Google patches two Chrome zero-days exploited in the wild, urging updates to version 146.0.7680.75/76 to prevent attacks.
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Microsoft: Windows 11 users can’t access C: drive on some Samsung PCs
Microsoft is investigating a new issue affecting some Samsung laptops running Windows 11 after installing the February 2026 security updates, in which users lose access to their C:\ drive and are unable to launch applications.
The company says it is working with Samsung to determine whether the problem is related to the Windows updates or Samsung software installed on affected devices.
“Users might encounter the error, ‘C:\ is not accessible – Access denied’, which prevents access to files and blocks the launch of some applications including Outlook, Office apps, web browsers, system utilities and Quick Assist,” explains Microsoft.
FBI seeks victims of Steam games used to spread malware
The FBI is asking gamers who installed Steam titles containing malware to provide information as part of an ongoing investigation into eight malicious games uploaded to the gaming platform.
In a notice published today by the FBI’s Seattle Division, the agency said it is attempting to identify individuals who were affected after installing one of the malicious games on Steam between May 2024 and January 2026.
“The FBI’s Seattle Division is seeking to identify potential victims installing Steam games embedded with malware. The FBI believes the threat actor primarily targeted users between the timeframe of May 2024 and January 2026,” reads the notice.
Fundamental constraints to the logic of living systems
Excellent review in which Solé et al. explore how physical/mathematical constraints may determine what subset of biological systems could theoretically evolve in the universe. Lots of fascinating ideas applying concepts like Turing machines, cellular automata, McCulloch-Pitts networks, energy minimization, and phase transitions to multiscale biological and evolutionary phenomena!
I found the description of how parasites almost inevitably emerge and drive increased biodiversity in computational models of evolution particularly fascinating. Interestingly, I recall this idea was featured in the Hyperion Cantos novels during an explanation of the history of artificial intelligence in their fictional universe!
Abstract. It has been argued that the historical nature of evolution makes it a highly path-dependent process. Under this view, the outcome of evolutionary dynamics could have resulted in organisms with different forms and functions. At the same time, there is ample evidence that convergence and constraints strongly limit the domain of the potential design principles that evolution can achieve. Are these limitations relevant in shaping the fabric of the possible? Here, we argue that fundamental constraints are associated with the logic of living matter. We illustrate this idea by considering the thermodynamic properties of living systems, the linear nature of molecular information, the cellular nature of the building blocks of life, multicellularity and development, the threshold nature of computations in cognitive systems and the discrete nature of the architecture of ecosystems. In all these examples, we present available evidence and suggest potential avenues towards a well-defined theoretical formulation.
The Abstraction Fallacy: Why AI Can Simulate But Not Instantiate Consciousness
The core issue: computation isn’t an intrinsic physical process; it’s an extrinsic, descriptive map. It logically requires an active, experiencing cognitive agent, a “mapmaker”, to alphabetize continuous physics into meaningful, discrete symbols.
Computational functionalism dominates current debates on AI consciousness. This is the hypothesis that subjective experience emerges entirely from abstract causal topology, regardless of the underlying physical substrate. We argue this view fundamentally mischaracterizes how physics relates to information. We call this mistake the Abstraction Fallacy. Tracing the causal origins of abstraction reveals that symbolic computation is not an intrinsic physical process. Instead, it is a mapmaker-dependent description. It requires an active, experiencing cognitive agent to alphabetize continuous physics into a finite set of meaningful states. Consequently, we do not need a complete, finalized theory of consciousness to assess AI sentience—a demand that simply pushes the question beyond near-term resolution and deepens the AI welfare trap. What we actually need is a rigorous ontology of computation. The framework proposed here explicitly separates simulation (behavioral mimicry driven by vehicle causality) from instantiation (intrinsic physical constitution driven by content causality). Establishing this ontological boundary shows why algorithmic symbol manipulation is structurally incapable of instantiating experience. Crucially, this argument does not rely on biological exclusivity. If an artificial system were ever conscious, it would be because of its specific physical constitution, never its syntactic architecture. Ultimately, this framework offers a physically grounded refutation of computational functionalism to resolve the current uncertainty surrounding AI consciousness.
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Oligodendrocyte molecular perturbations associated with tau in Alzheimer’s
The findings suggest that in AD, part of what happens in the brain may involve changes in DNA tagging that affect the function of oligodendrocytes, particularly in relation to the buildup of the toxic protein tau.
Oligodendrocytes are the brain cells that make myelin, the insulation that helps nerve cells communicate. Scientists have theorized that disrupting neuron communication contributes to symptoms for people with AD. Researchers in this study found that nearly all significant methylation changes — small chemical tags added to DNA that help control when genes are turned on or off — were linked to the tau protein. This supports the idea that this protein plays a key role in brain cell changes tied to AD.
“Our team has previously shown that oligodendrocytes are affected in Alzheimer’s and another tau-related disease, progressive supranuclear palsy (PSP),” says the author. “These new results further highlight that problems in oligodendrocytes and myelin are central to AD. They also point to specific molecular pathways, particularly epigenetic changes, that could be targeted in future therapies.”
The study results identified new genes that may play a role in AD, including one called LDB3, and confirmed many findings across multiple independent datasets, showing its reliability. The identification of specific genes provides potential targets for future research — for example, scientists might investigate whether interventions that reverse methylation or support oligodendrocyte health can slow or modify disease progression for patients with AD. ScienceMission sciencenewshighlights.
In a study published in Nature Communications, the researchers have identified specific DNA-level changes in the brains of people with Alzheimer’s disease (AD). Using advanced biological analysis, the team mapped alterations in the brain’s regulatory landscape that may help explain why Alzheimer’s presents and progresses differently from person to person. The findings could also open new avenues for understanding other neurodegenerative diseases.
Alzheimer’s disease is the most common cause of dementia. Biologically, the disease begins with the formation of protein deposits, known as amyloid plaques, and neurofibrillary tangles in the brain. This causes brain cells to die over time and the brain to shrink. About 6.9 million people in the U.S. age 65 and older live with Alzheimer’s disease. There is no cure, and in advanced stages, complications can result in a significant decline in quality of life and death.
A gain-of-function Retsat variant from high-altitude adaptation promotes myelination via a neuronal dihydroretinoic acid-RXR-γ pathway
High-altitude survival gene in mammals may help reverse nerve damage from conditions like multiple sclerosis.
Neuron.
Li et al. report that a gain-of-function Retsat variant, associated with high-altitude adaptation, promotes myelination by boosting neuronal synthesis of the signaling metabolite ATDRA. This molecule activates RXR-γ in oligodendrocyte progenitors. Administration of the prodrug ATDR promotes remyelination in models of myelin disease.
Stress-induced nucleolar rejuvenation via chaperone-mediated segregation in a filamentous fungus
Audra M. Rogers, Martin J. Egan et al. @UArkansas demonstrate that heat stress triggers nucleolar remodeling in filamentous fungi, enabling segregation of damaged material and selective inheritance of a new nucleolar compartment. This reveals a chaperone-mediated quality control mechanism that preserves nuclear function in highly polarized, multinucleate cells.
Model for nucleolar remodeling, partitioning, and quality control following heat shock. Schematic illustration of nucleolar remodeling in M. oryzae during recovery from heat stress. Heat shock damages the existing nucleolus. (2–3) A new nucleolar bud emerges from the old (preexisting) nucleolus and expands through de novo synthesis. Partial nuclear envelope breakdown permits entry of the molecular chaperones such as Hsp104 and Hsp70. The old nucleolar compartment accumulates SUMO-modified material and selectively recruits Hsp70 and Hsp104, mediating the partitioning of old and new nucleolar material. The newly formed nucleolus disassembles at mitotic onset and is preferentially inherited by daughter nuclei, while the old nucleolus is extruded and diminishes.
Figure 5.