Topology by Dissipation: Majorana Bosons in Metastable Quadratic Markovian Dynamics.

Majorana bosons, that is, tight bosonic analogs of the Majorana fermionic quasiparticles of condensed-matter physics, are forbidden for gapped free bosonic matter within a standard Hamiltonian scenario. We show how the interplay between dynamical metastability and nontrivial bulk topology makes their emergence possible in noninteracting bosonic chains undergoing Markovian dissipation. This leads to a distinctive form of topological metastability, whereby a conserved Majorana boson localized on one edge is paired, in general, with a symmetry generator localized on the opposite edge. We argue that Majorana bosons are robust against disorder and identifiable by signatures in the zero-frequency steady-state power spectrum. Our results suggest that symmetry-protected topological phases for free bosons may arise in transient metastable regimes, which persist over practical timescales.

Exploring itinerant states in divalent hexaborides using rare-earth L edge resonant inelastic x-ray scattering.

We present a study of resonant inelastic x-ray scattering (RIXS) spectra collected at the rare-earth L edges of divalent hexaborides YbB6 and EuB6. In both systems, RIXS-active features are observed at two distinct resonances separated by [Formula: see text] eV in incident energy, with angle-dependence suggestive of distinct photon scattering processes. RIXS spectra collected at the divalent absorption peak resemble the unoccupied 5d density of states calculated using density functional theory. We discuss possible origins of this correspondence including a scenario which changes the 4f  valence. In addition, anomalous resonant scattering is observed at higher incident energy, where no corresponding absorption feature is present. Our results demonstrate the potential for L-edge RIXS to assess the itinerant-state properties of f -electron materials.

Adenovirus-mediated inhibition of NF-kappaB confers chemo-sensitization and apoptosis in prostate cancer cells.

Acquirement of multi-drug resistance by tumor cells represents a major obstacle in the management of prostate cancer. Such resistance was demonstrated in the androgen-independent DU-145 cells in response to paclitaxel and the mechanisms by which these cell develops resistance was not understood. The objective of this study was to examine whether abrogation of the constitutively active NF-kappaB in the chemoresistant, androgen independent DU-145 prostate cancer cells will enhance their sensitivity to cytototoxic agents. Inhibition of NF-kappaB by a dominant negative super-repressor IkappaB mutant adenoviral construct enhanced the apoptotic potentials of paclitaxel and rhTNF-alpha in these cells. Using reporter assays and RT-PCR analysis, we demonstrate that paclitaxel-induced cell death was associated with an increase in NF-kappaB activation and MDR-1 gene expression. Abrogation of these effects by the dominant negative IkappaB adenoviral construct suggests that induction and/or constitutive activation of NF-kappaB can block the paclitaxel-induced apoptotic signaling pathways in this cell line, possibly by increasing the expression of anti-apoptotic and MDR-1 gene products, leading to development of chemoresistance in these cells. We conclude that inhibition of NF-kappaB activation may have therapeutic implications for prostate cancer.