20 research outputs found

    Manipulating disordered plasmonic systems by external cavity with transition from broadband absorption to reconfigurable reflection

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    Disordered biostructures are ubiquitous in nature, usually generating white or black colours due to their broadband optical response and robustness to perturbations. Through judicious design, disordered nanostructures have been realised in artificial systems, with unique properties for light localisation, photon transportation and energy harvesting. On the other hand, the tunability of disordered systems with a broadband response has been scarcely explored. Here, we achieve the controlled manipulation of disordered plasmonic systems, realising the transition from broadband absorption to tunable reflection through deterministic control of the coupling to an external cavity. Starting from a generalised model, we realise disordered systems composed of plasmonic nanoclusters that either operate as a broadband absorber or with a reconfigurable reflection band throughout the visible. Not limited to its significance for the further understanding of the physics of disorder, our disordered plasmonic system provides a novel platform for various practical application such as structural colour patterning

    The Alpha-1 Subunit of the Na<sup>+</sup>/K<sup>+</sup>-ATPase (ATP1A1) Is a Host Factor Involved in the Attachment of Porcine Epidemic Diarrhea Virus

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    Porcine epidemic diarrhea (PED) is an acute and severe atrophic enteritis caused by porcine epidemic diarrhea virus (PEDV) that infects pigs and makes huge economic losses to the global swine industry. Previously, researchers have believed that porcine aminopeptidase-N (pAPN) was the primary receptor for PEDV, but it has been found that PEDV can infect pAPN knockout pigs. Currently, the functional receptor for PEDV remains unspecified. In the present study, we performed virus overlay protein binding assay (VOPBA), found that ATP1A1 was the highest scoring protein in the mass spectrometry results, and confirmed that the CT structural domain of ATP1A1 interacts with PEDV S1. First, we investigated the effect of ATP1A1 on PEDV replication. Inhibition of hosts ATP1A1 protein expression using small interfering RNA (siRNAs) significantly reduced the cells susceptibility to PEDV. The ATP1A1-specific inhibitors Ouabain (a cardiac steroid) and PST2238 (a digitalis toxin derivative), which specifically bind ATP1A1, could block the ATP1A1 protein internalization and degradation, and consequently reduce the infection rate of host cells by PEDV significantly. Additionally, as expected, overexpression of ATP1A1 notably enhanced PEDV infection. Next, we observed that PEDV infection of target cells resulted in upregulation of ATP1A1 at the mRNA and protein levels. Furthermore, we found that the host protein ATP1A1 was involved in PEDV attachment and co-localized with PEDV S1 protein in the early stage of infection. In addition, pretreatment of IPEC-J2 and Vero-E6 cells with ATP1A1 mAb significantly reduced PEDV attachment. Our observations provided a perspective on identifying key factors in PEDV infection, and may provide valuable targets for PEDV infection, PEDV functional receptor, related pathogenesis, and the development of new antiviral drugs

    Genetic characterization of 11 porcine reproductive and respiratory syndrome virus isolates in South China from 2014 to 2015

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    Abstract Background Porcine reproductive and respiratory syndrome (PRRS) has leaded to an enormous loss per year to the swine industry, its etiology porcine reproductive and respiratory syndrome virus (PRRSV) is a highly mutated virus in pigs. To fully understand the genetic characteristics of PRRSV genome in South China, this study collected the lung samples infected with PRRSV in Guangdong and Hainan province from 2014 to 2015 and tried to isolate the PRRSV. Finally, the complete genomes of isolated strains were sequenced and analyzed. Methods Virus isolation was performed in MARC-145 cells. The 13 fragments of PRRSV genome were amplified by RT-PCR and the complete PRRSV genome sequence was obtained by SeqMan program of DNASTAR7.0 software. Nucleotide and deduced amino acid (AA) sequences of NSP2 and ORF5 were aligned using the MegAlign program of DNASTAR7.0 software to determine sequence homology. A phylogenetic tree was constructed using MEGA5.2 software with the neighbor-joining method to analyze the evolutionary relationship. Results 11 PRRSV strains were isolated in South China from 2014 to 2015. All the isolated strains clustered into subgenotype V along with the HP-PRRSV representative strains JXA1, HuN4 and JXwn06. The subgenotype V was furtherly divided into two groups. AA sequence alignment analysis indicated that all the isolated strains had 1 AA deletion and 29 AA continuous deletion at position 481 and 533-561. Notably, GDHY strain had another 120 AA continuous deletion at position 629-748. All the isolated strains had an A137S mutation in the residue A137 of GP5 which was considered to differentiate vaccine strains. All the isolated strains had a L39I mutation in the primary neutralizing epitope (PNE) of GP5. Except GDHZ had a N34T mutation, all the other isolated strains had conserved N30, N44 and N51 glycosylation sites in the four potential N-glycosylation sites (N30, N34, N44 and N51) of GP5. Conclusions Our study showed that the prevalent strains in this region were highly pathogenic PRRS virus-like. Moreover, one new strain having another 120 amino acids continuous deletion except the discontinuous 30 (29+1) amino acids deletion in NSP2 region had emerged. Besides, the isolated strains had extensive amino acids substitutions in the putative signal, extravirion and intravirion regions of GP5. These results showed that PRRSV has undergone extensive variation in South China, providing some theoretical basis for researching effective vaccince to better controling the PRRSV in this area

    Disorder‐Induced Material‐Insensitive Optical Response in Plasmonic Nanostructures: Vibrant Structural Colors from Noble Metals

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    Materials show various responses to incident light, owing to their unique dielectric functions. A well-known example is the distinct colors displayed by metals, providing probably the simplest method to identify gold, silver, and bronze since ancient times. With the advancement of nanotechnology, optical structures with feature sizes smaller than the optical wavelength have been routinely achieved. In this regime, the optical response is also determined by the geometry of the nanostructures, inspiring flourishing progress in plasmonics, photonic crystals, and metamaterials. Nevertheless, the nature of the materials still plays a decisive role in light–matter interactions, and this material-dependent optical response is widely accepted as a norm in nanophotonics. Here, a counterintuitive system—plasmonic nanostructures composed of different materials but exhibiting almost identical reflection—is proposed and realized. The geometric disorder embedded in the system overwhelms the contribution of the material properties to the electrodynamics. Both numerical simulations and experimental results provide concrete evidence of the insensitivity of the optical response to different plasmonic materials. The same optical response is preserved with various materials, providing great flexibility of freedom in material selection. As a result, the proposed configuration may shed light on novel applications ranging from Raman spectroscopy, photocatalysis, to nonlinear optics

    Effect of Fluoride Ions on the Surface Dissolution of Vanadium-Bearing Biotite

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    In shale vanadium ore, vanadium is mainly formed as a low-V(III) homogeneous phase to partially replace Si and exists in the lattice structure of aluminosilicate minerals such as biotite. During the acid leaching of shale vanadium ore, an activator is needed to effectively extract vanadium. Using biotite as a tetrahedral structure doped with Aluminum-Silicon tetrahedron structure, the interaction between leaching-agent ions (H+), activator ions (F&minus;), and vanadium-containing biotite surface was discussed by DFT quantum chemical calculations. The dissolution behavior of activator fluoride ions on the surface of vanadium-bearing biotite during sulfuric acid leaching was revealed. According to the simulated leaching results, the oxygen on the biotite surface first absorbed hydrogen ions to undergo complete hydroxylation, and then combined with hydrogen ions to form water molecules. However, in the presence of activator (NaF), fluoride ions were adsorbed on the surface cations, which catalyzed the formation of water molecules and promoted the dissolution of surface cations. SEM&ndash;EDS analysis showed that the surface of vanadium-bearing minerals became very irregular, and the number of voids and cracks greatly increased. At the same time, XPS showed that the addition of activator fluoride ions destroyed the Al-O tetrahedron structure. Many Al and V atoms dissolved in the solution, which improved the leaching rate of vanadium

    Effect of Fluoride Ions on the Surface Dissolution of Vanadium-Bearing Biotite

    No full text
    In shale vanadium ore, vanadium is mainly formed as a low-V(III) homogeneous phase to partially replace Si and exists in the lattice structure of aluminosilicate minerals such as biotite. During the acid leaching of shale vanadium ore, an activator is needed to effectively extract vanadium. Using biotite as a tetrahedral structure doped with Aluminum-Silicon tetrahedron structure, the interaction between leaching-agent ions (H+), activator ions (F−), and vanadium-containing biotite surface was discussed by DFT quantum chemical calculations. The dissolution behavior of activator fluoride ions on the surface of vanadium-bearing biotite during sulfuric acid leaching was revealed. According to the simulated leaching results, the oxygen on the biotite surface first absorbed hydrogen ions to undergo complete hydroxylation, and then combined with hydrogen ions to form water molecules. However, in the presence of activator (NaF), fluoride ions were adsorbed on the surface cations, which catalyzed the formation of water molecules and promoted the dissolution of surface cations. SEM–EDS analysis showed that the surface of vanadium-bearing minerals became very irregular, and the number of voids and cracks greatly increased. At the same time, XPS showed that the addition of activator fluoride ions destroyed the Al-O tetrahedron structure. Many Al and V atoms dissolved in the solution, which improved the leaching rate of vanadium

    Genome-Wide mRNA and Long Non-Coding RNA Analysis of Porcine Trophoblast Cells Infected with Porcine Reproductive and Respiratory Syndrome Virus Associated with Reproductive Failure

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    Porcine reproductive and respiratory syndrome (PRRS) is a vertically transmitted reproductive disorder that is typically characterized by miscarriage, premature birth, and stillbirth in pregnant sows after infection. Such characteristics indicate that PRRSV can infect and penetrate the porcine placental barrier to infect fetus piglets. The porcine trophoblast is an important component of the placental barrier, and secretes various hormones, including estrogen and progesterone, to maintain normal pregnancy and embryonic development during pregnancy. It is conceivable that the pathogenic effects of PRRSV infection on porcine trophoblast cells may lead to reproductive failure; however, the underlying detailed mechanism of the interaction between porcine trophoblast (PTR2) cells and PRRSV is unknown. Therefore, we conducted genome-wide mRNA and long non-coding RNA (lncRNA) analysis profiling in PRRSV-infected PTR2. The results showed that 672 mRNAs and 476 lncRNAs were significantly different from the control group after viral infection. Target genes of the co-expression and co-location of differential mRNAs and lncRNAs were enriched by GO (gene ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis, revealing that most of the pathways were involved in cell nutrient metabolism, cell proliferation, and differentiation. Specifically, the estrogen signaling pathway, the PI3K (PhosphoInositide-3 Kinase)-Akt (serine/threonine kinase) signaling pathway, and the insulin secretion related to embryonic development were selected for analysis. Further research found that PRRSV inhibits the expression of G-protein-coupled estrogen receptor 1 (GPER1), thereby reducing estrogen-induced phosphorylation of AKT and the mammalian target of rapamycin (mTOR). The reduction in the phosphorylation of AKT and mTOR blocks the activation of the GPER1- PI3K-AKT-mTOR signaling pathway, consequently restraining insulin secretion, impacting PTR2 cell proliferation, differentiation, and nutrient metabolism. We also found that PRRSV triggered trophoblast cell apoptosis, interrupting the integrity of the placental villus barrier. Furthermore, the interaction network diagram of lncRNA, regulating GPER1 and apoptosis-related genes, was constructed, providing a reference for enriching the functions of these lncRNA in the future. In summary, this article elucidated the differential expression of mRNA and lncRNA in trophoblast cells infected with PRRSV. This infection could inhibit the PI3K-AKT-mTOR pathway and trigger apoptosis, providing insight into the mechanism of the vertical transmission of PRRSV and the manifestation of reproductive failure

    A Nectin1 Mutant Mouse Model Is Resistant to Pseudorabies Virus Infection

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    The present study generated nectin1-mutant mice with single amino acid substitution and tested the anti-pseudorabies virus (PRV) ability of the mutant mice, with the aim to establish a model for PRV-resistant livestock. A phenylalanine to alanine transition at position 129 (F129A) of nectin1 was introduced into the mouse genome to generate nectin1 (F129A) mutant mice. The mutant mice were infected with a field-isolated highly virulent PRV strain by subcutaneous injection of virus. We found that the homozygous mutant mice had significantly alleviated disease manifestations and decreased death rate and viral loading in serum and tissue compared with heterozygous mutant and wild-type mice. In addition to disease resistance, the homozygous mutant mice showed a defect in eye development, indicating the side effect on animals by only one amino acid substitution in nectin1. Results demonstrate that gene modification in nectin1 is an effective approach to confer PRV resistance on animals, but the mutagenesis pattern requires further investigation to increase viral resistance without negative effect on animal development
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