Future

The People Do Not Yearn for AutomationNilay Patel | The Verge

“Not everything about our lives can be measured and automated and optimized, and it shouldn’t be. And so the tech industry is rushing forward to put AI everywhere at enormous cost—energy, emissions, manufacturing capacity, the ability to buy RAM—and locked into the narrow framework of software brain without realizing they are also asking people to be fundamentally less human.”

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A year after most robots failed to finish the Beijing race, nearly half the field autonomously ran a course of slopes, narrow passages, and 20 turns.

Humanoid robots are Silicon Valley’s latest obsession, but real-world performance has lagged the hype. That may be starting to change, however, after a robot beat the human record for a half marathon by nearly seven minutes in Beijing.

While tech companies around the world are piling into humanoid robots, China has made it a national priority. The government is pouring subsidies and infrastructure investment into the sector, and Chinese firms already account for around 80 percent of the humanoid machines shipped globally, according to the South China Morning Post.

Eager to show off its prowess, China has been staging sporting events for robots, most notably last year’s inaugural World Humanoid Robot Games. Another such event, the Beijing E-Town Half Marathon, pits humanoid robots against thousands of human runners over a 13-mile course. Last year, most of the non-human competitors failed to finish, and the fastest robots managed an unimpressive two hours and 40 minutes.

But this time around, four robots clocked times under an hour. And the winner, made by Chinese smartphone company Honor, registered a record-breaking 50 minutes, 26 seconds, eclipsing the benchmark set by Ugandan long-distance runner Jacob Kiplimo in Lisbon last month.

“Running faster may not seem meaningful at first, ​but it enables technology transfer, for example, into structural reliability and cooling, and eventually industrial applications,”  Du Xiaodi, an engineer on the winning team, told Reuters.

More than 100 teams fielded 300 robots at this year’s event, up from just 21 entries at the inaugural event last year. But Honor, a spinoff from Chinese telecom giant Huawei, dominated the competition, with separate teams from the company taking all three podium spots.

The winning robot, Lightning, navigated the course entirely autonomously. The bot stands 5 feet 6 inches tall but features legs 37 inches long to mimic the physical attributes of elite runners. It also boasts liquid cooling technology used in the company’s smartphones.

The growing sophistication of the robots’ control software is perhaps one of the starkest shifts since last year, with roughly 40 percent of teams operating autonomously. This is particularly impressive given the challenging course, according to Bernstein Research analysts.

“The course included flat sections, slopes, narrow passages, and ~ 20 turns, demonstrating rapid improvement in robots’ intelligence to handle generalized environments in the real world,” they wrote, according to Bloomberg.

But the technology isn’t bulletproof yet. One robot ran into a barricade and had to be carried off on a stretcher. Another veered into a bush after crossing the finish line. And one continued racing with its torso held together by packing tape after a heavy fall.

Nonetheless, the race showcased the rapid progress China’s tech industry is making, particularly in the raw components used to build these machines, like motors, joints, and batteries. Liu Xiangquan, a robotics professor at Beijing Information Science and Technology University told The South China Morning Post that long-distance running is a great test of how well these components can stand up to the kind of repeated strain that will occur in industrial settings.

And that’s likely to cause some consternation in US policy circles, where many see robotics as a key battlefront in the growing technological rivalry between the two superpowers.

Behind Sunday’s spectacle is a higher-stakes contest between China and the US over who will dominate the next generation of humanoids. US robotics firms have been lobbying Washington to draft a national strategy to counter China, which could include tariffs or bans on Chinese robots to help protect domestic producers.

However, running fast in a straight line is a very different challenge than the fine motor control and perception demanded by commercial applications. Experts told Reuters that despite impressive hardware, robotics companies are still a long way from developing the sophisticated software required to put these humanoids to practical use.

Still, these machines struggled to get over the starting line just a year ago. The gap between humanoid robots and human athletes has closed faster than anyone expected, so betting against further rapid progress seems unwise.

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That’s a few minutes longer than it takes to fill up the average gas-powered car—but still fast enough it might not matter.

For all their promise, electric cars have always had a big drawback: Charging takes much longer than filling up a gas tank.

But the gap has been closing, and this week, Chinese battery giant CATL announced battery technology nearing parity. On Tuesday, the company said its third-generation Shenxing fast-charging battery goes from 10 percent to 98 percent charged in 6 minutes and 27 seconds.

If you’re driving an electric car around town, charging is a breeze. You probably don’t have to do it more than a couple times a month. And when you do, you can plug your car in overnight at home.

For longer trips, you’ll need a charging station. Smartphone apps can help, and drivers learn to plan ahead, but it’s still a pain. Stations aren’t abundant, and when you find one, there may be a line. A full charge will then take the better part of an hour. Most people aim for 80 percent, but even that consumes up to a half hour. EV fans may find it’s worth the trouble, but range is a sticking point for many drivers.

It’s no wonder that battery makers have been hyper-focused on energy density, which determines how far EVs can go, and charging speed. They’ve improved both in recent years. But increasing range, which involves balancing a complex mix of battery chemistries, weight, and economics, may prove a tougher tradeoff to manage than bringing charging times in line with gas-powered cars at the pump.

In other words, if you can travel the same distance and charge or gas up in roughly the same amount of time, the two become interchangeable on long trips. (This also depends, of course, on infrastructure—more on that below.)

CATL has been pushing the boundaries of charging speeds with its Shenxing line of fast-charging batteries, first announced in 2023. The company is the world’s largest EV battery manufacturer. Its products power EVs in China but also American brands including Tesla and Ford.

The numbers are hard to compare generation to generation and company to company, as the specs reported vary. The second-generation Shenxing battery, announced last year, charged from 5 percent to 80 percent in 15 minutes, according to the Financial Times. Then in March of this year, rival battery maker BYD said its Blade 2.0 model charged 10 percent to 97 percent in 9 minutes.

Notching nearly a full charge in under 10 minutes was already an impressive mark.

But on Tuesday, CATL one-upped BYD with its third-generation Shenxing, which takes a full charge in a little over six minutes. At a maximum legal rate of 10 gallons per minute at gas stations in the US, that’s still a few minutes longer than it takes to fill up most gas-powered cars. But it might also be fast enough not to matter. Big gas-powered trucks are already in the same range. And CATL said charging to 80 percent takes just 3 minutes and 44 seconds—which is nearly a wash.

“This effectively closes the gap with ICE [internal combustion engine] vehicles,” Bernstein analysts wrote in a note quoted by the Wall Street Journal.

Fast-charging batteries have shorter lifespans due to excess heat. But CATL said it’s tamed the heat by decreasing the amount produced in operation, more effectively bleeding it off, and controlling how and when it’s generated. The battery retains over 90 percent capacity after 1,000 charging cycles.

“The boundaries of electrochemistry are still far from being reached, and the possibilities of materials science are still far from being exhausted,” CATL founder and CEO, Robin Zeng, told reporters and investors, per the Financial Times.

With 6-minute charging times, it’s easy to imagine charging station lines evaporating. Instead of drivers grabbing a meal while their car takes up real estate, they’d breeze in and out, like at a gas station.

That vision will take time to materialize, however. There are still far fewer charging stations than there are gas pumps. And those that do exist won’t include chargers that handle the bleeding edge anytime soon.

As for the batteries themselves, splashy press releases don’t usually translate to near-term availability and might not match real-world performance. The third-generation Shenxing isn’t likely to hit roads right away. When it does, it could show up in Chinese models first, be pricey (like BYD’s latest offering), and require fancy new chargers.

Still, it’s no longer theoretical: EVs can compete with the convenience of traditional cars at the gas station.

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A new tool that tethers healthy mitochondria to ailing cells has shown promise in mice with inherited blindness.

Our cells produce energy in biological power plants called mitochondria. These energy-makers have minds of their own. They operate using a unique set of DNA and can travel outside cells. Like astronauts, they often escape in fatty bubbles, land on other cells, explore them, and sometimes literally fuse with native mitochondria in their new homes.

This makes mitochondrial diseases hard to treat. Few gene editing tools can reach them and fix genetic typos. Even without mutations, mitochondria falter with age, contributing to diabetes, Alzheimer’s disease, heart failure, and other medical scourges.

But an experimental fix is gaining traction. Researchers are shuttling healthy mitochondria into cells—essentially transplanting them—to restore energy production and reboot metabolism.

There’s a major roadblock, however. Getting healthy mitochondria to the right cells is challenging. Scientists at the Institute of Molecular and Clinical Ophthalmology Basel have now developed a system that tethers donated mitochondria to their targets.

Called MitoCatch, the scientists engineered matching proteins and attached them to donor mitochondria and recipient cells. Like hook-and-eye fasteners, the binders pull the two partners into close contact. From there—by mechanisms that are still mysterious—the new mitochondria ride in on fatty bubbles, disembark inside the cell, and get to work.

In the study, the researchers delivered mitochondria to multiple cell types, and an injection of mitochondria saved vulnerable retinal cells in mice with inherited blindness.

“As a therapy, mitochondria transplantation has been hindered by the lack of tools to target healthy mitochondria directly to disease-affected cells,” wrote Samantha Krysa and Jonathan Brestoff at Washington University School of Medicine, who were not involved in the study.

MitoCatch overcomes this barrier.

Domesticated Bacteria

Roughly two billion years ago, an ancestral cell ate a bacterium. But rather than digesting it, the cell formed an unlikely alliance with its erstwhile prey. The bacterium converted oxygen into energy for the host, and received protection and nutrients in return. Over time, the bacterium gave up its independence and became a critical part of our cells: mitochondria.

Unlike other cell structures called organelles, mitochondria carry 37 unique genes that encode the core components of their energy-making machinery. Their stripped-down genome leaves little margin for error and is especially vulnerable to mutation. It’s also shielded by a double membrane, making it difficult to reach using conventional biotech tools.

But mitochondria have a superpower: They can leave host cells. Research from the last two decades shows that many cells export some mitochondria into the cellular void. The practice could be a way to rid themselves of damaged mitochondria or to deliver healthy ones to struggling neighbors, like an intercellular care package.

This quirk led to the idea of mitochondrial transplantation. Here, healthy mitochondria are injected into tissue or the bloodstream to treat damaged cells. Early results are encouraging. Transplant extends the healthy lifespan of mice with mitochondrial defects, limits injury after stroke or heart attack, accelerates wound healing in people, and hints at benefits for obesity.

Because nearly every human cell depends on mitochondria for energy—and falters when they break—transplantation could unlock treatments for a broad range of diseases hard to treat today. That is, if healthy replacements can reach their destination.

“Being able to deliver mitochondria efficiently to the right cell types has been a key hurdle for this therapeutic strategy,” wrote Krysa and Brestoff.

Catch Me if You Can

MitoCatch relies on a cellular “handshake.” All cell surfaces are densely studded with proteins, some universal, others unique to specific cell types. These proteins interact with surrounding molecules to drive biological processes. During infection, for example, antibodies latch onto proteins on bacteria to trigger an immune attack. CAR T cell therapy outfits T cells with protein “binders” so they can better recognize and eliminate cancer cells, senescent cells, or cells involved in autoimmune disorders. In each case, success hinges on matched protein pairs snapping together like hook-and-eye fasteners.

The new system works on the same principle and has three designs. MitoCatch-M helps donor mitochondria recognize markers unique to different types of recipient cells. MitoCatch-C flips the approach, modifying recipient cells with binders that better capture mitochondria. And a third version uses a “bispecific” tether that simultaneously grips mitochondria and target cells. Once in close proximity, mitochondria are packaged in fatty bubbles that drift into the cell.

Then comes a brief moment of terror.

Many of these bubbles are routed to the cell’s waste processing organelle, where their cargo is completely destroyed. The mitochondria must escape before it’s too late.

In cultured brain, retinal, heart, skin, and immune cells, the tailored mitochondria largely avoided death. How they managed this up for debate, and the team is trying to work it out now. But once inside, the donor mitochondria fused with the cell’s native mitochondrial network.

This “suggests that MitoCatch can be used to enhance the efficacy of mitochondria transplantation substantially,” wrote Krysa and Brestoff.

Of course, cells in a dish aren’t the same as those in bodies. In another test, the team injected the engineered mitochondria into the eyes of mice with a hereditary condition where a single mitochondrial genetic defect destroys cells in the retina, resulting in gradual vision loss.

Over 10 days, the healthy mitochondria revamped treated cells’ metabolisms, reduced damage, and boosted survival and response to light. Whether this translates to better vision remains to be seen, but the treatment didn’t trigger an immune response, a promising sign it might be safe. To be clear, the transplanted mitochondria didn’t correct the underlying mutation. Instead, they supplied enough working versions of the gene to bring energy production back to life.

It’s “a proof-of-principle that mitochondria transplantation can be used to correct mutations encoded in the mitochondrial genome that cause a severe form of vision loss,” wrote Krysa and Brestoff.

MitoCatch isn’t ready for prime time. It requires extensive genetic engineering, making the system difficult to translate for routine treatment. It’s also still unclear how long transplanted mitochondria last in their new hosts and whether they have a lasting benefit.

These early results highlight the ways scientists can boost the therapy’s potential. With more work, we may have a new way to tackle previously untreatable mitochondrial disorders.

The post Scientists Revive Failing Cells With Mitochondria Transplants appeared first on SingularityHub.

New artificial neurons fire so realistically they can activate living brain cells in mouse tissue.

As AI demands ever more power, researchers are looking to the brain for more efficient ways to process information. A new approach uses soft, flexible electronics to create artificial neurons that can mimic biological signaling and even directly interface with living neural tissue.

Researchers have long attempted to create so-called “neuromorphic” chips made of artificial neurons that mimic the spiking behavior of their biological counterparts. But there are still wide gaps between how these devices and brains operate.

Real neurons in the brain display a wide variety of activity patterns, which helps them encode and process information extremely efficiently. In contrast, most artificial neurons are carbon copies of each other with highly uniform spiking behavior, forcing neuromorphic chips to use millions of these neurons to achieve even modest functionality.

Now, a team from Northwestern University has designed a novel fabrication technique to create artificial neurons that mimic the complex signaling patterns found in the brain. The neurons’ output was so realistic that they successfully stimulated neurons in mouse brain tissue. More importantly, the approach could lay the groundwork for much more energy efficient AI.

“Silicon achieves complexity by having billions of identical devices,” Mark Hersam, who co-led the research, said in a press release. “Everything is the same, rigid and fixed once it’s fabricated. The brain is the opposite. It’s heterogeneous, dynamic and three-dimensional. To move in that direction, we need new materials and new ways to build electronics.”

The team created their artificial neurons, described in a paper in Nature Nanotechnology, by jet printing special electronic ink onto a flexible polymer. The ink contains nanoscale flakes of molybdenum disulfide, which acts as a semiconductor, and graphene, which serves as an electrical conductor.

The ink also contains a stabilizing polymer researchers typically burn off after printing to prevent it from interfering with the flow of current. But the researchers discovered that by leaving some of it behind, they could introduce imperfections that result in far more sophisticated signaling behavior.

Rather than completely burning the material away, they partially decomposed it. Then when they passed a current through the printed neurons, the polymer broke down further, but in an uneven pattern that created a conductive thread where current gets squeezed into a tight channel.

This constricted pathway rapidly switches on and off, firing sharp voltage spikes that look a lot like the spikes found in real neurons. The device doesn’t just produce simple on-off pulses, but everything from isolated spikes to sustained firing to rhythmic bursts, much like a real neuron.

With just two of these printable neurons and some basic circuit components, the researchers produced sophisticated spiking patterns. And crucially, they were able to tune the length and frequency of spikes to match the timing of biological action potentials, which could be useful for applications like bioelectronic medicine or brain-computer interfaces.

To test whether they could go beyond simply matching the numbers, the team worked with Northwestern neurobiology professor, Indira Raman, to hook up their artificial neurons to slices of mouse cerebellum and fire spikes into the tissue. The biological neurons fired in response, showing the synthetic signals were convincing enough to activate real neural circuits.

“You can see the living neurons respond to our artificial neuron,” said Hersam. “So, we’ve demonstrated signals that are not only the right timescale but also the right spike shape to interact directly with living neurons.”

While those capabilities could lead to some interesting applications, the researchers’ mainly hope the technology can reduce AI’s energy bill by mimicking the brain’s more efficient processing.

“To meet the energy demands of AI, tech companies are building gigawatt data centers powered by dedicated nuclear power plants,” Hersam said. This can only scale so far, in terms of power and cooling, he said. “However you look at it, we need to come up with more energy-efficient hardware for AI.”

Given the long, tortuous path from lab bench to factory floor, it seems unlikely this technology will be making a dent in the industry’s power bill any time soon. But it could lay the groundwork for a smarter way to do computation in the future.

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Robotics

Physical Intelligence, a Hot Robotics Startup, Says Its New Robot Brain Can Figure Out Tasks It Was Never TaughtConnie Loizos | TechCrunch

“Physical Intelligence, the two-year-old, San Francisco-based robotics startup that has quietly become one of the most closely watched AI companies in the Bay Area, published new research Thursday showing that its latest model can direct robots to perform tasks they were never explicitly trained on—a capability the company’s own researchers say caught them off guard.”

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Fewer than 10 people worldwide have eradicated the virus with stem cells. But this case was special—no one knew his brother’s cells carried a protective mutation until transplant day.

When the 63-year-old man received a bone marrow transplant from his brother, he got a two-for-one deal. The therapy was meant to tame a life-threatening blood disorder. But it also wiped out all signs of HIV, which he had been battling for 14 years.

Called the Oslo patient, he joins a small group of people with HIV who no longer need medication after a stem cell transplant. Four years later, the donor stem cells had completely overhauled his immune system, and there were no signs of lingering virus—even in hidden reservoirs that are notoriously hard to target.

His case is special. Previous successes in long-term remission had used donated stem cells carrying a mutation in the CCR5 gene. Called CCR5Δ32, this version of the gene blocks HIV’s ability to infect and destroy immune cells, rendering the virus incapable replicating. The Oslo patient carried one copy of the protective gene variant but was still infected. His donor brother, unexpectedly, had two copies.

In three months, the patient’s immune cells were clear of viral genetic material. Now, two years after ending antiviral medication, he is “having a great time” with more energy than he knows what to do with, study author Anders Eivind Myhre at the Oslo University Hospital told Agence France-Presse. “For all practical purposes, we are quite certain that he is cured.”

Sneaky Virus

Thanks to antiviral drugs, HIV is no longer a death sentence. And HIV preexposure prophylaxis, or PrEP, reduces the chances of infection in high-risk populations. Though it once required daily pills, the FDA recently approved a twice-a-year shot, making prevention less of a headache. But access remains uneven worldwide, and many hesitate to seek the drugs for fear of stigma.

Neither drug is a cure. The HIV virus attacks T cells and gradually destroys the body’s defenses. Over time, even mundane infections like a cold or the flu become harder to fight. As HIV replicates, it infiltrates hidden reservoirs—the gut is a common holdout—and embeds itself in DNA across the body.

Antiviral drugs keep active HIV in check but can’t touch reservoirs. Even after years of control, the virus rebounds as soon as treatment stops. To truly conquer HIV, we need a cure.

Fewer than 10 people worldwide have beaten the virus after an immune system reset. The first case, in 2009, was a lucky surprise. Known as the Berlin patient, a man received a stem cell transplant for a lethal blood cancer—and the cells kept HIV at bay for 20 months without drugs. The donor stem cells carried two copies of the CCR5Δ32 mutation, revealing its potent protective effect.

Other successes followed with stem cells carrying double and single copies of CCR5Δ32, and even normal versions of the gene—suggesting unknown factors are critical “for an eradicating HIV cure,” wrote the team.

Winning the Lottery, Twice

Treating HIV wasn’t the Norwegian man’s first priority when he agreed to a stem cell transplant.

Diagnosed in 2006, he’d kept the virus suppressed for over a decade with antiviral drugs. Repeated tests found no detectable viral genetic material in his blood, and he was able to live a relatively normal life.

But in 2017, he began struggling with extreme fatigue. His blood cell counts plummeted: Including the cells carrying oxygen, fighting off infections, and preventing uncontrolled bleeding. The life-threatening condition was eventually traced to a bone marrow disease. Several treatments briefly kept symptoms in check, but then they returned. His only option was a bone marrow transplant.

The patient’s care team searched for immune-compatible donors who also carried two copies of the CCR5Δ32 mutation, hoping to simultaneously treat the blood disorder and HIV. It’s like trying to find a needle in a haystack, said study author Marius Trøseid in a press release.

As the patient’s health rapidly declined, the team focused on treating the bone marrow disease with his 60-year-old brother as the donor. On transplant day, they realized they’d hit the jackpot—the brother carried both copies of CCR5Δ32.

“We had no idea…That was amazing,” said Myhre.

Brotherly Love

The HIV-resistant stem cells began replacing the patient’s own cells within 90 days. Two years on, the transplanted cells had fully repopulated his bone marrow—which is where blood cells are born—and cured the bone marrow disease.

The immune system reboot also allowed the patient to end antiviral medications. Four years after the transplant, the donor cells had completely taken over in multiple organs, including the lower gut—a known reservoir for HIV.

It’s the first time a bone marrow transplant has achieved total replacement in the gut, wrote the team.

Tests in more than 65 million T cells, HIV’s main targets, failed to detect intact genetic material needed for the virus to grow and spread. The results suggest the “HIV reservoir had been eliminated,” wrote the team.

The man’s immune system seemed to forget the virus. Viral antibodies gradually faded, and newly minted T cells patrolled the body as usual. Liberated from the constant threat of HIV, the body’s immune defenses returned to health—as if he had never been infected.

But the therapy wasn’t all smooth sailing. Roughly a month and a half after transplant, the man experienced severe graft-versus-host disease, where transplanted cells viciously attack the body. A combination of drugs eventually quelled the assault. In a twist, a deeper analysis suggests the drugs treating the immune attack might have also helped fight the virus.

A bone marrow transplant is a last resort and only used to treat people with HIV who also have deadly bone marrow disorders. Roughly 10 to 20 percent of patients die from the procedure within a year, regardless of underlying disease. For now, antivirals remain the first option for millions of people living with the virus. But these unique cases of full, long-term remission shed light on how the virus behaves.

Scientists are still trying to define what “cure” means when it comes to HIV.

“Moving forward, a critical step will be to compare existing cases of HIV cure to identify the most effective combination of biomarkers,” wrote the team. For example, do decreased viral load, antibodies, or a boost in healthy T cells amount to a cure? How long should the changes last? And did the patient struggle with HIV even though he had a single copy of CCR5Δ32?

Individual cases only offer a glimpse into HIV’s complexity. Projects like the European-led IciStem are underway to consolidate case results so scientists can better share findings and ideas—and potentially beat HIV once and for all.

As for the Oslo patient, he’s “perhaps no longer a patient. At least he doesn’t feel like it,” said Trøseid.

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New technologies rarely leave work untouched. They also rarely eliminate the need for human contribution altogether.

Forecasts of the impact of artificial intelligence range from the apocalyptic to the utopian. An October 2025 report from Senate Democrats, for example, predicted AI will destroy millions of US jobs. A couple of years earlier, consultant company McKinsey forecast AI will add trillions to the global economy, while emphasizing job losses can be mitigated by training workers to do new things.

The problem is that many of these claims are based on projections, overly simplified surveys, or thought experiments rather than observed changes in the economy. That makes it hard for the public, and often policymakers, to know what to trust.

As a labor economist who studies how technology and organizational change affect productivity and well-being, I believe a better place to start is with actual data on output, employment, and wages—which are all looking relatively more hopeful.

AI and Jobs

In one of my new research papers with economist Andrew Johnston, we studied how exposure to generative AI affected industries across America between 2017 and 2024, using administrative data that covers nearly all employers. Our analysis covered a crucial period when generative AI use exploded, allowing us to analyze the effect within businesses and industries.

We measured AI exposure using occupation-level task data matched to each industry and state’s occupational workforce mix prior to the pandemic. A state and industry with more workers in roles requiring language processing, coding, or data tasks scored higher on exposure, for example, compared with one with more plumbers and electricians.

We then took that exposure ranking by occupation and looked at changes in the standard deviation in occupational exposure, comparing that with labor market and GDP across states and industries from 2017 to 2024.

Think of a standard deviation as roughly the gap between a paramedic—whose work centers on physical assessment, emergency response, and hands-on care that AI cannot easily replicate—and a public relations manager, whose work involves drafting communications, analyzing sentiment, and synthesizing information that AI tools handle well. That gap in AI exposure is roughly what we’re measuring when we ask: Does being on the higher-exposure side of that divide change your industry’s trajectory?

This data allowed us to answer two questions: When AI tools became widely available following the public release of ChatGPT in late 2022, did states and industries that were more exposed to generative AI become more productive, and what happened to workers?

Our answers are more encouraging, and more nuanced, than much of the public debate suggests.

We found that industries in states that were more exposed to AI experienced faster productivity growth beginning in 2021—before ChatGPT reached the public—driven by enterprise tools already embedded in professional workflows, including GitHub Copilot for software development, Jasper for marketing and content writing, and Microsoft’s GPT-3-powered business applications. In 2024, for example, industries whose AI exposure was one standard deviation higher saw gains of 10% in productivity, 3.9% in jobs, and 4.8% in wages than comparable industries in the same state.

Those patterns suggest that, at least so far, AI has acted as a productivity-enhancing tool that boosts employment and wages rather than a simple substitute for labor.

Augmentation Versus Displacement

A crucial distinction in the data is between tasks where AI works with people and tasks where AI can act more independently. In sectors where AI mainly complements workers—think marketing, writing, or financial analysis—our data show that employment rose by about 3.6% per standard deviation increase in exposure.

In sectors where AI can execute tasks more autonomously—including basic data processing, generating boilerplate code, or handling standardized customer interactions—we found no significant employment change, though workers in those roles saw slower wage growth.

What these findings suggest is that when AI lowers the cost of completing a task and raises worker productivity, companies expand output enough to increase their demand for labor overall—the same logic that explains why power tools didn’t eliminate construction workers.

The economic question is not whether any given task disappears. It is whether businesses and workers can reorganize fast enough to create new productive combinations. And so far, in most sectors, our evidence suggests they can.

But state policies also matter: These benefits were concentrated in the states with more efficient labor markets, meaning that the impact of generative AI on workers and the economy also depends on the types of policies and institutions of the local economy.

Importantly, these findings hold beyond occupational exposure. In additional work with co-authors at the Bureau of Economic Analysis, we found a similar effect on GDP and employment when looking at actual AI utilization—that is, how often workers use AI. Drawing on the Gallup Workforce Panel, we measured workers actively using AI daily or multiple times a week. We found that each percentage-point increase in the share of frequent AI users in a state and industry is associated with roughly 0.1% to 0.2% higher real output and 0.2% to 0.4% higher employment.

To put that in context: The share of frequent AI users across all occupations rose from about 12% in mid-2024 to 26% by late 2025, a shift our estimates suggest corresponds to roughly 1.4% to 2.8% higher real output—or about 1 to 2 percentage points of annualized growth over that period.

New technologies rarely leave work untouched. But they also rarely eliminate the need for human contribution altogether. Instead, they change the composition of work, as our research shows. Some tasks shrink. Others expand. New ones emerge that were previously too costly or too hard to perform at scale. Put simply, some occupations might go away, but most of them just change.

If anything, the trends documented here are likely to strengthen rather than fade. Not only are generative AI tools rapidly improving, but also the experimentation and research and development that many workers and companies are engaging in are likely to pay large dividends. These investments—often referred to as intangible capital—tend to get unlocked a few years after a technology comes onto the scene, once complementary investments have been made.

The Role of Companies and Managers

Whether AI leads to anxiety or adaptation for workers depends in part on what happens inside organizations. Using additional data collected over many years in the Gallup Workforce Panel covering more than 30,000 US employees from 2023 to 2026, I found in a 2026 paper that workplace adoption of generative AI rose quickly over the period, with the share of workers using AI often increasing from 9% to 26%.

But the more important finding is that adoption was far more common where workers believed their organization had communicated a clear AI strategy and where employees said they trust leadership. This suggests that growing adoption and effective use of AI depends not only on the availability of the technology but on whether managers make its use clear, credible, and safe.

Where that clarity exists, frequent AI use is associated with higher engagement and job satisfaction, and it even reverses the burnout penalties that appear elsewhere.

In other words, the broader economic effects of AI depend not only on how sophisticated the tools are but on whether companies and managers create environments where workers can experiment, reorganize tasks, and integrate new tools into productive routines. That is, if employees do not feel the psychological safety to experiment, they are less likely to use AI, and they are especially less likely to use it for higher-value work.

That is precisely the kind of adaptation that I believe makes labor markets more resilient than the most alarmist forecasts suggest.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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A woman battling the conditions went from “two handfuls of pills” and blood transfusions daily to medication-free.

The 47-year-old woman was at the end of her rope.

In 2014, she was diagnosed with a rare form of anemia. Her body’s B cells, which normally produce antibodies to fight infections, had gone rogue, endlessly attacking oxygen-carrying red blood cells. Two other autoimmune disorders soon followed, one crippling her body’s ability to stop bleeding, the other increasing the risk of blood clots.

She had tried nine treatments. None helped. Her life was centered on blood transfusions, up to three daily, to keep the symptoms at bay. But constant fatigue made every day a struggle. The threat of deadly bleeding or blood clots loomed over her life.

Out of options, her care team tested an experimental treatment called CAR T cell therapy. They made a “living drug” out of the patient’s own T cells, editing the cells’ DNA so they would seek and destroy a specific biological enemy. Though CAR T is best known as a treatment for blood cancer, it’s also shown early promise in autoimmune disease. Trying to take on three conditions at the same time raised the bar, but it worked.

A single infusion of engineered cells rapidly killed off the misbehaving B cells. The woman was able to end blood transfusions within a week, and her red blood cell count was near normal in roughly a month. Her strength returned, and at the 11-month follow up, she was free of medication and able to enjoy life again.

“It was an entirely uncontrolled disease. And now she’s off any therapy. That tells you that, at least for now, we did something very right,” study author Fabian Müller at University Hospital Erlangen in Germany told Nature.

Runaway Train

The body’s B cells are powerful defenders. They watch for infections or cancer, generate antibodies to take out threats, and rally other immune cells to join the fight.

But sometimes B cells break down. Genetic mutations can lead to blood cancer. Some B cells struggle to produce antibodies, rendering them powerless to counter infection. And in autoimmune disorders, the cells mistakenly attack and damage healthy tissue—a kind of immune friendly fire—that can damage organs if left untreated.

In the woman’s case, malfunctioning B cells relentlessly attacked red blood cells, stripping them of their ability to carry oxygen. They also destroyed platelets—tiny, disc-shaped fragments in the blood that stem bleeding. The cells also attacked a protein that helps prevent clot formation.

This triple whammy ”can kill you very rapidly,” said CAR T pioneer Carl June at the University of Pennsylvania, who was not involved in the study.

Steroids to dampen the immune system didn’t work. Neither did antibodies that inhibit B cells or other classic autoimmune drugs. After attempting nine treatments and exhausting their options, the team offered CAR T cell therapy as a last resort.

CAR T drugs are usually made from a patient’s own T cells, genetically boosted to hunt down, grab onto, and destroy targets. Researchers originally developed CAR T for blood cancer, but efforts are underway to expand its use against solid cancers. In other studies, scientists have made these cancer-fighting soldiers directly inside the body to slash cost and time. Because CAR T cells can divide and replenish their numbers, a single dose could last over a decade.

The treatment is largely plug-and-play. The surfaces of all cells are dotted with protein beacons. Tumors have a unique protein signature. B cells have one too—a protein called CD19. Scientists have already had early success treating autoimmune diseases by designing CAR T cells that selectively hunt and destroy B cells.

A small CAR T trial in 2014 restored movement in patients with systemic sclerosis, a condition that causes tissue rigidity. Earlier this year, Müller helmed a clinical trial testing Zorpo-cel, T cells engineered to seek out CD19 in a variety of autoimmune conditions with promising results. Six months after treatment, all patients had ended their use of steroids and other treatments.

“For the very first time in severe autoimmune diseases, you actually have a treatment-free period,” Müller told Medscape at the time. “That is really a new perspective that has never been achieved before.”

One for All

Simultaneously tackling three autoimmune diseases was uncharted territory. Too many CAR T cells could trigger a deadly runaway immune reaction, which could risk even the brain.

The team turned to Zorpo-cel. They isolated the woman’s T cells and gene edited them to produce protein “hooks” targeting CD19 in the lab. The patient then underwent standard chemotherapy to wipe out most of her immune system. This step is obviously very tough on the body, but it’s needed to remove immune cells that would shut down CAR T.

A week after infusion, the woman’s red blood cells had rebounded, ending the need for blood transfusions. A month later, most of her disease-related blood work had improved, and she “experienced a rapid and remarkable increase in physical strength and has been able to carry out normal everyday activity,” wrote the team.

Now, a year on, she no longer needs the “two handfuls of pills” she took to manage the conditions. Her liver struggled at several points during the trial, but she avoided major immune reactions and other severe side effects. It’s not clear if the liver trouble was due to CAR T or lingering damage from earlier treatments.

Battling three autoimmune disorders with CAR T is unprecedented. But there are limitations. It’s a single-case study, and researchers will need to keep an eye on the patient’s health over time. Also, CAR T cells can dwindle and allow target cells to return. At the end of the study, the team found signs of newly formed B cells. However, they were “naïve,” in that they hadn’t learned to target normal tissues yet—and they may never learn.

Hundreds of CAR T clinical trials targeting autoimmune diseases are in the works. Multiple commercial companies have joined the race. “I think, within a year or two, there’s going to be approvals in the US,” said June.

The post One Shot Just Crushed Three Deadly Autoimmune Diseases appeared first on SingularityHub.

The technology harnesses the brain’s own blood chemistry to assemble soft, light-controlled electrodes around neurons.

A single shot transforms the mice’s brains into biomanufacturing machines. Blood proteins churn the injected chemicals into a soft, flexible electrode mesh that seamlessly wraps around delicate neurons. Pulses of light aimed at the mesh quiet hyperactive cells. All the while, the mice go about their merry ways, with no inkling they’ve been turned into cyborgs.

This science fiction-like invention is the brainchild of Purdue University scientists seeking to reimagine brain implants.

These devices, often composed of rigid microelectrode chips, have already changed lives. They can collect electrical signals from the brain or spinal cord and translate these signals into speech or movement—returning lost abilities to people with paralysis or diseases of the brain. Implants can also jolt brain activity and pull people out of severe depression.

Yet most implants require extensive surgery and risk damaging the brain’s delicate tissue. The new technology would avoid these downsides by building electrodes directly at the target.

“Our work points to a future where doctors could ‘grow’ soft, wire-free electronic interfaces inside the brain using the patient’s own blood, then gently dial brain activity up or down from outside the head using harmless near-infrared light,” study author Krishna Jayant said in a press release.

Probes Galore

The brain produces every one of our sensations, movements, emotions, and decisions. Scientists have long sought to decode and manipulate its activity with a range of hardware.

Some devices use electrodes to monitor single neurons in a lab dish. Others are physically inserted into brain regions that encode cognition and emotion. Some designs sit atop the brain, without puncturing its delicate tissue, and capture dynamic brain waves like a wide-lens camera.

But brain tissue is soft and squishy; microelectrodes are not. The mismatch often leads to scarring, signal loss, and shortened device lifetimes. Replacing broken or infected implants is surgically complex and can further damage the brain. Some experts have even raised ethical concerns about long-term care.

A recent explosion of soft, biocompatible materials suggests alternatives are possible, and we’ve seen a wave of creative new probes. In one example, a silk-like mesh drapes over the brain’s surface, and a related version maps electrical activity in brain organoids. Another device is smaller than a cell and, after injection, hitches a ride on immune cells into the brain. These systems can record and alter brain activity. But prebuilt implants often require surgery and struggle to integrate with their hosts without damaging surrounding tissue.

So, why not grow an electrode directly inside the brain?

“The ability to synthesize [conductive] materials on demand at a target site could overcome the limitations of conventional synthetic implants,” wrote M.R. Antognazza and G. Lanzani at the Italian Institute of Technology, who were not involved in the study.

Under Construction

Our cells are natural manufacturers, constantly assembling things like proteins, genetic messengers, and membranes. Cells rely on two essential ingredients to construct the complex structures of life: Biological building blocks and catalysts to bind them together. Synthetic materials work the same way. Monomers link like Lego blocks to form polymers with the help of a catalyst.

The discovery of electrically conductive polymers, meanwhile, has galvanized efforts to grow living bioelectronics directly inside the body. In a previous study, researchers genetically engineered cells to produce a protein catalyst that helps assemble conductive structures on the surfaces of living neurons. Another approach used hydrogen peroxide—a common first-aid staple—to compile monomers into reliable electrodes that monitor nerves in leeches.

These quirky early successes showcased the promise of brain-built electronics, but hit hard limits. The chemistry often relied on catalysts toxic to neurons. Even when successfully formed, the electrodes mostly just listened. Changing brain activity required additional physical cables.

The Purdue team rewrote the recipe. They designed a monomer, called BDF, that with the help of hemoglobin—a protein in red blood cells—becomes a soft, flexible, and electrically conductive mesh surrounding neurons at the site of injection. The willowy electrode hugs the brain’s anatomy and moves with it, minimizing physical damage. It’s responsive to near-infrared light and can translate light pulses from outside the skull into electrical signals that alter brain activity.

“Our key idea was to let the body’s own chemistry do the hard work,” said study author Sanket Samal.

The appeoach worked in several tests. Injecting BDF into store-bought beef and lamb steaks produced the electrode mesh within a day at human body temperature. In zebrafish embryos, a darling in neuroscience research, the reaction proceeded smoothly inside their yolks. Over 80 percent of the embryos survived, developed normally, and actively swam around—suggesting minimal harm.

But steak dinners and translucent fish are a far cry from our brains. Mice are closer. With the help of blood, BDF formed electrodes in mice’s motor cortexes after injection with minimal surgery. The mice’s brains maintained a normal balance of activity as they skittered around.

The team also coaxed dendrites, the tree-like input branches of a neuron, to produce the conductive mesh. Dendrites aren’t just passive cables, they’re “mini computers” that contribute to the brain’s computation and learning. Current methods struggle to precisely single out and control dendrite activity without messing with other parts of the neuron.

With near-infrared light, dendrite-built electrodes changed the way the neural branches behaved. The light temporarily lowered brain activity, and mice trained to press a lever were unable to perform the task. It didn’t wipe out their memory though: After turning off the light, the animals regained the skill. Their brains showed no signs of infection, inflammation, or over-heating throughout the study.

Inhibiting brain signals has upsides. Hyperactive brain activity in epilepsy and Parkinson’s disease, for example, is currently dampened with medication or—in severe cases—brain implants. If validated, brain-grown electrodes could be a less invasive alternative. Though to be clear, the method still requires surgery to inject the materials. Adding biocompatible magnetic ingredients, which can also control brain activity, could further boost the system’s potential.

How long the materials stay put and if they’re safe over the long term remains unclear. But in theory, the strategy could also control spinal cord nerves or heart tissue. Researchers could also adapt the strategy to use other types of materials that regulate brain activity in different ways, like ramping it up.

With further improvement, the electrode wouldn’t “just coexist with brain cells for months or years; it becomes part of them, stable across lifetimes,” said Jayant.

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