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NASA supercomputer just predicted Earth’s hard limit for life

Scientists have used a NASA-grade supercomputer to push our planet to its limits, virtually fast‑forwarding the clock until complex organisms can no longer survive. The result is a hard upper bound on how long Earth can sustain breathable air and liquid oceans, and it is far less about sudden catastrophe than a slow suffocation driven by the Sun itself. The work turns a hazy, far‑future question into a specific timeline for the end of life as we know it.

Instead of fireballs or rogue asteroids, the simulations point to a world that quietly runs out of oxygen, with only hardy microbes clinging on before even they disappear. It is a stark reminder that Earth’s habitability is not permanent, yet it also stretches over such vast spans of time that our immediate crises still depend on choices made this century, not on the Sun’s distant evolution.

The new modeling effort starts from a simple premise: if I know how the Sun brightens over time and how Earth’s atmosphere responds, I can calculate when conditions for complex life finally fail. Researchers fed a high‑performance system with detailed physics of the atmosphere, oceans and carbon cycle, then let it run through hundreds of thousands of scenarios until the planet’s chemistry tipped past a critical point. One study describes a supercomputer simulation that projects life on Earth ending in roughly 1 billion years, once rising solar heat strips away most atmospheric oxygen.

Smart Golden Cities of the Future: 1 Hour Exploring Nature & Sci-Fi Innovation in 2050

Step into the future with “Smart Golden Cities of the Future”, a 1-hour journey exploring how technology and nature will merge to create sustainable, intelligent cities by 2050. In this immersive video, we’ll dive deep into a world where urban spaces are powered by Sci-Fi innovation, green infrastructure, and advanced technologies. From eco-friendly architecture to autonomous transportation systems, discover how the cities of tomorrow will function in harmony with the environment. Imagine a future with clean energy, smart public services, and a thriving connection to nature—where sustainability and futuristic technology drive every aspect of life. Join us for an hour-long exploration of the Smart Cities of 2050, as we uncover the incredible possibilities and challenges of creating urban spaces that work for both people and the planet. ✨ This video was created with passion and love for sharing creative production using AI tools such as: • 🧠 Research: ChatGPT • 🖼️ Image Creation: Leonardo, Midjourney, ImageFX • 🎬 Video Production: Veo 3.1, Runway ML • 🎵 Music Generation: Suno AI • ✂️ Video Editing: CapCut Pro 💡 Note: All of the above AI tools are subscription-based. This project combines imagination and creativity from my perspective as a mechanical engineer who loves exploring the future. 🙏🏻 Please Support: • ✅ Subscribe • 👍 Like • 💬 Comment Thank you so much for watching!I hope you enjoy this journey and gain inspiration from this creative experience ❤️ #SmartCities #Sustainability #FutureOfLiving #SciFiInnovation #EcoFriendlyCities #midjourney #veo3 #sunoai

New smart chip reduces consumption and computing time, advancing high-performance computing

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.

Scientists identify promising new target for Alzheimer’s-linked brain inflammation

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.

Video: Why ‘basic science’ is the foundation of innovation

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.”

NF-κB activation enhances STING signaling by altering microtubule-mediated STING trafficking

(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.

CERN’s Future Circular Collider project gets $1 billion funding

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.

How beige fat keeps blood pressure in check

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.

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