A practical guide to PDF coordinate systems, font subset dictionaries, and client-side vector editing.

Nuix Neo BYO AI leverages the Nuix Neo Gen AI Framework and further tailors it to enable thorough AI analysis across every item in a dataset. Rather than relying on other approaches that prioritise or sample subsets, it applies repeatable workflows to systematically process every item and then crafts structured reports, with links back to source items and citations for rapid and forensically defensible action, all the while providing clarity and control over key issues like token usage. "With Nuix Neo's latest AI, we can move quickly to implement targeted solutions to digital evidence challenges and investigative bottlenecks, while satisfying our unique compliance needs. Being able to leverage the latest AI advancements while staying confined within our own environment is an accelerator," said Donn Hoffman, Chief Privacy Officer and Deputy District Attorney at Los Angeles County District Attorney's Office. Nuix Neo Agentic AI The Nuix Neo AI Agent, a conversational investigation capability built on the Gen AI Framework, is available for Early Adopter participants, via the Nuix Responsible Innovation Framework. The AI Agent extends the Nuix Neo platform, allowing analysts to interrogate their data with reasoning across text, metadata, and images, with access to the full power of Nuix's APIs,...

Severe dengue is characterized by systemic inflammation and vascular leakage. Recent evidence indicates that Toll-like receptor 2 (TLR2) supports early steps of dengue virus (DENV) infection in monocytes, whereas intracellular viral RNA sensing drives much of the subsequent inflammatory response. However, whether this entry-associated function of TLR2 differs among human monocyte subsets remains unknown. Here, we investigated how the TLR2 axis regulates DENV serotype 2 (DENV2) infection and inflammatory output in purified primary human monocytes and sorted monocyte subsets. Blocking TLR2 at the cell surface or targeting its intracellular TIR domain reduced virus-cell association, productive infection, and the release of inflammatory and antiviral mediators. Among TLR2-associated receptors, CD14 and, to a lesser extent, CD36 contributed to efficient infection, whereas TLR1, TLR6, and TLR10 were dispensable under the conditions tested. Notably, TLR2 blockade reduced viral production and cytokine release in CD16- classical monocytes but not in pooled CD16+ monocytes, identifying a subset-specific dependence on the TLR2 axis. TLR3 contributed to inflammatory and antiviral responses without affecting viral replication, consistent with post-entry recognition of viral RNA. Finally, blocking the TLR2 axis during monocyte infection prevented the loss of endothelial barrier integrity induced by monocyte-derived soluble mediators. Together, these findings identify a TLR2-associated entry route that preferentially supports productive DENV2 infection in classical monocytes and thereby enables RNA-sensor-dependent inflammatory responses that compromise endothelial function.

Recursive self-improvement (RSI) relies on evaluation feedback to assess progress and guide further research, yet repeatedly running complex benchmarks is costly and slows iteration. Human experts reduce this cost by selecting benchmark subsets or designing compact suites. We ask whether AI agents …

arXiv:2610.06527 · math.CO

Abstract page for arXiv paper 2610.06903: Component and Dimension Sparsity in Transformer Refusal Mechanisms

Current precision oncology strategies benefit only subsets of patients because cancer driving alterations are often infrequent or not readily tar-getable. Here, the authors identify MPZL1 as an amplified cell surface receptor broadly expressed across solid cancers and show that MPZL1-directed CAR T cells eliminate MPZL1 expressing tumors in multiple preclinical models.

The FBI is warning the public about In Real Life (IRL) Com, one of three subsets of the growing and evolving online threat group known as The Com, short for The Community.

Radiomic features may discriminate outcomes without identifying the image property responsible for that discrimination. We evaluated a patient-specific surrogate framework that tests feature responses to explicitly defined image modifications and diagnoses limitations of the surrogate procedure itself. Four public brain tumor magnetic resonance imaging collections contributed 1699 studies passing initial quality control. Core validation used smaller subsets, including 40 depth-stratified control evaluations from 38 glioma subjects, alongside a constructive counterexample and Gaussian-null diagnostics. Thirteen quantile-based morphological and topological descriptors were compared with conventional radiomics. Binary image pairs with exactly equal distance-1 co-occurrence counts differed in Euler characteristic beyond an independent ensemble’s range in 16/16 replicates, versus 0/16 negative controls. This establishes a specific limitation of those co-occurrence measurements. The Gaussian spectrum estimator was parameter-sensitive: only three of five evaluated settings satisfied an operational negative-control diagnostic, which does not establish statistical calibration. Under the depth-stratified null, the median fraction of descriptors detecting planted objects was 61.5% for the topological set, versus 13.7% and 31.5% for conventional features at 24 and 64 bins. These are descriptive, configuration-dependent comparisons; dependent features, control-based selection, and incomplete spectral convergence limit inference. Secondary clinical applications did not establish biological transferability or prognostic benefit. The framework provides reproducible tests of specified feature–null combinations, while exposing the controls and assumptions needed to interpret them.

Alt: Gretchen So Fetch

Recursive self-improvement (RSI) relies on evaluation feedback to assess progress and guide further research, yet repeatedly running complex benchmarks is costly and slows iteration. Human experts reduce this cost by selecting benchmark subsets or designing compact suites. We ask whether AI agents …

Severe dengue is characterized by systemic inflammation and vascular leakage. Recent evidence indicates that Toll-like receptor 2 (TLR2) supports early steps of dengue virus (DENV) infection in monocytes, whereas intracellular viral RNA sensing drives much of the subsequent inflammatory response. However, whether this entry-associated function of TLR2 differs among human monocyte subsets remains unknown. Here, we investigated how the TLR2 axis regulates DENV serotype 2 (DENV2) infection and inflammatory output in purified primary human monocytes and sorted monocyte subsets. Blocking TLR2 at the cell surface or targeting its intracellular TIR domain reduced virus-cell association, productive infection, and the release of inflammatory and antiviral mediators. Among TLR2-associated receptors, CD14 and, to a lesser extent, CD36 contributed to efficient infection, whereas TLR1, TLR6, and TLR10 were dispensable under the conditions tested. Notably, TLR2 blockade reduced viral production and cytokine release in CD16- classical monocytes but not in pooled CD16+ monocytes, identifying a subset-specific dependence on the TLR2 axis. TLR3 contributed to inflammatory and antiviral responses without affecting viral replication, consistent with post-entry recognition of viral RNA. Finally, blocking the TLR2 axis during monocyte infection prevented the loss of endothelial barrier integrity induced by monocyte-derived soluble mediators. Together, these findings identify a TLR2-associated entry route that preferentially supports productive DENV2 infection in classical monocytes and thereby enables RNA-sensor-dependent inflammatory responses that compromise endothelial function.