Poly[diaqua­(μ2-oxalato-κ4 O 1,O 2:O 1′,O 2′)(μ2-pyrazine-2-carboxyl­ato-κ4 N 1,O:O,O′)neodymium(III)]

In the title complex, [Nd(C5H3N2O2)(C2O4)(H2O)2]n, the NdIII atom is ten-coordinated by one N atom and three O atoms from two pyrazine-2-carboxyl­ate ligands, four O atoms from two oxalate ligands and two water mol­ecules in a distorted bicapped square-anti­prismatic geometry. The two crystallographically independent oxalate ligands, each lying on an inversion center, act as bridging ligands, linking Nd atoms into an extended zigzag chain. Neighboring chains are linked by the pyrazine-2-carboxyl­ate ligands into a two-dimensional layerlike network in the (10) plane. The layers are further connected by O—H⋯O and O—H⋯N hydrogen bonds, forming a three-dimensional supra­molecular network

Reinforcement of natural rubber with core-shell structure silica-poly(Methyl Methacrylate) nanoparticles

A highly performing natural rubber/silica (NR/SiO2) nanocomposite with a SiO2 loading of 2 wt% was prepared by combining similar dissolve mutually theory with latex compounding techniques. Before polymerization, double bonds were introduced onto the surface of the SiO2 particles with the silane-coupling agent. The core-shell structure silica-poly(methyl methacrylate), SiO2-PMMA, nanoparticles were formed by grafting polymerization of MMA on the surface of the modified SiO2 particles via in situ emulsion, and then NR/SiO2 nanocomposite was prepared by blending SiO2-PMMA and PMMA-modified NR (NR-PMMA). The Fourier transform infrared spectroscopy results show that PMMA has been successfully introduced onto the surface of SiO2, which can be well dispersed in NR matrix and present good interfacial adhesion with NR phase. Compared with those of pure NR, the thermal resistance and tensile properties of NR/SiO2 nanocomposite are significantly improved

Poly[(6-carboxy­picolinato-κ3 O 2,N,O 6)(μ3-pyridine-2,6-dicarboxyl­ato-κ5 O 2,N,O 6:O 2′:O 6′)dysprosium(III)]

In the title complex, [Dy(C7H3NO4)(C7H4NO4)]n, one of the ligands is fully deprotonated while the second has lost only one H atom. Each DyIII ion is coordinated by six O atoms and two N atoms from two pyridine-2,6-dicarboxyl­ate and two 6-carboxy­picolinate ligands, displaying a bicapped trigonal-prismatic geometry. The average Dy—O bond distance is 2.40 Å, some 0.1Å longer than the corresponding Ho—O distance in the isotypic holmium complex. Adjacent DyIII ions are linked by the pyridine-2,6-dicarboxyl­ate ligands, forming a layer in (100). These layers are further connected by π–π stacking inter­actions between neighboring pyridyl rings [centroid–centroid distance = 3.827 (3) Å] and C—H⋯O hydrogen-bonding inter­actions, assembling a three-dimensional supra­molecular network. Within each layer, there are other π–π stacking inter­actions between neighboring pyridyl rings [centroid–centroid distance = 3.501 (2) Å] and O—H⋯O and C—H⋯O hydrogen-bonding inter­actions, which further stabilize the structure

A novel image encryption scheme based on Kepler’s third law and random Hadamard transform

In this paper, a novel image encryption scheme based on Kepler’s third law and random Hadamard transform is proposed to ensure the security of a digital image. First, a set of Kepler periodic sequences is generated to permutate image data, which is characteristic of the plain-image and the Kepler’s third law. Then, a random Hadamard matrix is constructed by combining the standard Hadamard matrix with the hyper-Chen chaotic system, which is used to further scramble the image coefficients when the image is transformed through random Hadamard transform. In the end, the permuted image presents interweaving diffusion based on two special matrices, which are constructed by Kepler periodic sequence and chaos system. The experimental results and performance analysis show that the proposed encrypted scheme is highly sensitive to the plain-image and external keys, and has a high security and speed, which are very suitable for secure real-time communication of image data

4-(4-Pyrid­yl)pyridinium 3′,4,4′-tricarboxy­biphenyl-3-carboxyl­ate dihydrate

In the title compound, C10H9N2 +·C16H9O8 −·2H2O, both the cation and anion possess crystallographically imposed centres of symmetry, causing the nitro­gen-bound H atom in the 4-(4-pyrid­yl)pyridinium cation and the acidic H atom of the carboxyl­ate groups at the 3 and 3′ positions in the anion to be disordered over two positions with equal occupancies. In the crystal packing, the cations, anions and water mol­ecules are connected by O—H⋯O, C—H⋯O and N—H⋯N hydrogen bonds, forming layers parallel to (20). These layer are further connected into a three-dimensional supra­molecular network by O—H⋯O hydrogen bonds involving the water mol­ecules as H-atom donors and by weak π–π stacking inter­actions between neighbouring benzene and pyridine rings, with centroid–centroid distances of 3.756 (5) Å

Bis(2,2′-bipyridine)(2-hy­droxy-2,2-diphenyl­acetato)­copper(II) nitrate dihydrate

In the title complex, [Cu(C14H11O3)(C10H8N2)2]NO3·2H2O, the CuII atom is coordinated by four N atoms from two 2,2′-bipyridine ligands and two O atoms from one benzilate ligand in a distorted octa­hedral geometry. A supra­molecular network is formed via inter­molecular O—H⋯O and C—H⋯O hydrogen-bonding inter­actions. π–π stacking inter­actions between neighboring pyridine rings are also present, the centroid—centroid distance being 3.808 (2) Å

Antiviral activity and mechanism of action of arbidol against Hantaan virus infection

Purpose: To investigate the activity and mechanism of action of arbidol against Hantaan virus (HTNV) activity by modulating inflammation via TLR-4 pathway.Methods: HUVEC cells infected with HTNV 76-118 were treated with serially diluted arbidol solutions at -2h (2 h before viral infection, pre-treatment mode), 0 h (at the same time as viral infection, simultaneous treatment mode) or 2 h (2 h after viral infection, post-treatment mode). The transcript levels of TLR4 were detected by semi-quantitative reverse transcription-PCR (RT-PCR) at 6, 12, 18, and 24 h later. The levels of iNOS and TNF-α were examined using enzyme-linked immunosorbent assay (ELISA).Results: Pre-treatment with arbidol, rather than simultaneous treatment or  post-treatment, effectively inhibited up-regulation of cellular TLR4 expression (up to 40 ± 6.1 % inhibition) and activity of supernatant iNOS induced by HTNV  infection(up to 44.1 ± 9.4 % inhibition), as well as in a LPSstimulated inflammatory endothelial cell. Arbidol decreased the elevated TNF-α levels induced by LPSstimulation.Conclusion: These results are the first evidence that arbidol modulates viral PRRs signaling and its consequential inflammatory cytokine/chemokine response during hantavirus infection.Keywords: Hantavirus, Arbidol, Toll-like receptors, inducible nitric oxide synthase, Antiviral activity, Inflammatio

Maslinic acid potentiates the anti-tumor activity of tumor necrosis factor α by inhibiting NF-κB signaling pathway

<p>Abstract</p> <p>Background</p> <p>Tumor necrosis factor alpha (TNFα) has been used to treat certain tumors in clinic trials. However, the curative effect of TNFα has been undermined by the induced-NF-κB activation in many types of tumor. Maslinic acid (MA), a pharmacological safe natural product, has been known for its important effects as anti-oxidant, anti-inflammatory, and anti-viral activities. The aim of this study was to determine whether MA potentiates the anti-tumor activity of TNFα though the regulation of NF-κB activation.</p> <p>Results</p> <p>In this study, we demonstrate that MA significantly enhanced TNFα-induced inhibition of pancreatic cancer cell proliferation, invasion, and potentiated TNFα-induced cell apoptosis by suppressing TNFα-induced NF-κB activation in a dose- and time-dependent manner. Addition of MA inhibited TNFα-induced IκBα degradation, p65 phosphorylation, and nuclear translocation. Furthermore, MA decreased the expression levels of NF-κB-regulated genes, including genes involved in tumor cell proliferation (Cyclin D1, COX-2 and c-Myc), apoptosis (Survivin, Bcl-2, Bcl-xl, XIAP, IAP-1), invasion (MMP-9 and ICAM-1), and angiogenesis (VEGF). In athymic nu/nu mouse model, we further demonstrated that MA significantly suppressed pancreatic tumor growth, induced tumor apoptosis, and inhibited NF-κB-regulated anti-apoptotic gene expression, such as Survivin and Bcl-xl.</p> <p>Conclusions</p> <p>Our data demonstrate that MA can potentiate the anti-tumor activities of TNFα and inhibit pancreatic tumor growth and invasion by activating caspase-dependent apoptotic pathway and by suppressing NF-κB activation and its downstream gene expression. Therefore, MA together with TNFα could be new promising agents in the treatment of pancreatic cancer.</p