detailed record so you can see the full picture. Draw your own conclusions. I have drawn mine. I am going to keep publishing. A note about Pablo Torre Finds Out After the episode aired I posted publicly, calling out Pablo Torre Finds Out for concerns I had about the integrity of their investigation, and about an interview directly with Pablo Torre which had been offered but never happened. I have since spoken with a producer at PTFO. The offer had rested on a misunderstanding about where things stood between us, and it fell away as the Science Vs part of the production widened past the science. He apologized for the miscommunication and I accepted. The producer also confirmed to me that they did essentially hand off the entire investigation to Science Vs for narrative purposes — so Pablo would be genuinely curious or potentially surprised by their findings — while still taking responsibility for what went out under their name. I appreciated the candor and the accountability, and I am comfortable with where we left things. So this post is not about PTFO. My disagreement is with Science Vs. What they left out about childhood leukemia Childhood leukemia appears at three milligauss. They gave no number at all. 1. They built an EMF ruler, then discussed childhood cancer without it. The sequence on air went like this: First I measured almost 9 mG, then I measured up to 50 milligauss. Torre reacts with concern — “that sounds high.” Cut to Karipidis: the public limit is 2,000 milligauss. Torre reacts again — “What happens at 2,000?” Karipidis explains that nothing happens at 2,000, that safety factors are built in. Then: at more than 50,000 milligauss you get flickers of light in the retina, and higher still, nerve stimulation. The listener now has a ruler (their ruler) to measure these numbers with. Fifty is nothing by their ruler. Then the episode turns to childhood leukemia and states, accurately, that there is a real association — but tellingly, they never give the exposure level at which that association appears. Childhood leukemia appears at three milligauss. They conveniently left that out. The pooled analyses that produced the World Health Organization’s carcinogen classification found roughly a doubling of childhood leukemia risk above three to four milligauss. That is the number that belongs in that segment, and it is more than ten times below the reading that had just been dismissed as trivial. I gave them that number myself, on tape, in the interview. Describing my own threshold, I said my comfort level for long-term chronic exposure is three to four milligauss, but preferably one. 2. Six children in thirteen million. The episode reports that these fields might explain one to four percent of childhood leukemias, then reframes it as a German estimate of perhaps six cases among thirteen million children. Torre, to his credit, is uncomfortable. What never gets explained is why that number is small. Almost no children lives above three milligauss in Europe. Fewer than two children in a hundred, in the Italian data. So even if the risk to those children doubles, the number of additional cases across an entire country stays small — not because the hazard is small, but because hardly anyone is exposed to it. Count the whole population and the few who are exposed disappear. And the reason hardly anyone is exposed is that siting rules keep housing away from transmission lines. In Europe, at least. The Dutch government has a standing precautionary policy against building new homes in any zone where the annual average magnetic field exceeds 4 milligauss — the same number the episode never mentioned. Denmark and Norway treat 4 milligauss as the level that triggers a look at mitigation. That is five hundred times below the ICNIRP figure quoted on air. The United States has no federal equivalent. That is evidence of infrastructure siting policy working. It is not evidence that there is no hazard. It is evidence that we already act as though there is one. If you listen to the raw audio you will hear that my proposed solution is EMF exposure is to build better infrastructure. What they left out about the mechanism 3. They accused me of cherry-picking, and then cherry-picked themselves. On air, Zukerman tells Torre that people who worry about electromagnetic fields dismiss the studies showing null results and collect the ones showing harm, and that this is why you have to be careful not to cherry-pick. They had two papers I had rattled off in a hurry, and a second email containing a carefully chosen set. They ran the two weakest, graded them on air, and presented the result as the state of the evidence for not only my theory, but the whole question of oxidative stress from magnetic fields. That is cherry-picking from my emails. The bigger picture is what they did with the literature as a whole. Zukerman acknowledges it exists, dismisses it, and disposes of it in a single stroke. You can go online right now, she tells Torre, and find scores of studies showing these fields increase oxidative stress. The issue, she says, is that they are not studies in people. Many of them are in people. The occupational studies in my second email are in people. That email had been in her inbox for five weeks. She waved off the literature on a factual claim that the documents in her possession contradict. (I have written separately about the evidentiary standard at work here). The effect was that they essentially baited me: ask the subject to supply the evidence, take the weakest thing he sends, and let that stand as a proxy for the whole argument. Wendy has been doing this show for ten years and clearly knows how to extract what she needs for her desired narrative. 4. They presented the collagen-improvement research as a gotcha, but I had already addressed it. The episode treats the existence of studies showing that EMF can improve collagen as a surprise that undercuts me, but I had pre-emptively addressed that five weeks earlier in the email they ignored. Those studies use measured, high-intensity pulsed dosing. The mechanism by which they work is oxidative signalling. The cell reads a controlled rise in reactive oxygen species as a warning, upregulates its antioxidant defenses, mounts a repair response, and the therapy stops before the system is overwhelmed. The key point is that it induces an oxidative response, which means those studies are actually evidence for my proposed mechanism, not against it. A field that produces a therapeutic effect cannot be biologically inert (which is the implication when they say “Nothing happens at 2,000 milligauss). Chronic ambient exposure is the same pathway with no off switch, and it is most consequential during the evening and while sleeping, when the body is in repair mode and the exposure does not stop. Section 5 of my email is titled What about the study showing improved collagen synthesis. I raised the counter-evidence myself, explained why I did not think it refuted the theory, and wrote that I was disappointed the question had not come up in the interview. That is worth holding against the cherry-picking charge in the item above: the studies they presented as inconvenient for me were studies I had gone out of my way to put in front of them. 5. Section 1 of my email stated a critical argument that was never put to the expert directly responsible for it. My email says the exposure limits exist to prevent acute effects and do not address chronic exposure at all, and that my dispute is with the entire framework. Zukerman gestures at this once. After Karipidis gives the 2,000 milligauss figure, she tells Torre that I would object because those levels do not capture “more subtle effects.” That is not my argument, and “subtle” is doing a lot of work here. My argument is that the limits are built to prevent acute effects — nerves firing, muscles twitching, etc — and were not designed to address chronic exposure at all. In fact, ICNIRP’s own documents state as much themselves. Mine is a structural objection to what the standard measures, reduced as a concern about subtlety, it becomes a matter of degree, rather than a categorical difference. They interviewed Ken Karipidis, vice chair of ICNIRP — the body that writes those limits. He was asked what the limit is, but he was never asked how it applies to chronic exposure. The scientists Science Vs interviewed and did not air 6. They interviewed four officials of the standards body. The episode credits roughly a dozen researchers. Four of them are associated with ICNIRP. Ken Karipidis is the vice chair. Rodney Croft chaired ICNIRP from 2020 to 2024 and led the development of its current guidelines. Dan Baaken is ICNIRP’s scientific secretary. Frank de Vocht sits on the Main Commission. One of them speaks in the episode. Their institution’s position is more than adequately represented — the 2,000 milligauss figure, the safety factors, the assurance that nothing happens below the line. 7. The four who were left out. Dr. Beatrice Golomb is Professor of Medicine at UC San Diego — a physics undergraduate degree, a PhD in biology, an MD. She directs a research group whose stated focus is the relationship between oxidative stress, mitochondrial function and health. That is the mechanism the episode spent its first half dismissing. Her published work includes the fluoroquinolone case series behind the FDA’s black box warning on an antibiotic class that ruptures tendons, where the accepted mechanism is oxidative stress and mitochondrial toxicity — the back half of my chain, already on a drug label. She is in the credits. She is not in the episode. She has told me she finds my theory biologically plausible, and that she has a recording of her interview. Dr. David Carpenter directed the Institute for Health and the Environment at the University at Albany for decades and is the most prominent academic voice arguing these fields cause harm. Childhood leukemia is the reason these fields carry a WHO classification at all, and Carpenter is the person you call if you want that case made by someone who has spent a career on it. He is in the credits. He is not in the episode. He has told me that when he was interviewed they could not have been less interested in what he had to say. Dr. Joel Moskowitz directs the Center for Family and Community Health at UC Berkeley’s School of Public Health. He told me directly that they interviewed him and that he thought it went well. He does not appear in the episode, and unlike Golomb and Carpenter, he does not even appear in the credits. Dr. Paul Héroux at McGill is the researcher whose work provides the foundation for the oxidative stress mechanism my theory rests on. I gave Rose his email address and phone number. He was never interviewed. They never even called him. 8. “He’s not a scientist.” The episode leans hard on the fact that I am not a credentialed scientist. Zukerman says it. Torre repeats it. “At all.” Having built a segment on that, they then left out the physicist-biologist-physician, the professor of public health, the director of a university environmental health institute, and the McGill researcher whose work the primary mechanism comes from. They spent the episode telling their audience I am not a scientist, and then kept four actual scientists who support the theory off because their argument does not survive otherwise. How they misrepresented me and my case 9. They played my words as a response to an interview I had never heard. Near the end of the hour, Zukerman says she went to me and told me the evidence was lacking. Then she plays me saying I am not wedded to it being an EMF, that I have staked my reputation on it needing more study, and that I am not certain of anything. That segment was placed immediately after Karipidis had finished taking the cherry-picked papers apart. It plays as a man folding under expert scrutiny. Commenters have used it against me since, but it is incorrect. Here is the sequence as it happened. I was interviewed. Karipidis was interviewed weeks later. I was never told what he said, or even who he was. I was never asked to respond to it. I did not know his name until the episode aired. That is not a simple editing decision. That is a quote from one interview, moved to follow a critique from a different interview it was not a response to, so that it would land as a concession. A friend of mine who has spent thirty years as a journalist read that sequence and called it sleazy. She is right. The full passage is reproduced in Appendix A, and it is worth reading. What airs is the preamble. Four paragraphs later I say “to directly answer your question” — and that answer, about what would change my mind if the team relocated, is not in the episode. Neither is the sentence two paragraphs on, where I say the EMF might turn out to be ten percent of the problem. I will say the underlying point again, though, because I meant it and I still do. I am not wedded to my theory that magnetic fields from the substation are contributing to the 49ers injuries. I could be wrong. What I am wedded to is the process of scientific inquiry, and the fact that we should be cautious around these exposures and we need more independently funded studies. 10. Three telling edits. They cut “I’m not a scientist” mid-sentence. What I said: “...and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS...” What aired: “...and that I am not certain of anything. I’m not.” The clip ends on the first two words of the sentence in which I say I am not a scientist, in an episode that spends considerable energy establishing that I am not a scientist. The full sequence is in Appendix A. They cut my own description of my work. Asked what I do, I said I run a wellness business, that I am focused on writing software to help people navigate environmental stressors, that environmental health is my focus, and that I also do independent journalism and research. What aired is the wellness business and the environmental health, with the software and the journalism removed from my own answer. The software engineering does come up later — narrated by them, as a hacker who grew up to write firmware — but my current work, in my own words, arrives as “wellness guy.” Thousands of commercial routers became home Wi-Fi. What I described: working at a wireless networking company surrounded by thousands of Wi-Fi routers, and a stress-induced health collapse afterward that working in that environment contributed to. What aired: Wi-Fi, the kind you have at home — reinforced by a clip of Christian McCaffrey talking about turning his router off at night. Three cuts, and every one of them makes me seem less credible. That is not a coincidence. 11. I gave them my own caveats and the test that would disprove me. In the first email I wrote that a well-designed chronic, ambient-level exposure study in tendon showing no collagen degradation, run over many months, would undercut my confidence in the theory. That is a specific, testable condition, stated in advance and in writing. There was a second interview, weeks later, which was not used in the episode, but in that I asked again for the falsification criterion to be included. What the episode presents instead is a man saying “we need more study,” which reads as a hedge, an open-ended request for the benefit of the doubt. It is the opposite of a hedge. Section 6 of my second email says, unprompted, that as far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human in vivo or in human tendon in a lab. I wrote that because it is true and because it is the first thing anyone should check. Under their standard it becomes the hinge of the entire first half, framed as something they had to surface without my cooperation. I had handed it to them five weeks earlier. And in the interview I said that my 25 to 50 milligauss readings were taken at knee level, and that these fields attenuate quickly, so by the time it reaches your head it is not that high anymore. That did not air either. The qualification arrives later, from Karipidis, as a correction. How you would actually study the injuries 12. They measured the wrong thing. The episode spends its final act on whether the 49ers are the most injured team in the NFL, finds no clean ranking, and lands on “injuries are random”. That is the wrong test. You would define the exposure — measured field levels at the facility — and the outcome narrowly: soft-tissue injuries, not a single MSK injury count that a broken finger and a ruptured Achilles both land in. Then you would compare the 49ers to themselves before and after the exposure changed, and compare that change against every other team over the same window. That controls for league-wide shifts in rules, turf and training load. It is a difference-in-differences design, and it is standard. I sent them that argument on July 28th, in writing, along with the fact that in eleven of the past twelve seasons the 49ers had finished top ten in Adjusted Games Lost. And by the episode’s own reporting, the 49ers are second in games lost to injury over the past decade, with FTN’s Aaron Schatz confirming that once you adjust for starters they come out second worst in the league — after having been one of the healthiest teams for years before that. A finding like that is where an investigation starts, not where it stops. 13. I did a lot of substation research for the episode that was never aired. I had reported that the substation next to the facility was expanded in 2014. That was wrong, and Rose Rimler and I sorted it out together. They gave me credit on air, which I appreciated, but framed it as a concession on my part to something they had found. In fact I had been investigating it myself, was uncertain before they asked, but was waiting for clarification from Silicon Valley Power. The uncertainty centered around a substation named “Esparanca” that was proposed right behind the facilities as part of the stadium construction, but now appears to never have been built. I spent days in Silicon Valley Power’s records, and did eventually reach Silicon Valley Power for confirmation and indentified the mistake myself. I also gave them highly detailed documents on what we do know about those facilities: new equipment installed between 2010 and 2014, and load growth across the system with an inflection around 2013–2014, with the Northern Receiving Station carrying the highest capacity in the system and sitting closest to the data center corridor. None of that is in the episode. I have a separate piece about it coming out soon. *I cut 2 seconds from the raw audio to remove personal information that had no connection to anything in the episode. Appendix A: the passage the clip was taken from This is the sequence from my first interview, in full. The episode uses one fragment of it. It’s tricky because my understanding is that there’s something like a 15-year half-life on collagen remodeling issues. They’re going to get a new crop of players. What I really need, though, is for the injuries to be broken down so we can see the soft tissue injuries. Right now, they’re categorized as MSK injuries, but let’s say we can actually identify them more specifically. Is that right? He was able to do that? Oh, cool. I wasn’t able to find that information. Interesting — I didn’t know that data existed. I tried so hard to get it, and I didn’t know it was available. Maybe you could connect me with that person. That would be amazing. I’m not wedded to it being an EMF, honestly. I’m not. I would say that, to a certain extent, I’ve staked my reputation on the fact that it needs more study. It’s important to look into it, and I am not certain of anything. I’m not a scientist. To me, I find the mechanisms compelling. I will go back to the fact that I got into this not because of the 49ers, but because of clients I was working with who suffer from EDS, Ehlers-Danlos Syndrome, a tendon hypermobility issue. This condition is documented to be partially caused by oxidative stress. I’ve worked with them to mitigate their EMF exposure and have seen people improve. I think it’s a bigger story. In a way, the 49ers represent an occupational cluster with specific exposure risks. If someone would conduct a study on this, I believe we could learn a lot. Perhaps we would discover that it’s like, okay, maybe it’s 10% of the problem. I don’t know the exact number, but I think either way, conducting the study would provide valuable insights. To directly answer your question, it’s challenging for me because it’s part of a bigger story. If the 49ers move and stop having injuries, I might conclude that it was related to the substation. However, if they move and still experience injuries, I would want to analyze the nature of those injuries. Are they primarily soft tissue injuries? I don’t think it’s necessarily a case closed, but the story might lose traction at that point regardless. Three things are worth noting. The aired fragment stops immediately before the sentence in which I say I am not a scientist — the cut described in item 10. It also stops four paragraphs before the words “to directly answer your question.” What the episode plays is the throat-clearing. The actual answer, about what would change my mind, never airs. And two paragraphs in, I say the EMF might turn out to be ten percent of the problem. That is the ranking the episode says I never gave. Appendix B: the full email, July 6th, 1:39 PM Hi Rose, You asked me to send you some studies a couple of weeks ago. I apologize for the delay. I have been incredibly busy. I also wanted to give you a chance to dig in yourself, and get your own perspective before I influenced you too much with mine. That said, I do want to make sure that the actual argument is abundantly clear, so here it is! One note before I begin, there are really two separate questions here: Does the substation cause the soft-tissue injuries? That was my specific claim, and what the podcast is about. Is the theory biologically sound? Can 50/60 Hz fields at these levels do anything biological below the safety limits? Question two is why people have been calling me a conspiracy theorist. The regulatory and advisory bodies (ICNIRP, etc) maintain that anything below their exposure limits is biologically inert, and that position is broadly accepted within the mainstream, but the actual science paints a different picture. To defend my theory I’ve had to defend a much larger claim: that the advisory bodies have the biology wrong. I can’t honestly answer question 1 without first addressing that. Here’s is a simplified outline of my theory, with links to studies: 1. Advisory body thresholds for biological effects The ELF magnetic-field limits (ICNIRP’s ~2,000 mG public / 10,000 mG occupational) exist to prevent acute effects from exposure. If a magnetic field is strong enough, it makes nerves fire and muscles contract. Muscles twitch. You can see faint flashes of light in your vision. People can even feel tingling or even a shock. That happens due to Faraday’s law, which states that a time-varying magnetic field induces an electric field inside the body via the creation of Eddy currents.The standards assume that those currents do nothing below the twitch threshold. They do not consider chronic effects at all. My argument is that they are biologically active and do have chronic effects. 2. There are multipe ELF-EMF mechanisms for inducing oxidative stress. This is basic biophysics. Below are the two primary mechanisms. Simplest first. Dr. Paul Héroux of McGill has the most intuitive explanation, which rests on Maxwell’s principle of superposition: because Maxwell’s equations are linear, two sets of electromagnetic waves sharing the same space simply add together. In the interview I pictured a pebble dropped into a pond, sending out clean ripples. Then a boat motors past at distance, sending larger waves, and where they meet the ripples, the two add together and the original pattern gets distorted. In our cells, the mitochondria run on continuous currents of electrons and protons that carry their own faint electromagnetic fields. An external field from a substation, by the principle of superposition, adds to those internal currents and shifts the pattern. The electron transport chain in the mitochondria leaks a fraction of its electrons by design as reactive oxygen species (ROS), which act as signalling molecules in a healthy cell. Distorting that field increases that electron leakage, creating oxidative stress. A tiny electromagnetic interference results in a large downstream effect. https://www.sciencedirect.com/science/article/pii/S2405844025006474 The more complex pathway is Dimitris Panagopoulos’s Ion Forced-Oscillation / Voltage-Gated Ion Channel (IFO-VGIC) mechanism. Weak, polarized, low-frequency fields force the ions (calcium, potassium, sodium) next to an ion channel’s voltage sensor to oscillate; because that force scales with the inverse cube of the distance involved, fields far below the stimulation threshold can still force the channel open, disrupting the cell’s ion balance and driving ROS overproduction (Nitric oxide and superoxide interact and produce peroxynitrite, a highly unstable cytotoxin that breaks down into free radicals). https://www.researchgate.net/publication/366088934 https://www.spandidos-publications.com/ijo/59/5/92 https://www.mdpi.com/1422-0067/22/18/10041 https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2025.1585441/full https://pmc.ncbi.nlm.nih.gov/articles/PMC3772193/ 3. Evidence of oxidative stress, in vivo, in humans from ELF-EMF There are many studies, and the strongest are occupational, which applies to the 49ers situation. 115 power-plant workers vs. 145 office controls. Serum malondialdehyde (MDA, the standard lipid-peroxidation marker), superoxide dismutase, and catalase were all significantly higher in the exposed group, and the markers rose with increasing field exposure. https://journals.sagepub.com/doi/abs/10.3233/WOR-203244 A follow-up where they reversed the oxidative stress in power plant workers. A double-blind randomized controlled trial: 91 power-plant workers given vitamin E, vitamin C, both, or placebo for 90 days. The antioxidant groups showed reduced lipid peroxidation and raised antioxidant capacity versus controls. https://pubmed.ncbi.nlm.nih.gov/32191586/ A spot-welder study: 46 welders occupationally exposed at 50 Hz, showed significantly altered red-blood-cell antioxidant enzyme activity and concluded ELF-MF “might act as an oxidative stressor… even at the recommended levels of exposure.” https://pubmed.ncbi.nlm.nih.gov/18504600/ A substation-specific study found oxidative stress and DNA damage https://pubmed.ncbi.nlm.nih.gov/24460415/ 4. Oxidative stress degrades collagen This half isn’t controversial at all. Oxidative stress activates the matrix metalloproteinases (MMPs) that break collagen down and suppresses its synthesis. Here are three example studies: Siwik et al. 2001: Oxidative stress raises MMPs and lowers collagen synthesis in cardiac fibroblasts. https://pubmed.ncbi.nlm.nih.gov/11121376/ Fisher et al. 2009: Collagen fragmentation drives oxidative stress and elevates MMP-1 in aged human skin. https://pmc.ncbi.nlm.nih.gov/articles/PMC2631323/ Varani et al. 2006: Decreased collagen production in oxidatively aged skin. https://pubmed.ncbi.nlm.nih.gov/16723701/ 5. What about the study showing improved collagen synthesis I’m glad you asked this question, and I’m bummed we didn’t get to it in the interview because it is a great question, and very important to understand. Superficially it may appear to be a refutation of my theory, but I would argue that it actually supports the underlying argument. That study used a short, high-intensity pulsed dose: therapeutic-PEMF, the same type of field used clinically to stimulate bone and tissue healing. The reason this works is because it triggers the very same biological pathways that can lead to oxidative stress. The exposure still stimulates ROS production, but done at a controlled dosage, for a limited duration it has a different effect. The cell reads the ROS as a warning signal and it upregulates its antioxidant defenses, and mounts a repair/proliferation response. The therapy is then stopped before the cell gets overwhelmed. That is essentially a hormetic response: a small dose of a stressor producing a beneficial adaptation. Two things follow: At the very least, this means the field is biologically active, which by itself undercuts the regulatory claim that these fields are inert below their thresholds. There is a wealth of literature on PEMF (pulsed EMF) bone regeneration and calcium channel signalling (which is the second mechanims in section one). Here is one. https://www.nature.com/articles/srep13856 At best, it leads us straight to my actual concern, which is that under chronic, chaotic and unregulated exposure, the cell’s antioxidant capacity gets overwhelmed, resulting in oxidative stress. There are plentiful examples of things that are beneficial at controlled doses, but harmful at uncontrolled doses. Excecise is one obvious, uncontroversial example. Botox is perhaps a more interesting example. 6. What about a study that shows EMF causing collagen degradation in humans? As far as I am aware there is not a single study showing EMF-driven oxidative stress degrading collagen in a human, in vivo, or in human tendon in a lab. There are studies involving isolated fibroblasts though, which secrete collagen. The most relevant one showed that human fetal scleral fibroblasts exposed to 50 Hz ELF-EMF showed a significant decrease in collagen synthesis and that MMP-2 expression was upregulated, which is the exact mechanism I described in section 2. https://pmc.ncbi.nlm.nih.gov/articles/PMC3626379/ That’s it! Thanks again for the interview. Best, Peter Anthony Cowan Environmental Health · Wellness Tech · Researcher & Journalist Publisher & Editor, Living Energy Bio: petercowan.comSocial: X · Instagram · TikTokApp: sunlightis.lifePhone: [redacted]
This giant tropical fruit could help reverse gum disease damage
A new biomaterial made from jackfruit latex, pomegranate peel, and simvastatin could transform the treatment of severe gum disease. Early tests suggest it not only combats infection and inflammation but may also help rebuild lost bone and tissue around teeth.
Can This New Enzyme Turn Back the Clock in Bodily Tissues?
In a recent study, scientists devised a way of reversing the buildup of compounds that lead to some age-related diseases.
Scientists are uncovering how common viruses may quietly increase cancer risk
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'Voicemails for Isabelle' is Netflix's latest big hit — but viewers should expect tears
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Stanford Scientists Identify Enzyme That May Promote Cartilage Regeneration in Arthritis
Stanford researchers identified an enzyme that may restore cartilage repair signals in arthritic joints, offering a potential drug target backed by mouse and human tissue results.
A grad student’s wild idea sparks a major aging breakthrough
A casual conversation between graduate students helped spark a breakthrough in aging research at Mayo Clinic. Researchers discovered that tiny synthetic DNA molecules called aptamers can selectively attach to senescent “zombie cells,” which are linked to aging, cancer, and neurodegenerative disease. The method could eventually help scientists identify and target these cells in living tissue with far greater precision.
Reducing muscle protein activity strengthens bone health, study suggests
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Scientist Jay Hoying explores frontiers of tissue therapeutics
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Bones communicate with the rest of the body to support overall health – here’s the science behind your skeleton
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This common pesticide may be quietly wiping out future bumblebees
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Beyond 'healthy' obesity: New framework weighs organ damage and daily limitations
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How scientists are trying to repair the body from within: Regenerative medicine and anti-aging
At Scripps Research and its drug discovery arm, the Calibr-Skaggs Institute for Innovative Medicines, scientists are developing regenerative medicine therapies designed to help the body repair itself from within. Unlike traditional medicines that primarily manage symptoms or slow disease progression, regenerative medicine aims to restore damaged tissues and rebuild function lost to aging and disease. Researchers are advancing programs focused on the heart, lungs, digestive tract and eyes, including investigational therapies for heart failure, idiopathic pulmonary fibrosis, inflammatory bowel disease, age-related macular degeneration and other chronic conditions that become more common as we age. Learn how scientists are activating the body’s natural repair mechanisms to explore a future where medicine may not only treat disease, but help reverse its damage.
Supercharged “natural killer” cells could be a powerful new cancer weapon
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August Monthly Review: ChatGPT In Epic
Death, taxes, another frontier lab healthcare launch inspiring truly insane LinkedIn takes. As much as I want to stay away, I repeatedly am the crewman unplugging his ears whenever we pass these sirens. So it’s not the first and probably not the last time we dial up the typewriter rather than tie ourselves to the mast. The full blow-by-blow timeline: Health API Guy is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Subscribe The End of the Standalone PHR (Jan 8): ChatGPT Health arrives for consumers, at the time powered by b.well. I was bullish on the approach in that the best way for the PHR to finally solve distribution was to meet consumers were they already are (i.e. When Horizontal Meets Healthcare (Jan 9): OpenAI for Healthcare puts out the shingle for enterprises, with SharePoint ingestion standing in for the EHR integration the product actually needed. Another One: Anthropic’s Healthcare Debut (Jan 16): Claude's version, on HealthEx rails instead of b.well, with Agent Skills for FHIR development as the one true vertical-specific investment. ChatGPT for Clinicians: The Trap Sprung (Apr 24): OpenAI filled in the missing GTM middle with a free product for verified clinicians, effectively peeling the enterprise wrapper off ChatGPT for Healthcare and taking the PLG fight directly to OpenEvidence. OpenAI’s Second Attempt at Health (Jul 31): a relaunch of their patient specific app, now branded Health in ChatGPT, where the privacy partition came out, the connectors thinned, and b.well disappeared in favor of first-party FHIR work against a smaller network Beyond a Shingle So what was announced now? Today, we’re introducing a new electronic health record integration that brings authorized patient context from Epic into ChatGPT for Healthcare, along with the Healthcare Public Data plugin for direct, structured access to official healthcare datasets like PubMed, DailyMed, and CMS Coverage. Together, these capabilities bring ChatGPT closer to the systems and sources healthcare teams trust, while supporting the controls and compliance healthcare work requires. The core portfolio is unchanged from prior announcements we delineated and discussed (aside from the relaunch of patient-facing). Since trade publications still seem to be confusing them by using the wrong names: Enterprise sales motion: ChatGPT for Healthcare Protecting their core product / PLG: ChatGPT for Clinicians Consumer/patient-facing product: Health in ChatGPT So really, this is a feature release (specifically for ChatGPT for Healthcare when it comes to EHR integration). What’s cool about it, though, is that we are moving beyond just putting out a shingle. Everything in the January enterprise launch was horizontalizable: Horizontal tech companies thus generally start verticalization with their “putting out a shingle phase”. Telling the world you’re open for business as a horizontal tech company reliably attracts early inbound interest from buyers who are already trying to force-fit horizontal tools into domain-specific workflows and are eager for any signal that the vendor intends to support their use case more directly. Nothing was really vertical specific, which is exactly what you'd expect from the ultimate hypergrowth horizontal company dipping their toes into specific industries. But eventually you have to stop changing the sign on the door and start changing the product. Can you guess where the horizontal product was going to run out of road? This is the core dilemma writ large: verticalization requires differentiation, while scale economics of consumer and horizontal push toward unification. I’ve buried the lede so deep here it will be painful to some readers, but what should be shocking to no one is that my perspective is that EHR integration is the only path that meaningfully resolves this tension for ChatGPT for Healthcare. Integration with Microsoft Sharepoint is fine, but it is categorically insufficient for any product that hopes to influence clinical decision-making. SMART Money Well here we are, eight months later! Real vertical investment has begun, which surprised a few people. One friend in the industry messaged me: “Absolutely no way Epic gave ChatGPT API access.” Looking forensically at the announcements, the integration is notably read-only across appointment notes, laboratory results, medications, and specialist documentation. So while I’m not a betting man, I'd wager the house this is a SMART on FHIR launch: That sounds a lot like USCDI! The recommended path for the workflow they outline would be SMART on FHIR Their Health AI lead’s post is evocative of both standalone and EHR launch SMART, which another termed “ChartGPT” and “EHR Plugin” The implementation burden for SMART on FHIR is the lowest of the available integrative paths This is the team who literally did patient-facing SMART on FHIR with Epic last month Most importantly, if you’re a horizontal company, you generally still haven’t taken the full plunge and thus (overly) value reusability. SMART on FHIR is the logical compromise: healthcare-specific enough to matter, but standardized enough to reuse. Nobody Asked Judy Another friend asked “I thought they had to go to each health system, or did they go direct to Epic and now health systems opt in?” Given the trust paradigms in healthcare, this functionally cannot be Epic hoovering up all the data for OpenAI and shoving ChatGPT in their customers’ faces (or they would revolt). However, I do believe the aforementioned terrible coverage by TechCrunch and other outlets is probably responsible for that question, given the 325 million reference. When using FHIR as a business associate to an Epic customer, there is no EHR gatekeeping to speak of, as that isn’t how fhir.epic.com works: You register an app You pick your APIs You test against the sandbox APIs You list as “Ready for Production” Hospitals pick your app You test and go live with them Bluntly, nobody had to say yes or no in Verona (nor were they given the chance). Vendor Services (their next developer tier up that I doubt OpenAI is using quite yet in this initial release) certainly has contractual paperwork that some resent, but even there, the twin pressures of mounting antitrust and information blocking make outright gatekeeping increasingly fraught. My friend’s sentiment is, to me, representative of a broader industry neurosis, perhaps a sort of scar tissue of prior eras: people assume the gate is still there and never actually try the door. There are certainly other ways Epic (and any EHR) can put its thumb on the scale, but they are not so dumb as to stand in front of a federally mandated API and play bouncer at this exact moment in time. So I think they can and probably should go deeper, as this release is at best parity and at worst behind vertical-specific competition. OpenEvidence did a basic SMART launch with Sutter Health in February, allowing for more convenient evidence search by providers. They then add patient-context (the equivalent SMART on FHIR flow to what we see here) when Cedars-Sinai went enterprise-wide in May. UpToDate has four distinct applications across deeper workflows like patient engagement listed in Epic Showroom and announced a partnership with Epic to power Art at UGM Abridge and other ambient scribes have invested deeply into the deepest bidirectional clinical copilot workflow with integrations well beyond SMART on FHIR. In that light, the “Who is OpenAI primarily targeting here?” is clear. This release brings them into striking distance of OpenEvidence, but not the others quite yet. They are the only one of the three you can reach without building something truly Epic-specific. When will they go further? Competition is a great motivator to overcome the horizontal demons and start building things that can’t be reused: not across industries, not across EHRs, maybe not past the customer you built them for. That’s the price of actually verticalizing. The question is if and when OpenAI will be willing to pay it. Month in Review Here is the monthly review. As a reminder, this is a regular round-up of the month’s posts and other content to surface things you may have missed across regulation, litigation, interoperability, and beyond. AI assistance is used in these bullet summaries so I can focus on articles. Articles Published: None this month Video Content: The Information Exchange: Standards-based Thruple Edition (Aug 14): Back to school for us too, with Brad reporting in from the CMS Health Tech Ecosystem’s one year anniversary in DC. We get into the January CMS-0057 deadline, the fall rulemaking reading list, and why enrollment still keeps most apps off FHIR. The Information Exchange: Epic Dúnadan Edition (Aug 25): A UGM roundup with Ryan Brickner joining for the first time to check our takes against what the building actually thinks. Rangers, Ergo sitting on top of EHI, and a down-market lineup that needs some cuts. Regulatory: Stacked Deck, Bad Hand (Aug 05): ONC’s website refresh took the entire HIT Policy Committee record with it, so I rebuilt the archive and went looking for the regulatory capture story everyone assumes is buried in there. Stacking the deck and winning the hand turn out to be very different things. The Sixth Generation of Patient Access (Aug 19): A quick catalog of the five generations of patient access we’ve layered on since HIPAA, and the two candidates now competing to be the sixth. One is planned. The other is the market routing around the plan entirely. Court cases: Three Cases Walk Into a Docket (Aug 06): Two surprise settlements cleared the board in a single week, and then Judge Maddox dropped ninety-four pages on Vyne v. Henry Schein. The sleeper is a DMCA holding that makes direct-to-database a considerably riskier business model. Epic v. Health Gorilla: Into the MDL (Aug 10): Nine class actions are headed to Miami, and the Panel signaled it wants to bring the case that spawned them along too. That would leave Epic arguing the requests were obviously fraudulent in one courtroom and unknowable in the other. Amazon v. Perplexity: Agents Are Legalized! (Aug 11): The Ninth Circuit vacated the injunction against Comet, holding that the user is the one accessing the servers rather than the company that built the agent. A real win for agentic access, and a much narrower one than the headline suggests. Veeva v. Epic: Come At Me, Bro (Aug 26): Epic’s response brief wants the dismissal affirmed and, unusually, wants the opinion published as precedent. Buried in it is Epic’s own description of what its non-competes actually prohibit, which current and former employees should read closely. EHRs: The Contract Epic Would Never Sign Today (Aug 04): A 1999 SEC exhibit catches Epic licensing nearly its entire product line, Tapestry included, to the company that became TriZetto. The marketing services menu attached to it is the part that will make you blink. Forecast from Verona (Aug 07): The Epic Almanac makes one argument six different ways: the AI is only as good as the networks behind it. Emmie headlines, Art’s context stack is the most ambitious part, and Penny finally gets an autonomous coding date on the calendar. Works With Epic MyChart (Aug 17): Epic’s first new Showroom category since the death of Workshop certifies hardware instead of software, badge on the box and all. Made for iPhone, but for blood pressure cuffs, and rough news for anyone selling the RPM stack sitting in between. UGM Hot Takes 2026 (Aug 20): Everyone else covered the AI announcements, so I went after Savvy deleting the payment gateway, Rangers as Boost with the timer removed, and a down-market lineup with too many entries. Plus the Health Grid tidbits I cannot help myself on. MyChart Central Grows Up (Aug 24): Device data and Emmie turn Epic’s identity hub into a full consumer platform, which is both a logical answer to ChatGPT and a bit of a mistake. It also happens to be the best scraping target Epic has ever shipped. Industry Analysis: The Wrong Yardstick (Aug 12): Vertical software keeps getting judged against Superhuman and Notion, which is the wrong bar entirely. Your user is comparing your product to a whiteboard and forty phone calls before lunch. Primitives vs. Abstractions (Aug 27): Developers want building blocks, systems of record prefer to hand out business logic, and both sides have a real case. There’s no test from the outside that separates the engineering reason from the competitive one, which is why this keeps ending up in court. Cross-industry Comparisons: The Two Kinds of Platform Power (Aug 18): Attention power and record power are different problems that keep getting handed the same regulatory toolkit. Congress’s latest swing at Big Tech shows both what’s possible and where it falls apart. The Dogs of (Platform) War (Aug 21): A CourtListener alert turned up a property management fight with healthcare’s exact shape and none of the Cures Act. Shell prospects, ghost accounts, a notetaker bot that came back to haunt someone, and a lawyer arguing both sides of the same theory in two states. Fractals All the Way Down (Aug 31): Yardi dominates property management right up until you zoom into one segment, where AppFolio owns it outright and Yardi doesn’t appear at all. Where you draw the line around a B2B software market is about to decide an awful lot of cases. Other News: If Judy Had the Courage (Aug 13): A short eulogy for the era when software was allowed to look insane: WinAMP, bold colors, and everything the grey chatbot era has taken from us. External Media: Portland Monthly Health Tech Meetup: Erin O’Brien channeled my own feelings - maybe it’s just because it’s August and beautiful, but the monthly edition of the PDX Health community meetup was a ripper. Make sure to reach out if interested to join for the next one. STAT’s Coverage of Epic This Month: Brittany Trang of STAT did a fantastic job of breaking the FTC investigation that’s been lurking, as well as UGM related coverage, so I had to give her her wish of a meme. Fall Conferences: I’m pumped to be kicking off my fall conference season in NYC at Nabla Accelerate next month, which Chrissy provided the link to apply for. Here’s the rest of my schedule in case you want to meet up: Commonwell (Redwood Shores, CA): Oct 13-14 Open@Epic (Madison, WI): Oct 21-22 eHealthExchange (Austin, TX): Oct 27 Sequoia Project (Austin, TX): Oct 28-29 HLTH (Vegas): Nov 15-18 RSNA (Chicago): Nov 29-Dec 3 Posts I Liked: HTI-6 Should Unbundle API Certification: Josh Mandel makes the case that HTI-6 should split (g)(10) into separate authorization and data certifications, so a PACS or a genomics platform can certify only the role it actually performs. Imaging is the urgent example, but the structure solves a much bigger problem. On implementing ePrior Auth with Epic: Scott Rossignol’s field notes from a live ePrior Auth build on Epic, including the two app registrations nobody warns you about and the CPT mapping problem waiting at the end. CMS-0057 implementations are going to be such a beast. Healthcare point solutions are starting to look a lot like streaming services: Spencer Dorn runs the cable-to-streaming arc against health IT and lands squarely on the bundling half of the cycle. Bundling can be good! It can also be bad! Life is nuanced. Health API Guy is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Subscribe
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UF Health researchers uncover biological clues behind childhood scoliosis
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Virginia Tech leads multimillion-dollar project for women's health
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This shark can live 400 years. Its eyes barely seem to age
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Scientists Discovered ‘Zombies’ With ‘Immortal’ Body Parts. This Could Redefine What We Think Life Is.
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New Molecular Monitoring Offers Scientists a ‘Live Video’ Look at Cells
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Fossilized tissue reveals largest known T. rex died from broken rib
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AI tech uses cardiac CT scans to evaluate inflammation, predict stroke risk
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Scientists built implants that talk to each other through body tissue
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Without this protein, damaged muscle turns to fat and scar tissue
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A hidden conversation inside injured tissue may hold clues to regeneration
When tissue is damaged, healing isn't simply a matter of growing new cells. The body also has to know when to stop growing and begin rebuilding. If those steps happen out of order, the tissue may never fully recover.Researchers, led by Arizona State University Associate Professor Rob Harris, have discovered what appears to be a previously unrecognized communication system that helps coordinate those two stages of repair.
A severed piece of sea cucumber refused to die, and what happened next could transform medicine
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A stress hormone may help the brain repair itself
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Science & Medicine: Tooth pain with a purpose
Anibal Diogenes, D.D.S., Ph.D., is an endodontist, the branch of dentistry that deals with the innermost part of the tooth called pulp, a connective tissue that has immunological, reparative functions.
Retired Middle School Teacher Brings the Science of Organ Donation into Wyoming Classrooms
Donor Alliance's Transplantation Science program gives students and their families a reason to talk about organ, eye and tissue donation
Lena Dunham welcomes her first baby via surrogacy
(CNN) — Actress and writer Lena Dunham and her husband Luis Felber have welcomed a baby daughter via surrogate.Writing in an op-ed published by Vogue on Wednesday, Dunham, 40, who is best known as the creator of hit TV series “Girls,” revealed that the couple’s first child had arrived 13 days late, before describing the moment of her birth.“I was so focused on our surrogate — in awe at her concentration, her period of quiet followed by what sounded like a roar — I forgot to look down until I heard our baby’s cry,” she wrote.“I saw her face, gasping just as she did. Her eyes, wide and unfocused, taking in the light and shadow, blinking rapidly.”Dunham said she was “bashful and dizzy with joy.”In 2018, Dunham revealed that she’d had a hysterectomy in an attempt to end the pain caused by endometriosis.Endometriosis is a common and often painful condition that happens when tissue similar to the lining of the uterus grows outside the uterus itself. It’s estimated to affect more than 11% of women between the ages of 15 and 44 across the United States.The surgery removed her cervix and uterus, meaning that she was unable to conceive naturally.On meeting her surrogate, Dunham wrote in the Vogue piece: “While I’ve been known to make friends quickly — airport terminals, veterinary offices — this was the quickest leap from first coffee to gynecological procedure I’d ever done.”Dunham said in the months before the embryo transfer date, as she “got to know our surrogate and to trust her,” she thought she would feel “jealousy” towards her, but she did not.“Instead, I felt a different kind of jealousy — toward said baby, for the chance to be tucked into someone who radiated such safety. I could just tell she knew how to steer an SUV in the snow,” Dunham added.The pregnancy came after “12 years circling the fertility drain,” Dunham wrote, and revealed how she dealt with the nerves of the intervening months.“Powerless and unable to feel the physical changes that signal a growing fetus, I horrified friends and family who adhere to the Jewish superstition prohibiting anticipatory purchases, and I started shopping,” said Dunham, before recounting her journey into the world of baby fashion.“I was looking for garments that allowed her personality to develop and express itself rather than announcing an identity she didn’t yet have,” she said.“She would be a person that we helped to dress, who made an impression on the world based on our choices, until she was old enough to do it herself.”The-CNN-Wire™ & © 2026 Cable News Network, Inc., a Warner Bros. Discovery Company. All rights reserved.THE-CNN-WIRE (TM) & © 2026 CABLE NEWS NETWORK, INC., A TIME WARNER COMPANY. ALL RIGHTS RESERVED.
Continual integration of single-cell multimodal data with MIRACLE
Nature Computational Science - MIRACLE is an online continual learning framework that efficiently integrates single-cell multimodal data across batches, modalities, tissues, and diseases.
Scientists just found something weird inside moss
UC Riverside researchers have found evidence, for the first time, that desert mosses may host fungi inside their tissues. The finding offers a clue about how ancient life crawled from oceans onto dry land.
Scientists Trace How Cancer Spread Between Identical Twins Before Birth
Scientists have used DNA analysis to trace how a rare soft tissue cancer spread from one identical twin to her sister before birth.
Scientists discover cells that cheat death and rebuild damaged tissue
Scientists discovered a population of cells that can start the process of programmed cell death, survive it, and then help rapidly rebuild damaged tissue. Their descendants become far more resistant to future damage, revealing a mechanism that could improve healing but may also help cancers return after treatment.
Science on Target: Q3 Publications from our Innovation Ecosystem
Antisense Oligonucleotide Tofersen Distribution in the Central Nervous System of SOD1-ALS Autopsy Tissue Donors. Guise AJ, Sellon MT, Roemer SF, Monine M, Comfort Harris NT, […] Plowey ED. JAMA Neurol. 2026 Jul 6:e262195. doi: 10.1001/jamaneurol.2026.2195. Epub ahead of print. PMID: 42406382; PMCID: PMC13338845. Using human 3D organoid models to gain mechanistic insight in motor neuron […]
Koning Health secures Australian TGA approval for breast CT system
The platform is designed to provide volumetric images to assist clinicians in evaluating breast tissue.
What happens to the body in the first hour after death? Science reveals a surprising sequence of changes
Death can look like a single moment: the heart stops, breathing ends and the person is declared dead. At the level of individual organs, tissues and cells, however, the transition is not synchronized....
Peng Gao receives NIH New Innovator Award for research measuring chemical exposure in blood and tissues | Harvard T.H. Chan School of Public Health
Peng Gao was awarded an NIH Director's New Innovator Award from the NIH's High-Risk, High-Reward Research program.
Double Success for ISTA at the Lower Austrian Science Awards
3D-printed thermoelectric materials and expansion microscopy of brain tissue—these are the contributions that earned two researchers from the Institute of Science and Technology Austria (ISTA) distinctions at the Lower Austrian Science Awards. Maria Ibáñez and Johann Danzl accepted their awards at a
Lab-grown mini brains may predict which Alzheimer’s treatments will work
Miniature brain models grown from patients’ cells revealed striking differences in how Alzheimer’s-related tissue responds to an antidepressant. The organoids and the particles they release could eventually guide more personalized treatments and provide new clues for diagnosing the disease.