Neutrino emission from a GRB afterglow shock during an inner supernova shock breakout

The observations of a nearby low-luminosity gamma-ray burst (GRB) 060218 associated with supernova SN 2006aj may imply an interesting astronomical picture where a supernova shock breakout locates behind a relativistic GRB jet. Based on this picture, we study neutrino emission for early afterglows of GRB 060218-like GRBs, where neutrinos are expected to be produced from photopion interactions in a GRB blast wave that propagates into a dense wind. Relativistic protons for the interactions are accelerated by an external shock, while target photons are basically provided by the incoming thermal emission from the shock breakout and its inverse-Compton scattered component. Because of a high estimated event rate of low-luminosity GRBs, we would have more opportunities to detect afterglow neutrinos from a single nearby GRB event of this type by IceCube. Such a possible detection could provide evidence for the picture described above.Comment: 6 pages, 2 figures, accepted for publication in MNRA

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

Short-time critical dynamics at perfect and non-perfect surface

We report Monte Carlo simulations of critical dynamics far from equilibrium on a perfect and non-perfect surface in the 3d Ising model. For an ordered initial state, the dynamic relaxation of the surface magnetization, the line magnetization of the defect line, and the corresponding susceptibilities and appropriate cumulant is carefully examined at the ordinary, special and surface phase transitions. The universal dynamic scaling behavior including a dynamic crossover scaling form is identified. The exponent $\beta_1$ of the surface magnetization and $\beta_2$ of the line magnetization are extracted. The impact of the defect line on the surface universality classes is investigated.Comment: 11figure

New Approach on the General Shape Equation of Axisymmetric Vesicles

The general Helfrich shape equation determined by minimizing the curvature free energy describes the equilibrium shapes of the axisymmetric lipid bilayer vesicles in different conditions. It is a non-linear differential equation with variable coefficients. In this letter, by analyzing the unique property of the solution, we change this shape equation into a system of the two differential equations. One of them is a linear differential equation. This equation system contains all of the known rigorous solutions of the general shape equation. And the more general constraint conditions are found for the solution of the general shape equation.Comment: 8 pages, LaTex, submit to Mod. Phys. Lett.

Discussion on Event Horizon and Quantum Ergosphere of Evaporating Black Holes in a Tunnelling Framework

In this paper, with the Parikh-Wilczek tunnelling framework the positions of the event horizon of the Vaidya black hole and the Vaidya-Bonner black hole are calculated respectively. We find that the event horizon and the apparent horizon of these two black holes correspond respectively to the two turning points of the Hawking radiation tunnelling barrier. That is, the quantum ergosphere coincides with the tunnelling barrier. Our calculation also implies that the Hawking radiation comes from the apparent horizon.Comment: 8 page

Intrinsic Percolative Superconductivity in Heavily Overdoped High Temperature Superconductors

Magnetic measurements on heavily overdoped $La_{2-x}Sr_xCuO_4$, $Tl_2Ba_2CuO_6$, $Bi_2Sr_2CuO_6$ and $Bi_2Sr_2CaCu_2O_8$ single crystals reveal a new type magnetization hysteresis loops characterized by the vanishing of usual central peak near zero field. Since this effect has been observed in various systems with very different structural details, it reflects probably a generic behavior for all high temperature superconductors. This easy penetration of magnetic flux can be understood in the picture of percolative superconductivity due to the inhomogeneous electronic state in heavily overdoped regime.Comment: 4 pages, 5 figure

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