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The ability to actively regulate heat flow at the nanoscale could be a game changer for applications in thermal management and energy harvesting. Such a breakthrough could also enable the control of heat flow using thermal circuits, in a manner analogous to electronic circuits. Here we demonstrate switchable thermal transistors with an order of magnitude thermal on/off ratio, based on reversible electrochemical lithium intercalation in MoS₂thin films. We use spatially-resolved time-domain thermoreflectance to map the lithium ion distribution during device operation, and atomic force microscopy to show that the lithiated state correlates with increased thickness and surface roughness. First principles calculations reveal that the thermal conductance modulation is due to phonon scattering by lithium rattler modes,c-axis strain, and stacking disorder. This study lays the foundation for electrochemically-driven nanoscale thermal regulators, and establishes thermal metrology as a useful probe of spatio-temporal intercalant dynamics in nanomaterials.

Circadian dysfunction is a common attribute of many neurodegenerative diseases, most of which are associated with neuroinflammation. Circadian rhythm dysfunction has been associated with inflammation in the periphery, but the role of the core clock in neuroinflammation remains poorly understood. Here we demonstrate that Rev-erbα, a nuclear receptor and circadian clock component, is a mediator of microglial activation and neuroinflammation. We observed time-of-day oscillation in microglial immunoreactivity in the hippocampus, which was disrupted in Rev-erbα^−/−mice. Rev-erbα deletion caused spontaneous microglial activation in the hippocampus and increased expression of proinflammatory transcripts, as well as secondary astrogliosis. Transcriptomic analysis of hippocampus from Rev-erbα^−/−mice revealed a predominant inflammatory phenotype and suggested dysregulated NF-κB signaling. Primary Rev-erbα^−/−microglia exhibited proinflammatory phenotypes and increased basal NF-κB activation. Chromatin immunoprecipitation revealed that Rev-erbα physically interacts with the promoter regions of several NF-κB–related genes in primary microglia. Loss of Rev-erbα in primary astrocytes had no effect on basal activation but did potentiate the inflammatory response to lipopolysaccharide (LPS). In vivo, Rev-erbα^−/−mice exhibited enhanced hippocampal neuroinflammatory responses to peripheral LPS injection, while pharmacologic activation of Rev-erbs with the small molecule agonist SR9009 suppressed LPS-induced hippocampal neuroinflammation. Rev-erbα deletion influenced neuronal health, as conditioned media from Rev-erbα–deficient primary glial cultures exacerbated oxidative damage in cultured neurons. Rev-erbα^−/−mice also exhibited significantly altered cortical resting-state functional connectivity, similar to that observed in neurodegenerative models. Our results reveal Rev-erbα as a pharmacologically accessible link between the circadian clock and neuroinflammation.