Semiclassical Theory of Quantum Chaotic Transport: Phase-Space Splitting, Coherent Backscattering and Weak Localization

We investigate transport properties of quantized chaotic systems in the short wavelength limit. We focus on non-coherent quantities such as the Drude conductance, its sample-to-sample fluctuations, shot-noise and the transmission spectrum, as well as coherent effects such as weak localization. We show how these properties are influenced by the emergence of the Ehrenfest time scale \tE. Expressed in an optimal phase-space basis, the scattering matrix acquires a block-diagonal form as \tE increases, reflecting the splitting of the system into two cavities in parallel, a classical deterministic cavity (with all transmission eigenvalues either 0 or 1) and a quantum mechanical stochastic cavity. This results in the suppression of the Fano factor for shot-noise and the deviation of sample-to-sample conductance fluctuations from their universal value. We further present a semiclassical theory for weak localization which captures non-ergodic phase-space structures and preserves the unitarity of the theory. Contrarily to our previous claim [Phys. Rev. Lett. 94, 116801 (2005)], we find that the leading off-diagonal contribution to the conductance leads to the exponential suppression of the coherent backscattering peak and of weak localization at finite \tE. This latter finding is substantiated by numerical magnetoconductance calculations.Comment: Typos in central eqns corrected (this paper supersedes cond-mat/0509186) 20page

Counselor Educators Lean-In to Walk the Talk: A Team Approach to Strengthening Faculty Multicultural Sensitivity

This session offers an innovative approach for engaging faculty in the development and deepening of their own multicultural sensitivity, for improving pedagogy, and in turn promoting second-order change within students as they engage with multicultural competencies. Broader systemic issues are also addressed given the university\u27s contextual setting as a faith-based, primarily Caucasian institution

The Hyperfine Spin Splittings In Heavy Quarkonia

The hyperfine spin splittings in heavy quarkonia are studied using the recently developed renormalization group improved spin-spin potential which is independent of the scale parameter $\mu$. The calculated energy difference between the $J/\psi$ and the $\eta_c$ fits the experimental data well, while the predicted energy difference $\Delta M_p$ between the center of the gravity of $1^3P_{0,1,2}$ states and the $1^1P_1$ state of charmonium has the correct sign but is somewhat larger than the experimental data. This is not surprising since there are several other contributions to $\Delta M_p$, which we discuss, that are of comparable size ($\sim 1$ MeV) that should be included, before precise agreement with the data can be expected. The mass differences of the $\psi'-\eta_c'$, $\Upsilon(1S)-\eta_b$, $\Upsilon(2S)-\eta_b'$, and $B_c^*-B_c$ are also predicted.Comment: 17 page

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts