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When danger sounds, mice draw closer to familiar companions via a newly identified brain circuit

When mice heard a sound they thought signaled danger, they moved closer to a familiar companion, according to Virginia Tech researchers. They did not do the same when paired with a mouse they didn’t know. The study, led by Alexei Morozov of the Fralin Biomedical Research Institute at VTC and published in Neuropsychopharmacology, begins to reveal how the brain turns a warning signal into a drive to seek familiar company.

Scientists have long observed that animals gather when confronted with immediate threats such as predators. The new study asked whether a learned warning signal could produce a similar response and, if so, which biological mechanisms might be involved.

Researchers first trained mice individually to associate a tone with a short, mild foot shock. One to two days later, they placed the mice in pairs and played the tone again. Mice that had previously lived together drew closer when the tone played, while those paired with strangers showed no consistent change in distance.

Why AI consciousness could become the next great societal divide

As AI systems grow more human-like, the question of their consciousness is becoming unavoidable and could rival abortion or climate change as a polarising issue. Surveys reveal deep public splits, and experts disagree on whether biology is required.

From the start, the solar system chose fire over ice to build its first bodies

When the solar system first took up the task of building solid bodies—such as planets, moons and protoplanets—it basically had a choice between two ingredients: heat-forged chondrules, which were millimeter-sized bits of rock, and matrix, a fine-grained, cold dust loaded with water ice and organic molecules. And from the get-go, the solar system chose fire.

In a new Yale-led study, researchers provide the first geochemical evidence that within the first million years after the solar system began to form, it was already preferentially sorting for chondrules over matrix. Prior research had only been able to document this sorting process in objects that formed 2–4 million years after the solar system’s origin.

The study is published in the journal Nature Astronomy.

Clearing Damaged Mitochondria to Fight Skin Photoaging

Researchers publishing in Aging Cell have found that a cocktail of molecules released by human umbilical cord mesenchymal stem cells (hUC-MSCs) can mitigate sun-induced skin aging (photoaging) in mice by restoring their cells’ ability to get rid of their own damaged mitochondria (mitophagy).

Wrinkles are only a small part of the problem

Chronic exposure to ultraviolet light is the main driver of photoaging, which is characterized by the accumulation of senescent cells in the skin along with the depletion of DNA-protecting lamins [1]. It causes skin to become thickened, wrinkled, and rough while accumulating visible veins [2]. This damage is more than cosmetic; photoaging can lead to precancerous lesions along with cancer itself [3]. Retinoids and other antioxidants have been found to have some effects but cannot completely reverse this damage [4], and laser-based treatments may be expensive and painful while causing other symptoms [5].

MOLOCH | Official Teaser Trailer HD | When AI Replaces Us All

MOLOCH — Premiering 29 September on Omeleto.

Subscribe so you don’t miss it: / @omeleto.

As the technology she built rips her family apart and triggers worldwide job loss, an AI engineer battles spiritual forces — and the CEO of her own company — to pull the plug.

Everyone sees the danger. No one can afford to stop.

Starring Fiona Hampton, Parker Sawyers, David Buttle, and Buddy Wignall-Ho.
Written & directed by Tom Cozens.
An Owl In Space production in collaboration with the Future of Life Institute.

#Moloch #ShortFilm #SciFi #AI #AISafety #Superintelligence #Omeleto

Google cofounder Larry Page’s wife, a Stanford-trained scientist, has built an ocean-tech organisation; company has donated $120 million-plus in science projects

Around the world, ultra-wealthy individuals and institutions are pouring massive fortunes into projects designed to heal the planet. One of them is Lucinda Southworth, wife of Google co-founder Larry Page, a Stanford-trained scientist and one of the most prolific backers of high-tech ocean conservation.

Insilico Medicine AI Drug Rentosertib Cuts Biological Age on Six Independent Protein Clocks

Didn’t say by how much unless I skimmed over it.


Not proven yet. The study found a coordinated shift in blood proteins associated with younger predicted biological age in treated IPF patients. It cannot prove the drug reversed the aging process itself, because all study participants had IPF — a disease that alters the very protein patterns the clocks are trained on. The critical next test, which Nobel laureate Michael Levitt explicitly named, is a trial in healthy volunteers without IPF. If the biological age signal persists in people without the disease confound, the case for systemic geroprotective activity becomes substantially stronger. The ongoing Phase III trial in IPF (320 patients, 47 centers in China) is designed to assess lung function, not aging per se — but its larger sample may provide additional proteomic data over a longer time horizon.

What makes rentosertib different from other longevity drugs like rapamycin or metformin?

Rapamycin, metformin, and the senolytic combination dasatinib plus quercetin are repurposed drugs: they were developed for other indications (organ transplant, diabetes, and cancer, respectively) and discovered through subsequent research to interact with aging-relevant pathways. None was designed with aging biology as the primary specification. Rentosertib was. Insilico’s AI platform scored TNIK — the drug’s molecular target — against the 12 hallmarks of aging framework, found it relevant to six hallmarks, and designed a molecule specifically to inhibit it. That makes rentosertib, if its geroprotective effects are confirmed in further studies, the first drug created from scratch specifically for the biology of aging to produce a clinical signal in humans.

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