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2026-07-15 05:48:06

Stress does more than take a toll on mental health. After a particularly taxing week or month, it’s easier to catch a cold and harder to recover. Health issues build up as stress lingers, raising the risk of heart disease, diabetes, cancer, and a weakened immune system.

Chronic stress is often treated as an unavoidable part of modern life. While therapy can help people cope, researchers are increasingly asking a deeper question: How do stress signals in the brain ripple through the rest of the body, and can that damage be stopped?

A new study offers one of clearest answers yet. In mice modeling chronic stress, activity dropped in two brain regions governing emotional resilience. By way of a large nerve to the digestive track, the change wiped out a beneficial bacterial strain key to a healthy microbiome.

Without those microbes, the gut produced less of a crucial molecule that helps cells clear damaged proteins and other molecular  junk. These effects impacted the bone marrow, where stem cells generate oxygen-carrying blood cells and components of the immune system. Over time, these stem cells dwindled, leaving signs of premature immune aging in stressed mice.

“One surprising finding of our study was that suppression of only two specific brain regions was sufficient to produce many of the hematopoietic [blood stem cell] defects caused by psychological stress,” study author Linjia Jiang at Sun Yat-sen University said in a press release.

By tracing a direct pathway from brain to gut microbiome and bone marrow, the results could inspire new ways to blunt the biological toll of stress, from targeted probiotics to non-invasive brain stimulation.

Three-Piece Puzzle

De-stressing has become synonymous with self-care. Whether it’s work, family obligations, or a stream of notifications stressing you out, escaping into a good book or a walk in the woods feels like a deep mental exhale.

Stress has its perks. A product of the “fight-or-flight” response, it activates the sympathetic nervous system, a kind of highway connecting brain and body. In extreme cold, the system redirects blood from the skin to vital organs and temporarily slows digestion to prioritize muscles during a marathon. Brief bursts of stress aren’t detrimental. They’re an evolutionary survival hack.

But chronic stress is another story. Decades of research have found that prolonged or repeated mental strain disrupts brain activity and increases the vulnerability to a range of diseases. This is largely related to stress hormones released by the brain. But direct electrical signals traveling to the gut—which is often nicknamed the “second brain”—may also play a major role.

The garden of microbes in our gut roughly matches the number of cells in the body. These bacteria regulate digestion, metabolism, and immunity. They also communicate with the brain. When the ecosystem falls out of balance, it contributes to conditions ranging from diabetes to brain disease.

These beneficial effects can be traced to chemicals gut microbes manufacture. Lactobacillus reuteri, for example, boosts production of spermidine, a molecule that helps cells and tissues clear toxic debris. The process, called autophagy, is essential for the maintenance of healthy tissues but declines with age.

Stress also makes blood stem cells less resilient. Studies have linked prolonged stress to shortened telomeres, the protective caps at the ends of chromosomes, and an accumulation of senescent “zombie” cells. Both are hallmarks of accelerated biological aging.

The brain, gut microbiome, and bone marrow all respond to chronic stress. The new study aimed to find out if they’re connected.

Chain Reaction

To trace how chronic stress ages the body, the team tested four mouse models. Some experienced mild nerve injury. Others faced subtle disruptions to their daily routines, such as lights switching on earlier than expected or their home cages gently rocking at unpredictable times.

The changes put the mice on edge based on established behavioral tests. Mapping brain activity, the team zeroed in on two regions that consistently quieted. One, the medial prefrontal cortex, orchestrates executive control, or the ability to keep ideas in mind while reaching towards a goal. The other, the periaqueductal grey, coordinates attention to potential threats.

As activity decreased in both regions, blood stem cells struggled to divide and replenish immune cells. Inflammation and other toxic pathways flared up, and the cells developed molecular signatures similar to those seen in much older animals. Silencing either brain region with genetic tools reproduced many of the same symptoms, suggesting neural changes are a cause, not just a correlation.

But how was the brain communicating with the bone marrow? The answer lay in the gut microbiome.

Comparing the levels of chemicals surrounding the bone marrow in stressed and unstressed mice, the team zeroed in on spermidine. The molecule is made by gut bacteria and boosts autophagy, a process that’s linked to healthy aging.

Spermidine levels plummeted in stressed mice due to the loss of Lactobacillus reuteri, a beneficial strain of bacteria in the gut ecosystem that supports spermidine production. Stress-related nerve signals from the brain depleted these microbes, which caused spermidine levels to collapse and leaves blood stem cells unable to maintain themselves.

In another test, transplanting gut microbes from a stressed mouse into a happy-go-lucky mouse triggered early blood stem cell aging in the recipient—even though it didn’t experience stress itself. The results strengthen the case that the gut microbiome is a major link between the brain and bone marrow.

Rather than stress hormones, the pathway seems largely driven by electrical signals traveling from stress-sensitive brain regions to the gut. This means targeted brain stimulation could interrupt the cascade. Supplementing Lactobacillus reuteri as a probiotic or directly providing spermidine in a pill may also restore the missing molecule and slow blood stem cell aging.

This is just speculation though. Stress is deeply personal, and mice can’t capture the entire human experience. The team is now investigating whether the same brain circuits operate in people and if targeting this brain-gut-bone marrow axis can benefit the immune system.

“Our findings raise the possibility that managing psychological stress may not only improve mental well-being but also help preserve immune function and promote healthy aging,” said Jiang.

The post Scientists Find a Surprising New Way Stress Cascades From Brain to Body appeared first on SingularityHub.

2026-07-14 07:10:32

Watchers held their breath as the robot made its first incision. Hovering over its patient, an anesthetized pig, with a robotic assistant standing nearby, it navigated to the gallbladder and gently removed it.

The operation marked the debut of humanoid robots in a standard surgical setting. The robot, named Surgie, wasn’t autonomous—it was controlled by an expert surgeon—but the study is a step toward using humanoid robots as collaborators in minimally invasive surgery.

“Remotely operated and autonomous humanoid robots have real potential for amplifying access to critical surgeries to which patients would otherwise not have access,” said study author Michael Yip at UC San Diego.

The study included two successful surgeries. Human surgeons remained on standby for emergencies, but the teleoperated robot completed the task with only minimal intervention.

Feedback from surgeons operating Surgie was positive. They reported less physical strain and frustration, along with better overall performance. But they also pointed to practical problems like intermittent overheating and the need to frequently reposition the robot.

Despite a long road ahead, humanoid robots “have a viable future,” said Yip. “You can imagine these robots being deployed in remote communities where staffing is challenging, or in austere environments like search and rescue scenarios where a massive deployment of field medicine is needed in a short period of time.”

Smooth Operator

Robots have assisted surgeons for years. With a human surgeon at the helm, they excel at delicate procedures requiring precision and dexterity. They’re especially well-equipped for laparoscopic surgery, a minimally invasive technique that uses tiny incisions to reduce pain, speed recovery, and lower the risk of infection.

Despite the promise, surgeons face tradeoffs when they use surgical robots. The robots are highly specialized and often require operating rooms to be redesigned to accommodate them.

A major reason for this is the way they’re built. Intuitive Surgical’s Da Vinci system, for example, uses a robot with multiple arms, each independently controlled from a remote console. Other systems, such as Versius from CMR Surgical, deploy several lightweight independent arms, each attached to a mobile base. The robots have to be carted near the patient.

Surgeons operate all these systems from a console using a magnified, high-definition, 3D view of the surgical field, which is often better than what they’d see with their own eyes. Da Vinci 5 adds sharper visuals and depth perception with two cameras, one for each eye. And because the cameras are held by a robot rather than a human assistant, the image is far more stable.

These platforms are already used in a range of operations. But they have weaknesses. Most require proprietary surgical instruments and methods to make extra space for robot docking and maneuvering during procedures. Staff training adds further complexity and cost, limiting where the systems can be deployed.

Humanoid robots, in contrast, are far more mobile and compact. Their human-like bodies could move through standard operating rooms, use conventional surgical instruments, and potentially be easier to incorporate into existing operating rooms.

The timing may also be right. Recent advances in electric components controlling their motion have made humanoid robots faster and more stable than their awkward, stumbling predecessors. Newer AI systems that predict full-body movement and provide feedback have improved robots’ balance and ability to adjust to real-world complexities. Humanoid robots are already stocking warehouses and winning marathons.

But surgery sets a higher bar.

We still don’t know how close humanoid robots are to meeting the requirements for surgical procedures, wrote the team. That’s what they set to find out.

Hello, Surgie

The new system consists of a surgeon’s control console and the robot itself. The surgeon wears a stereoscopic headset with a magnified 3D view of the surgical field and controls the robot with an input device. The robot translates the surgeon’s commands into movements in real time.

The team chose the commercially available Unitree G1 for the job. Unlike Da Vinci, which was built for surgery, G1 is a more general-purpose humanoid with dexterous wrists and multiple joints. The researchers customized the robot’s hands so that it can rapidly switch between surgical tools. Standing just over four feet tall and weighing roughly 77 pounds, the robot takes up a fraction of the space needed by conventional surgical robots.

Precision is key for laparoscopic surgery. Surgical instruments must pivot around a fixed site at the incision, allowing them to move freely inside the body without stretching or tearing neighboring tissues. After extensively mapping Surgie’s movements, the team identified a safe set-up with enough range of motion for most minimally invasive surgeries.

Surgie passed standard robotics benchmarks evaluating surgical skill for both humans and robots. But the real challenge came next. The team performed two gallbladder removal surgeries in a standard operating room. Both operations followed a typical workflow, with a lead surgeon and an assistant responsible for placing the camera, cleaning lenses, and swapping instruments.

Surgie collaborated with the human assistant to locate, identify, and remove the gallbladder with minimal damage to surrounding tissues, including the liver. During part of one procedure, a second humanoid briefly took over camera handling while the human assistant stepped aside.

Both operations went relatively smoothly. One involved minor bleeding and bile leakage from the gallbladder, but both were easily managed. In interviews, surgeons said controlling humanoid robots felt intuitive, particularly because they had two arms and could use standard surgical tools.

“We were surprised at how well Surgie meshed with our workspace and workflow,” said study author Nikita Thareja.

The system is still in early development. Surgie’s restricted reach required frequent repositioning and recalibration, adding more than three minutes each time. The robot also occasionally needed cooling breaks after overheating. In a real operating room, interruptions like these could increase risk by forcing surgeons to split their attention between the procedure and supervising the robot.

Still, Surgie has a leg up on conventional surgical robots: It can walk. Beyond assisting with an operation, it could potentially fetch surgical tools or help clean operation rooms between procedures.

The team is now refining the system to reduce control lag, particularly during long-distance teleoperation, and exploring ways to safely sterilize—or “scrub in”—a humanoid robot for the operating room.

“Our goal is an operating theater of the future, where humanoid robots and humans work side by side as an integrated team to deliver procedures to those in need, both in traditional hospital settings as well as in non-traditional, field medicine scenarios,” said Yip.

The post In a First, a Humanoid Robot Performed Live Surgery Under a Surgeon’s Control appeared first on SingularityHub.

2026-07-11 22:00:00

The post This Week’s Awesome Tech Stories From Around the Web (Through July 11) appeared first on SingularityHub.

2026-07-10 22:00:00

Cancer researchers just found a new way to take on tumors.

CAR T cell therapy revolutionized blood cancer treatment by supercharging a patient’s own immune cells to hunt down cancers. But the approach has struggled in solid cancers. These are some of our top killers—breast, lung, prostate. Roughly two million Americans are expected to be diagnosed with cancer in 2026, and over 600,000 will likely succumb to the disease.

Unlike blood cancers, solid tumors rarely share a single, universal target for CAR T cells. Even cells within the same tumor are a mishmash. Some have little or none of a target protein, allowing them to evade the engineered immune cells, survive treatment, and fuel relapse.

“Target discovery remains a considerable challenge in the development and translation of

CAR T cell therapies for solid tumors,” wrote Christopher Mount and Marcela Maus at the Massachusetts General Brigham Cancer Institute.

Now, two independent teams have converged on the same promising target: A cell-surface protein called GPNMB. In one study, CAR T cells engineered to recognize GPNMB rapidly destroyed glioblastoma—a lethal brain cancer—in tissues taken from patients and shrank tumors in mice.

A second team used a similar strategy against an aggressive soft tissue cancer to fight tumors in organoids and mice. In an early clinical trial involving a single participant, one infusion stabilized the disease for three months without serious side effects.

CAR T designers are often wary of broadly shared targets because they can trigger dangerous attacks on healthy tissue. But GPNMB is an odd duck. In addition to cancer cells, it also sits on immune cells that spur cancer growth or suppress the body’s innate ability to get rid of tumors.

“Our approach attacks both the tumor and the environment that allows it to thrive,” said Sheila Singh at McMaster, who led the glioblastoma study, in a press release. “We’re going beyond targeting the cancer alone and eliminating the immune cells that help shield it from treatment.”

Cancer Fortress

Solid cancers have plenty of tricks to outsmart CAR T cells.

Researchers make these supercharged immune cells  by extracting a patient’s own T cells and genetically engineering them to produce protein “claws” that latch onto a specific cancer target. After infusing the cells back into the body, they seek and destroy tumor cells. CAR T has transformed treatment for several blood cancers and is showing promise in autoimmune diseases and excessive heart and kidney scarring. To simplify the procedure, researchers are also exploring ways to directly transform T cells inside the body with gene therapy.

Solid cancers, however, are far tougher opponents. Unlike blood cancers, which are heavily coated with a shared target called an antigen, solid tumors are molecular patchworks. Cells within the same tumor can display different targets—or none at all—allowing some to evade a CAR T attack and trigger relapse. Many of these targets also appear on healthy tissues, raising the risk of dangerous side effects. And then there’s the tumor microenvironment: A toxic, glue-like “fortress” that hijacks immune cells and uses them to battle incoming CAR T cells.

These barriers aren’t impenetrable. Previous work enlisted  bacteria to help CAR T cells burrow into tumors. Other efforts engineered ultra-sensitive CAR T cells capable of detecting tiny amounts of a cancer target shared across multiple solid tumors.

“Recent reports of activity in several clinical trials reinforce optimism that these efforts may result in true clinical benefit,” wrote Mount and Maus, who were not involved in either study.

But these strategies require additional engineering steps, increasing complexity and cost. And most still leave one major roadblock intact: The tumor’s immune defenses.

One-Two Punch

In the glioblastoma study, the team at McMaster University scoured donated tumors for proteins that distinguished the most aggressive cancer cells. They found one standout: GPNMB. Another test of every protein dotting the cell surface confirmed it as a promising target. The protein is evident across a cancer cell’s membrane, making it readily accessible to CAR T cells.

In lab tests, CAR T cells engineered against GPNMB performed well, nearly eliminating tumors grown from patient samples and extending survival in mice.

The target turned out to be far more valuable than expected. The team soon realized that GPNMB also marked the immune cells that suppress anti-cancer drugs. CAR T cells attacked both fronts simultaneously, weakening the tumor’s immune shield and killing the cancer itself.

“Most approaches have focused on killing cancer cells alone,” said study author Shan Grewal. “Our work suggests we may also need to dismantle the immune support system that helps the tumor survive.”

The second team focused on alveolar soft-part sarcoma, a rare soft-tissue cancer that often spreads to the lungs, brain, and bones before it’s diagnosed. Treatment often comes too late.

The disease is driven by a type of “fusion” gene created when pieces of genetic material are accidentally stitched together. These genes are extremely tough to target directly. Instead, the team screened all surface proteins on the cancer cells and again landed on GPNMB as a top candidate for intervention. The protein’s levels closely tracked the activity of the fusion gene.

CAR T cells targeting GPNMB cleared tumors and prevented metastasis in mice. But because an earlier antibody drug against the protein caused severe skin toxicity in patients, the team also tested their CAR T cells in mice carrying small human skin grafts. Although inflammation initially flared, there were no signs of ongoing skin damage.

Encouraged, the team treated a patient with relapsed, metastasized alveolar soft-part sarcoma. After a single infusion, the engineered cells rapidly divided in the bloodstream and remained detectable for roughly a month. The treatment didn’t trigger skin rashes or more dangerous side effects, like cytokine release syndrome where the body mounts a hyperactive immune defense that harms healthy organs.

The treatment’s benefits outlasted the engineered cells themselves. For roughly three months, imaging tests found fewer of the small, round spots on the patient’s lungs that often signal metastatic cancer, suggesting the disease had stabilized.

A final analysis identified another roadblock: Clusters of cells that suppress the immune system and could blunt the benefits. Adding drugs to block these immune molecules boosted tumor killing in mice. Because the same kind of gene fusion drives other cancers, including kidney, the CAR T cells could have reach beyond this specific type of sarcoma.

Together, the studies underscore that the best CAR T targets might extend beyond cancer cells to expose and attack cancer’s immune cell supporters too. Finding a viable target is a delicate balancing act. Chosen well, and CAR T cells could tackle multiple drivers for cancer growth. Choose poorly, and healthy tissues could get hurt in the crossfire.

Even so, “these two studies indicate that GPNMB represents an actionable target for CAR T cell therapies in several solid tumors,” wrote Mount and Maus.

The post CAR T Revolutionized How We Treat Blood Cancers. Now It’s Closing In on Solid Tumors. appeared first on SingularityHub.

2026-07-10 06:34:39

Synthetic biologists have long dreamed of constructing artificial cells from the bottom up. Researchers have now taken a major step in this direction by demonstrating that non-living components can be assembled into a system that grows, copies its DNA, and divides.

The genomic revolution transformed our ability to understand and manipulate cellular machinery, allowing scientists to rewire cells’ genetic circuitry to fight disease, produce valuable chemicals, and make crops more resilient. The holy grail for the field, however, has been to use these tools to create entirely synthetic cells—a milestone that would signal humanity’s mastery of life’s key ingredients.

How best to do this has long been an open question. Genomics pioneer Craig Venter made significant progress by stripping living bacteria back to their bare essentials, culminating in the 2016 unveiling of a minimal cell with just 473 genes. The Synthetic Yeast Genome Project has taken the opposite approach, building artificial versions of all 16 yeast chromosomes from scratch, though they’ve yet to get them working together in a single cell.

Now, researchers from the University of Minnesota, have assembled a synthetic cell out of engineered, non-living components housed inside an artificial, cell-like membrane. Their creation was capable of the four hallmarks of a living entity—the ability to feed, grow, copy genetic material, and produce offspring.

“We’ve replicated in chemistry what only used to be possible in biology: the complete set of behaviors of a cell,” Kate Adamala, who led the project, said in a press release. “It proves that the most fundamental functions of life, like growth and replication, do not need a mysterious magical spark.”

The researchers outline the design for their synthetic organism—nicknamed SpudCell for its potato-like shape under the microscope—in a non-peer reviewed paper uploaded to bioRxiv. SpudCell features a genome 90,000 base pairs long, which is considerably smaller than the 113,000 base pairs researchers had previously predicted would be the bare minimum needed to support a viable cell.

Rather than housing all the genes in a single chromosome, the team split them across several small, circular DNA molecules called plasmids, each specialized to fulfill specific functions. The researchers say this makes it possible to modify different aspects of the organism more easily.

To read the genome and build proteins, SpudCell uses a pre-defined kit of 36 purified enzymes drawn largely from E. coli. The whole assembly sits inside a liposome, a hollow bubble of the same fatty molecules that form natural cell membranes.

The artificial cell feeds in two distinct ways. Small molecules pass directly into the cell through protein pores implanted across the membrane. Molecules too large to squeeze through—like ribosomes and enzymes—are packaged inside tiny lipid bubbles that fuse with the membrane and empty their contents inside.

While the cell can feed, it’s entirely reliant on the researchers providing it with specially prepared meals. This means it’s a long way from surviving in the wild, which is both a major limitation and a key safety mechanism. “It’s a bed-ridden Frankenstein’s monster that has to be spoon-fed,” Adamala told New Scientist. “There’s no danger of it running amok.”

After ingesting “food,” SpudCell’s genes use the material to churn out proteins, while folding the incoming lipids into its membrane. This causes the whole cell structure to swell. Within a few hours, it’s bulked up enough to reproduce by dividing into two smaller cells.

Replicating cell division has been a longstanding challenge in the field. Natural cells split using an intricate protein scaffold called a cytoskeleton that’s fiendishly difficult to recreate. Adamala’s team sidestepped this problem by using a completely different mechanism, in which proteins bunch up on the membrane’s surface, putting it under mechanical strain. Eventually this squeezes two parts of the membrane together to pinch off a new cell.

The cells even manage a crude form of evolution. When the researchers introduced a genetic tweak boosting the cells’ ability to feed, those with the variant outcompeted the original lineage within five generations, and their edge widened when the researchers exposed the population to nutrient scarcity.

However, no one is claiming SpudCell is alive. Crucially, the cells cannot make their own ribosomes—the machines that build proteins from genetic instructions—and the ribosomes provided by the researchers degrade over time, limiting the cells to five to ten divisions.

The University of Chicago’s Jack Szostak told Quanta the work is an “impressive step” but the inability to produce ribosomes seriously limits potential for sustained growth. “If their system was able to generate its own ribosomes and other proteins and RNAs, it would be much closer to existing biological cells such as bacteria,” he said.

Nonetheless, the researchers think these artificial cells are a promising way to manufacture drugs, fuels, and materials without the toxic, energy-hungry industrial chemistry we rely on today. And they’ve created a new nonprofit called Biotic to share the tools they’ve developed with researchers.

The post This Synthetic Cell Grows, Copies Its DNA, and Produces Offspring—But It Isn’t Alive appeared first on SingularityHub.

2026-07-07 22:00:00

Researchers at the University of Cambridge have developed what they describe as a fundamentally new type of vaccine using artificial intelligence. The vaccine’s key component was designed entirely by AI and has now been tested in people for the first time.

The goal is ambitious: a single vaccine that works not just against all known human coronavirus variants, but against related bat viruses that could jump from animals to humans and cause future pandemics.

Traditional vaccines train our immune system to recognize one specific virus. The problem is that viruses mutate. When they change enough, the vaccine stops working, which is why we need a new flu shot every year and why Covid vaccines have been updated repeatedly since 2021.

AI offers a way around this. By analyzing genetic data from thousands of related viruses, it can identify the parts that stay the same across different strains and that are unlikely to change over time. Target those stable features, and you have a vaccine that should work against the whole family, not just the strain you started with.

This is exactly what the Cambridge team did. They used AI to scan viruses from the sarbecovirus family, which includes the viruses that cause both SARS and Covid, as well as a range of animal coronaviruses—looking for shared features that evolution has left largely untouched. Those features became the basis of the vaccine.

DNA Vaccines

While many people are familiar with the mRNA shots used during the pandemic, this new vaccine uses DNA. DNA vaccines are generally more stable than mRNA vaccines, making them easier to store and transport. This is a significant advantage in lower-income countries where “cold-chain” infrastructure is limited.

They can also be administered without needles. A high-pressure stream of liquid delivers the vaccine through the skin, making administration less painful and easier to scale up during an outbreak.

Could It Protect Against Future Pandemics?

These practical advantages matter most if the vaccine itself can do something no existing jab can: protect against viruses we haven’t encountered yet.

Broad-spectrum vaccines could change the way the world responds to emerging infectious diseases. By offering much wider protection than traditional vaccines, they could provide rapid immunity against new and emerging viral threats. This would equip public health officials with tools to stop future outbreaks in their tracks before they have a chance to turn into global pandemics.

They could also transform our approach to more familiar diseases. Influenza is a prime target because it exists in many different strains and evolves so rapidly. Scientists have to predict which strains will dominate each flu season, and if they guess wrong, vaccine effectiveness can suffer. A universal flu vaccine that targets features shared across multiple strains could eventually end the annual race to keep up with the virus.

The Ebola virus shows why this matters right now. The recent outbreak in the Democratic Republic of the Congo and Uganda is driven by the Bundibugyo strain, which bypasses existing vaccines. While researchers rush to create a new vaccine specifically for this strain, local communities remain at high risk. A broad-spectrum vaccine designed to cover an entire virus family could transform that picture.

What the Trial Found

This is the first human trial of an AI-designed vaccine. The results showed that this DNA vaccine was able to stimulate the immune system to produce antibodies that can recognize different types of sarbecoviruses. The technology was found to be safe and well tolerated.

This is an exciting advance because it demonstrates how AI has the potential to design variant-proof vaccines against future pandemic threats. The needle-free delivery system could also make the vaccine easier to administer and distribute worldwide.

However, there is more work to do. Although the results in this study are encouraging, the immune responses following vaccination were modest. It was also uncertain how long the protection lasts and whether further boosters will be required. Larger trials are also needed to determine whether the vaccine can prevent or reduce viral infections in the real world.

A universal vaccine remains a few years away. And any new vaccine must still pass larger trials to prove it is safe, effective, and provides lasting protection. But this study shows the goal is getting closer—and AI may help us get there faster.

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

The post The First AI‑Designed Vaccine Has Been Tested in People. Here’s What Happened. appeared first on SingularityHub.