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Human Flourishing In The Age Of AI And Robots — The Futurists X Summit 2025

See my Comment below for a link to David Orban’s 20 minute talk.


In this keynote, delivered at The Futurists X Summit, on September 22 in Dubai, David Orban maps how AI and humanoid robotics shift us from steady exponential progress to an acceleration of acceleration—what he calls the Jolting Technologies Hypothesis. He argues we’re not in a zero-sum economy; as capability compounds and doubling times shrink, we unlock new degrees of freedom for individuals, firms, and society. The challenge is to steer that power with clear narratives, robust safety, and deliberate design of work, value, and purpose.

You’ll hear:
• Why narratives (optimism vs. doom) shape which futures become real.
• How shortening doubling times in AI capabilities pull forward timelines once thought 20–30 years out.
• Why trust in AI is task-relative: if +5% isn’t enough, aim for 10× reliability.
• The coming phase transformation as intelligence becomes infrastructure (homes, mobility, industry).
• Concrete social questions (e.g., organ donation post–road-death decline) that demand AI-assisted governance.
• Why the nature of work will change: from jobs as status to human aspiration as value.

Key ideas:
• Humanoid robots at scale: rapid iteration, non-fragile recovery, and human-complementary performance.
• Designing agency: go from idea → action with near-instant execution; experiment, learn, and iterate fast.
• From zombies to luminaries: use newfound freedom to architect lives worth living.

Resources & Links:

A ‘universal’ therapy against the seasonal flu? Antibody cocktail targets virus weak spot

An unusual therapy developed at The Jackson Laboratory (JAX) could change the way the world fights influenza, one of the deadliest infectious diseases. In a new study in Science Advances, researchers report that a cocktail of antibodies protected mice—including those with weakened immune systems—from nearly every strain of influenza tested, including avian and swine variants that pose pandemic threats.

Unlike current FDA-approved flu treatments, which target viral enzymes and can quickly become useless as the virus mutates, this therapy did not allow viral escape, even after a month of repeated exposure in animals. That difference could prove crucial in future outbreaks, when survival often depends on how quickly and effectively doctors can deploy treatments and vaccine development will take about six months.

“This is the first time we’ve seen such broad and lasting protection against flu in a living system,” said Silke Paust, an immunologist at JAX and senior author of the study. “Even when we gave the therapy days after infection, most of the treated mice survived.”

How nearly dying helped me discover my own cure (and many more)

Physician-scientist David Fajgenbaum was dying from a rare disease that didn’t have a cure — until he discovered a lifesaving drug that wasn’t originally intended for his condition. In an astonishing talk, he shares how his near-death experience led him to cofound the nonprofit Every Cure, which is using AI to uncover hidden treatments in existing medicines in order to save lives. (This ambitious idea is part of The Audacious Project, TED’s initiative to inspire and fund global change.)

Cancer cells can use backup routes to fuel their growth

When it comes to their survival, cancer cells have a host of backup plans.

This is especially true of the nutrients that cancers use to grow and spread. In addition to relying on sugars like glucose to power their proliferation, some cancer cells also use ketones — metabolites produced from fats when the body is fasting or on a low carb diet — as an alternate fuel source.

Now, a new study scientists suggest that the routes cancer cells use to process these different nutrients deeply influence cell behavior. They discovered an alternate, or non-canonical, path by which cancer cells convert a ketone called β-hydroxybutyrate (β-OHB) into acetyl-CoA, an essential metabolic building block for fatty acids and cholesterol that supports cell proliferation.

The findings, published in the journal Nature Metabolism, could reshape how the relationship between diet and cancer is viewed.

The authors also found that cancer cells can leverage this alternative β-OHB pathway even when glucose, the body’s main source of energy, is plentiful. This suggests that, depending on the circumstances, glucose may not always be the nutrient of choice for cells.

Stem cell models show epilepsy genes disrupt different brain regions

Using patient-derived induced pluripotent stem cells, the researchers generated advanced models known as 3D assembloids of two key brain areas: the cortex, which is essential for movement and higher-order thinking, and the hippocampus, which supports learning and memory. The results revealed strikingly different effects depending on the brain region.

In cortical models, the SCN8A variants made neurons hyperactive, mimicking seizure activity. In hippocampal models, however, the variants disrupted the brain rhythms associated with learning and memory. This disruption stemmed from a selective loss of specific hippocampal inhibitory neurons — the brain’s traffic cops that regulate neural activity.

These findings may help explain why patients with epilepsy often struggle with symptoms beyond seizures.

To confirm their findings, the researchers compared brain recordings from people with epilepsy to stem cell-derived hippocampal assembloids. They looked at seizure-prone regions of the patients’ hippocampi as well as regions unaffected by seizures. Abnormal brain rhythms appeared in both the patients’ seizure “hot spots” and in assembloids carrying SCN8A variants. In contrast, seizure-free brain regions and assembloids without the variants showed normal activity.


For families of children with severe epilepsy, controlling seizures is often just the beginning of their challenges. Even in cases where powerful medications can reduce seizures, many children continue to face difficulties with learning, behavior and sleep that can be just as disruptive to daily life.

New stem cell-based research published in Cell Reports, provides an early step toward understanding why current treatments often fall short, pointing to the distinct effects that single disease-causing gene variants can have across different regions of the brain.

Engineered gut bacteria improve survival outcomes in colorectal cancer tumors

In a new study that combines synthetic biology with cancer immunotherapy, researchers from the Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine) and Central South University in China have developed an engineered strain of gut-homing bacteria that stimulates potent antitumor immune responses against colorectal cancer (CRC).

Antitumor immune responses refer to the actions taken by the body’s immune system to recognize, attack, and destroy . It operates like the body’s internal surveillance system, spotting rogue cells (like ) and activating its defense forces to eliminate them.

Harnessing the immune system to fight cancer offers a powerful and precise approach to disease control. Unlike traditional treatments such as chemotherapy or radiation, which can harm healthy cells, immune responses can selectively target and destroy cancer cells with high specificity.

Single drug provides first evidence of ‘nearly universal’ pharmacological chaperone for rare disease

A study published in Nature Structural & Molecular Biology is the first time researchers have shown evidence that a single drug, already licensed for medical use, can stabilize nearly all mutated versions of a human protein, regardless of where the mutation is in the sequence.

The researchers engineered seven thousand versions of the vasopressin V2 receptor (V2R), which is critical for normal kidney function, creating all possible mutated variants in the lab.

Faulty mutations in V2R prevent from responding to the hormone vasopressin, leading to the inability to concentrate urine and resulting in excessive thirst and large volumes of dilute urine, causing nephrogenic diabetes insipidus (NDI), also known as arginine vasopressin resistance, a rare disease affecting roughly one in 25,000 people.

Stem Cells Repair Brain Damage Caused by Stroke in Mice

Brain damage caused by blocked blood vessels may be treatable using injections of stem cells, according to a new study by researchers from the University of Zurich and the University of Southern California.

The results could one day help patients who have experienced some forms of stroke recover lost functions.

Using mice with stroke-induced brain damage, the researchers found that injections of human stem cells could successfully develop into immature brain cells. The results were dramatic: most of the implanted cells remained in place, developing features of fully functioning neurons and communicating with surrounding cells.

A mobile robot scientist capable of carrying out experiments by itself

We live in a time when robots can clean our homes, drive our vehicles, deactivate bombs, offer prosthetic limbs, help healthcare workers, read the news, entertain, teach, and many more. And now, there is a robot scientist that can work on behalf of humans 24 hours a day, seven days a week.

Researchers at the University of Liverpool have built an intelligent “robot scientist” capable of moving around a laboratory and carrying out scientific experiments by itself. The first of its kind machine with humanoid dimensions are designed to work in a standard laboratory, using instruments much as a human researcher does. It can also make its own decisions about which chemistry experiments to perform next.

The robot scientist is 1.75-meter tall, weighs around 400 kg, and can roam around the laboratory, performing a wide range of different tasks. Unlike a human being, the robot has infinite patience, can think in 10 dimensions, and works for 21.5 hours each day, pausing only to recharge its battery for two hours. This will allow scientists to automate time-consuming and tedious research they wouldn’t otherwise tackle.

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