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Adaptive Entangled Game Modules in Artificial General Intelligence

arXiv:2609.09226v1 Announce Type: new Abstract: We introduce a probability-wave framework for modeling the collective behavior of interacting adaptive agents, deriving testable eigenmodes through a generalized behavioral intelligence (GBI) nonlocal probability-wave equation. This framework captures a broad range of human intelligence behaviors with analytical mechanisms and offers an indirect method to examine the Liu-Chen-Ao (LCA) hypothesis of nonlocal entangled nerve fibers in the brain through collective trader behaviors. Our empirical analysis of Chinese intraday stock market data demonstrates that adaptive entangled game modes explain 82-94% (89% overall) of observed decision patterns, a sharp contrast to the predictions of neoclassical finance based on independent rational agents. Moreover, 2-12% of behaviors show adaption to intraday news, events, and environments, characterized by dual equilibrium states and abrupt reference point shifts, while purely independent modes occur in less than 5% of cases. These findings empirically support the LCA hypothesis, as observable trading behaviors reflect underlying brain mechanisms and internal intelligence decision-making in behavioral psychology. Our results highlight the necessity of incorporating adaptive entangled game modules into artificial general intelligence (AGI) architectures, addressing the limitations of conventional artificial neural network (ANN)-based AI, which relies on trillions of opaque parameters. By integrating ANN-based AI with probability-wave-based entangled-brain simulations, machine learning can enrich AGI foundation models (FMs) and facilitate the development of human-like processing units (HPUs) that leverage brain-inspired mechanisms. Such HPUs may ultimately create more compact, efficient, and robust AGI systems, particularly for embodied intelligence and robotics.
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What Should an Agent Forget? Separating What Is Stored from What Is Used

arXiv:2609.10263v1 Announce Type: new Abstract: Persistent language agents need stored experience to remain available across time, while each answer requires evidence suited to a particular question. A superseded fact can mislead a current-state answer and still be essential for a historical query. We present RD-Forget, a training-free framework that separates what an agent stores from what it uses. A retained source archive preserves observations, and a query-conditioned memory view controls their influence on the current answer. A frozen language-model curator extracts relevant evidence, groups facts into semantic slots, and preserves the relations needed for multi-hop reasoning. Same-slot replacement links suppress superseded values in current-state contexts, while intent-aware retrieval makes earlier evidence eligible again. A rate-distortion formulation guides construction of the answer-time view within a memory budget. Experiments span conversational memory, knowledge updating, fact consolidation, long-context reasoning, and personalization under a shared answering pipeline. The results associate accurate answers with both query-relevant evidence construction and control over obsolete alternatives. Configurations without forgetting or query conditioning have the largest score deficits, while slot grouping, historical access, and relation preservation contribute complementary functions. Retaining history while selectively controlling its use offers a practical way to accommodate changing facts and future questions.
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EEGBind: Detecting Source-Level Interictal Epileptiform Discharges via EEG-Centric Multimodal Binding

arXiv:2609.09728v1 Announce Type: cross Abstract: Source-level analysis of interictal epileptiform discharges (IEDs) is relevant to presurgical evaluation and treatment planning because it helps characterize where epileptiform activity is likely to arise. Beyond detecting whether an IED is present, this setting requires assigning IED-positive activity to clinically meaningful brain-region categories. This setting is challenging because source-region evidence in short electroencephalography (EEG) windows can be subtle, partial, and affected by subject variability, class imbalance, and imperfect multimodal context. We present EEGBind, an EEG-centric multimodal binding framework for five-class source-level IED classification. EEGBind treats EEG as the primary modality and binds synchronized video-context features around an EEG-centric representation. Instead of relying on early or overly strong multimodal fusion, which may perturb the source-sensitive EEG representation, EEGBind uses video context as auxiliary evidence for robust classification. A view-consistent repair stage is further used to improve hidden-set robustness while preserving the learned source-class boundary. On the NeuroMM 2026 Grand Challenge Track 3 NMM-Source-IED benchmark, EEGBind achieves 0.8395 on weighted-F1 and outperforms strong competitors. These results support EEG-centric multimodal binding as a practical strategy for source-level IED classification. The open-source code is available at https://github.com/HKUSTGZ-ML4Health-Lab/NeuroMM2026_IED_Detection.
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Genomics and social practices at Mogou and other Gansu sites during prehistoric trans-Eurasian exchange

Ancient DNA from 149 individuals at 11 sites in Gansu, China, dated to around 4,700–3,000 years ago, reveals human population history during early transcontinental exchanges of agriculture and technology, as well as contemporary social practices, at the large Mogou cemetery.
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Macrophage spatiotemporal plasticity in pulmonary diseases: decoding the niche at single-cell resolution

Front Immunol. 2026 Jun 18;17:1855906. doi: 10.3389/fimmu.2026.1855906. eCollection 2026.

ABSTRACT

Pulmonary gas exchange and host defense depend on the dynamic coordination of resident and recruited macrophage populations. Historically, macrophage functions have often been interpreted through the classic M1/M2 dichotomy; however, this binary framework does not capture the heterogeneity and context-dependent plasticity of macrophage states within the lung microenvironment. Advances in single-cell RNA sequencing and spatial multi-omics have substantially refined our understanding of this complex macrophage network. Here, we synthesize evidence from human studies and experimental models to summarize macrophage functional states in homeostasis and across chronic obstructive pulmonary disease, asthma, idiopathic pulmonary fibrosis, pulmonary hypertension, acute lung injury/acute respiratory distress syndrome, and lung cancer. We highlight how macrophage transcriptional programs are shaped by ontogeny, tissue niche, and epigenetic-metabolic regulation, and how these programs are linked to disease-specific remodeling of the pulmonary microenvironment. Across diverse respiratory diseases, persistent tissue injury and microenvironmental stress remodel resident macrophage programs and are frequently accompanied by the expansion and context-dependent differentiation of recruited monocyte-derived macrophages. These macrophage states are associated with inflammatory amplification, epithelial and endothelial barrier dysfunction, extracellular matrix remodeling, and tumor immune evasion. Ligand-receptor and spatial analyses further identify candidate communication axes linking macrophages with stromal, epithelial, endothelial, and immune cells, some of which appear partially conserved across disease contexts. Emerging macrophage-targeted strategies are increasingly being explored beyond broad depletion, with growing interest in context-specific reprogramming and niche modulation, including antibody-based, nanocarrier-mediated, and engineered-cell approaches. Decoding the spatiotemporal trajectories and cell-cell communication networks of specific macrophage subsets, while considering tissue context, species differences, and levels of experimental support, may help clarify mechanisms of tissue remodeling, therapeutic resistance, and macrophage-targeted intervention in complex pulmonary diseases.

PMID:42396453 | PMC:PMC13322945 | DOI:10.3389/fimmu.2026.1855906

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