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Explicit Quantum Circuit Simulation of Nonlinear 1-Dimensional Fluid with Carleman-linearized Boltzmann Method

arXiv:2606.12770v1 Announce Type: new Abstract: Quantum computation of fluid dynamics has attracted growing attention as a key application of fault-tolerant quantum computers anticipated in the coming decade, with lattice Boltzmann methods emerging as a particularly promising approach. Explicit and efficient elementary-gate-level circuit simulations, however, have so far been demonstrated only in the linear case. Here we include the leading nonlinearity through second-order Carleman linearization of the one-dimensional Boltzmann equation, and demonstrate, via explicit quantum-circuit simulation, the preparation of the final-time state using a Taylor-expansion-based ODE solver based on the quantum singular value transformation. With this construction, we analyze the gate and qubit complexities, which scale logarithmically with the grid size, the nonlinearity captured by the higher-order Carleman linearization, and the practical utility of higher-order expansions in the Taylor ODE solver. The construction provides a concrete baseline for computational cost reduction and further developments such as extensions to higher dimensions, complex geometries, and the extraction of physical quantities, towards industrially useful quantum CFD.

A non-invasive liquid biopsy resolves the diagnostic blind spot in chronic kidney disease

Chronic kidney disease is a major global health burden, and its early detection is critical for delaying progression to kidney failure using recently developed targeted therapies. However, current diagnostic screening relies heavily on blood markers that are confounded by muscle mass, and on urine tests that frequently miss structural damage occurring without protein leakage. This creates a critical diagnostic blind spot that hinders timely intervention. Here we show a non-invasive liquid biopsy platform that quantifies a specific protein marker, MUC1, on urinary extracellular vesicles to accurately assess renal parenchymal integrity. By bypassing the systemic metabolic noise of traditional blood tests, our assay provides a remarkably stable, person-specific functional signature. Following extensive validation across diverse cohorts, our longitudinal analysis demonstrated that the discrepancy between this novel urine-based readout and standard blood tests unmasks hidden renal vulnerability, successfully predicting rapid functional decline. By comprehensively evaluating both tubular and glomerular integrity from a single spot urine sample, these findings establish a completely non-invasive, highly scalable prescreening tool that resolves the diagnostic blind spot, enabling broader early detection strategies and ushering in a new era of proactive risk management.

Trajectory inference of epithelial-centered neighborhood profiles reconstructs a pseudo-temporal continuum in idiopathic pulmonary fibrosis

Idiopathic pulmonary fibrosis (IPF) is characterized by complex lung architecture and spatially heterogeneous remodeling, which have hindered integrated analysis of cell-intrinsic activity and intercellular communication during disease progression. Here we profiled six IPF lung specimens comprising more than 630,000 cells using the Xenium 5k panel and developed an epithelial-centered neighborhood profiling framework based on the local cellular composition around each epithelial cell. This approach captured fibrosis-associated variation in epithelial niches without requiring predefined histological regions. Pseudo-temporal continuum inference of these profiles reconstructed a continuous axis that reflected the spatial progression of fibrotic remodeling from relatively preserved alveolar regions to fibrotic and airway-like remodeled regions. Within this spatial dataset, we mapped coordinated changes in epithelial states, local microenvironments, epithelial intracellular pathway activities, and directional interactions with neighboring cell types along the same axis. Our findings provide a spatial framework that generates testable hypotheses for progressive epithelial niche remodeling in IPF.

Where Does Social Reasoning Come From? Capability Provenance in Language Models

We use training-data attribution as an interpretable tool for capability discovery, mapping which regions of the pretraining corpus support social-reasoning versus STEM-reasoning in OLMo3-7B. Training-data attribution measures how strongly each training document influences a model's predictions on a benchmark, but document-level scores are too noisy to identify which corpus regions support which capabilities, and prior work has emphasized factual knowledge rather than reasoning. We compute gradient-based attribution (TrackStar via Bergson) over a working set drawn from the de-duplicated Dolma3 mix, aggregate influence across WebOrganizer's 24-format x 24-topic taxonomy (576 bins), and contrast benchmark pairs in a 2x2 design that varies domain (social vs. STEM) and capability type (reasoning vs. knowledge): SocialIQA and MMLU Social Sciences against ARC-Challenge and MMLU STEM. Social and STEM reasoning draw on qualitatively distinct corpus regions, and the contrast is sharper at the reasoning level than at the knowledge level. Targeted machine unlearning provides partial causal validation: forgetting high-attribution topic bins (e.g., Literature for SocialIQA) degrades the aligned benchmark more than within-bin random baselines, and we open-source all code, sampling manifests, the bin-level influence matrix, and unlearning checkpoints.