AI News Archive: July 25, 2026 — Part 6
Sourced from 500+ daily AI sources, scored by relevance.
- Flint AI
Build, share & chat with custom AI agents.
- TinTin AI Virtual Try-on
Your garment on a photoreal model - in minutes, in bulk
- Mindivo AI
Understand the people who matter most.
- WishDay: AI Birthday Reminder
Never miss a birthday. Always send the perfect greeting.
- EstateReel AI
Turn listing photos into property videos instantly.
- Claude
Building reliable, interpretable AI systems
- Neuronsy
Learn until you can explain it without the source.
- Claude Opus 5
Claude Opus 5: Powerful AI for Coding and Work
- Photogenerator
Photogenerator
- Flaq AI
Flaq AI
- Generative replay across hippocampal-neocortical circuits
To make flexible decisions, the brain needs to make inferences between events that were not directly experienced together. In sharp-wave ripple (SWR) events, during periods of rest and sleep, spiking activity in the hippocampus appears to support this process, by co-activating mnemonic representations of discrete cues and events that have not been experienced together. However, it remains unclear whether this 'generative replay' also occurs in other brain regions to update beliefs across the brain. To address this question, here we use multi-unit electrophysiology and calcium imaging in freely moving mice during a multi-day inference task. We show evidence for a putative anatomical pathway from the dorsal CA1 (dCA1) region of the hippocampus to primary visual cortex (V1), via the granular Retrosplenial Cortex (RSCg). We then characterise the neuronal activity across this pathway during an inference task and in subsequent periods of sleep. We show that during inference, mnemonic activity in V1 mirrors that observed in dCA1 to represent learned associations. In sleep, we show evidence for generative replay in V1, where co-activity can be observed between cells representing inferred relationships between cues that have not been directly experienced together. This activity in V1 is predicted by activity in dCA1, suggesting that the hippocampus coordinates generative replay across neocortical circuits. This coordinated generative replay may underpin the formation of a hierarchical generative model capable of predicting future scenarios that extend beyond direct experience.
- AI segmentation requires accounting for brain size to maintain performance on developmental MRI cohorts
The human brain undergoes rapid developmental changes through early life, underpinning the emergence of function but also marking a period of vulnerability to a range of neurodevelopmental disorders. With dynamic changes to brain size, morphology, and imaging contrast, consistent and accurate computational neuroanatomy remains a challenge. Deep learning tools for segmentation, like SynthSeg, offer robustness to heterogeneously acquired MRI contrast but remain unproven in early development. Here, we aggregated a large cohort (26k) of MRI scans spanning infant to adult development, and evaluated SynthSeg performance. Automated quality control scores, visual inspection, and spatial overlap with expert-segmented MRI scans revealed poor quality output segmentations during development. In the infant period only 36% of scans (1094/3069) passed automated QC. Rescaling infant scans to adult brain sizes significantly improved spatial overlap, and cropping scans to match adult fields of view retrieved automated quality control. Evaluation of the SynthSeg rescale + crop pipeline demonstrated visible and quantitative improvements in segmentation throughout infancy and childhood. There were marked increases in successful segmentations in infant scans, with 91% of scans now passing QC (2803/3069). These findings facilitate computational analysis of typical and disrupted neurodevelopment and should be considered when training the next generation of computational tools.
- Deep Phenotyping with Global Brain Activity and Plasticity Mapping Identify the Dorsal Raphe-Basolateral Amygdala Circuit as a Mediator of Adaptive Stress Responses
Exposure to chronic environmental challenges triggers divergent behavioral trajectories across individuals. At the core, these different trajectories can be classified as individuals actively adapting to the challenges (responders) and those displaying a rigid, non-responsive phenotype (non-responders). The brain system-wide network configurations that dictate why individuals diverge along these differential coping strategies, which can also lead to disease vulnerability or resilience, remain poorly understood. Here, we paired machine-learning-based deep behavioral phenotyping with multi-modal whole-brain imaging, integrating longitudinal Manganese-Enhanced MRI (MEMRI) and post-challenge cFOS mapping, to chart the functional landscape of individual stress trajectories in mice subjected to chronic social defeat stress. High-dimensional behavioral phenotyping revealed that active stress adaptation is a complex trajectory marked by latent, pre-stress kinetic signatures in vigilance-like and locomotive behaviors. At the neural level, longitudinal MEMRI captured distinct, consolidated activity reconfigurations across canonical valence and stress-regulatory circuits that segregated responders from non-responders. Complementary whole-brain cellular cFOS network analysis after an additional acute challenge revealed that non-responders exhibited marked hyper-modularity and network fragmentation, whereas responders featured a tightly integrated functional module co-clustering the periaqueductal gray, ventral tegmental area, basolateral amygdala (BLA), and dorsal raphe (DR). Notably, functional network connectivity along the DR-BLA axis was completely lost in non-responsive animals. Finally, pathway-specific chemogenetic inhibition of BLA-projecting DR neurons during a social challenge significantly attenuated social avoidance and reversed anxiety-like behavioral deficits, effectively shifting active behavioral adaptation toward a non-responsive phenotype. Together, these findings demonstrate that individual stress-coping strategies are driven by coordinated, system-wide reconfigurations of activity and plasticity, identifying the DR-BLA circuit as a critical gatekeeper of adaptive stress responses.
- Microbial Metabolites Potentiate MAIT Cell Anti-Tumor Immunity Against Solid Tumors
Mucosal-associated invariant T (MAIT) cells sense riboflavin metabolites through the monomorphic antigen-presenting molecule MR1, providing a unique opportunity to therapeutically mobilize a broadly shared T cell population without genetic engineering. Here, we show that the highly potent microbial metabolites, 5-OP-RU and 5-OE-RU, can be exploited as pharmacologic precision immune activators to drive human MAIT cell responses against solid tumors. Ligand stimulation in human co-culture systems elicited robust MAIT cell cytotoxicity, inflammatory cytokine secretion, and transcriptional states transformation. In vivo administration of riboflavin ligands 5-OP-RU significantly suppressed tumor growth in xenograft liver cancer models. Metabolite-driven MAIT activation also reprogrammed the local immune landscape, enhancing effector function and overcoming features of the immunosuppressive niche by markedly eliminating tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) within the tumor microenvironment (TME). These findings reveal that microbial riboflavin metabolites can power and redirect MAIT cells to solid tumors, establishing MR1-metabolite signaling as a tractable therapeutic axis for liver cancer and other solid malignancies.
- Deletion of Ferritin Heavy Chain Limits Tumor Growth and Promotes Iron-Dependent Stress in Medulloblastoma
Iron is essential for tumor proliferation and metabolic adaptation but becomes cytotoxic when unbuffered, creating a potential metabolic vulnerability. Ferritin, a conserved iron-storage complex, limits labile iron and establishes the upper threshold of iron tolerance in cancer cells. Here, we report the first ferritin heavy chain (FTH) knockout in a brain tumor model system. Although FTH loss was tolerated under basal conditions through adaptive remodeling of iron metabolism, it exposed profound vulnerabilities under iron stress. FTH deficiency lowered the threshold for iron toxicity, sensitizing medulloblastoma (MB) cells to both canonical ferroptosis and a mechanistically distinct iron-dependent cell death pathway. Oxidative iron stress impaired tumor growth and prolonged survival in orthotopic xenografts, whereas vitamin C-induced iron reduction triggered a selective, iron-dependent, but non-ferroptotic elimination of MB-like cells in tumor organoids. Notably, sensitivity to iron toxicity correlated strongly with cellular phenotype, with mesenchymal-like cells displaying greater susceptibility than epithelial-like counterparts. Collectively, these findings identify ferritin as a central regulator of iron tolerance in MB and establish iron toxicity, not via iron deprivation, as a therapeutically exploitable vulnerability. More broadly, this work provides a mechanistic framework for targeting iron metabolism through modulation of ferritin-dependent iron buffering and iron redox homeostasis in cancers.
- Bidirectional Electron Transfer in Far-Red-Light Adapted Photosystem I. Implications for the Photosystem's Functionality
Far-Red (FR) Light Photoacclimation (FaRLiP) enables cyanobacteria to extend photosynthetic activity into the far-red region by extensively remodelling Photosystem I (PSI), including the replacement of several core subunits with paralogs that coordinate the red-shifted chlorophyll f (Chl f). The binding positions of Chls f are still a matter of debate, with the most recent structural findings supporting the location of a single Chl f molecule within the reaction centre (RC) at the so-called A-1B site. This was in turn suggested to strongly affect electron transfer (ET) directionality leading to an almost monodirectional transfer along the B branch in FR-PSI RC. Here, we directly probe ET in FR-PSI by characterising the photogenerated [P700A1-] spin-correlated radical pair using complementary pulse and Time-Resolved (TR) Electron Paramagnetic Resonance (EPR) spectroscopy at cryogenic temperature. Electron spin-echo decay kinetics are distinctly biexponential, indicating the formation of two charge-separated states. Consistently, out-of-phase ESEEM traces are quantitatively described by two modulation frequencies arising from different dipolar interactions, while TR-EPR spectra are accurately simulated by the combined contributions of [P700A1A-] and [P700A1B-] radical pairs. These results provide direct spectroscopic evidence that both the A and B branches remain photochemically active in FR-PSI. The conservation of bidirectional ET, even when considering the presence of a single Chl f molecule in the RC, further implies that the two radical pairs originate from a common primary electron donor. This finding identifies P700 as the most likely primary donor and argues against a mechanism in which the RC Chl f initiates charge separation.
- Optimized cryo-FIB milling strategy to generate thin, minimally damaged biological lamellae
Focused ion beam (FIB)-milling has been adapted to thin frozen cells for visualization of macromolecular structures in situ with cryogenic electron microscopy. However, only a few large and abundant complexes have been annotated to date. FIB-milling introduces damage which limits the recoverable information from cellular sections. Here, we present Nilas, a low-energy milling strategy optimized to minimize damage and produce thin lamellae. Nilas-milled lamellae show minimal FIB-milling damage, contain areas at or below 50 nm and produce higher resolution in situ 3D reconstructions. Nilas improves the recovery of ribosomal subunits and reduces the predicted minimal detectable molecular mass with two-dimensional template matching (2DTM) to approximately 220 kDa. Consistently, we recover additional non-ribosomal complexes including RNA polymerase III with 2DTM in Nilas-milled lamellae. Nilas is compatible with common milling hardware, making it accessible to diverse users. By extending the size limit for in situ structural biology we bring visual proteomics closer to reality.
- Characterization of NPR-14 in the Regulation of Sleep-Like Behaviour in Caenorhabditis elegans
Sleep-like quiescence is an evolutionarily conserved state essential for physiological homeostasis; however, its dysregulation can lead to sleep disorders such as narcolepsy, which can be caused by abnormal neuropeptide signaling. In Caenorhabditis elegans, the G-protein-coupled receptor NPR-14 belongs to the orexin/allatotropin receptor family and has been proposed as a homolog of mammalian orexin receptors. Using npr-14 loss-of-function (lf) mutants, we demonstrate that NPR-14 promotes arousal and inhibits sleep-like quiescence. npr-14(lf) mutants exhibit prolonged quiescence, reduced locomotion, impaired sensory responses, and metabolic defects including elevated fat accumulation and decreased feeding and egg-laying. NPR-14 is expressed in ASH and ASI sensory neurons and in GABAergic DD, VD, and VC motor neurons, positioning it to modulate both sensory-motor integration and motor output directly. Genetic epistasis analysis revealed that NPR-14 functions upstream of EGL-4/protein kinase G (PKG): egl-4 loss-of-function suppressed the enhanced quiescence of npr-14 mutants, while egl-4 gain-of-function phenotypes were not enhanced by loss of npr-14. Caffeine treatment partially suppressed npr-14 mutant quiescence, suggesting convergence with adenosine-sensitive arousal pathways. These findings establish NPR-14 as a wake-promoting GPCR that inhibits EGL-4/PKG signalling to regulate quiescence and arousal. The NPR-14EGL-4 axis suggests functional parallels to arousal regulation in other systems.
- Outbreak of Dermatophilus congolensis skin infection among contact sport practitioners, Norway, summer 2025
Dermatophilus congolensis is a zoonotic gram-positive bacterium causing dermatophilosis, a skin infection primarily affecting animals and uncommonly reported in humans. Although human infections have traditionally been associated with animal contact, recent reports suggest alternative transmission pathways. We investigated an outbreak among contact sport athletes in Trondheim, Norway, during July to September 2025, using structured interviews and whole-genome sequencing. Nine confirmed cases were identified. Symptoms were mild and consisted mainly of pustular lesions affecting the face, arms, back, and chest. None of the cases reported animal contact. Genomic analysis confirmed species identity and showed that outbreak isolates were highly related, differing by only 0-7 core-genome single nucleotide polymorphisms. The Trondheim isolates clustered with strains from recent outbreaks in Spain and France, suggesting international dissemination of a shared clone. These findings identify contact sports as a potential setting for transmission of human dermatophilosis and highlight the value of genomic surveillance for outbreak investigation.
- Intrafilament nucleotide exchange in a prokaryotic actin homolog
Polymerisation and disassembly govern the cellular functions of cytoskeletal proteins. In canonical nucleotide-dependent polymers such as actin and tubulin, nucleotide exchange occurs in soluble subunits but not within intact protofilaments. By contrast, the assembly dynamics and nucleotide dependency of the prokaryotic actin homolog MreB, whose polymerization into membrane associated filaments is essential for bacterial cell morphogenesis, remain poorly understood. We used total internal reflection fluorescence microscopy and high-speed atomic force microscopy to monitor the assembly of MreB on supported lipid bilayers in real time. ATP binding triggers MreB polymerization into symmetrically elongating pairs of filaments on cardiolipin-containing membranes. While ATP hydrolysis occurs within filaments and contributes to endwise disassembly, continuous nucleotide exchange within filaments tunes their stability on the membrane. Nucleotide cycling within MreB filaments defines a new class of biological polymer behavior and highlights the evolutionary divergence of mechanisms governing actin homologs assembly dynamics.
- Structural and Stereochemical Elucidation of Cyanochelin C, a Siderophore Associated with Novel Class of Cyanobacterial Acyl Hydrolases
Iron is a key micronutrient that constrains microbial growth and productivity in many aquatic and terrestrial environments due to its limited bioavailability. Microorganisms evolved sophisticated acquisition strategies, including the production of siderophores, high-affinity iron-chelating molecules that facilitate iron solubilisation and uptake. Cyanobacteria, photosynthetic prokaryotes and major contributors to global primary production, also depend on iron as a cofactor to their core metabolic enzymes. However, very few cyanobacterial siderophores were described so far, and cyanobacteria remain an underxplored source of possibly novel siderophores. Here we report a novel cyanobacterial siderophore, cyanochelin C, that employs two {beta}-hydroxyaspartate residues for iron chelation. We provide extensive nuclear magnetic resonance (NMR) and mass spectrometry (MS) evidence on the molecular structure and identify the corresponding biosynthetic gene cluster (BGC). Bioinformatic analysis of the BGC further revealed the presence of an acylase CcsQ clustering with a broader cyanobacteria-specific family of acylases associated with predicted siderophore-encoding BGCs. Discovery of cyanochelin C and its deacylation by CcsQ expands the known structural diversity of cyanobacterial siderophores and improves the understanding of important enzymatic reactions.
- Prevalent phenotypic mutation impairs binding of broadly neutralizing antibodies to influenza hemagglutinin
Mistakes during protein synthesis, such as transcription errors, occur often and lead to non-inheritable amino acid replacements generally known as phenotypic mutations. We recently used a consensus approach in high-throughput sequencing to determine the error landscape for influenza-hemagglutinin mRNA. We found single-site errors to occur with widely different frequencies. Here we show that the most prevalent transcription error encodes a phenotypic mutation that impairs binding of broadly neutralizing antibodies. The error occurs in 0.2-0.5% of mRNA molecules and, consequently, many virions will expose hemagglutinin variants bearing the encoded amino acid replacement. Our results point to a mechanism of antibody evasion, akin to programmed recoding, in which evading mutations are encoded by transcription errors promoted by inheritable RNA sequence/structure patterns.
- Cryo-electron microscopy structure of Jabs, a bacteriophage infecting the multidrug-resistant pathogen Mycobacterium abscessus
Exploring bacteriophage structural diversity is essential for understanding phage biology and for advancing phage-based therapies. Here, we determine the cryo-electron microscopy structure of Jabs, providing, to our knowledge, the first high-resolution view of a phage infecting the multidrug-resistant human pathogen Mycobacterium abscessus. Although Jabs displays the canonical organization of a siphophage, its virion combines several unusual architectural features. The T=9 icosahedral capsid is assembled from two distinct major capsid proteins, with one forming the hexons and the other the pentons, revealing an unprecedented capsid assembly strategy among icosahedral phages. An extensive network of ~1,700 disulfide bonds stabilize individual structural components and covalently links the capsid, connector, tail, and adhesion device into a continuous assembly. At the distal end of the tail, an elaborate and conformationally dynamic adhesion device comprises multiple candidate receptor-binding proteins organized into complex multidomain architectures, including carbohydrate-binding modules and {beta}-sandwich hetero- and homotrimers resembling the receptor-binding proteins of phages infecting lactic acid bacteria. Together, these findings expand our understanding of phage structural diversity and provide a framework for investigating phage-host interactions and guiding the engineering of therapeutic phages.
- Intracellular pathogen targeting by IL32 elicits cell-autonomous immunity
Interferon gamma safeguards humans against intracellular pathogens, yet how most interferon-stimulated genes protect host cells, and how human-adapted pathogens evade these defenses is unclear. Here, we discover a potent immune surveillance and effector circuit executed by an intracellularly acting cytokine, IL32, that targets and restricts phylogenetically distinct vacuolar pathogens, including the bacterium Chlamydia and the microsporidian Encephalitozoon. Quantitative proteomics coupled to a tailored CRISPR screen, uncovered components of the cysteine/Arg N-degron pathway that modify IL32 through oxidation-dependent arginylation, thereby enabling the recruitment of the autophagy machinery to pathogen-containing vacuoles. A forward genetics screen in Chlamydia trachomatis, the leading cause of sexually transmitted bacterial infection, identified the secreted virulence factor IncS as an evasion factor that blocks IL32 targeting and shields this human pathogen from xenophagy. These findings establish an IL32-dependent intracellular sensing mechanism linking IFN gamma signaling to N-degron-mediated xenophagy, revealing a broadly relevant axis of human host-pathogen conflict
- A Circulating TLR2pos CD14neg CD16neg '' Unclassified Subset '' is Decreased in Multiple Myeloma Patients and May Comprise CD163pos Dendritic Cells.
Background: Strategies to define human monocytes by flow cytometry vary considerably across studies. Recently, toll-like receptor 2 (TLR2) has been proposed as a marker to identify '' all monocytes ''in human peripheral blood. However, the TLR2-defined monocytes also contained a previously ignored TLR2posCD14dim/negCD16neg population, which we termed the unclassified subset (UCS). Methods: Peripheral blood mononuclear cells (PBMCs) from healthy donors and patients with multiple myeloma (MM) or monoclonal gammopathy of undetermined significance (MGUS) were analyzed by multiparameter flow cytometry using TLR2pos gating. PBMCs from additional healthy donors were analyzed to characterize the UCS population, including the impact of using either TLR2pos or a negative selection-based gating strategy. Results: The TLR2pos CD14dim/neg CD16neg UCS population was present in healthy controls, MGUS, and MM patients. The UCS expressed the monocyte-macrophage scavenger receptor CD163 and was significantly reduced in MM patients compared to healthy donors (P<0.002). Further phenotypic characterization in healthy blood donors revealed that approximately 80% of UCS cells expressed CD163 at levels comparable to classical monocytes, yet phenotypically resembled CD163pos dendritic cells (DCs). Importantly, gating strategies influenced the composition of the UCS: negative selection-based gating captured all DC subsets, whereas TLR2pos gating primarily included CD1cpos DCs that were highly CD163pos. Conclusions: These findings demonstrate that circulating CD163pos CD1cpos DCs are included in the TLR2pos cell population previously described as exclusively monocytes, highlighting the impact of gating strategy on monocyte subset identification. Further, the lower level of TLR2pos CD14dim/neg CD16neg CD163pos cells in MM patients may represent decreased levels of circulating DCs that may contribute to the immune dysregulation in this disease.
- Concept-Level Semantic Representations Remain Decodable in Chronic Post-Stroke Aphasia
Aphasia is characterized by impaired word retrieval, yet most cognitive models of word production assume that underlying conceptual-semantic representations are largely preserved. This study investigated whether concept-level semantic structure remains decodable from BOLD signals in chronic post-stroke aphasia and which semantic models best explain neural representational geometry during covert semantic feature generation. Eight healthy adults and six individuals with chronic aphasia completed a dense-sampling fMRI protocol in which they viewed 57 pictured nouns while silently generating semantic features. Representational similarity analysis showed that an experiential model (Exp48) best matched neural geometry in both people with aphasia and controls, outperforming taxonomic (WordNet) and distributional (Word2Vec, GloVe) models. Using representational similarity decoding, concept identity was recovered well above chance in both groups. No relationship was found between decoding accuracy and language measures from individuals with aphasia. These findings suggest that experiential semantic structure remains robustly represented and decodable in chronic aphasia despite lesion-related language impairments, highlighting preserved conceptual representations alongside altered anatomy.
- Developmental tuning of functional manifold dimensionality across the human brain
Neural representations vary in their complexity across brain regions and tasks. How this variation emerges over human development remains poorly understood. We estimated intrinsic dimensionality in five naturalistic fMRI datasets (N = 781 unique participants, aged 3 months to 53 years) with T-PHATE -- a nonlinear manifold learning method robust to noisy, autocorrelated signals. In adults, brain regions relevant to a task had higher-dimensional activity than task-irrelevant regions across auditory, visual, and audiovisual stimuli. The modulation of representational complexity by tasks was absent in infants, emerged in early childhood, and strengthened logarithmically through adolescence. It reflected a selective collapse in dimensionality in task irrelevant regions, relative to a resting-state baseline, rather than an expansion of dimensionality in task-relevant regions. Such compression followed a trajectory from global and nonselective in infants to local and precise by adulthood. These results identify selective compression as a developmental engine of functional specialization: rather than adding complexity where it is needed, the brain dynamically pares it away where it is not.
- Live-imaging of endogenous neurofascins reveals glial adhesion shapes developing nodes of Ranvier
The organisation of myelinated axons into specialised domains is essential for saltatory conduction and depends on the polarised distribution of neuronal and glial cell-adhesion molecules, including neurofascins. However, how these domains assemble and refine in vivo remains unclear, as longitudinal imaging of endogenous proteins within intact nervous systems remains challenging. Here, we generated knock-in zebrafish in which endogenous neuronal and glial neurofascins are fused to fluorescent proteins, which enabled live-imaging without perturbing node assembly or introducing overexpression artefacts. Using these reporters, we visualised neuronal and glial neurofascin dynamics, and the formation of nodes of Ranvier and paranodes in vivo. We find that nascent nodes progressively compact in developing peripheral nerves, and that this process depends on glial neurofascin. Our novel toolkit for imaging endogenous neurofascins reveals a glia-dependent mechanism that shapes the developmental refinement of nodal architecture after their initial assembly. Our findings imply that glia-driven modulation of paranodes can be a mechanism for nervous systems to regulate circuit function.
- Distinct forms of dopamine transmission control locomotion and learning
The neuromodulator dopamine is essential for voluntary movement and learning from experience. While these behaviors often occur simultaneously and rely on overlapping nigrostriatal dopamine circuits, they are also separable and can manifest independently. How a single neuromodulatory system controls such disparate aspects of behavior in parallel remains poorly understood. Here we show that striatal dopamine is released through two spatially and functionally distinct modes that are independently regulated and serve distinct behavioral roles. Eliminating dopamine release underlying bulk extracellular accumulation reveals a spatially restricted mode of transmission that maintains phasic dopamine receptor activation on striatal projection neurons. We find that selective loss of diffuse dopamine impairs striatal circuit excitability and reduces locomotion, while point-to-point transmission is sufficient to maintain striatal spine density and support motor and associative learning. We propose that the geometry of dopamine release determines its behavioral output, a principle that explains the breadth of dopamine's functions and more broadly elucidates how neurons multiplex different forms of information.
- A significant enrichment that is not: spatial nulls, co-expression, and the imaging transcriptomics of EEG alpha-power genetics
Background. Imaging transcriptomics routinely asks whether a trait-associated gene set is over-expressed in a region of interest, and the field standard is to guard that inference with a spatial-autocorrelation-preserving spin test. Electroencephalographic (EEG) oscillatory power is among the most heritable human neurophysiological traits, and the cortical generators of the alpha rhythm have been characterised independently from resting-state magnetoencephalography - making this a natural test bed both for asking whether trait genetics is regionally organised, and for asking what such a test actually establishes. Objective. To test whether alpha-associated genetic signal is spatially enriched in the cortical generators of the alpha rhythm, and to evaluate that inference against complementary null models. Methods. MAGMA gene-based analysis of ENIGMA-EEG summary statistics for six phenotypes: central and occipital alpha power, occipital alpha peak frequency, and theta, beta and delta power. Regional transcription was obtained from the Allen Human Brain Atlas (AHBA) with abagen in the Glasser HCP-MMP1.0 atlas, with Schaefer-100 and Yan-600 as sensitivity analyses. Enrichment in the 41 cortical alpha-source regions was quantified with a threshold-free continuous score and a top-100 gene-set composite, and assessed against three complementary nulls: a spin test (10,000 rotations, cross-checked against brainsmash surrogates), a co-expression-aware gene-set null (10,000 matched random gene sets), and a positive control on a known expression gradient. Results. Judged by the field-standard spin test alone, this study would have reported a positive, biologically coherent finding: alpha-power genes are enriched in the cortical alpha generators (continuous p_spin = 0.022; top-100 p_spin = 0.030), with the spin result corroborated by an independent surrogate model (p = 0.018) and the pipeline validated by a positive control (p_spin = 2 x 10^-4). Three further tests dissolve that conclusion. First, it is not band-specific: theta, beta and delta enrich comparably or more strongly (top-100 beta p_spin = 0.011; delta 0.042; continuous theta 0.042). Second, it does not replicate across alpha phenotypes (occipital alpha continuous p_spin = 0.20; alpha peak frequency non-significant, p_spin >= 0.066). Third, against random gene sets of matched size the alpha set is unremarkable (p_geneset = 0.33) - the apparent enrichment is a generic property of arbitrary gene sets in this cortical territory, and is invisible to a spatial-only null. No test survived false-discovery-rate correction across the 24-cell phenotype x score x region-set grid (minimum q = 0.127), and nominal significance did not survive a change of parcellation. Conclusion. EEG alpha-power genetics shows no regionally specific transcriptomic signature in the cortical generators of the rhythm; the weak tendency that is present is shared across frequency bands, consistent with their known genetic correlation. Methodologically, this is a worked demonstration that correcting for spatial autocorrelation is necessary but not sufficient: a spin-significant, surrogate-corroborated, mechanistically plausible enrichment can be fully accounted for by gene-set co-expression. Enrichment claims in imaging transcriptomics should report a gene-set null alongside the spatial null.
- remio: Your Personal ChatGPT
Get Tailored Answer with Your Personal ChatGPT
- Global structure of new relational knowledge networks is represented in retrosplenial complex, and node-distance in hippocampus
Much of our knowledge is structured in networks, but how the brain represents such networks remains unclear. In most nested knowledge structures a subset of the nodes will be highly connected to other nodes in the network. High levels of connection can exist either locally (high degree centrality) or at a global level (high closeness/betweenness centrality). Here, we explored how the human brain represents network structure using functional magnetic resonance imaging (fMRI) and a novel learning paradigm. During training, participants learned the transition structure for travel between a set of fictious partially connected alien planets. Despite encountering only individual connections, participants choices indicated they could infer the broader network structure. Next day, they viewed each stimulus during a cover task while undergoing fMRI. Representational-similarity analysis showed that shortest-path distances within the learned graph were encoded in the posterior hippocampus and right retrosplenial complex, whereas global connectivity (closeness/ betweenness centrality) was represented in the left retrosplenial complex. These findings extend the view that brain networks associated with spatial navigation also process abstract relational knowledge using principles akin to mapping physical space. The results are also consistent with proposals that the hippocampus represents distance information and that the retrosplenial cortex acts as hub for integrating recently acquired knowledge.
- Hugging Face CEO shares his demands of OpenAI after 'rogue' agent hack: 'It deserves an unprecedented response'
Hugging Face CEO shares his demands of OpenAI after 'rogue' agent hack: 'It deserves an unprecedented response' Business Insider
- Its AI agent spent days hacking a company, but sources say OpenAI did not notice for a week
As OpenAI faces backlash from its AI agent’s breach of Hugging Face, experts warn about the implications for AI safety and risks of more autonomous systems
- Its AI agent spent days hacking a company, but sources say OpenAI did not notice for a week
Its AI agent spent days hacking a company, but sources say OpenAI did not notice for a week
- New reports reveal the extent of OpenAI's loss of control during the autonomous hack on Hugging Face
In a cybersecurity test, OpenAI's most advanced models breached the boundaries of their isolated test environment, reached the open internet, and hacked the AI platform Hugging Face on their own. The attack took hours, not the weeks a human hacker would need. At least seven days passed before OpenAI realized what had happened. By then, the FBI was already involved. Earlier warning signs had apparently gone ignored. The article New reports reveal the extent of OpenAI's loss of control during the autonomous hack on Hugging Face appeared first on The Decoder .
- OpenAI agent hack: AI safety concerns
OpenAI agent hack: AI safety concerns The Straits Times
- OpenAI's rogue agent went on a hacking spree that lasted days, Reuters says
Reuters reports that the OpenAI agent that hacked Hugging Face had been free for a week before the company noticed.
- OpenAI agent goes rogue and hacks popular AI community — left escape plans for future models inside the company's infrastructure
OpenAI tests multiple autonomous AI agents at once and has difficulty identifying the threats each of them represents, if a new report from Reuters is accurate.
- OpenAI didn't realize its agent was responsible for hack for a week: report
One of OpenAI's models autonomously breached AI company Hugging Face's systems during an internal evaluation, and OpenAI didn't catch it for days.
- OpenAI model unintentionally hacks another company's system
OpenAI model unintentionally hacks another company's system marketplace.org
- OpenAI’s rogue AI hack was just the beginning, Hugging Face warns
OpenAI calls its autonomous Hugging Face breach unprecedented, while security and AI experts say the episode raises an equally uncomfortable question about the company’s own safeguards.
- DeepSeek said to tell backers of funding pause after viral posts
DeepSeek said to tell backers of funding pause after viral posts Fortune
- Nvidia chief says will announce $500 bln partnership with SK Group in meeting with Lee
President Lee Jae Myung held a meeting with Nvidia Chief Executive Officer Jensen Huang on Friday, during which the tech executive said his company will announce a $500 billion business partnership with South Korea's SK Group. The meeting took place on the first day of Lee's two-day trip to San Francisco aimed at promoting AI investment and cooperation between global tech giants and South Korea. During the meeting, Huang also announced plans to jointly develop a self-driving Genesis sedan with S
- Nvidia chief pledges massive investment, cooperation with S. Korea in meeting with Lee
President Lee Jae Myung held a meeting with Nvidia Corp. Chief Executive Officer (CEO) Jensen Huang on Friday, during which the tech executive unveiled a series of large cooperation projects with South Korean tech firms, including a US$500 billion business partnership with SK Group. The meeting took place on the first day of Lee's two-day trip to San Francisco aimed at promoting AI investment and cooperation between global tech giants and South Korea. Huang was referring to investment plans that
- Microsoft, Meta, Nvidia, OpenAI, and Palantir have a message for Washington
Microsoft, Meta, Nvidia, OpenAI, and Palantir have a message for Washington Business Insider
- Tech leaders lobby against restrictions on open-source AI
Tech leaders lobby against restrictions on open-source AI PitchBook
- Nvidia, other tech giants caution against open-source AI ban in open letter
A group of tech firms has released an open letter that calls on policymakers not to ban open-source artificial intelligence models. The development follows a report that some Trump administration officials sought to limit the use of such algorithms. Many of the world’s most popular open-source AI models were developed by Chinese companies. According to […] The post Nvidia, other tech giants caution against open-source AI ban in open letter appeared first on SiliconANGLE .
- Why Nvidia, Microsoft and Meta want the US to support open-weight AI
Why Nvidia, Microsoft and Meta want the US to support open-weight AI
- Nvidia, Microsoft and other tech giants back open-source AI models
Tech leaders have also chafed at controls that OpenAI and Anthropic build into their models. Hugging Face, the AI coding collaboration site that was hacked by a rogue OpenAI model, this week said that it had to use a Chinese open-source model to defend against the attack because closed-source models have restrictions on use for cybersecurity work.