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A single crystal of Bi2ZnOB2O6 has been grown with sizes up to 18 x 13 x 6 mm(3) by the top-seeded growth method for the First time with high quality. It crystallizes in the orthorhombic system, space group Pba2 with unit-cell parameters a = 10.8200(7) angstrom, b = 11.00 14(7) angstrom, c = 4.8896(3) angstrom, Z = 4, V = 582.03(6) angstrom(3). Bi2ZnOB2O6 has a three-dimensional network consisting of ZnB2O76- layers alternating with six-coordinated Bi3+ cations along the c axis. Transmission spectrum of Bi2ZnOB2O6 crystal was reported. The refractive indices of the crystal were measured by the minimum deviation technique and fitted to the Sellmeier equations. The powder second-harmonic generation (SHG) properties measured by the Kurtz-Perry method indicate that Bi2ZnOB2O6 is phasematchable.

Two new tartratoborate nonlinear optical materials, KSr[C4H2O6B(OH)2]·4H2O (KSCB) and RbSr[C4H2O6B(OH)2]·4H2O (RSCB), have been prepared through slow evaporation at room temperature. Single-crystal X-ray diffraction data reveal that KSCB crystallizes in the triclinic system, space group P1 (no. 1). It consists of KO8 polyhedra, SrO9 polyhedra, BO4 tetrahedra, tartrate molecules and H2O molecules. The isolated tartratoborate anions are connected to form a three-dimensional network structure by sharing oxygen atoms with K+ and Sr2+. The structural data show that KSCB and RSCB are isostructural and noncentrosymmetric. KSCB and RSCB produce second-harmonic generation intensities of 1.5 × KH2PO4 and 1.7 × KH2PO4, respectively, and they are both type I phase-matchable. The UV-Vis diffuse reflectance spectra of these compounds indicate that they are both transparent from 250 to 850 nm. Related infrared spectra and thermal analyses were also performed.

A new non-centrosymmetric polyborate, Li5Rb2B7O14, has been synthesized. The structure of the title compound was solved by single-crystal X-ray diffraction analysis. The infinite three-dimensional structure of Li5Rb2B7O14 is constructed from bridged LiOn (n = 4, 5, 6) and RbO10 polyhedra with two kinds of one-dimensional B–O chain fundamental building blocks through their vertex oxygen atoms. It melts congruently and exhibits a short-wavelength absorption onset at 190 nm. The feature of a short UV cut off edge is favourable in practical applications. The calculated band structure and the density of states of Li5Rb2B7O14 suggest that its indirect energy gap is 4.247 eV. The materials have also been characterized by infrared spectroscopy and thermal analysis.

Single crystals of Li3Cs2B5O10 have been synthesized and its structure determined by single-crystal X-ray diffraction. Li3Cs2B5O10 crystallizes in the non-centrosymmetric space group C222(1) ( No. 20). The structure consists of isolated B5O10 groups that are bridged by LiOn (n = 4, 5) and CsOn (n = 8, 10) polyhedra through their vertex oxygen atoms to form an infinite three-dimensional structure. Li3Cs2B5O10 melts congruently and exhibits a short-wavelength absorption onset at 175 nm. As-prepared Li3Cs2B5O10 is both non-centrosymmetric and phase matchable as supported by second harmonic generation measurements.

In the crystal structure of the title compound, C8H5N3O3, intermolecular N—H...O hydrogen bonds link molecules into centrosymmetric dimers. These dimers are, in turn, linked though weak intermolecular C—H...O and C—H...N hydrogen bonds and π–π stacking interactions, with centroid–centroid distances of 3.678 (3) Å, into a three-dimensional network.

Background: Mitogen-activated protein kinase (MAPK) signaling pathway plays an important role in response to viral infection. The aim of this study was to explore the function and mechanism of MAPK signaling pathway in enterovirus 71 (EV71) infection of human rhabdomyosarcoma (RD) cells. Methods: Apoptosis of RD cells was observed using annexin V-FITC/PI binding assay under a fluorescence microscope. Cellular RNA was extracted and transcribed to cDNA. The expressions of 56 genes of MAPK signaling pathway in EV71-infected RD cells at 8 h and 20 h after infection were analyzed by PCR array. The levels of IL-2, IL-4, IL-10, and TNF-α in the supernatant of RD cells infected with EV71 at different time points were measured by ELISA. Results: The viability of RD cells decreased obviously within 48 h after EV71 infection. Compared with the control group, EV71 infection resulted in the significantly enhanced releases of IL-2, IL-4, IL-10 and TNF-α from infected RD cells (p

Background The mitogen-activated protein kinase kinase/extracellular-signal-regulated kinase (MEK/ERK) signaling pathway is involved in viral life cycle. However, the effect of MEK/ERK pathway in enterovirus 71(EV71)-infected immature dendritic cells (iDCs) is still unclear. Methods Human peripheral blood mononuclear cells (PBMCs) were isolated and induced to generate iDCs. Unifected iDCs and EV71-infected iDCs with a multiplicity of infection (MOI = 5) were analyzed by flow cytometry. Differential gene expressions of MEK/ERK signaling pathway molecules in EV71-infected iDCs were performed by PCR arrays. The phosphorylation of MEK/ERK pathway molecules in EV71-infected iDCs preincubated without or with U0126 (20 μM) at indicated times was detected by Western blot. The concentrations of IL-1α, IL-2, IL-6, IL-12, TNF-α, IFN-α1, IFN-β and IFN-γ in culture supernatant were analyzed by the luminex fluorescent technique. Results When iDCs were infected with EV71 for 24 h, the percentage of CD80, CD83, CD86 and HLA-DR expressed on iDCs significantly increased. PCR arrays showed that gene expressions of molecules in MEK/ERK signaling pathway were remarkably upregulated in EV71-infected iDCs. EV71 infection activated both MEK1/2 and ERK1/2, which phosphorylated their downstream transcription factor c-Fos, c-Jun, c-myc and Elk1. Importantly, the treatment of U0126 significantly inhibited MEK/ERK signaling pathway molecules and severely impaired virus replication., Additionally, EV71 infection promoted the expression of son of sevenless (SOS1) and increased the secretion of IL-1α, IL-2, IL-6, IL-12, TNF-α,IFN-β and IFN-γ. Furthermore,the release of IL-1α, IL-2,IL-6 and TNF-α could be effectively suppressed by inhibitor U0126. Conclusions Our data suggest that the MEK/ERK signaling pathway plays an important role in EV71-infected iDCs and these molecules may be potential targets for the development of new anti-EV71 drugs.

Background Enterovirus 71 (EV71) infection can induce the apoptosis of infected cells. The aim of this study is to explore the effect of EV71 infection on apoptosis mechanisms in virus-infected human rhabdomyosarcoma (RD) cells. Methods The apoptosis of RD cells was examined using annexin V-FITC/PI by flow cytometry and cytokines were detected by ELISA. Cellular RNA was extracted and transcribed to cDNA. PCR array was employed to analyze the expressions of 84 apoptotic genes from EV71-infected RD cells at 8 and 20 h postinfection, respectively. In addition, the expressions of FasL, caspase, AKT2, JNK1/2, c-Jun and NF-κB proteins were detected by western blotting. Results Flow cytometry demonstrated that the apoptosis or death of EV71-infected RD cells was increased by 37.1% with a multiplicity of infection (MOI) of 5 at 20 h postinfection. The production of IL-4, IL-10 and TNF-α was enhanced by the subsequent EV71 infection. PCR array revealed significant changes in the expressions of apoptotic genes. Among 84 genes, 42 genes were down-regulated after EV71 infection at 8 h, whereas 32 genes were up-regulated at 20 h postinfection. Moreover, the ligands of TNF superfamily such as FasL, CD40L and TNF-α were significantly up-regulated and enhanced the expressions of apoptosis-related cysteine peptidases, including caspase-10, -8, -7 and -3. In addition, EV71 infection induces the phosphorylation of AKT2, JNK1/2, c-Jun and NF-κB at 20 h postinfection. Conclusion PCR array for the determination of apoptosis gene expressions is an informative assay in elucidating biological pathways. During the early stage of EV71 infection, the apoptotic process of RD cells is significantly delayed. EV71 infection can also induce the expressions of FasL, TNF-α and CD40L, which contribute to the apoptosis of RD cells.