Paper List
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Evolutionarily Stable Stackelberg Equilibrium
通过要求追随者策略对突变入侵具有鲁棒性，弥合了斯塔克尔伯格领导力模型与演化稳定性之间的鸿沟。
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Recovering Sparse Neural Connectivity from Partial Measurements: A Covariance-Based Approach with Granger-Causality Refinement
通过跨多个实验会话累积协方差统计，实现从部分记录到完整神经连接性的重建。
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Atomic Trajectory Modeling with State Space Models for Biomolecular Dynamics
ATMOS通过提供一个基于SSM的高效框架，用于生物分子的原子级轨迹生成，弥合了计算昂贵的MD模拟与时间受限的深度生成模型之间的差距。
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Slow evolution towards generalism in a model of variable dietary range
通过证明是种群统计噪声（而非确定性动力学）驱动了模式形成和泛化食性的演化，解决了间接竞争下物种形成的悖论。
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Grounded Multimodal Retrieval-Augmented Drafting of Radiology Impressions Using Case-Based Similarity Search
通过将印象草稿基于检索到的历史病例，并采用明确引用和基于置信度的拒绝机制，解决放射学报告生成中的幻觉问题。
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Unified Policy–Value Decomposition for Rapid Adaptation
通过双线性分解在策略和价值函数之间共享低维目标嵌入，实现对新颖任务的零样本适应。
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Mathematical Modeling of Cancer–Bacterial Therapy: Analysis and Numerical Simulation via Physics-Informed Neural Networks
提供了一个严格的、无网格的PINN框架，用于模拟和分析细菌癌症疗法中复杂的、空间异质的相互作用。
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Sample-Efficient Adaptation of Drug-Response Models to Patient Tumors under Strong Biological Domain Shift
通过从无标记分子谱中学习可迁移表征，利用最少的临床数据实现患者药物反应的有效预测。
Imperfect molecular detection renormalizes apparent kinetic rates in stochastic gene regulatory networks
Department of Mathematical Analysis and Numerical Mathematics, Comenius University, Slovakia | University of Edinburgh, UK
30秒速读
IN SHORT: This paper addresses the core challenge of distinguishing genuine stochastic dynamics of gene regulatory networks from artifacts introduced by imperfect molecular detection in single-cell experiments.
核心创新
- Methodology Extends the binomial capture model from simple gene expression to general gene regulatory networks (GRNs) with explicit regulation, enabling analysis of technical noise in complex systems.
- Theory Establishes precise mathematical conditions under which technical noise leads to a renormalization (rescaling) of kinetic rates versus when it introduces non-absorbable distortions.
- Methodology Derives results valid for networks of arbitrary connectivity and under time-dependent kinetic rates, significantly generalizing previous steady-state analyses.
主要结论
- Technical noise systematically reduces the apparent mean burst size of gene products by a factor of p (the capture probability), e.g., from b(t) to b(t)*p.
- Rate renormalization occurs when promoter-state transitions are on a distinct timescale (much slower/faster) than other reactions or under high transcription factor abundance.
- The framework shows that for the telegraph model, the observed mRNA dynamics are equivalent to the true system with a renormalized transcription rate: k₃(t) → p*k₃(t).
摘要: 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 emerges either under significant transcription factor abundance or when promoter-state transitions occur on a distinct (much slower or faster) timescale than other reactions. In these cases, technical noise causes the apparent mean burst size of synthesized gene products to appear reduced while transcription factor binding reactions appear faster. These effects hold for gene regulatory networks of arbitrary connectivity and remain valid under time-dependent kinetic rates.