Lattice supersolid phase of strongly correlated bosons in an optical cavity

We numerically simulate strongly correlated ultracold bosons coupled to a high-finesse cavity field, pumped by a laser beam in the transverse direction. Assuming a weak classical optical lattice added in the cavity direction, we model this system by a generalized Bose-Hubbard model, which is solved by means of bosonic dynamical mean-field theory. The complete phase diagram is established, which contains two novel self-organized quantum phases, lattice supersolid and checkerboard solid, in addition to conventional phases such as superfluid and Mott insulator. At finite but low temperature, thermal fluctuations are found to enhance the buildup of the self-organized phases. We demonstrate that cavity-mediated long-range interactions can give rise to stable lattice supersolid and checkerboard solid phases even in the regime of strong s-wave scattering. In the presence of a harmonic trap, we discuss coexistence of these self-organized phases, as relevant to experiments.Comment: 4 pages, 3 figure

In Situ Formation of Crystallographically Oriented Semiconductor Nanowire Arrays via Selective Vaporization for Optoelectronic Applications

Direct transformation of bulk crystals to single-crystalline crystallographically oriented semiconductor nanowire arrays is presented. Real-time imaging during in situ environmental scanning electron microscopy experiment clearly demonstrates that the nanowire arrays form through a selective vaporization process with respect to the crystallography of wurtzite crystals. Due to the high quality of the prepared semiconductor nanowire arrays, photodetectors constructed from them can present superior optoelectronic performances

Scaling analysis of Schottky barriers at metal-embedded semiconducting carbon nanotube interfaces

We present an atomistic self-consistent tight-binding study of the electronic and transport properties of metal-semiconducting carbon nanotube interfaces as a function of the nanotube channel length when the end of the nanotube wire is buried inside the electrodes. We show that the lineup of the nanotube band structure relative to the metal Fermi-level depends strongly on the metal work function but weakly on the details of the interface. We analyze the length-dependent transport characteristics, which predicts a transition from tunneling to thermally-activated transport with increasing nanotube channel length.Comment: To appear in Phys.Rev.B Rapid Communications. Color figures available in PRB online versio

The role of anti-aquaporin 4 antibody in the conversion of acute brainstem syndrome to neuromyelitis optica

Background: Acute brainstem syndrome (ABS) may herald multiple sclerosis (MS), neuromyelitis optica (NMO), or occur as an isolated syndrome. The aquaporin 4 (AQP4)-specific serum autoantibody, NMO-IgG, is a biomarker for NMO. However, the role of anti-AQP4 antibody in the conversion of ABS to NMO is unclear. Methods: Thirty-one patients with first-event ABS were divided into two groups according to the presence of anti-AQP4 antibodies, their clinical features and outcomes were retrospectively analyzed. Results: Fourteen of 31 patients (45.16 %) were seropositive for NMO-IgG. The 71.43 % of anti-AQP4 (+) ABS patients converted to NMO, while only 11.76 % of anti-AQP4 (-) ABS patients progressed to NMO. Anti-AQP4 (+) ABS patients demonstrated a higher IgG index (0.68 ± 0.43 vs 0.42 ± 0.13, p < 0.01) and Kurtzke Expanded Disability Status Scale (4.64 ± 0.93 vs 2.56 ± 0.81, p < 0.01) than anti-AQP4 (-) ABS patients. Area postrema clinical brainstem symptoms occurred more frequently in anti-AQP4 (+) ABS patients than those in anti-AQP4 (-) ABS patients (71.43 % vs 17.65 %, p = 0.004). In examination of magnetic resonance imaging (MRI), the 78.57 % of anti-AQP4 (+) ABS patients had medulla-predominant involvements in the sagittal view and dorsal-predominant involvements in the axial view. Conclusions: ABS represents an inaugural or limited form of NMO in a high proportion of anti-AQP4 (+) patients

PP1A-Mediated Dephosphorylation Positively Regulates YAP2 Activity

Background: The Hippo/MST1 signaling pathway plays an important role in the regulation of cell proliferation and apoptosis. As a major downstream target of the Hippo/MST1 pathway, YAP2 (Yes-associated protein 2) functions as a transcriptional cofactor that has been implicated in many biological processes, including organ size control and cancer development. MST1/Lats kinase inhibits YAP2’s nuclear accumulation and transcriptional activity through inducing the phosphorylation at serine 127 and the sequential association with 14-3-3 proteins. However, the dephosphorylation of YAP2 is not fully appreciated. Methodology/Principal Findings: In the present study, we demonstrate that PP1A (catalytic subunit of protein phosphatase-1) interacts with and dephosphorylates YAP2 in vitro and in vivo, and PP1A-mediated dephosphorylation induces the nuclear accumulation and transcriptional activation of YAP2. Inhibition of PP1 by okadiac acid (OA) increases the phosphorylation at serine 127 and cytoplasmic translocation of YAP2 proteins, thereby mitigating its transcription activity. PP1A expression enhances YAP2’s pro-survival capability and YAP2 knockdown sensitizes ovarian cancer cells to cisplatin treatment. Conclusions/Significance: Our findings define a novel molecular mechanism that YAP2 is positively regulated by PP1mediate

An essential role for the IL-2 receptor in Treg cell function

Regulatory T cells (Treg cells), which have abundant expression of the interleukin 2 receptor (IL-2R), are reliant on IL-2 produced by activated T cells. This feature indicates a key role for a simple network based on the consumption of IL-2 by Treg cells in their suppressor function. However, congenital deficiency in IL-2R results in reduced expression of the Treg cell lineage–specification factor Foxp3, which has confounded experimental efforts to understand the role of IL-2R expression and signaling in the suppressor function of Treg cells. Using genetic gain- and loss-of-function approaches, we found that capture of IL-2 was dispensable for the control of CD4+ T cells but was important for limiting the activation of CD8+ T cells, and that IL-2R-dependent activation of the transcription factor STAT5 had an essential role in the suppressor function of Treg cells separable from signaling via the T cell antigen receptor