Image tag completion by local learning

The problem of tag completion is to learn the missing tags of an image. In this paper, we propose to learn a tag scoring vector for each image by local linear learning. A local linear function is used in the neighborhood of each image to predict the tag scoring vectors of its neighboring images. We construct a unified objective function for the learning of both tag scoring vectors and local linear function parame- ters. In the objective, we impose the learned tag scoring vectors to be consistent with the known associations to the tags of each image, and also minimize the prediction error of each local linear function, while reducing the complexity of each local function. The objective function is optimized by an alternate optimization strategy and gradient descent methods in an iterative algorithm. We compare the proposed algorithm against different state-of-the-art tag completion methods, and the results show its advantages

Candidate chiral doublet bands in the odd-odd nucleus 126^{126}Cs

The candidate chiral doublet bands recently observed in $^{126}$Cs have been extended to higher spins, several new linking transitions between the two partner members of the chiral doublet bands are observed, and $\gamma$$-$intensities related to the chiral doublet bands are presented by analyzing the $\gamma$$-$$\gamma$ coincidence data collected earlier at the NORDBALL through the $^{116}$Cd$($$^{14}$N, 4n$)$$^{126}$Cs reaction at a beam energy of 65 MeV. The intraband $B(M1)/B(E2)$ and interband $B(M1)_{in}/B(M1)_{out}$ ratios and the energy staggering parameter, S(I), have been deduced for these doublet bands. The results are found to be consistent with the chiral interpretation for the two structures. Furthermore, the observation of chiral doublet bands in $^{126}$Cs together with those in $^{124}$Cs, $^{128}$Cs, $^{130}$Cs and $^{132}$Cs also indicates that the chiral conditions do not change rapidly with decreasing neutron number in these odd-odd Cesium isotopes

Quantum speed limit for relativistic spin-0 and spin-1 bosons on commutative and noncommutative planes

Quantum speed limits of relativistic charged spin-0 and spin-1 bosons in the background of a homogeneous magnetic field are studied on both commutative and oncommutative planes. We show that, on the commutative plane, the average speeds of wave packets along the radial direction during the interval in which a quantum state evolving from an initial state to the orthogonal final one can not exceed the speed of light, regardless of the intensities of the magnetic field. However, due to the noncommutativity, the average speeds of the wave packets on noncommutative plane will exceed the speed of light in vacuum provided the intensity of the magnetic field is strong enough. It is a clear signature of violating Lorentz invariance in quantum mechanics region.Comment: 8 pages, no figures. arXiv admin note: text overlap with arXiv:1702.0316

Quantum broadcast communication

Broadcast encryption allows the sender to securely distribute his/her secret to a dynamically changing group of users over a broadcast channel. In this paper, we just consider a simple broadcast communication task in quantum scenario, which the central party broadcasts his secret to multi-receiver via quantum channel. We present three quantum broadcast communication schemes. The first scheme utilizes entanglement swapping and Greenberger-Horne-Zeilinger state to realize a task that the central party broadcasts his secret to a group of receivers who share a group key with him. In the second scheme, based on dense coding, the central party broadcasts the secret to multi-receiver who share each of their authentication key with him. The third scheme is a quantum broadcast communication scheme with quantum encryption, which the central party can broadcast the secret to any subset of the legal receivers

Multiparty simultaneous quantum identity authentication based on entanglement swapping

We present a multiparty simultaneous quantum identity authentication protocol based on entanglement swapping. In our protocol, the multi-user can be authenticated by a trusted third party simultaneously

ZIKV infection activates the IRE1-XBP1 and ATF6 pathways of unfolded protein response in neural cells.

BACKGROUND: Many viruses depend on the extensive membranous network of the endoplasmic reticulum (ER) for their translation, replication, and packaging. Certain membrane modifications of the ER can be a trigger for ER stress, as well as the accumulation of viral protein in the ER by viral infection. Then, unfolded protein response (UPR) is activated to alleviate the stress. Zika virus (ZIKV) is a mosquito-borne flavivirus and its infection causes microcephaly in newborns and serious neurological complications in adults. Here, we investigated ER stress and the regulating model of UPR in ZIKV-infected neural cells in vitro and in vivo. METHODS: Mice deficient in type I and II IFN receptors were infected with ZIKV via intraperitoneal injection and the nervous tissues of the mice were assayed at 5 days post-infection. The expression of phospho-IRE1, XBP1, and ATF6 which were the key markers of ER stress were analyzed by immunohistochemistry assay in vivo. Additionally, the nuclear localization of XBP1s and ATF6n were analyzed by immunohistofluorescence. Furthermore, two representative neural cells, neuroblastoma cell line (SK-N-SH) and astrocytoma cell line (CCF-STTG1), were selected to verify the ER stress in vitro. The expression of BIP, phospho-elF2α, phospho-IRE1, and ATF6 were analyzed through western blot and the nuclear localization of XBP1s was performed by confocal immunofluorescence microscopy. RT-qPCR was also used to quantify the mRNA level of the UPR downstream genes in vitro and in vivo. RESULTS: ZIKV infection significantly upregulated the expression of ER stress markers in vitro and in vivo. Phospho-IRE1 and XBP1 expression significantly increased in the cerebellum and mesocephalon, while ATF6 expression significantly increased in the mesocephalon. ATF6n and XBP1s were translocated into the cell nucleus. The levels of BIP, ATF6, phospho-elf2α, and spliced xbp1 also significantly increased in vitro. Furthermore, the downstream genes of UPR were detected to investigate the regulating model of the UPR during ZIKV infection in vitro and in vivo. The transcriptional levels of atf4, gadd34, chop, and edem-1 in vivo and that of gadd34 and chop in vitro significantly increased. CONCLUSION: Findings in this study demonstrated that ZIKV infection activates ER stress in neural cells. The results offer clues to further study the mechanism of neuropathogenesis caused by ZIKV infection