Lifeboat Foundation: Safeguarding Humanity
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Astronomers have recently identified a colossal black hole lurking in the shadows of our cosmic neighborhood. This celestial giant, estimated to be 600,000 times more massive than our Sun, resides in the Magellanic Clouds and is gradually approaching the Milky Way. The discovery has sparked significant interest among scientists who are now contemplating the potential consequences of an eventual collision between our galaxy and this massive cosmic entity.

A team of researchers from the Harvard & Smithsonian Center for Astrophysics has detected compelling evidence of a supermassive black hole within the Magellanic Clouds. These findings, published in The Astrophysical Journal on April 7, 2025, reveal a cosmic giant that dwarfs our Sun by a factor of 600,000 in terms of mass. The black hole’s enormous gravitational influence has long remained hidden from direct observation.

The Magellanic Clouds consist of two satellite galaxies orbiting our Milky Way at a distance of approximately 160,000 light-years. Their gradual approach toward our galaxy suggests an eventual merger that could dramatically reshape our cosmic neighborhood. Scientists are particularly concerned about the fate of this newly discovered black hole during such a collision event.

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Neutron star mergers are collisions between neutron stars, the collapsed cores of what were once massive supergiant stars. These mergers are known to generate gravitational waves, energy-carrying waves propagating through a gravitational field, which emerge from the acceleration or disturbance of a massive body.

Collisions between neutron stars have been the topic of many theoretical physics studies, as a deeper understanding of these events could yield interesting insights into how matter behaves at extreme densities. The behavior of matter at extremely high densities is currently described by a known as the equation of state (EoS).

Recent astrophysics research has explored the possibility that EoS features, such as or a quark-hadron crossover, could be inferred from the gravitational wave spectrum observed after neuron stars have merged. However, most of these theoretical works did not consider the effects of magnetic fields on this spectrum.

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When Demis Hassabis won the Nobel Prize last year, he celebrated by playing poker with a world champion of chess. Hassabis loves a game, which is how he became a pioneer of artificial intelligence. The 48-year-old British scientist is co-founder and CEO of Google’s AI powerhouse, called DeepMind. We met two years ago when chatbots announced a new age. Now, Hassabis and others are chasing what’s called artificial general intelligence—a silicon intellect as versatile as a human but with superhuman speed and knowledge. After his Nobel and a knighthood from King Charles, we hurried back to London to see what’s next from a genius who may hold the cards of our future.

Demis Hassabis: What’s always guided me and— the passion I’ve always had is understanding the world around us. I’ve always been— since I was a kid, fascinated by the biggest questions. You know, the— meaning of— of life, the— nature of consciousness, the nature of reality itself. I’ve loved reading about all the great scientists who worked on these problems and the philosophers, and I wanted to see if we could advance human knowledge. And for me, my expression of doing that was to build what I think is the ultimate tool for advancing human knowledge, which is— which is AI.

Scott Pelley: We sat down in this room two years ago. And I wonder if AI is moving faster today than you imagined.

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There are several physiological reasons why biological organisms sleep. One key one concerns brain metabolism. In our article we discuss the role of metabolism in myelin, based on the recent discovery that myelin contains mitochondrial components that enable the production of adenosine triphosphate (ATP) via oxidative phosphorylation (OXPHOS). These mitochondrial components in myelin probably originate from vesiculation of the mitochondrial membranes in form from mitochondrial derived vesicles (MDVs). We hypothesize that myelin acts as a proton capacitor, accumulating energy in the form of protons during sleep and converting it to ATP via OXPHOS during wakefulness. Empirical evidence supporting our hypothesis is discussed, including data on myelin metabolic activity, MDVs, and allometric scaling between white matter volume and sleep duration in mammals.

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Capitalizing on the flexibility of tiny cells inside the body’s smallest blood vessels may be a powerful spinal cord repair strategy, new research suggests.

In mouse experiments, scientists introduced a specific type of recombinant protein to the site of a spinal cord injury where these cells, called pericytes, had flooded the lesion zone. Once exposed to this protein, results showed, pericytes change shape and inhibit the production of some molecules while secreting others, creating “cellular bridges” that support regeneration of axons—the long, slender extensions of nerve cell bodies that transmit messages.

Researchers observed axon regrowth in injured mice that received a single treatment injection of the growth-factor protein, and the animals also regained movement in their hind limbs. An experiment involving suggests the results are not restricted to mice.

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A team of researchers from the University of Chicago, in collaboration with researchers from the University of Pittsburgh, has identified a novel oncometabolite that accumulates in tumors and impairs immune cells’ ability to fight cancer.

The study, published in Nature Cell Biology, highlights how the metabolic environment of tumors influences the function of T cells, which are critical immune cells responsible for eliminating cancer. The finding opens new possibilities for improving cancer immunotherapy by targeting .

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A new way to deliver disease-fighting proteins throughout the brain may improve the treatment of Alzheimer’s disease and other neurological disorders, according to University of California, Irvine scientists. By engineering human immune cells called microglia, the researchers have created living cellular “couriers” capable of responding to brain pathology and releasing therapeutic agents exactly where needed.

The study, published in Cell Stem Cell, demonstrates for the first time that derived from induced pluripotent stem cells can be genetically programmed to detect disease-specific brain changes—like in Alzheimer’s disease—and then release enzymes that help break down those toxic proteins. As a result, the cells were able to reduce inflammation, preserve neurons and synaptic connections, and reverse multiple other hallmarks of neurodegeneration in mice.

For patients and families grappling with Alzheimer’s and related diseases, the findings offer a hopeful glimpse at a future in which microglial-based cell therapies could precisely and safely counteract the ravages of neurodegeneration.

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