We develop an effective medium model of thermal conductivity that accounts for both percolation and interface scattering. This model accurately explains the measured increase and decrease of thermal conductivity with loading in composites dominated by percolation and interface scattering, respectively. Our model further predicts that strong interface scattering leads to a sharp decrease in thermal conductivity, or an insulator transition, at high loadings when conduction through the matrix is restricted and heat is forced to diffuse through particles with large interface resistance. The accuracy of our model and its ability to predict transitions between insulating and conducting states suggest it can be a useful tool for designing materials with low or high thermal conductivity for a variety of applications.
All-dielectric metamaterials utilizing Mie resonances in high-permittivity dielectric resonators offer a low-loss alternative to plasmonic metamaterials. Here we present the demonstration of a single-negative all-dielectric metamaterial, comprised of a single layer of cylindrical silicon resonators on a silicon-on-insulator substrate, that possesses peak reflectance over 99% and an average reflectance over 98% across a 200 nm wide bandwidth in the short-wavelength infrared region. The study is also extended to disordered metamaterials, demonstrating a correlation between the degree of disorder and the reduction in reflectance. It is shown that near-unity reflection is preserved as long as resonator interaction is avoided. Realization of near-unity reflection from disordered metamaterials opens the door to large-area implementations using low-cost self-assembly based fabrication techniques.
The sleep disorder narcolepsy results from loss of hypothalamic orexin/hypocretin neurons. Although narcolepsy onset is usually postpubertal, current mouse models involve loss of either orexin peptides or orexin neurons from birth. To create a model of orexin/hypocretin deficiency with closer fidelity to human narcolepsy, diphtheria toxin A (DTA) was expressed in orexin neurons under control of the Tet-off system. Upon doxycycline removal from the diet of postpubertal orexin-tTA;TetO DTA mice, orexin neurodegeneration was rapid, with 80% cell loss within 7 d, and resulted in disrupted sleep architecture. Cataplexy, the pathognomic symptom of narcolepsy, occurred by 14 d when ∼5% of the orexin neurons remained. Cataplexy frequency increased for at least 11 weeks after doxycycline. Temporary doxycycline removal followed by reintroduction after several days enabled partial lesion of orexin neurons. DTA-induced orexin neurodegeneration caused a body weight increase without a change in food consumption, mimicking metabolic aspects of human narcolepsy. Because the orexin/hypocretin system has been implicated in the control of metabolism and addiction as well as sleep/wake regulation, orexin-tTA; TetO DTA mice are a novel model in which to study these functions, for pharmacological studies of cataplexy, and to study network reorganization as orexin input is lost.
SRI Authors: Srini Krishnamurthy