A new chip aims to dramatically reduce energy consumption while accelerating the processing of large amounts of data.
A paper on this work appears in the journal Nature Electronics.
The chip was developed by a group of researchers from the Department of Electronics, Information and Bioengineering–DEIB at the Politecnico di Milano, led by Professor Daniele Ielmini, with researcher Piergiulio Mannocci as the first author.
A multidisciplinary team has developed a selective compound that inhibits an enzyme tied to inflammation in people at genetic risk for Alzheimer’s, while preserving normal brain function and crossing the blood-brain barrier.
The findings are published in the journal npj Drug Discovery.
The driver is an enzyme called calcium-dependent phospholipase A2 (cPLA2). The team discovered its role in brain inflammation by studying people who carry the APOE4 gene —the strongest genetic risk factor for Alzheimer’s disease. While many people who have the APOE4 gene don’t develop the disease, those with elevated levels of cPLA2 generally do.
At first glance, some scientific research can seem, well, impractical. When physicists began exploring the strange, subatomic world of quantum mechanics a century ago, they weren’t trying to build better medical tools or high-speed internet. They were simply curious about how the universe worked at its most fundamental level.
Yet without that “curiosity-driven” research—often called basic science—the modern world would look unrecognizable.
“Basic science drives the really big discoveries,” says Steve Kahn, UC Berkeley’s dean of mathematical and physical sciences. “Those paradigm changes are what really drive innovation.”
(Cell Reports 42, 112185; March 28, 2023)
In our article published on March 28, 2023, the representative image for the cGAMP-treated group was inadvertently replaced with that of the control group in STING-KO cells in Figure 7A, resulting in two control panels being displayed. Similarly, the representative image of the control group of WT cells was inadvertently replaced with that of STING-KO cells in Figure S8A, resulting in two control panels of STING-KO cells being displayed. The errors occurred during figure preparation. The authors have carefully re-examined the original data and now provide the corrected version of the figure panels, which accurately present the appropriate control and treated groups.
The errors and their corrections do not affect any of the conclusions reported in the original manuscript. The authors sincerely apologize for any confusion or inconvenience these errors may have caused.
In a historic first for the laboratory, CERN has received $1 billion in private donations to support the development of the Future Circular Collider (FCC).
This philanthropic backing marks a shift in CERN’s 72-year funding history as it seeks to bridge the gap for the project’s estimated $18 billion price tag.
It comes from the Breakthrough Prize Foundation, the Eric and Wendy Schmidt Fund, and billionaire entrepreneurs John Elkann and Xavier Niel. Together, they pledged a combined $1 billion in late December 2025 to jumpstart the project.
In this report, researchers link thermogenic adipose tissue (brown/beige fat), best known for heat production, to blood-pressure control via direct fat–blood vessel communication. Using mouse models engineered to lose beige fat identity (via adipocyte-specific disruption of PRDM16), they observed elevated arterial pressure alongside perivascular remodeling, including fibrotic tissue accumulation and marked vascular hypersensitivity to the vasoconstrictor hormone angiotensin II. Mechanistically, loss of beige fat identity increased secretion of QSOX1 (quiescin sulfhydryl oxidase 1), which activated pro-fibrotic gene programs in vascular cells and promoted vessel stiffening; blocking this pathway (including genetic removal of QSOX1 in the model) restored healthier vascular signaling and function. The authors characterize this as a previously underappreciated, obesity-independent axis by which the “quality” (thermogenic vs white-like) of perivascular fat influences vascular stiffness and responsiveness to pressor signals, suggesting QSOX1 and related adipose-derived signals as potential precision targets for future antihypertensive therapies.
A mouse aorta with immunofluorescent tagging, emphasizing the close connection between vasculature and fat. (Credit: Cohen lab)
Obesity causes hypertension. Hypertension causes cardiovascular disease. And cardiovascular disease is the leading cause of death worldwide. While the link between fat and high blood pressure is clearly central to this deadly chain, its biological basis long remained unclear. What is it about fat that impacts vascular function and blood pressure control?
Now, a new study demonstrates how thermogenic beige fat—a type of adipose tissue, distinct from white fat, that helps the body burn energy—directly shapes blood pressure control. Building on clinical evidence that people with brown fat have lower odds of hypertension, the researchers created mouse models that cannot form beige fat (the thermogenic fat depot in mice that most closely resembles adult human brown fat) to watch what happens when this tissue is lost. They found that the loss of beige fat increases the sensitivity of blood vessels to one of the most important vasoconstricting hormones (angiotensin II)—and that blocking an enzyme involved in stiffening vessels and disrupting normal signaling can restore healthy vascular function in mice. These results, published in Science (opens in new window), reveal a previously unknown mechanism driving high blood pressure and point toward more precise therapies that target communication between fat and blood vessels.
Ray, you’ve made two predictions that I think are important. The first one, as you said, was the one you announced back in 1989: that we would reach human-level AI by 2029. And as you said, people laughed at it.
But there’s another prediction you’ve made: that we will reach the Singularity by 2045. There’s a lot of confusion here. In other words, if we reach human-level AI by 2029 and it then grows exponentially, why do we have to wait until 2045 for the Singularity? Could you explain the difference between these two?
It’s because that’s the point at which our intelligence will become a thousand times greater. One of the ways my view differs from others is that I don’t see it as us having our own intelligence—that is, biological intelligence—while AI exists somewhere else, and we interact with it by comparing human intelligence to AI.
Founder of XPRIZE and pioneer in exponential technologies. Building a world of Abundance through innovation, longevity, and breakthrough ventures.
