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“Truly Extraordinary” — Supermassive Black Hole Found in the Last Place Scientists Expected

Dr. Sfaradi, who led the research, is a former graduate student of Prof. Assaf Horesh. “This is one of the fascinating discoveries I’ve been part of,” said Prof. Horesh. “The fact that it was led by my former student, Itai, makes it even more meaningful. It’s another scientific achievement that places Israel at the forefront of international astrophysics.”

A black hole far from home

Tidal disruption events occur when a star ventures too close to a massive black hole and is torn apart by its immense gravity.

Europol dismantles SIM box operation renting numbers for cybercrime

European law enforcement in an operation codenamed ‘SIMCARTEL’ has dismantled an illegal SIM-box service that enabled more than 3,200 fraud cases and caused at least 4.5 million euros in losses.

The cybercriminal online services had about 1,200 SIM-box devices with 40,000 SIM cards to provide phone numbers that were used in telecommunication crimes ranging from phishing and investment fraud to impersonation and extortion.

In an announcement today, Europol says that the cybercrime service operated through two websites, gogetsms.com and apisim.com, which have been seized and now display a law enforcement banner.

AGI is still a decade away

Reinforcement learning is terrible — but everything else is worse.

Karpathy’s sharpest takes yet on AGI, RL, and the future of learning.

Andrej Karpathy’s vision of AGI isn’t a bang — it’s a gradient descent through human history.

Karpathy on AGI & Superintelligence.

* AGI won’t be a sudden singularity — it will blend into centuries of steady progress (~2% GDP growth).

* Superintelligence is uncertain and likely gradual, not an instant “explosion.”

LLMs Can Get “Brain Rot”!

We propose and test the LLM Brain Rot Hypothesis: continual exposure to junk web text induces lasting cognitive decline in large language models (LLMs). To causally isolate data quality, we run controlled experiments on real Twitter/X corpora, constructing junk and reversely controlled datasets via two orthogonal operationalizations: M1 (engagement degree) and M2 (semantic quality), with matched token scale and training operations across conditions. Contrary to the control group, continual pre-training of 4 LLMs on the junk dataset causes non-trivial declines (Hedges’ $g

Cambridge lab-grown human embryo model produces blood cells

Prof Azim Surani, senior author of the paper, said: “Although it is still in the early stages, the ability to produce human blood cells in the lab marks a significant step towards future regenerative therapies — which use a patient’s own cells to repair and regenerate damaged tissues.”

Human blood stem cells, also known as hematopoietic stem cells, are immature cells that can develop into any type of blood cell.

These include red blood cells that carry oxygen and various types of white blood cells crucial to the immune system.

Surprising gene mutation in brain’s immune cells linked to increased Alzheimer’s risk

In a study published in Neuron, a research team at the Department of Neurology at Massachusetts General Hospital, aimed to understand how immune cells of the brain, called microglia, contribute to Alzheimer’s disease (AD) pathology. It’s known that subtle changes, or mutations, in genes expressed in microglia are associated with an increased risk for developing late-onset AD.

The study focused on one such mutation in the microglial gene TREM2, an essential switch that activates microglia to clean up toxic amyloid plaques (abnormal protein deposits) that build up between in the brain. This mutation, called T96K, is a “gain-of-function” mutation in TREM2, meaning it increases TREM2 activation and allows the gene to remain super active.

The researchers explored how this mutation impacts microglial function to increase risk for AD. The team generated a mutant mouse model carrying the mutation, which was bred with a mouse model of AD to have brain changes consistent with AD. They found that in female AD mice exclusively, the mutation strongly reduced the capability of microglia to respond to toxic amyloid plaques, making these cells less protective against brain aging.

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