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Mozilla announces switch to disable all Firefox AI features

In response to user feedback on AI integration, Mozilla announced today that the next Firefox release will let users disable AI features entirely or manage them individually.

The new “Block AI enhancements” toggle will be available in Firefox 148 on February 24 and will help block current and future generative AI features in the desktop browser from a single location. Users will also have the option to enable specific AI tools while keeping others disabled.

“We’ve heard from many who want nothing to do with AI. We’ve also heard from others who want AI tools that are genuinely useful. Listening to our community, alongside our ongoing commitment to offer choice, led us to build AI controls,” said Firefox head Ajit Varma.

New GlassWorm attack targets macOS via compromised OpenVSX extensions

A new GlassWorm malware attack through compromised OpenVSX extensions focuses on stealing passwords, crypto-wallet data, and developer credentials and configurations from macOS systems.

The threat actor gained access to the account of a legitimate developer (oorzc) and pushed malicious updates with the GlassWorm payload to four extensions that had been downloaded 22,000 times.

GlassWorm attacks first appeared in late October, hiding the malicious code using “invisible” Unicode characters to steal cryptocurrency wallet and developer account details. The malware also supports VNC-based remote access and SOCKS proxying.

Malicious MoltBot skills used to push password-stealing malware

More than 230 malicious packages for the personal AI assistant OpenClaw (formerly known as Moltbot and ClawdBot) have been published in less than a week on the tool’s official registry and on GitHub.

Called skills, the packages pretend to be legitimate tools to deliver malware that steals sensitive data, like API keys, wallet private keys, SSH credentials, and browser passwords.

Originally named ClawdBot and switching to Moltbot and now OpenClaw in under a month, the project is a viral open-source AI assistant designed to run locally, with persistent memory and integrate with various resources (chat, email, local file system). Unless configured properly, the assistant introduces security risks.

2024–2026 Global Memory Supply Shortage

Following a severe market downturn in 2022–2023, major memory manufacturers— Samsung Electronics, SK Hynix, and Micron Technology —implemented strategic production cuts to stabilize pricing. [ 4 ] By mid-2024, the rapid expansion of generative AI services triggered unprecedented demand for specialized memory products, particularly High Bandwidth Memory (HBM) used in AI accelerators and data center GPUs. [ 5 ] [ 6 ] [ 7 ] Specialized components of chip-making technology are also experiencing supply constraints due to high demand in AI application. For example, glass cloth, a high-performance glass fiber substrate used for power efficient high speed data transfer and a crucial component of chip-making, is experiencing supply crisis as Nitto Boseki, a Japanese firm having overwhelming monopoly in its production, is not able to meet increased demands making chip-makers such as Qualcomm, Apple, Nvidia and AMD compete for securing supply for their chips. [ 8 ] [ 9 ]

A 2024 McKinsey analysis projected that global demand for AI-ready data center capacity would grow at approximately 33% annually through 2030, with AI workloads consuming roughly 70% of total data center capacity by the decade’s end. [ 10 ]

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Cancer-associated fibroblast-derived extracellular vesicles deliver ATP6V1C1 to promote lung adenocarcinoma metastasis via the ID1-IGFBP3 axis

Chen et al. reveal the V-ATPase subunit ATP6V1C1 as a non-canonical transcriptional repressor delivered by CAF-derived EVs to drive LUAD metastasis. By suppressing IGFBP3, ATP6V1C1 simultaneously triggers EMT and amplifies stromal IGF1 signaling, creating a potent pro-metastatic feedforward loop.

A Parasite Carried by Billions Has a Secret Life Inside the Brain

A common parasite hiding in the brain turns out to be far more active and organized than anyone realized.

A team of scientists at the University of California, Riverside, has discovered that Toxoplasma gondii, a parasite estimated to infect up to one-third of the world’s population, is far more biologically complex than previously understood. Their findings, published in Nature Communications, provide new insight into how the parasite causes disease and why it has proven so difficult to eliminate with current treatments.

How Toxoplasmosis Spreads in Humans.

Scientists Identified a New Blood Group After a 50-Year Mystery

It represents a huge achievement, and the culmination of a long team effort.

A pregnant woman’s blood sample taken in 1972 was mysteriously missing a surface molecule found on all other known red blood cells at the time.

More than 50 years later, that strange absence finally led researchers from the UK and Israel to describe a new blood group system in humans. The team published a paper on the discovery in 2024.

“It represents a huge achievement, and the culmination of a long team effort, to finally establish this new blood group system and be able to offer the best care to rare, but important, patients,” hematologist Louise Tilley from the UK National Health Service said in September 2024, after nearly 2 decades of personally researching this bloody quirk.

Cells adapt to aging by actively remodeling endoplasmic reticulum, study reveals

Improvements in public health have allowed humankind to survive to older ages than ever before, but, for many people, these added golden years are not spent in good health. Aging is a natural part of life, but it is associated with a greatly increased incidence of most chronic diseases, including various cancers, diabetes, and Alzheimer’s disease.

The laboratory of Kris Burkewitz, assistant professor of cell and developmental biology, wants to figure out if there is a way to break the links between the aging process and disease so that we can stay healthy longer, allowing us to better enjoy our later years. To accomplish this goal, the Burkewitz lab focuses on how cells organize their internal compartments, or organelles, and how organelle structures can influence cellular function, metabolism, and disease risk.

In his most recent paper, published in Nature Cell Biology, Burkewitz describes a new way by which cells adapt to the aging process: by actively remodeling the endoplasmic reticulum, one of the cell’s largest and most complex organelles. His team found that aging cells remodel their ER through a process called ER-phagy, which selectively targets specific ER subdomains for breakdown. The discovery that ER-phagy is involved in aging highlights this process as a possible drug target for age-related chronic conditions such as neurodegenerative diseases and various metabolic disease contexts.

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