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。
ATP Level and Phosphorylation Free Energy Regulate Trigger-Wave Speed and Critical Nucleus Size in Cellular Biochemical Systems
School of Physics, Center for Quantitative Biology, Peking University, Beijing 100871, China
30秒速读
IN SHORT: This work addresses the core challenge of quantitatively predicting how the cellular energy state (ATP level and phosphorylation free energy) governs the speed, direction, and critical initiation size of propagating biochemical trigger waves.
核心创新
- Methodology Develops a thermodynamically consistent reaction-diffusion framework that treats ATP concentration ([ATP]) and the nonequilibrium parameter γ (=[ATP]/(Keq[ADP][Pi])) as independent control variables for analyzing trigger waves.
- Biology Identifies the intracellular energetic state as a direct regulator of trigger-wave behavior, quantitatively linking metabolic conditions (ATP/ADP/Pi ratio) to spatiotemporal propagation dynamics.
- Theory Derives analytical expressions showing that the critical excitation radius (Rc) for sustained wave propagation depends on both [ATP] and γ, with scaling Rc ∝ 1/√[ATP] under specific approximations.
主要结论
- ATP concentration ([ATP]) and the phosphorylation free energy parameter (γ) jointly regulate trigger-wave speed (c0), with a dominant scaling c0 ∝ √[ATP] in the forward propagation regime.
- The sign of the potential difference (ΔF) between bistable states, determined by [ATP] and γ, dictates wave propagation direction (forward for ΔF<0, reverse for ΔF>0), with a stationary interface at ΔF=0.
- The critical nucleus radius (Rc) for sustained spherical wave propagation is inversely related to wave speed (Rc = D(d-1)/c0), leading to the prediction that higher [ATP] reduces the minimum trigger size required (Rc ∝ 1/√[ATP]).
摘要: Trigger waves are self-regenerating propagating fronts that emerge from the coupling of nonlinear reaction kinetics and diffusion. In cells, trigger waves coordinate large-scale processes such as mitotic entry and stress responses. Although the roles of circuit topology and feedback architecture in generating bistability are well established, how nonequilibrium energetic driving shapes wave propagation is less well understood. Here, we employ a thermodynamically consistent reaction–diffusion framework to investigate trigger-wave dynamics in ATP-dependent phosphorylation–dephosphorylation systems. We first recapitulate general expressions for trigger-wave speed in the bistable regime and analyze curvature-induced corrections that determine the minimum critical nucleus required for sustained propagation in higher dimensions. We then apply this framework to two representative systems, treating ATP concentration and the nonequilibrium parameter γ=[ATP]/(Keq[ADP][Pi]) as independent control variables to examine how energetic driving regulates wave propagation. Our results show that ATP and γ not only modulate wave speed, but can also reverse the direction of propagation and reshape the parameter regime supporting trigger waves. The critical excitation radius also depends on both ATP concentration and phosphorylation free energy. These findings identify the intracellular energetic state as a regulator of trigger-wave behavior, linking metabolic conditions to the spatial dynamics of wave propagation. More broadly, this framework connects classical reaction–diffusion theory with ATP-driven biochemical regulation and provides a general perspective on related energy-dependent cellular decision-making processes.