The push to reshape the utility liability system has become a keystone issue of Newsom’s final legislative session.

Agency employees have feared blowback from the president after their emails were sought by right-leaning operatives since he last left the White House.

To improve the chances of having a race in cooler weather, organizers are shifting race dates, starting earlier and even giving options for participants to cut their runs short.

Roughly 97 million people from the central Plains to the Southeast face heat advisories.

Mining has stripped away vast areas of rainforest, leaving behind a scarred landscape of contaminated pools and altered rivers.

As we move through everyday life, our brains engage in a huge variety of cognitive tasks. For example, during a grocery run, we might have to recall the items for a recipe, remember where the clerk said the flour was located, and count out money to pay.  

Scientists have long theorized that the brain contains modules, or clusters of neurons, that perform the same computation across many different types of tasks. This type of modularity could help explain why our brains are able to take on so many functions, with little difficulty.

In a new study of mice, MIT neuroscientists have found the first evidence for the existence of these flexible modules. They identified neurons in the prefrontal cortex that can be used to store either a sensory input or an action plan in working memory.

“We found that the brain doesn’t dedicate a separate group of neurons for every type of information. Instead, it uses the same populations of neurons to perform the same computation on different kinds of information, which means the same subset of neurons can hold both an action and a sensory stimulus in working memory,” says Yuma Osako, an MIT postdoc and the lead author of the new study.

The discovery supports the theory that reusable circuits allow the brain to mix and match components to generate a rich variety of behavior, the researchers say. 

Mriganka Sur, the Newton Professor of Neuroscience at MIT’s Picower Institute for Learning and Memory, and Timothy Buschman PhD ’08, a professor at the Princeton Neuroscience Institute, are the senior authors of the paper, which appears today in Nature Neuroscience. MIT graduate student Greggory Heller and postdoc Sofie Ahrlund-Richter are also authors of the study.

Cognitive building blocks

Dating back to his time as a graduate student at MIT, Buschman has been interested in understanding how the brain is able to perform so many different kinds of behavior. 

“One of the solutions that’s always been proposed has been this idea of compositionality — that you can take pieces of cognition that perform part of a task and reuse them in another task,” he says. 

In a study published last year, Buschman’s lab at Princeton showed that when animals perform a task such as categorizing objects based on their shape or color, they assemble neural circuits that perform different pieces of the task. Just like “cognitive Legos,” these building blocks can be flexibly combined to generate new behaviors.

Osako, who joined Sur’s lab several years ago, was also interested in studying cognitive flexibility. He and Sur teamed up with Buschman to explore a related question: whether individual neural circuits can be repurposed to perform different functions. 

“Our everyday life requires us to temporarily hold many different kinds of information. One big question is how the brain can represent an unlimited variability of information using only a finite number of neurons,” Osako says.

To get at that question, the researchers trained mice on a task in which they have to determine whether two sensory stimuli (high or low pitched tones) are the same, and respond accordingly. 

The researchers recorded electrical impulses from the brain while the mice performed this task, focusing on the prefrontal cortex, which is involved in executive functions such as planning and decision-making, and the parietal cortex, which processes sensory information and plans movement.

After measuring electrical activity from thousands of neurons, the researchers performed computational analyses that allowed them to identify groups of neurons that encode specific pieces of information.

They focused on two time periods — the time between the first and second tone, when the animals are holding a memory of the first tone, and the time between the second tone and the point where they have to decide on an action. During that second period, the animals are holding their decision and action plan in their working memory.

Within the parietal cortex, the researchers found that neurons appeared to exclusively store memory of the tone. But in the prefrontal cortex, they identified a cluster of neurons that could switch between the two types of memory. During the first period, they stored a memory of the first tone, but during the second, they were responsible for remembering the plan of action.

Re-using these clusters for different purposes allows the animals to flexibly store different types of information, the researchers say.

“When mice do tasks that test whether memory computations can be reused, the answer is they are. There are subspaces of functional activity in the prefrontal cortex that can be the substrate of mixing and matching toward flexible cognition,” Sur says.

Computational flexibility

The new findings offer support for the idea that the same computational circuits can be used for different purposes, Buschman says.

“The main result from this study is that there’s a circuit in the brain that maintains items in working memory, and you can put either sensory or motor information into it, and flexibly reuse it depending on what your current task is,” he says. “This means you do not have to build an entire new circuit for holding information in mind every time you want to learn a new task.”

The researchers now plan to study whether inhibiting these modules during different parts of the task affects the animals’ behavior, which could offer additional evidence that the flexible modules they identified participate in a variety of functions.

The research was funded by the National Institutes of Health, a MURI Grant, the Picower Institute Innovation Fund, the Japan Society for the Promotion of Science Overseas Research Fellowships, and the Uehara Memorial Foundation Postdoctoral Fellowship. 

Nature Climate Change, Published online: 17 August 2026; doi:10.1038/s41558-026-02712-y

The influence of fine particulate pollution (PM2.5) on plant water-use efficiency remains poorly understood. The authors highlight that PM2.5 exerts a primarily negative effect across scales due to asymmetric effects on photosynthesis and evapotranspiration.

Fascinating video about searching for life undersea. The video basically makes the point that our bright white searchlights are scaring everything away, and that red light is more neutral. That, plus bait to attract sea creatures, is teaching us a lot about what’s going on down there. Lots of footage of giant squid, and speculation about the colossal squid. Worth watching.

As usual, you can also use this squid post to talk about the security stories in the news that I haven’t covered.

Blog moderation policy.

Chiang Chung "C.C." Mei, professor emeritus in the MIT Department of Civil and Environmental Engineering (CEE), a renowned hydrodynamicist whose work shaped the field’s understanding of ocean waves and their interactions with coastal and offshore structures, passed away peacefully at home in Waltham, Massachusetts, on July 16. He was 91. 

For more than four decades, Mei was a defining presence in CEE. Since joining the MIT faculty as an associate professor in 1965, he became one of the world's foremost authorities on theoretical hydrodynamics, fluid mechanics, and ocean and coastal wave phenomena, retiring in 2010 after 45 years on the faculty. Throughout his career, he earned a reputation among colleagues and students as a generous mentor and thoughtful leader.

An elegant, rigorous scholar

Mei's research advanced the science of ocean wave hydrodynamics, spanning nearly every aspect, including nearshore currents, sediment transport and resuspension, the formation of sand ripples and bars on beaches, wave-induced stresses and seabed deformation, and the removal of contaminants from soils. In later years, he extended his mathematical approach to biofluid dynamics, publishing on flow problems in blood vessels and the inner ear, including a paper on "Streaming and diffusion in the cochlea" that appeared in the Journal of Fluid Mechanics in July 2025.

He authored over 300 publications, was cited more than 14,000 times, and coauthored the landmark books "Theory and Applications of Ocean Surface Waves" and "Homogenization Methods for Multiscale Mechanics." Mei published decades of influential research on wave power extraction, harbor oscillations, waves over muddy seabeds, coastal vegetation, landslide-generated waves, tsunamis, and hydrodynamic resonance. His work combined mathematical elegance with practical engineering application and continues to guide solutions to some of the world's most complex ocean-based environmental challenges, including coastal defenses against storms and oil spill response strategies.

"C.C. tackled deep, diverse, difficult, and important fluid dynamics questions with utmost finesse and elegance," says Lydia Bourouiba, the Japan Steel Industry Professor. "He was an inspiring scholar, an intellectual leader, and a wonderful mentor, whose rigor set the standard we should continue to uphold. We lost a true giant in our field."

His excellence and leadership in research and teaching earned numerous prestigious recognitions, including a Guggenheim Fellowship in 1972, election to the National Academy of Engineering in 1986, fellowship in the American Physical Society, the Theodore von Kármán Medal in 2007, and appointment as a Ford Professor of Engineering at MIT. 

Beyond his scientific achievements, Mei devoted himself to the MIT community, serving as interim head of CEE from 2001 to 2002 and helping guide the department through a period of transition with the same humility and steadiness that characterized his scholarly contributions. In 2015, the department established the C.C. Mei Distinguished Speaker Series in his honor — an idea that grew out of the initiative of Bourouiba to revive CEE's environmental seminar series and honor its strong historical legacy in fluid dynamics. "Discussing the idea with C.C., he thought it was an excellent idea and was so generously supportive. He embodied the excellence I wanted the new series to reflect; naturally, we named it in his honor," she says. The series continues to bring internationally renowned scholars to MIT. 

A mentor whose students became family

Mei's influence was equally profound in the lives of his students. Over more than 45 years at MIT, Mei advised and mentored generations of engineers, many of whom became leaders in academia, industry, and government. Even in his final days, those relationships endured. 

One of his first doctoral students, Professor Emertius Ole Madsen, visited him just hours before his passing. Former student Yile Li SM '01, PhD '06, who continued collaborating with Mei on biofluid dynamics research in his later years, remained in close conversation with him throughout his final days. Li recalls the highlight of his discussions with Mei. "He told me there are three stages of doing research: solving problems using mathematical methods, modeling problems by capturing core physics, and ultimately discovering entirely new problems," Li says. "His own work proved he was a master of all three."

For Mei's family, MIT was never simply his workplace. "CEE was truly the center of my father's life," says his daughter Deborah Mei. "For more than 50 years, it shaped not just his career, but our whole family's world. His students, colleagues, and collaborators weren't separate from our home life — they were part of it, for as long as I can remember."

Colleagues consistently remember not only Mei's intellectual brilliance, but also his extraordinary generosity. Mei was known for the warmth he extended to junior colleagues finding their footing at MIT. 

"He was so respectful and kind to me when I was hired in 1976, and feeling like a fish out of water," says Institute Professor Sallie “Penny” Chisholm. "I will never forget that. A great gentleman, indeed." 

Heidi Nepf, the Donald and Martha Harleman Professor, recalls Mei as "an exceptional scholar and a wonderful colleague."

Rafael L. Bras, professor emeritus, remembers Mei as the model of the gentleman scholar. "He cared deeply about people, loved his profession, and touched countless lives, both directly and indirectly. Everybody loved him."

A full and joyful life

Mei was born on April 4, 1935, in Wuchang, Hubei Province, China, the only son and first child of Ju-Long Mei and Wu Yu-Ling. He earned his BS from National Taiwan University in 1955, his MS from Stanford University in 1958, and his PhD from Caltech in 1963.

Those who knew him describe a man who was passionate, playful, endlessly curious, and quick with both words and affection. The home he shared with his wife, Caroline, became a gathering place for generations of the Mei family, his MIT colleagues and students alike with animated conversation, humor, and his familiar loving banter with his wife and siblings, as those close to him remember it.

To generations of students and colleagues, Mei was known as much for his patience, kindness, intellectual curiosity, and quiet encouragement as for his scientific accomplishments. He was always willing to discuss an idea, help a student work through a difficult problem, or offer thoughtful guidance to a young colleague beginning an academic career. His legacy lives on not only in the theories that continue to shape coastal and ocean engineering, but also in the worldwide community of scholars he mentored, inspired, and welcomed over more than half a century at MIT.

Mei is survived by his wife, Caroline (Schmitt) Mei of Waltham; his daughter, Deborah Yupin Mei, and her husband, Juan Ignacio Garcia De Motiloa Ubis of Singapore; his sisters Helen Chiang-Hua Mei Chao of Potomac, Maryland; Teresa Chiang-Ming Mei Wu of Bethesda, Maryland; Heidi Chiang-Kuo Mei Hsia and her husband, Jack, of Potomac, Maryland; and Christine Chiang Ying Mei and her husband, Paul Tung, of Rancho Palos Verdes, California; his grandchildren, Juan Ignacio Jr. and Lauren; and many nieces, nephews, grand-nieces, and grand-nephews.

Gifts may be made in Mei's memory to the Chiang and Caroline Mei Fund 

Every year, lung cancer kills more than 100,000 people in the United States. Smoking is the leading risk factor for lung cancer, but other environmental exposures can also contribute to the disease.

In an advance that could help prevent some of those lung cancer deaths, MIT researchers have shown that blocking an enzyme involved in lung inflammation appears to reduce the risk of developing tumors. 

The researchers found that this enzyme, caspase-1, is active in developing tumors in mice. When they treated the mice with a small-molecule drug that inhibits caspase-1, the mice were much less likely to develop lung tumors.

That drug has already gone into clinical trials for other diseases, and the researchers now hope to test it as a preventative drug in people with elevated risk for lung cancer. 

“If you look at global cancer deaths, lung cancer causes most of them, and most of that is driven by tobacco smoking. Additionally, people who are ‘never smokers’ are showing up with lung cancer. You can imagine a future where you get a test and if you’re deemed high-risk, you go on a preventative medicine. This concept is called cancer interception, and it could help millions of people,” says Sangeeta Bhatia, the John and Dorothy Wilson Professor of Health Sciences and Technology and of Electrical Engineering and Computer Science at MIT, and a member of MIT’s Koch Institute for Integrative Cancer Research and the Institute for Medical Engineering and Science (IMES).

Bhatia is the senior author of the new study, which appears today in Science Advances. Cathy Wang PhD ’26 is the lead author of the paper. 

Blocking inflammation

Preventing lung cancer in patients who are at high risk could significantly reduce the death toll of the disease. In 2017, a clinical trial run by Novartis yielded a tantalizing hint that targeting lung inflammation could prevent some lung cancer cases. That trial, known as CANTOS, was designed to examine whether an anti-inflammatory drug — an antibody that blocks the cytokine IL-1 beta — could reduce the risk of strokes and heart attacks. Unexpectedly, the researchers found that this treatment led to lower rates of lung cancer in a subset of people.

Later trials showed that the antibody had little effect in patients who had established lung cancer, but researchers are still exploring the possibility of using it to prevent progression of lung cancer in high-risk patients. A recent study by the Swanton lab at the Francis Crick Institute identified a set of proteins, across several biological pathways and cell types, that could be used to predict which patients would respond to treatment with an IL-1 beta antibody. 

IL-1 beta requires protease cleavage to be converted to its mature, active form. Thus, Bhatia and her team wondered if enzymes called proteases, which cleave other proteins, might be involved in driving the inflammatory pathway that includes IL-1 beta.

For several years, Bhatia’s lab has been developing tools to track and visualize proteases, since the activity of these enzymes can contribute to cancer development. Proteases can help tumor cells escape their original locations by cutting through proteins of the extracellular matrix, and they also play essential roles in guiding inflammatory cell migration, which can influence tumor growth and immune system targeting.

By coming up with ways to detect these enzymes, Bhatia’s lab has created diagnostic nanosensors for cancer and other diseases. The sensors consist of nanoparticles decorated with peptides that can be cleaved by certain proteases, revealing when proteases are active in a particular tissue or disease state.

In addition to their role in cancer, proteases are known to be involved in the regulation of inflammation. In their new study, Bhatia and her colleagues adapted their nanosensors to identify proteases that may participate in IL-1 beta-mediated inflammatory pathways. 

“We know that proteases are very important in inflammation, and we wanted to pinpoint which ones might be the most active during early lung cancer development,” Wang says.

For this study, the researchers used a mouse model developed by Tyler Jacks, the David H. Koch Professor of Biology at MIT and a member of the Koch Institute. This model, known as KPS, is engineered to turn on cancer-causing mutations in the p53 and Kras genes. The mice also express a peptide called SIINFEKL, which helps to activate T cells and stimulate inflammation in the lung.

The researchers designed their experiments to allow them to model increased cancer risk, beginning before tumor formation was detectable. Five weeks after they induced the cancer-causing mutations, the researchers injected some of the mice with an antibody that blocks IL-1 beta, while others were untreated. Three weeks later, the researchers used their nanosensors to detect proteases that were active in the lungs. 

Those experiments showed that in untreated mice, which all developed lung tumors, caspase-1 was very active. However, in the treated mice, which had fewer tumors, caspase-1 activity was significantly reduced. The researchers also found that in untreated mice, the active caspase-1 was found primarily in lung tumors, not in nearby healthy tissue.

Working with Lecia Sequist, a professor of medicine at Havard Medical School and physician at Mass General Brigham, the researchers also analyzed a small number of human lung fluid samples. In these samples, they also found higher levels of caspase-1 activity from patients with lung cancer compared to healthy donors, despite a common smoking history.

A repurposed drug

The observation that caspase-1 activity is interrelated with the IL-1 beta inflammation pathway was not completely surprising, given IL-1 beta itself required protease cleavage to be converted to its mature, active form. The MIT team then investigated whether inhibitors of caspase-1 might also provide the same protective effects as inhibitors of IL-1 beta, or even improve them. 

Before tumors developed, the researchers began treating the at-risk KPS mice with either a caspase-1 inhibitor, an IL-1 beta antibody, or both. In mice that received both drugs, nearly 20 percent never developed tumors at all. In the mice that received either the caspase-1 inhibitor or the IL-1 beta antibody alone, tumors were much smaller and less numerous than in untreated mice.

Unlike antibodies, which need to be given intravenously, caspase-1 inhibitors can be taken orally, which could make them more appealing as a preventative treatment. Another opportunity provided by these drugs is that they have previously been tested in clinical trials for treatment of rheumatoid arthritis and other diseases.

“What’s so attractive about using this caspase-1 inhibitor is that it has actually been tested in humans. It’s already been through safety studies, and we think it could potentially be repurposed for cancer prevention,” Bhatia says.

The researchers hope to test the drug in a clinical trial, potentially using the biomarkers that were identified by the Swanton team to identify subjects who are likely responsive to IL-1 beta antibody treatment. 

The authors of the study also include MIT researchers Qian Zhong, Shih-Ting Wang, Carmen Martin-Alonso, Sofia Neaher, Sahil Patel, Tiziana Parisi, Jesse Kirkpatrick, and Tyler Jacks. 

The study was funded by Johnson & Johnson, Upstage Lung Cancer through the Koch Institute Frontier Research Program, the Virginia and D.K. Ludwig Fund for Cancer Research, the Koch Institute’s Marble Center for Cancer Nanomedicine, the Koch Institute Support (core) Grant from the National Cancer Institute, and a core center grant from the National Institute of Environmental Health Sciences. 

This is a current list of where and when I am scheduled to speak:

• I’m speaking, signing books, and participating in panel discussions at LAcon V in Anaheim, California, USA. My full schedule is here.
• I’m speaking online (via Zoom) at a League of Women Voters event on Tuesday, September 22, 2026, at 5 PM ET.
• I’m speaking at Elevate Festival in Toronto, Canada. The conference runs September 22–24, 2026; my talk is on Wednesday, September 23.
• I’m speaking at CanSecWest 2026 in Vancouver, Canada. The conference runs September 30–October 1, 2026; the time of my talk is TBD...

Epithelial cells are the tiny shields that line and protect our body. In a developing embryo, epithelial cells grow, divide, and move into positions to form the outer layers of our skin and the surfaces of our organs and blood vessels. When we scrape our skin, suffer an internal tear, or undergo surgery, epithelial cells will migrate to the site of injury to heal a wound. And when epithelial cells go haywire, they can turn malignant and spread through the body as cancer. 

MIT engineers have now discovered that as they migrate, epithelial cells can synchronize and collectively pulse. In a study appearing today in the journal Newton, the researchers report observing groups of epithelial cells repeatedly moving in, then out, like a circle of dancers coming together and pulling apart. 

The team measured this collective rhythmic pulsing in different types of epithelial cells, including healthy cells, cells from benign tumors, and cancerous cells. 

Surprisingly, they discovered that malignant epithelial cells were more persistent in their synchronization, pulsing together for twice as long as healthier cells. It’s unclear why the cells sync up in this way. But the researchers suspect that this cellular dance can serve as a clinical signal.

“More aggressive cancer cells tend to have a steadier and more persistent rhythm as compared to healthy ones,” says study author Ming Guo, professor of mechanical engineering at MIT. “We think this coordination could serve as an early warning sign of how likely a tumor is to spread. The same coordinated waves may help shape embryos during development and close wounds upon injury.”

The study includes first author and former MIT graduate student Wenhui Tang SM ’20, PhD ’24; Mehrana Nejad and L. Mahadevan of Harvard University; and Adrian Pegoraro of the Metrology Research Centre of the National Research Council Canada. 

Cells got rhythm

When studying how epithelial cells organize and develop into whole organs and tissues, scientists have focused mainly on how the cells coordinate in space. Where cells move, where they are in relation to the growing tissue, and where they end up, are questions of spatial coordination that scientists including Guo have looked to investigate. How the movement of cells relate over time is less well-understood. 

Guo’s group at MIT studies cell interactions to identify patterns that relate to healthy versus diseased states. As part of this work, the team takes microscopic snapshots of cells that they grow in the lab, to identify interesting behaviors among cells. Recently, Tang, then a member of Guo’s lab, was looking at a series of movies of epithelial cells when she started to see a rhythm, or pattern over time.

“I was studying collective cell migration, and I observed cells were swelling, then squeezing together, then swelling, again and again, forming local patterns,” Tang recalls. “That’s when I realized there might be something more interesting happening with these cells over time.”

Taking a pulse

In their new study, the researchers focused on the timing of cellular movements. They started by studying healthy, live epithelial cells that they cultured in the lab. They stained the cells with fluorescent dye to illuminate each cell’s nucleus. This way, they could easily identify one cell from another. They kept the cells in dishes with nutrients to help them naturally grow, divide, and move about. 

“We’re looking at their natural migration process, related to how they would migrate during different processes in the body, such as when forming skin and organs, and healing wounds,” Guo explains.

Using a confocal microscope, the team took snapshots of the cells every few minutes, for up to 30 hours. When they strung the images together as a sort of movie, a distinct pattern emerged. 

“If you just stare at any one location, you can see those dots are coming together, and then going further away, then coming together again, and going further away, like waves,” Tang says. 

They observed that a single pulse occurred over about an hour. This pulsing persisted in healthy cells, as a slow and steady rhythm over the 30-hour period. 

Curious as to whether other types of epithelial cells would sync up in similar fashion, the team tried the same experiment with several different lines of human breast cancer epithelial cells. They studied the movement of cells from benign tumors and cells of increasing malignancy. They observed similar pockets of synchronized pulsing in every cell type, especially in the most cancerous cells. 

“We found the really dangerous cancer cells team up over time, and do this persistent oscillation, twice as long as healthy cells,” Guo says. “This is unexpected. We see they really team up, synchronize, and oscillate together, which potentially facilitates their invasion.”

The researchers also observed a correlation between cell synchronization, and cell density: In each dish of cells, regardless of type, the cells continued to grow, divide, and pulse. As their numbers grew, more cells pulsed together, and their synchronization increased, up to a point. Once the cells reached a certain density, their pulsing began to die down.

“There’s a peak of synchrony before it decreases as cell density continues to increase,” Tang says.

This connection is especially interesting in the context of certain conditions such as asthma. Epithelial cells line the inside of many organs and tissues, including the airways. In healthy people, these cells pack together and “jam” up to form a solid, stable lining that protects the airways. In asthmatic airways, however, epithelial cells are less able to jam together. This results in airways that are loose and fragile, easily irritated, and difficult to heal. 

Guo and Tang suspect that, as there appears to be a connection between cell density and cell synchronization, there may be a way to target asthma treatments, by watching how potential drugs affect asthma cell synchronization. A similar approach could be taken for the screening of cancer drugs.

“More malignant cells would be better synchronized. After treating them with a drug, if their synchronization is disrupted, then it might be an efficient drug where we can consider the next step,” Guo envisions.

This research was supported, in part, by the National Institutes of Health.

This essay was written with Nathan E. Sanders, and originally appeared in The Guardian.

OpenAI, and then Anthropic, were each formed by AI developers who feared unrestrained corporate AI development—specifically, that companies like Google and Meta would steer the technology towards deleterious, maybe even catastrophically unsafe, outcomes for society. Their founders proclaimed that their new labs, uniquely, could be trusted to develop the technology in humanity’s best interest. But each, in turn, were themselves co-opted by the same market incentives, themselves becoming corporate behemoths zealously guarding future investor value rather than the public interest...

Justice Department lawyers are defending a FEMA program that environmentalists support.

Drivers are buying more electric cars and using less gasoline in plug-in hybrids, the International Energy Agency said.

A strategy outlined this week by Republican Gov. Patrick Morrisey highlights a state law that would steer half the sector’s tax revenue toward reducing and possibly eliminating statewide income taxes.

A Dutch bank published an analysis that estimated heat waves and drought could reduce gross domestic product across the European Union by 1 percent for 2026.

Bolsa Chica and Huntington state beaches reported more than 3,100 incidents so far this year, twice the number for all of 2025.

Dozens of miles of underground water pipes could prove useful beyond the winter months as the risk of wildfires grows.

The initial figures are based on an extrapolation of costs compiled by France’s official statistics agency.