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A Study on Robustness, Adaptation, and Generalization for Visual and Multimodal Learning
No full textAdaptive Online Learning and Portfolio Optimization: Regret Minimization, Robustness, and Efficient Algorithms
No full textA Cyclodepsipeptide Nature Product from <em>Saccharothrix Syringae</em> Targets DNA in Its Mode of Action
No full textMechanisms of Volume-Dependent Debris Flow Impact on Multiple Barriers Using an Efficient Two-Phase MPM
No full textDecoding Marine Community Interactions and Stability through Environmental DNA Metabarcoding
No full textMobility-Aware Robust Design for Secure and Energy-Efficient Integrated Sensing and Communication Systems
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Threshold Voltage Swing Caused by Intense Phonon-Electron Interaction in High-k Dielectrics
No full textThe dynamic charge trapping/releasing behavior of oxygen vacancies (VO) in the high-k dielectric layer of advanced multi-gate devices is investigated through a combination of first-principles calculations, non-radiative multi-phonon (NMP) model and TCAD simulations. Under the effect of phonon-electron interactions, the extremely large electron captures cross-sections (ECCS) for VO defects illustrates easy trapping/releasing of electrons, resulting in uncontrollable charge quantity in the dielectric layer and significant leakage current. Consequently, significant Vth swing of the operated device can be expected due to the electron capture and emission, thus degrading the reliability. These findings elucidate the fundamental mechanisms behind reliability degradation in scaled devices and establish a defect optimization foundation to optimize fabrication processes in future technology nodes.<br/
ROS and the cell cycle: Cycling in and out of the comfort zone of redox control
No full textThe cell cycle is marked by dynamic fluctuations in reactive oxygen species (ROS). While low levels of ROS can stimulate cell proliferation, excessive ROS lead to cell cycle arrest. Notably, cell cycle arrest can further generate more ROS, creating a bidirectional relationship that underscores the necessity for cells to finely tune ROS levels to maintain homeostasis and ensure proper cell cycle progression. Unlike classical cell cycle checkpoint systems, ROS directly oxidise cysteine residues in critical cell cycle regulators, with examples ranging from cyclins and cyclin-dependent kinases to APC/C, CDK inhibitors, and other CDK regulators, altering their functions. This review explores the interplay between ROS and the cell cycle, emphasizing how understanding their relationship could enhance therapeutic outcomes.</p
