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Reactions of Strained Cycloalkanes with Radicals and Diradicaloids: The Roles of Diradical Character and Strain Release
Copper-Mediated Radical Transformation of Protection-Free Glycosylsulfonohydrazide for Access to Diverse Glycosides
Divergent Asymmetric Synthesis of Glutinosasins A–E
Subtropical gyre expansion causes Southern Ocean salinification contrary to freshening predictions
Abstract The “salty-gets-saltier, fresh-gets-fresher” paradigm predicts that an intensifying hydrological cycle should freshen the climatologically fresh Southern Ocean. Here we show the opposite: sea surface salinity increased at ~0.03 decade − 1 across 40–50°S during 2004–2024, most coherently in the Pacific and Atlantic sectors. We attribute this salinification to the poleward expansion of the southern subtropical gyres, which advects saline subtropical water into latitudes of steepest meridional salinity gradient. The Subtropical and Subantarctic Fronts, tracked via the 35 and 34 isohalines, migrate poleward at unequal rates (–0.46° and –0.18° decade −1 ), narrowing the frontal corridor and sharpening the cross-frontal gradient. A mixed-layer budget shows that horizontal advection dominates the salinity trend, roughly tripling the opposing contribution from surface freshwater flux. Forced by poleward-intensifying westerlies and a positive Southern Annular Mode trend, this circulation-driven salinification demonstrates that ocean dynamics can override freshwater forcing, cautioning against interpreting salinity trends as direct fingerprints of the hydrological cycle.
A Modular PMDA Linker Enables Lysine-Selective Cyclization of Unprotected Peptides and Automated Macrocycle Assembly
Tubulin autoregulation tunes microtubule dynamics to support multicellular architecture and viability
Abstract Alpha- and beta-tubulin heterodimers dynamically assemble into microtubules, key cytoskeletal elements involved in intracellular trafficking, cell adhesion, and division. The availability of free tubulins regulates the synthesis of new subunits. In response to excessive soluble αβ-tubulins, tetratricopeptide protein 5 (TTC5) selectively recognizes nascent tubulins at the ribosome, recruiting downstream effectors that degrade their encoding messenger RNAs, in a process known as tubulin autoregulation. Despite its well-characterized molecular framework, the biological relevance of this regulatory pathway remains unknown. Here, using human 3D cellular models, advanced optics, and genetic perturbation of tubulin biosynthesis, we reveal that loss of TTC5-dependent tubulin autoregulation elevates soluble tubulin levels, increasing microtubule stability and disrupting cytoskeletal organization. These defects impair the localization of adhesion molecules at cell-cell junctions and extracellular matrix interfaces, compromising tissue architecture and reducing overall cell viability. Our findings establish tubulin autoregulation as a critical mechanism that tunes microtubule dynamics to sustain cellular integrity and tissue homeostasis.
Utilizing Vibrational Probes to Monitor Polaron–Anion Interactions during Polymer Electrochemical Doping
A multimodal vision-language model for comprehensive dental diagnosis and enhanced clinical practice
Author Correction: Contextual gating of whisker-evoked responses by frontal cortex supports flexible decision making
Direct α-Trifluoromethyl Amidation and Three-Component Alkene Trifluoroalkylamidation via Merging Halogen-Atom Transfer and Nickel-Mediated Nitrenoid Transfer
Anomalous charge density wave in a two-dimensional superatomic superconductor
Transporter-Mimicking MXene for Uric Acid Capture and Sensing in Biofluids
Crew Resource Management — Navigating AI’s Automation Paradox
A neural signature of sleep deprivation in the human brain
Abstract Insufficient sleep disrupts cognitive and emotional functioning, yet the precise neural consequences of sleep loss and their persistence remain unclear. Here, we leverage machine learning and large neuroimaging datasets to identify a candidate neural signature that robustly distinguishes sleep-deprived from well-rested brains. We validate this signature across multiple independent datasets spanning both controlled experimental and real-world settings. The signature not only detects residual neural disturbances following a night of recovery sleep, but also demonstrates sensitivity to partial sleep deprivation. Additionally, it captures natural variations in sleep duration in the general population, independent of experimental manipulation. We further identify distributed connectivity patterns that contribute to the signature, highlighting networks vulnerable to sleep manipulations and those that are resistant or rapidly normalized after recovery sleep. The reliability and generalizability of this neural signature underscore its potential as a biomarker for understanding and monitoring the neural impacts of acute and chronic sleep loss.