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Schr\"odinger's Navigator: Imagining an Ensemble of Futures for Zero-Shot Object Navigation

arXiv:2512.21201v2 Announce Type: replace-cross Abstract: Zero-shot object navigation (ZSON) requires robots to locate target objects in unseen environments without task-specific fine-tuning or pre-built maps, a capability crucial for service and household robotics. Existing methods perform well in simulation but struggle in realistic, cluttered environments where heavy occlusions and latent hazards make large portions of the scene unobserved. These approaches typically act on a single inferred scene, making them prone to overcommitment and unsafe behavior under uncertainty. To address these challenges, we propose Schr\"odinger's Navigator, a belief-aware framework that explicitly reasons over multiple trajectory-conditioned imagined 3D futures at inference time. A trajectory-conditioned 3D world model generates hypothetical observations along candidate paths, maintaining a superposition of plausible scene realizations. An adaptive, occluder-aware trajectory sampling strategy focuses imagination on uncertain regions, while a Future-Aware Value Map (FAVM) aggregates imagined futures to guide robust, proactive action selection. Evaluations in simulation and on a physical Go2 quadruped robot demonstrate that Schr\"odinger's Navigator outperforms strong ZSON baselines, achieving more robust self-localization, object localization, and safe navigation under severe occlusions and latent hazards. These results highlight the effectiveness of reasoning over imagined 3D futures as a scalable and generalizable strategy for zero-shot navigation in uncertain real-world environments.

RFC4 drives temozolomide resistance in glioblastoma by activating STK38-BECN1-dependent autophagy

Nat Commun. 2026 Mar 23. doi: 10.1038/s41467-026-70798-1. Online ahead of print.

ABSTRACT

Glioblastoma (GBM) remains a lethal brain tumor due to therapy resistance. While autophagy contributes to temozolomide (TMZ) resistance, its regulation is incompletely understood. This study investigates the role of replication factor RFC4, which is associated with poor prognosis and TMZ resistance in GBM. Multi-omics analyses and molecular experiments reveal that TMZ-induced chromatin accessibility enables transcription factor YY1 to bind the RFC4 promoter and upregulate its expression. RFC4, in turn, stabilizes the kinase STK38, which is essential for autophagosome formation. The RFC4-STK38 interaction facilitates BECN1 recruitment, thereby activating autophagy. Phosphorylation of STK38 at T444 stabilizes this complex, whereas a phospho-deficient mutant impairs autophagy. In vivo, RFC4 overexpression confers TMZ resistance, reversible by autophagy inhibition. Thus, our findings identify the RFC4-STK38-BECN1 axis as a mechanism underlying TMZ resistance and a potential target for precision therapy in GBM.

PMID:41872171 | DOI:10.1038/s41467-026-70798-1

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