11 research outputs found

    Universal behavior of highly-confined heat flow in semiconductor nanosystems: from nanomeshes to metalattices

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    Nanostructuring on length scales corresponding to phonon mean free paths provides control over heat flow in semiconductors and makes it possible to engineer their thermal properties. However, the influence of boundaries limits the validity of bulk models, while first principles calculations are too computationally expensive to model real devices. Here we use extreme ultraviolet beams to study phonon transport dynamics in a 3D nanostructured silicon metalattice with deep nanoscale feature size, and observe dramatically reduced thermal conductivity relative to bulk. To explain this behavior, we develop a predictive theory wherein thermal conduction separates into a geometric permeability component and an intrinsic viscous contribution, arising from a new and universal effect of nanoscale confinement on phonon flow. Using both experiments and atomistic simulations, we show that our theory is valid for a general set of highly-confined silicon nanosystems, from metalattices, nanomeshes, porous nanowires to nanowire networks. This new analytical theory of thermal conduction can be used to predict and engineer phonon transport in boundary-dominated nanosystems, that are of great interest for next-generation energy-efficient devices

    Obesity-induced PARIS (ZNF746) accumulation in adipose progenitor cells leads to attenuated mitochondrial biogenesis and impaired adipogenesis

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    Abstract White adipose tissue (WAT) is critical for whole-body energy metabolism, and its dysfunction leads to various metabolic disorders. In recent years, many studies have suggested that impaired mitochondria may contribute to obesity-related decline in adipose tissue function, but the detailed mechanisms remain unclear. To investigate these mechanisms, we carried out a comprehensive analysis of WAT from mice with diet-induced obesity. We discovered the transcription factor Parkin interactive substrate (PARIS or ZNF746), which suppresses the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), a key regulator of mitochondrial biogenesis, to be accumulated in adipose progenitor cells from obese mice. Furthermore, we demonstrated that 3T3-L1 preadipocytes with overexpression of PARIS protein exhibited decreased mitochondrial biogenesis and impaired adipogenesis. Our results suggest that the accumulation of PARIS protein may be a novel component in the pathogenesis of obesity-related dysfunction in WAT

    Opposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5

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    IL-2, a cytokine linked to human autoimmune diseases, limits IL-17 production. We show that deletion of STAT3 in T cells abrogates IL-17 production and attenuates autoimmunity associated with IL-2 deficiency. While STAT3 induces IL-17 and RORγt and inhibits FOXP3, IL-2 inhibited IL-17 independently of FOXP3 and RORγt. We found that STAT3 and STAT5 bound to multiple common sites across the Il17 genetic locus. The induction of STAT5 binding by IL-2 was associated with a reduction in STAT3 binding at these sites and the inhibition of associated active epigenetic marks. Titrating the relative activation of STAT3 and STAT5 modulated Th17 cell specification and thus, the balance rather than the absolute magnitude of these signals determine the propensity of cells to make a key inflammatory cytokine
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