Large magnetothermal conductivity of HoMnO_3 single crystals and its relation to the magnetic-field induced transitions of magnetic structure

We study the low-temperature heat transport of HoMnO_3 single crystals to probe the magnetic structures and their transitions induced by magnetic field. It is found that the low-T thermal conductivity (\kappa) shows very strong magnetic-field dependence, with the strongest suppression of nearly 90% and the biggest increase of 20 times of \kappa compared to its zero-field value. In particular, some ``dip"-like features show up in \kappa(H) isotherms for field along both the ab plane and the c axis. These behaviors are found to shed new light on the complex H-T phase diagram and the field-induced re-orientations of Mn^{3+} and Ho^{3+} spin structures. The results also demonstrate a significant spin-phonon coupling in this multiferroic compound.Comment: 5 pages, 4 figures, accepted for publication in Phys. Rev.

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

Possible DDˉD\bar{D} and BBˉB\bar{B} Molecular states in a chiral quark model

We perform a systematic study of the bound state problem of $D\bar{D}$ and $B\bar{B}$ systems by using effective interaction in our chiral quark model. Our results show that both the interactions of $D\bar{D}$ and $B\bar{B}$ states are attractive, which consequently result in $I^G(J^{PC})=0^+(0^{++})$ $D\bar{D}$ and $B\bar{B}$ bound states.Comment: arXiv admin note: substantial text overlap with arXiv:1204.395