Unification of bulk and interface electroresistive switching in oxide systems

We demonstrate that the physical mechanism behind electroresistive switching in oxide Schottky systems is electroformation, as in insulating oxides. Negative resistance shown by the hysteretic current-voltage curves proves that impact ionization is at the origin of the switching. Analyses of the capacitance-voltage and conductance-voltage curves through a simple model show that an atomic rearrangement is involved in the process. Switching in these systems is a bulk effect, not strictly confined at the interface but at the charge space region.Comment: 4 pages, 3 figures, accepted in PR

High-quality all-oxide Schottky junctions fabricated on heavily Nb-doped SrTiO3 substrates

We present a detailed investigation of the electrical properties of epitaxial La0.7Sr0.3MnO3/SrTi0.98Nb0.02O3 Schottky junctions. A fabrication process that allows reduction of the junction dimensions to current electronic device size has been employed. A heavily doped semiconductor has been used as a substrate in order to suppress its series resistance. We show that, unlike standard semiconductors, high-quality oxide-based Schottky junctions maintain a highly rectifying behavior for doping concentration of the semiconductor larger than 10^20 cm^(-3). Moreover, the junctions show hysteretic current-voltage characteristics.Comment: 10 pages, 9 figure

Quantum Communications with Compressed Decoherence Using Bright Squeezed Light

We propose a scheme for long-distance distribution of quantum entanglement in which the entanglement between qubits at intermediate stations of the channel is established by using bright light pulses in squeezed states coupled to the qubits in cavities with a weak dispersive interaction. The fidelity of the entanglement between qubits at the neighbor stations (10 km apart from each other) obtained by postselection through the balanced homodyne detection of 7 dB squeezed pulses can reach F=0.99 without using entanglement purification, at same time, the probability of successful generation of entanglement is 0.34.Comment: 4 pages, 2 figure

Implementing Unitarity in Perturbation Theory

Unitarity cannot be perserved order by order in ordinary perturbation theory because the constraint UU^\dagger=\1 is nonlinear. However, the corresponding constraint for $K=\ln U$, being $K=-K^\dagger$, is linear so it can be maintained in every order in a perturbative expansion of $K$. The perturbative expansion of $K$ may be considered as a non-abelian generalization of the linked-cluster expansion in probability theory and in statistical mechanics, and possesses similar advantages resulting from separating the short-range correlations from long-range effects. This point is illustrated in two QCD examples, in which delicate cancellations encountered in summing Feynman diagrams of are avoided when they are calculated via the perturbative expansion of $K$. Applications to other problems are briefly discussed.Comment: to appear in Phys. Rev.

SUMOylation inhibits FOXM1 activity and delays mitotic transition

The forkhead box transcription factor FOXM1 is an essential effector of G2/M-phase transition, mitosis and the DNA damage response. As such, it is frequently deregulated during tumorigenesis. Here we report that FOXM1 is dynamically modified by SUMO1 but not by SUMO2/3 at multiple sites. We show that FOXM1 SUMOylation is enhanced in MCF-7 breast cancer cells in response to treatment with epirubicin and mitotic inhibitors. Mutation of five consensus conjugation motifs yielded a SUMOylation-deficient mutant FOXM1. Conversely, fusion of the E2 ligase Ubc9 to FOXM1 generated an auto-SUMOylating mutant (FOXM1-Ubc9). Analysis of wild-type FOXM1 and mutants revealed that SUMOylation inhibits FOXM1 activity, promotes translocation to the cytoplasm and enhances APC/Cdh1-mediated ubiquitination and degradation. Further, expression of the SUMOylation-deficient mutant enhanced cell proliferation compared with wild-type FOXM1, whereas the FOXM1-Ubc9 fusion protein resulted in persistent cyclin B1 expression and slowed the time from mitotic entry to exit. In summary, our findings suggest that SUMOylation attenuates FOXM1 activity and causes mitotic delay in cytotoxic drug response

Discrete symmetries and models of flavor mixing

Evidences of a discrete symmetry behind the pattern of lepton mixing are analyzed. The program of "symmetry building" is outlined. Generic features and problems of realization of this program in consistent gauge models are formulated. The key issues include the flavor symmetry breaking, connection of mixing and masses, {\it ad hoc} prescription of flavor charges, "missing" representations, existence of new particles, possible accidental character of the TBM mixing. Various ways are considered to extend the leptonic symmetries to the quark sector and to reconcile them with Grand Unification. In this connection the quark-lepton complementarity could be a viable alternative to TBM. Observational consequences of the symmetries and future experimental tests of their existence are discussed.Comment: 14 pages, 5 figures. Talk given at the Symposium "DISCRETE 2010", 6 - 11 December 2010, La Sapienza, Rome, Ital

Selective Over-Expression of Endothelin-1 in Endothelial Cells Exacerbates Inner Retinal Edema and Neuronal Death in Ischemic Retina

The level of endothelin-1 (ET-1), a potent vasoconstrictor, was associated with retinopathy under ischemia. The effects of endothelial endothelin-1 (ET-1) over-expression in a transgenic mouse model using Tie-1 promoter (TET-1 mice) on pathophysiological changes of retinal ischemia were investigated by intraluminal insertion of a microfilament up to middle cerebral artery (MCA) to transiently block the ophthalmic artery. Two-hour occlusion and twenty-two-hour reperfusion were performed in homozygous (Hm) TET-1 mice and their non-transgenic (NTg) littermates. Presence of pyknotic nuclei in ganglion cell layer (GCL) was investigated in paraffin sections of ipsilateral (ischemic) and contralateral (non-ischemic) retinae, followed by measurement of the thickness of inner retinal layer. Moreover, immunocytochemistry of glial fibrillary acidic protein (GFAP), glutamine synthetase (GS) and aquaporin-4 (AQP4) peptides on retinal sections were performed to study glial cell reactivity, glutamate metabolism and water accumulation, respectively after retinal ischemia. Similar morphology was observed in the contralateral retinae of NTg and Hm TET-1 mice, whereas ipsilateral retina of NTg mice showed slight structural and cellular changes compared with the corresponding contralateral retina. Ipsilateral retinae of Hm TET-1 mice showed more significant changes when compared with ipsilateral retina of NTg mice, including more prominent cell death in GCL characterized by the presence of pyknotic nuclei, elevated GS immunoreactivity in Müller cell bodies and processes, increased AQP-4 immunoreactivity in Müller cell processes, and increased inner retinal thickness. Thus, over-expression of endothelial ET-1 in TET-1 mice may contribute to increased glutamate-induced neurotoxicity on neuronal cells and water accumulation in inner retina leading to edema