Ballistic Thermal Rectification in Asymmetric Three-Terminal Mesoscopic Dielectric Systems

By coupling the asymmetric three-terminal mesoscopic dielectric system with a temperature probe, at low temperature, the ballistic heat flux flow through the other two asymmetric terminals in the nonlinear response regime is studied based on the Landauer formulation of transport theory. The thermal rectification is attained at the quantum regime. It is a purely quantum effect and is determined by the dependence of the ratio $\tau_{RC}(\omega)/\tau_{RL}(\omega)$ on $\omega$, the phonon's frequency. Where $\tau_{RC}(\omega)$ and $\tau_{RL}(\omega)$ are respectively the transmission coefficients from two asymmetric terminals to the temperature probe, which are determined by the inelastic scattering of ballistic phonons in the temperature probe. Our results are confirmed by extensive numerical simulations.Comment: 10 pages, 4 figure

IM3D: A parallel Monte Carlo code for efficient simulations of primary radiation displacements and damage in 3D geometry

SRIM-like codes have limitations in describing general 3D geometries, for modeling radiation displacements and damage in nanostructured materials. A universal, computationally efficient and massively parallel 3D Monte Carlo code, IM3D, has been developed with excellent parallel scaling performance. IM3D is based on fast indexing of scattering integrals and the SRIM stopping power database, and allows the user a choice of Constructive Solid Geometry (CSG) or Finite Element Triangle Mesh (FETM) method for constructing 3D shapes and microstructures. For 2D films and multilayers, IM3D perfectly reproduces SRIM results, and can be ∼10[superscript 2] times faster in serial execution and > 10[superscript 4] times faster using parallel computation. For 3D problems, it provides a fast approach for analyzing the spatial distributions of primary displacements and defect generation under ion irradiation. Herein we also provide a detailed discussion of our open-source collision cascade physics engine, revealing the true meaning and limitations of the “Quick Kinchin-Pease” and “Full Cascades” options. The issues of femtosecond to picosecond timescales in defining displacement versus damage, the limitation of the displacements per atom (DPA) unit in quantifying radiation damage (such as inadequacy in quantifying degree of chemical mixing), are discussed.National Natural Science Foundation (China) (Grant 11275229)National Natural Science Foundation (China) (Grant 11475215)National Natural Science Foundation (China) (Grant NSAF U1230202)National Natural Science Foundation (China) (Grant 11534012)National Basic Research Program of China (973 Program) (Grant 2012CB933702)Hefei Center for Physical Science and Technology (Grant 2012FXZY004)Chinese Academy of Sciences (Hefei Institutes of Physical Science (CASHIPS) Director Grant)National Science Foundation (U.S.) (DMR-1410636)National Science Foundation (U.S.) (DMR-1120901

VOLTAGE FLICKER ASSESSMENT OF A WEAK SYSTEM INTEGRATED WIND FARM

ABSTRAC

(Z)3,4,5,4'-trans-tetramethoxystilbene, a new analogue of resveratrol, inhibits gefitinb-resistant non-small cell lung cancer via selectively elevating intracellular calcium level.

Calcium is a second messenger which is required for regulation of many cellular processes. However, excessive elevation or prolonged activation of calcium signaling would lead to cell death. As such, selectively regulating calcium signaling could be an alternative approach for anti-cancer therapy. Recently, we have identified an effective analogue of resveratrol, (Z)3,4,5,4′-trans-tetramethoxystilbene (TMS) which selectively elevated the intracellular calcium level in gefitinib-resistant (G-R) non-small-cell lung cancer (NSCLC) cells. TMS exhibited significant inhibitory effect on G-R NSCLC cells, but not other NSCLC cells and normal lung epithelial cells. The phosphorylation and activation of EGFR were inhibited by TMS in G-R cells. TMS induced caspase-independent apoptosis and autophagy by directly binding to SERCA and causing endoplasmic reticulum (ER) stress and AMPK activation. Proteomics analysis also further confirmed that mTOR pathway, which is the downstream of AMPK, was significantly suppressed by TMS. JNK, the cross-linker of ER stress and mTOR pathway was significantly activated by TMS. In addition, the inhibition of JNK activation can partially block the effect of TMS. Taken together, TMS showed promising anti-cancer activity by mediating calcium signaling pathway and inducing apoptosis as well as autophagy in G-R NSCLC cells, providing strategy in designing multi-targeting drug for treating G-R patients