Human cognition depends on large scale communication constrained by white matter architecture. Although weak connections are abundant in mammalian connectomes, they have long been treated as noise and downweighted because of tractography uncertainty in the human brain, and their relevance to human cognition and large scale functional organization remains unresolved. Across multiple datasets and tractography pipelines, we show that, when tractography derived connectivity weights are interpreted through a nonlinear weighting framework, weak connections make measurable contributions to cognitive prediction, functional connectivity simulation, and structure-function coupling. These effects are selective: nonlinear weighting improves the prediction of general cognitive ability and memory more than that of crystallized intelligence or processing speed, consistent with the notion that weak connections preferentially expand the modal repertoire of brain networks to enhance both large scale integration and fine grained segregation, thereby supporting the functional balance essential for diverse cognitive abilities. Importantly, these effects are replicated in a reliability aware connectome generated by integrating two post tractography filtering methods, in which preserving weak links consistently outperforms conventional thresholding strategies. Finally, we show that weak connections contain functionally informative subsets organized along systems level and transcriptomic gradients. In particular, a specific class of weak connections, predominantly linking visual and motor systems with limbic regions and characterized by negative gene coexpression, exerts a disproportionately large influence on brain function.

Learning, inference, memory, and emergence in biological and artificial systems are often described using disparate theoretical frameworks. Here we develop a cognitive field theory in which cognition is described as a collective nonequilibrium phenomenon governed by the geometry and collective spectrum of a learned cognitive manifold. Starting from a stochastic cognitive-field equation on an adaptive Riemannian manifold, we derive an effective cognitive field theory incorporating nonlocal memory kernels and retarded self-energy feedback. The learned cognitive geometry generates a complex collective spectrum characterized by the time-scale density of states $ρ(λ,ω)$, whose relaxation and circulation sectors govern memory persistence and temporal coherence. Integrating out latent slow collective modes produces non-Markovian memory feedback that renormalizes the cognitive forgetting gap $r_{\rm cog}$, enhances collective susceptibility, and drives the system toward a protected near-critical regime characterized by long-time contextual persistence and scale-free temporal organization. The observable cognitive field emerges as a macroscopic order parameter, $ϕ=Ae^{iψ}$, whose amplitude encodes collective cognitive organization and whose phase encodes temporal coherence across distributed collective modes. Within this framework, learning organizes cognitive geometry, cognitive geometry generates a collective spectrum, and the resulting memory feedback stabilizes a memory-dressed cognitive field. The theory provides a unified dynamical description of learning, memory, inference, selfhood, and emergent intelligence in terms of the infrared organization of collective cognitive dynamics.

Imperfect molecular detection in single-cell experiments introduces technical noise that obscures the true stochastic dynamics of gene regulatory networks. While binomial models of molecular capture provide a principled description of imperfect detection, they have so far been analyzed only for simple gene-expression models that do not explicitly account for regulation. Here, we extend binomial models of capture to general gene regulatory networks to understand how imperfect capture reshapes the observed time-dependent statistics of molecular counts. Our results reveal when capture effects correspond to a renormalization of a subset of the kinetic rates and when they cannot be absorbed into effective rates, providing a systematic basis for interpreting noisy single-cell measurements. In particular, we show that rate renormalization depends on the level of regulatory detail in the model. For implicit regulatory models based on promoter state transitions, it arises whenever gene product synthesis does not trigger a promoter state change, as in the absence of promoter-proximal pausing or when pausing is short-lived. For models with explicit transcription factor binding, the same condition holds, together with sufficiently high transcription factor abundance, which in practice requires only a few tens of molecules per cell. In these cases, technical noise reduces the apparent mean burst size of synthesized gene products and accelerates the apparent rates of transcription factor binding reactions. This acceleration becomes stronger as the number of protein species and/or molecules involved in promoter switching increases. These effects hold for gene regulatory networks of arbitrary connectivity and remain valid under time-dependent kinetic rates.

Resting-state EEG provides a non-invasive view of spontaneous brain activity, but extracting meaningful patterns is often limited by scarce high-quality data and reliance on manually engineered features. Generative adversarial networks (GANs) can synthesize neural signals and learn transferable representations directly from raw data, a dual capability that remains underexplored in EEG research. Here, we introduce REST-GAN, a GAN-based framework for resting-state EEG that combines adversarial training with an auxiliary self-supervised reconstruction objective to support signal synthesis and unsupervised feature extraction. Although trained only on raw time-domain signals, without explicit frequency-domain or sensor-topographic supervision, the generated time series reproduced key temporal, spectral, and connectivity properties of real EEG. In band-power feature space, generated samples showed high precision and recall across eyes-open and eyes-closed conditions (EO: 0.91/0.67; EC: 0.87/0.65), while group-average spectral coherence matrices showed low mean absolute differences from real data across frequency bands (~0.01-0.03). The representations learned by the model's critic transferred to independent resting-state demographic classification tasks, outperforming models trained directly on raw EEG and showing competitive performance relative to a recent EEG foundation model, while requiring substantially less training data and computational resources. These findings highlight a computationally efficient, architecture-driven strategy in which generative models serve not only as EEG signal generators, but also as unsupervised feature extractors. This approach may support more data-efficient EEG analysis while reducing reliance on manual feature engineering. The implementation code for REST-GAN is available at: https://github.com/Yeganehfrh/REST-GAN.

Human bone marrow stromal cells (BMSC) include skeletal stem cells with ground-breaking therapeutic potential. However, BMSC colonies have very heterogeneous in vivo behaviour, due to their different potency; this unpredictability is the greatest hurdle to the development of skeletal regeneration therapies. Colony-level heterogeneity urges a fundamental question: how is it possible that one colony as a collective unit behaves differently from another one? If cell-to-cell variability were just an uncorrelated random process, a million cells in a transplant-bound colony would be enough to yield statistical homogeneity, hence washing out any colony-level traits. A possible answer is that the differences between two originating cells are transmitted to their progenies and collectively persist through an hereditary mechanism. But non-genetic inheritance remains an elusive notion, both at the experimental and at the theoretical level. Here, we prove that heterogeneity in the lineage topology of BMSC clonal colonies is determined by heritable traits that regulate cell-cycle exit. The cornerstone of this result is the definition of a novel entropy of the colony, which measures the hereditary ramifications in the distribution of inactive cells across different branches of the proliferation tree. We measure the entropy in 32 clonal colonies, obtained from single-cell lineage tracing experiments, and show that in the greatest majority of clones this entropy is decisively smaller than that of the corresponding non-hereditary lineage. This result indicates that hereditary epigenetic factors play a major role in determining cycle exit of bone marrow stromal cells.

Graph symmetries identify structural regularities and reduce the computational complexity of network analysis. In weighted graphs, however, exact automorphisms are rare because real-valued weights seldom coincide. We introduce a general framework for detecting approximate symmetries by aggregating weights into discrete categories, generating a sequence of coarser graphs on which classical automorphism analysis applies. The approximation path is fully configurable, based on interaction magnitudes, and can be matched to the empirical weight distribution. Applied to 250 empirical food webs using logarithmic aggregation, the method reveals that automorphisms emerge even at low approximation levels and almost always form small orbits. Orbit sizes rarely exceed two or three vertices, reflecting the combinatorial fragility of larger symmetric sets. Even so, symmetric vertices occupy diverse structural positions in the network and high connectivity does not imply asymmetry. The observation of just local permutations confirms the conclusions of trophic species and niche analysis. A case study demonstrates that automorphisms can also recover latent ecological structure. The minimal aggregation level at which two vertices become substitutable provides a quantitative measure of role similarity. The framework offers a principled, automorphism-based approach for quantifying similarity and redundancy in weighted complex networks.