Gluon GPDs and Exclusive Photoproduction of a Quarkonium in Forward Region

Forward photoproduction of $J/\psi$ can be used to extract Generalized Parton Distributions(GPD's) of gluons. We analyze the process at twist-3 level and study relevant classifications of twist-3 gluon GPD's. At leading power or twist-2 level the produced $J/\psi$ is transversely polarized. We find that at twist-3 the produced $J/\psi$ is longitudinally polarized. Our study shows that in high energy limit the twist-3 amplitude is only suppressed by the inverse power of the heavy quark mass relatively to the twist-2 amplitude. This indicates that the power correction to the cross-section of unpolarized $J/\psi$ can have a sizeable effect. We have also derived the amplitude of the production of $h_c$ at twist-3, but the result contains end-point singularities. The production of other quarkonia has been briefly discussed.Comment: Discussions of results are adde

Measurement of the c-axis optical reflectance of AFe2_2As2_2 (A=Ba, Sr) single crystals: Evidence of different mechanisms for the formation of two energy gaps

We present the c-axis optical reflectance measurement on single crystals of BaFe$_2$As$_2$ and SrFe$_2$As$_2$, the parent compounds of FeAs based superconductors. Different from the ab-plane optical response where two distinct energy gaps were observed in the SDW state, only the smaller energy gap could be seen clearly for \textbf{E}$\parallel$c-axis. The very pronounced energy gap structure seen at a higher energy scale for \textbf{E}$\parallel$ab-plane is almost invisible. We propose a novel picture for the band structure evolution across the SDW transition and suggest different driving mechanisms for the formation of the two energy gaps.Comment: 4 page

Effect of nonlinear filters on detrended fluctuation analysis

We investigate how various linear and nonlinear transformations affect the scaling properties of a signal, using the detrended fluctuation analysis (DFA). Specifically, we study the effect of three types of transforms: linear, nonlinear polynomial and logarithmic filters. We compare the scaling properties of signals before and after the transform. We find that linear filters do not change the correlation properties, while the effect of nonlinear polynomial and logarithmic filters strongly depends on (a) the strength of correlations in the original signal, (b) the power of the polynomial filter and (c) the offset in the logarithmic filter. We further investigate the correlation properties of three analytic functions: exponential, logarithmic, and power-law. While these three functions have in general different correlation properties, we find that there is a broad range of variable values, common for all three functions, where they exhibit identical scaling behavior. We further note that the scaling behavior of a class of other functions can be reduced to these three typical cases. We systematically test the performance of the DFA method in accurately estimating long-range power-law correlations in the output signals for different parameter values in the three types of filters, and the three analytic functions we consider.Comment: 12 pages, 7 figure

Integrable impurities in Hubbard chain with the open boundary condition

The Kondo problem of two impurities in 1D strongly correlated electron system within the framework of the open boundary Hubbard chain is solved and the impurities, coupled to the ends of the electron system, are introduced by their scattering matrices with electrons so that the boundary matrices satisfy the reflecting integrability condition. The finite size correction of the ground state energy is obtained due to the impurities. Exact expressions for the low temperature specific heat contributed by the charge and spin parts of the magnetic impurities are derived. The Pauli susceptibility and the Kondo temperature are given explicitly. The Kondo temperature is inversely proportional to the density of electrons.Comment: 6 pages, Revtex, To appear in Europhysics Letter

Evidence for the band broadening across the ferromagnetic transition in Cr1/3_{1/3}NbSe2_2

The electronic structure of Cr$_{1/3}$NbSe$_2$ is studied via optical spectroscopy. We observe two low-energy interband transitions in the paramagnetic phase, which split into four peaks as the compound enters the ferromagnetic state. The band structure calculation indicates the four peaks are interband transitions to the spin up Cr e$_g$ states. We show that the peak splitting below the Curie temperature is \emph{not} due to the exchange splitting of spin up and down bands, but directly reflects a band broadening effect in Cr-derived states upon the spontaneous ferromagnetic ordering.Comment: 6 pages, 5 figures, to be published 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

Tick-borne encephalitis virus induces chemokine RANTES expression via activation of IRF-3 pathway.

BACKGROUND: Tick-borne encephalitis virus (TBEV) is one of the most important flaviviruses that targets the central nervous system (CNS) and causes encephalitides in humans. Although neuroinflammatory mechanisms may contribute to brain tissue destruction, the induction pathways and potential roles of specific chemokines in TBEV-mediated neurological disease are poorly understood. METHODS: BALB/c mice were intracerebrally injected with TBEV, followed by evaluation of chemokine and cytokine profiles using protein array analysis. The virus-infected mice were treated with the CC chemokine antagonist Met-RANTES or anti-RANTES mAb to determine the role of RANTES in affecting TBEV-induced neurological disease. The underlying signaling mechanisms were delineated using RANTES promoter luciferase reporter assay, siRNA-mediated knockdown, and pharmacological inhibitors in human brain-derived cell culture models. RESULTS: In a mouse model, pathological features including marked inflammatory cell infiltrates were observed in brain sections, which correlated with a robust up-regulation of RANTES within the brain but not in peripheral tissues and sera. Antagonizing RANTES within CNS extended the survival of mice and reduced accumulation of infiltrating cells in the brain after TBEV infection. Through in vitro studies, we show that virus infection up-regulated RANTES production at both mRNA and protein levels in human brain-derived cell lines and primary progenitor-derived astrocytes. Furthermore, IRF-3 pathway appeared to be essential for TBEV-induced RANTES production. Site mutation of an IRF-3-binding motif abrogated the RANTES promoter activity in virus-infected brain cells. Moreover, IRF-3 was activated upon TBEV infection as evidenced by phosphorylation of TBK1 and IRF-3, while blockade of IRF-3 activation drastically reduced virus-induced RANTES expression. CONCLUSIONS: Our findings together provide insights into the molecular mechanism underlying RANTES production induced by TBEV, highlighting its potential importance in the process of neuroinflammatory responses to TBEV infection

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