In the 1960s the Hungarian-born American mathematician John von Neumann wrote about machines that could make exact copies of themselves. He envisaged a kind of robot equipped with a computer brain that could be programmed to reproduce itself from raw materials taken from its surroundings. It wasn’t long before some people suggested that von Neumann machines, in the form of robot spacecraft, would be a great way for us to explore the Galaxy.
Yann LeCun, Turing Award winner and former Chief AI Scientist at Meta, joins Jacob Effron. The conversation centers on Yann’s contrarian thesis that LLMs are a dead-end on the path to human-level intelligence, despite being useful products — because they can’t predict the consequences of their actions, can’t plan, and fundamentally can’t model the messy, high-dimensional real world. He unpacks his alternative architecture, JEPA (Joint Embedding Predictive Architecture), which learns abstract representations rather than generating pixel-level predictions, and explains why this approach is essential for robotics, industrial applications, and any system that needs to operate beyond the substrate of language. Yann also reveals the real story behind his departure from Meta (he had zero technical influence on Llama, contrary to public narrative), the genesis of his Tapestry project for sovereign open-source AI, why he believes LLMs are intrinsically unsafe, where he diverges from his fellow Turing laureates Hinton and Bengio, and why he predicts the industry will recognize the paradigm shift by early 2027. Throughout, he offers candid reflections on the tension between research and product at major labs, and why he intentionally headquartered AMI Labs in Paris with zero Silicon Valley VC money.
0:00 Intro. 01:45 Why LLMs Aren’t the Path to Intelligence. 07:51 AMI and World Models. 12:07 The JEPA Architecture Explained. 15:55 Problems with Robotics Models Today. 20:37 Silicon Valley Herd Behavior. 28:18 Tapestry: Sovereign AI for the Rest of the World. 35:49 OpenAI Is the Next Sun Microsystems. 40:51 Why Yann’s Views Diverged from Hinton & Bengio. 44:32 LLMs Are Intrinsically Unsafe. 58:00 Why Yann Left Meta. 1:00:26 Reflections on FAIR 1:12:11 Advice for PhD Students.
A newly developed targeted radiopharmaceutical treatment can effectively slow tumor growth in pancreatic ductal adenocarcinoma (PDAC), according to new research published in the May issue of The Journal of Nuclear Medicine. In preclinical models, the treatment achieved complete remission of the disease, highlighting its potential to transform care for this highly aggressive cancer.
PDAC accounts for more than 90% of pancreatic cancer cases and remains one of the most lethal malignancies, with a five-year survival rate of less than 5% in patients with metastatic disease. Although surgery is the only curative approach, it is feasible only in 10%–20% of patients with localized disease.
“PDAC is very difficult to treat, and new options are urgently needed,” said Marika Nestor, professor in the Department of Immunology, Genetics and Pathology at Uppsala University in Sweden. “Our previous findings suggest a possible new targeted treatment approach for pancreatic cancer patients whose tumors express CD44v6, which may help make treatment more precise and effective.”
Potassium ions (K⁺) are essential for all cells and living organisms. Scientists have long believed that K⁺ merely passes through ion channels and transporters, rather than acting as an extracellular ligand or molecular “switch.” Indeed, there had been no clear evidence that K⁺ functions as a ligand for membrane proteins in animals or plants—until now.
“Unexpectedly, we made this discovery serendipitously while testing the effect of aspartic acid, with K⁺ added as a counter cation, on Alka, an ion channel located in the brain of Drosophila melanogaster,” said the author. “The compound was effective. At first, we thought the effect was due to aspartic acid, but we ultimately realized that it was caused by K⁺, meaning that Alka functions as a membrane receptor that detects extracellular K⁺ as a ligand.”
Ion channel currents in Alka-expressing cells changed significantly in response to K⁺ levels. The researchers combined electrophysiological analysis with AlphaFold3, an AI-based protein structure prediction tool. This allowed them to identify the K⁺-binding site in Alka. This site creates a chemical environment favorable for K⁺, similar to that found in aqueous solution or in the well-known selectivity filter of K⁺ channels.
This study aimed to explore the alleviating effects of fisetin, a polyphenolic flavonoid, on ovarian dysfunction in a D-galactose (D-gal)-induced aging mouse model, as well as the underlying mechanisms, using both in vivo and in vitro experiments. Mice were subcutaneously injected with D-gal (100 mg/kg/day) for 60 days to establish the ovarian aging model; during the final 30 days, fisetin (10, 20, 30 mg/kg/day) was given orally. In addition, a senescent model of granulosa cell (GC) was established using D-gal and treated with fisetin. Fisetin supplementation improved ovarian endocrine function and reproductive capacity in aging mice, as reflected by regularized estrous cycles, elevated estradiol levels, and increased embryo numbers.
This study aimed to explore the alleviating effects of fisetin, a polyphenolic flavonoid, on ovarian dysfunction in a D-galactose (D-gal)-induced aging mouse model, as well as the underlying mechanisms, using both in vivo and in vitro experiments. Mice were subcutaneously injected with D-gal (100 mg/kg/day) for 60 days to establish the ovarian aging model; during the final 30 days, fisetin (10, 20, 30 mg/kg/day) was given orally. In addition, a senescent model of granulosa cell (GC) was established using D-gal and treated with fisetin. Fisetin supplementation improved ovarian endocrine function and reproductive capacity in aging mice, as reflected by regularized estrous cycles, elevated estradiol levels, and increased embryo numbers. Furthermore, fisetin reduced the number of atretic follicles and the extent of ovarian fibrosis and senescence, while simultaneously restoring the proliferation-apoptosis balance in follicular GCs, as well as alleviating oxidative stress. RNA-sequencing revealed that AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR) signaling and mitophagy were involved in the protective effects of fisetin against ovarian aging. Consistently, fisetin treatment promoted mitophagy, accompanied by AMPK/mTOR activation in ovarian tissues and GCs following D-gal exposure. Inhibition of AMPK attenuated the effect of fisetin on mitophagy. Additionally, blockage of mitophagy also reversed the beneficial effects of fisetin on mitochondrial injury, oxidative stress, cell cycle arrest, and cellular senescence in D-gal-induced senescent GCs. These findings indicate that fisetin prevents ovarian aging by suppressing follicular GC oxidative damage and ameliorating cell cycle arrest via activation of AMPK/mTOR-mediated mitophagy, thereby preserving female fertility.
Researchers at UCLA Health have identified a key gene that may help explain why women are more likely than men to develop a certain type of artery plaque linked to heart disease.
In a study published in Circulation Research, investigators found that a gene known as MYH9 plays an important role in the formation of fibrous plaques. These buildups in the arteries are generally more stable than those more prone to rupture, but they can still lead to heart attacks and other serious cardiac events through plaque erosion.
Atherosclerosis, the buildup of plaque in the arteries, is the underlying cause of most heart disease. Research has mainly focused on unstable plaques, which can rupture and trigger heart attacks. Fibrous, scar-like plaques tend to have thicker caps and different biological characteristics.
Researchers develop LinCx, a biological “wire” that creates precision electrical bypasses in the brain to restore function without drugs or external stimulation.
One of the inventions that may be realized by advances in nanotechnology is the creation of a Von Neumann probe, which is essentially a virus, a self-replicating probe that can then explore the universe near the speed of light.
Dr. Michio Kaku is the co-founder of string field theory, and is one of the most widely recognized scientists in the world today. He has written 4 New York Times Best Sellers, is the science correspondent for CBS This Morning and has hosted numerous science specials for BBC-TV, the Discovery/Science Channel. His radio show broadcasts to 100 radio stations every week. Dr. Kaku holds the Henry Semat Chair and Professorship in theoretical physics at the City College of New York (CUNY), where he has taught for over 25 years. He has also been a visiting professor at the Institute for Advanced Study as well as New York University (NYU).
TRANSCRIPT:
Dr. Michio Kaku: Recently there was a conference, the One Hundred Year Starship, and of course many people came in with designs to have gigantic fusion rockets take us to Mars and beyond Jupiter, into the stars. Other people said yes, antimatter rockets, that’s the way to go, and we all had this mental vision of the Enterprise going to the nearby star systems… here is another way to do it. Think of Mother Nature. When Mother Nature wants to propagate life, one possibility is to send out seeds, not just one or two, but millions of seeds. Most of the seeds never make it, but one or two do and as a consequence that’s how trees in forests propagate. So why not create a nano ship using nanotechnology? How big would it be? Some people like Paul Davies say it could be as big as a bread box. Other people say it could be even smaller than that. Why not something the size of a needle? And because they’re so small it wouldn’t take much to accelerate them to near the speed of light.
The relationship between sleep and disease suggests that there exists a connection between the brain and the body that extends beyond merely influencing the brain itself.
Among brain-related disorders, short sleep was significantly associated with depressive episodes and anxiety disorders, as seen in other studies of sleep and mental health. Short sleep was also associated with obesity, type 2 diabetes, hypertension, ischemic heart disease, and heart arrhythmias.
Short and long sleep were associated with chronic obstructive pulmonary disease, asthma, and a cluster of digestive disorders, including gastritis and gastroesophageal reflux disease.
