Controllable Persistent Atom Current of Bose-Einstein Condensates in an Optical Lattice Ring

In this paper the macroscopic quantum states of Bose-Einstein condensates in optical lattices is studied by solving the periodic Gross-Pitaevskii equation in one-dimensional geometry. It is shown that an exact solution seen to be a travelling wave of excited macroscopic quantum states resultes in a persistent atom current which can be controlled by adjusting of the barrier height of the optical periodic potential. A critical condition to generate the travelling wave is demonstrated and we moreover propose a practical experiment to realize the persistent atom current in a toroidal atom waveguide.Comment: 9 pages, 1 figure

Phase diagram of two-species Bose-Einstein condensates in an optical lattice

The exact macroscopic wave functions of two-species Bose-Einstein condensates in an optical lattice beyond the tight-binding approximation are studied by solving the coupled nonlinear Schrodinger equations. The phase diagram for superfluid and insulator phases of the condensates is determined analytically according to the macroscopic wave functions of the condensates, which are seen to be traveling matter waves.Comment: 13 pages, 2 figure

Fermi-liquid ground state in n-type copper-oxide superconductor Pr0.91Ce0.09LaCuO4-y

We report nuclear magnetic resonance studies on the low-doped n-type copper-oxide Pr_{0.91}LaCe_{0.09}CuO_{4-y} (T_c=24 K) in the superconducting state and in the normal state uncovered by the application of a strong magnetic field. We find that when the superconductivity is removed, the underlying ground state is the Fermi liquid state. This result is at variance with that inferred from previous thermal conductivity measurement and contrast with that in p-type copper-oxides with a similar doping level where high-T_c superconductivity sets in within the pseudogap phase. The data in the superconducting state are consistent with the line-nodes gap model.Comment: version to appear in Phys. Rev. Let

SUMO Modification Stabilizes Enterovirus 71 Polymerase 3D To Facilitate Viral Replication.

Accumulating evidence suggests that viruses hijack cellular proteins to circumvent the host immune system. Ubiquitination and SUMOylation are extensively studied posttranslational modifications (PTMs) that play critical roles in diverse biological processes. Cross talk between ubiquitination and SUMOylation of both host and viral proteins has been reported to result in distinct functional consequences. Enterovirus 71 (EV71), an RNA virus belonging to the family Picornaviridae, is a common cause of hand, foot, and mouth disease. Little is known concerning how host PTM systems interact with enteroviruses. Here, we demonstrate that the 3D protein, an RNA-dependent RNA polymerase (RdRp) of EV71, is modified by small ubiquitin-like modifier 1 (SUMO-1) both during infection and in vitro Residues K159 and L150/D151/L152 were responsible for 3D SUMOylation as determined by bioinformatics prediction combined with site-directed mutagenesis. Also, primer-dependent polymerase assays indicated that mutation of SUMOylation sites impaired 3D polymerase activity and virus replication. Moreover, 3D is ubiquitinated in a SUMO-dependent manner, and SUMOylation is crucial for 3D stability, which may be due to the interplay between the two PTMs. Importantly, increasing the level of SUMO-1 in EV71-infected cells augmented the SUMOylation and ubiquitination levels of 3D, leading to enhanced replication of EV71. These results together suggested that SUMO and ubiquitin cooperatively regulated EV71 infection, either by SUMO-ubiquitin hybrid chains or by ubiquitin conjugating to the exposed lysine residue through SUMOylation. Our study provides new insight into how a virus utilizes cellular pathways to facilitate its replication. IMPORTANCE: Infection with enterovirus 71 (EV71) often causes neurological diseases in children, and EV71 is responsible for the majority of fatalities. Based on a better understanding of interplay between virus and host cell, antiviral drugs against enteroviruses may be developed. As a dynamic cellular process of posttranslational modification, SUMOylation regulates global cellular protein localization, interaction, stability, and enzymatic activity. However, little is known concerning how SUMOylation directly influences virus replication by targeting viral polymerase. Here, we found that EV71 polymerase 3D was SUMOylated during EV71 infection and in vitro Moreover, the SUMOylation sites were determined, and in vitro polymerase assays indicated that mutations at SUMOylation sites could impair polymerase synthesis. Importantly, 3D is ubiquitinated in a SUMOylation-dependent manner that enhances the stability of the viral polymerase. Our findings indicate that the two modifications likely cooperatively enhance virus replication. Our study may offer a new therapeutic strategy against virus replication

A Dispersive Analysis on the f0(600)f_0(600) and f0(980)f_0(980) Resonances in γγ→π+π−,π0π0\gamma\gamma\to\pi^+\pi^-, \pi^0\pi^0 Processes

We estimate the di-photon coupling of $f_0(600)$, $f_0(980)$ and $f_2(1270)$ resonances in a coupled channel dispersive approach. The $f_0(600)$ di-photon coupling is also reinvestigated using a single channel $T$ matrix for $\pi\pi$ scattering with better analyticity property, and it is found to be significantly smaller than that of a $\bar qq$ state. Especially we also estimate the di-photon coupling of the third sheet pole located near $\bar KK$ threshold, denoted as $f_0^{III}(980)$. It is argued that this third sheet pole may be originated from a coupled channel Breit-Wigner description of the $f_0(980)$ resonance.Comment: 24 pages and 13 eps figures. A nuerical bug in previous version is fixed. Some results changed. References and new figures added. Version to appear in Phys. Rev.

Optical properties of MgCNi3MgCNi_3 in the normal state

We present the optical reflectance and conductivity spectra for non-oxide antiperovskite superconductor $MgCNi_{3}$ at different temperatures. The reflectance drops gradually over a large energy scale up to 33,000 cm$^{-1}$, with the presence of several wiggles. The reflectance has slight temperature dependence at low frequency but becomes temperature independent at high frequency. The optical conductivity shows a Drude response at low frequencies and four broad absorption features in the frequency range from 600 $cm^{-1}$ to 33,000 $cm^{-1}$. We illustrate that those features can be well understood from the intra- and interband transitions between different components of Ni 3d bands which are hybridized with C 2p bands. There is a good agreement between our experimental data and the first-principle band structure calculations.Comment: 4 pages, to be published in Phys. Rev.

Zika virus promotes CCN1 expression via the CaMKIIα-CREB pathway in astrocytes.

Zika virus (ZIKV) infection in the human central nervous system (CNS) causes Guillain-Barre syndrome, cerebellum deformity, and other diseases. Astrocytes are immune response cells in the CNS and an important component of the blood-brain barrier. Consequently, any damage to astrocytes facilitates the spread of ZIKV in the CNS. Connective tissue growth factor/Nephroblastoma overexpressed gene family 1 (CCN1), an important inflammatory factor secreted by astrocytes, is reported to regulate innate immunity and viral infection. However, the mechanism by which astrocyte viral infection affects CCN1 expression remains undefined. In this study, we demonstrate that ZIKV infection up-regulates CCN1 expression in astrocytes, thus promoting intracellular viral replication. Other studies revealed that the cAMP response element (CRE) in the CCN1 promoter is activated by the ZIKV NS3 protein. The cAMP-responsive element-binding protein (CREB), a transacting factor of the CRE, is also activated by NS3 or ZIKV. Furthermore,a specific inhibitor of CREB, i.e. SGC-CBP30, reduced ZIKV-induced CCN1 up-regulation and ZIKV replication. Moreover, co-immunoprecipitation, overexpression, and knockdown studies confirmed that the interaction between NS3 and the regulatory domain of CaMKIIα could activate the CREB pathway, thus resulting in the up-regulation of CCN1 expression and enhancement of virus replication. In conclusion, the findings of our investigations on the NS3-CaMKIIα-CREB-CCN1 pathway provide a foundation for understanding the infection mechanism of ZIKV in the CNS