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Being able to dynamically shape light at the nanoscale is one of the ultimate goals in nano-optics1. Resonant light–matter interaction can be achieved using conventional plasmonics based on metal nanostructures, but their tunability is highly limited due to a fixed permittivity2. Materials with switchable states and methods for dynamic control of light–matter interaction at the nanoscale are therefore desired. Here we show that nanodisks of a conductive polymer can support localized surface plasmon resonances in the near-infrared and function as dynamic nano-optical antennas, with their resonance behaviour tunable by chemical redox reactions. These plasmons originate from the mobile polaronic charge carriers of a poly(3,4-ethylenedioxythiophene:sulfate) (PEDOT:Sulf) polymer network. We demonstrate complete and reversible switching of the optical response of the nanoantennas by chemical tuning of their redox state, which modulates the material permittivity between plasmonic and dielectric regimes via non-volatile changes in the mobile charge carrier density. Further research may study different conductive polymers and nanostructures and explore their use in various applications, such as dynamic meta-optics and reflective displays.PEDOT nanodisks show near-infrared plasmonic resonances that can be reversibly switched by chemical redox reactions.

Demands are growing rapidly in the operational prediction and applications communities for forecasts that fill the gap between medium-range weather and long-range or seasonal forecasts. Based on the potential for improved forecast skill at the subseasonal to seasonal time range, the Subseasonal to Seasonal (S2S) Prediction research project has been established by the World Weather Research Programme/World Climate Research Programme. A main deliverable of this project is the establishment of an extensive database containing subseasonal (up to 60 days) forecasts, 3 weeks behind real time, and reforecasts from 11 operational centers, modeled in part on the The Observing System Research and Predictability Experiment (THORPEX) Interactive Grand Global Ensemble (TIGGE) database for medium-range forecasts (up to 15 days). The S2S database, available to the research community since May 2015, represents an important tool to advance our understanding of the subseasonal to seasonal time range that has been considered for a long time as a “desert of predictability.” In particular, this database will help identify common successes and shortcomings in the model simulation and prediction of sources of subseasonal to seasonal predictability. For instance, a preliminary study suggests that the S2S models significantly underestimate the amplitude of the Madden–Julian oscillation (MJO) teleconnections over the Euro-Atlantic sector. The S2S database also represents an important tool for case studies of extreme events. For instance, a multimodel combination of S2S models displays higher probability of a landfall over the islands of Vanuatu 2–3 weeks before Tropical Cyclone Pam devastated the islands in March 2015.

We recently showed that FoxM1 is overexpressed in human glioblastomas and that forced FoxM1B expression in anaplastic astrocytoma cells leads to the formation of highly invasive glioblastoma multiforme (GBM) in nude mice. However, the molecular mechanisms by which FoxM1 enhances glioma invasion are unknown. In this study, we found that FoxM1 overexpression increased matrix metalloproteinase (MMP)-2 expression in glioma cells, whereas blockade of FoxM1 expression suppressed MMP-2 expression. Transfection of FoxM1 into glioma cells directly activated the MMP-2 promoter, whereas inhibition of FoxM1 expression by FoxM1-siRNA suppressed its activation. We identified a FoxM1-binding site in the MMP-2 promoter and demonstrated that FoxM1 protein bound directly to it. Mutation of this FoxM1-binding site significantly attenuated MMP-2 promoter activity. Furthermore, FoxM1 overexpression increased the invasiveness of glioma cells, whereas inhibition of FoxM1 expression suppressed the invasiveness of GBM cells. Inhibition of MMP-2 by a specific MMP-2 inhibitor reversed the invasive phenotype of glioma cells overexpressing FoxM1. Finally, immunohistochemical analysis of 45 human GBM specimens showed a significant correlation between FoxM1 overexpression and elevated MMP-2 expression. Collectively, these findings provide evidence that FoxM1 contributes to glioma progression by enhancing MMP-2 gene transcription and thus tumor-cell invasion.

Detailed crystallographic data on high-quality Li 2 MnO 3 material has been obtained using a combination of X-ray diffraction (XRD), selected-area electron diffraction (SAED), high-resolution electron microscopy (HREM), and 0.1 nm probe high-angle annular dark-field imaging (HAADF) in a scanning transmission electron microscope. A high-purity Li 2 MnO 3 powder was annealed at 950 °C for 3 days to obtain predominantly defect-free grains which average size was 3.0 ± 1.5 μm. Rietveld refinement indicated that the C2/m spacegroup provided the best fit for the XRD data. Electron diffraction patterns obtained along various zone axes, on defect-free oxide particles, could be uniquely indexed to the monoclinic structure. HREM and HAADF images of defect-free grains were consistent with a Li–Mn–Mn– arrangement, i.e., lithium ordering in the transition metal planes. Low-magnification TEM images occasionally revealed stacking defects within oxide particles. HREM images of sample areas containing defects revealed a low density of stacking faults within the monoclinic sequence, resulting in a trigonal P3 1 12 local arrangement.

Background: DJ-1 (PARK7) was reported as an oncogene in a Ras-dependent manner. Recent studies have shown that DJ-1 stimulates cell proliferation, cell invasion, and cancer metastasis. However, the molecular mehchanism by which DJ-1 induces cancer cell invasion and metastasis remains unclear. Methods: Breast cancer cells were transfected with DJ-1 siRNA or DJ-1 overexpression to investigate the effect of DJ-1 on KLF17 expression. ID-1 luciferase promoter assay was performed to evaluate DJ-1-dependent KLF17 expression changes. In addition, Epistasis analysis of DJ-1 and KLF17 was performed to evaluate their regulatory interactions. Ras inhibitors were pretreated to determine whether DJ-1 regulates cell invasion in a Ras-dependent manner. Results: In the present study, we found increased DJ-1 expression in highly invasive breast cancer cells as compared with non-metastatic cells. Furthermore, DJ-1 promoted breast cancer cell invasion by downregulating E-cadherin and increasing Snail expression. Interestingly, exogenous DJ-1 overexpression markedly decreased mRNA and protein expression of KLF17, the EMT negative regulator. These data were confirmed by ID-1 promoter activity, which is directly regulated by DJ-1-dependent KLF17 transcription factor. Epistasis analysis showed that KLF17 overexpression overcomes increased cell invasion by DJ-1, suggesting that KLF17 might be one of the downstream signalling molecules of DJ-1. Acceleration of cell invasion by DJ-1 was alleviated by Ras inhibitors, suggesting that DJ-1 cooperates with Ras to increase cell invasion. Conclusion: Altogether, these data suggest for the first time that DJ-1 acts as an EMT-positive regulator in breast cancer cells via regulation of the KLF17/ID-1 pathway.

Background and aims:Activated hepatic stellate cells (HSCs) but not quiescent HSCs express cyclo-oxygenase-2 (COX-2), suggesting that the COX-2/prostanoid pathway has an active role in hepatic fibrogenesis. However, the role of COX-2 inhibitors in hepatic fibrogenesis remains controversial. The aim of this study was to investigate the antifibrotic effects of celecoxib, a selective COX-2 inhibitor.Methods:The effects of various COX inhibitors—that is, ibuprofen, celecoxib, NS-398 and DFU, were investigated in activated human HSCs. Then, the antifibrotic effect of celecoxib was evaluated in hepatic fibrosis developed by bile duct ligation (BDL) or peritoneal thioacetamide (TAA) injection in rats.Results:Celecoxib, NS-398 and DFU inhibited platelet-derived growth facor (PDGF)-induced HSC proliferation; however, only celecoxib (⩾50 μM) induced HSC apoptosis. All COX inhibitors completely inhibited prostaglandin E2 (PGE2) and PGI2 production in HSCs. Separately, PGE2 and PGI2 induced cell proliferation and extracellular signal-regulated kinase (ERK) activation in HSCs. All COX inhibitors attenuated ERK activation, but only celecoxib significantly inhibited Akt activation in HSCs. Celecoxib-induced apoptosis was significantly attenuated in HSCs infected with adenovirus containing a constitutive active form of Akt (Ad5myrAkt). Celecoxib had no significant effect on PPARγ (peroxisome proliferator-activated receptor γ) expression in HSCs. Celecoxib inhibited type I collagen mRNA and protein production in HSCs. Oral administration of celecoxib (20 mg/kg/day) significantly decreased hepatic collagen deposition and α-SMA (α-smooth muscle actin) expression in BDL- and TAA-treated rats. Celecoxib treatment significantly decreased mRNA expression of COX-2, α-SMA, transforming growth factor β1 (TGFβ1) and collagen α1(I) in both models.Conclusions:Celecoxib shows a proapoptotic effect on HSCs through Akt inactivation and shows antifibrogenic effects in BDL- and TAA-treated rats, suggesting celecoxib as a novel antifibrotic agent of hepatic fibrosis.

An ideal material has yet to be discovered that can completely treat dentin hypersensitivity; however, calcium phosphate precipitation has exhibited potential value for the treatment of dentin hypersensitivity by the occlusion of dentinal tubules. We hypothesized that a novel mesoporous silica biomaterial (nano CaO@mesoporous silica, NCMS) containing nano-sized calcium oxide particles mixed with 30% phosphoric acid can efficiently occlude dentinal tubules and significantly reduce dentin permeability, even with the presence of pulpal pressure. This highly supersaturated Ca2+-and HPO4 2−ion-containing NCMS paste was brushed onto dentin surfaces, and the ions diffused deeply into the dentinal tubules and formed a CaHPO4·2H2O precipitation with a depth of 100 μm. The results of the dentin permeability tests showed that the novel mesoporous material exhibited a significant reduction in dentin permeability (p < 0.05), even under simulated pulpal pressure, as compared with our previously developed material, DP-bioglass, and a commercial desensitizing material, Seal & Protect®.

Optical nanoantennas provide control of light at the nanoscale, which makes them important for diverse areas ranging from photocatalysis and flat metaoptics to sensors and biomolecular tweezing. They have traditionally been limited to metallic and dielectric nanostructures that sustain plasmonic and Mie resonances, respectively. More recently, nanostructures of organic J‐aggregate excitonic materials have been proposed capable of also supporting nanooptical resonances, although their advance has been hampered from difficulty in nanostructuring. Here, the authors present the realization of organic J‐aggregate excitonic nanostructures, using nanocylinder arrays as model system. Extinction spectra show that they can sustain both plasmon‐like resonances and dielectric resonances, owing to the material providing negative and large positive permittivity regions at the different sides of its exciton resonance. Furthermore, it is found that the material is highly anisotropic, leading to hyperbolic and elliptic permittivity regions. Nearfield analysis using optical simulation reveals that the nanostructures therefore support hyperbolic localized surface exciton resonances and elliptic Mie resonances, neither of which has been previously demonstrated for this type of material. The anisotropic nanostructures form a new type of optical nanoantennas, which combined with the presented fabrication process opens up for applications such as fully organic excitonic metasurfaces. Optical nanoantennas based on organic anisotropic J‐aggregate materials with strong exciton absorption provide dual functionality in the same nanostructure. They can support hyperbolic localized surface‐exciton polariton resonances on one spectral side of the exciton resonance while they support elliptic Mie resonances on the other side.

Steep slope, heavy rainfall and forested cover have unique soil erosion and sediment transport in South Korea. Sediment transport pattern in the monsoon region (from June to September) is complex and sediment transport modeling in these areas is often difficult as sediment load in the river varies largely from year to year. This paper describes a GIS-based soil erosion model and then developed a sediment transport model to estimate sediment yield (SY) at different basin scales. The model for estimating suspended sediment is based on Revised Universal Soil Loss Equation and suspended delivery ratio (SDR) models. For applying SDR model, basin-specific parameter was validated on the basis of field data, which ranged from 0.6 to 1.2 based on observed SY. In the study region, the high flow rates lasted for 4 months (from July to September) and over 90 % of total SY discharged during that time. At that time, it was found that annual bed loads in this area are 56–84 % of total sediment loads.

Background:Deletions in the 17p13.3 region are associated with abnormal neuronal migration. Point mutations or deletion copy number variants of the PAFAH1B1 gene in this genomic region cause lissencephaly, whereas extended deletions involving both PAFAH1B1 and YWHAE result in Miller–Dieker syndrome characterised by facial dysmorphisms and a more severe grade of lissencephaly. The phenotypic consequences of YWHAE deletion without deletion of PAFAH1B1 have not been studied systematically.Methods:We performed a detailed clinical and molecular characterization of five patients with deletions involving YWHAE but not PAFAH1B1, two with deletion including PAFAH1B1 but not YWHAE, and one with deletion of YWHAE and mosaic for deletion of PAFAH1B1.Results:Three deletions were terminal whereas five were interstitial. Patients with deletions including YWHAE but not PAFAH1B1 presented with significant growth restriction, cognitive impairment, shared craniofacial features, and variable structural abnormalities of the brain. Growth restriction was not observed in one patient with deletion of YWHAE and TUSC5, implying that other genes in the region may have a role in regulation of growth with CRK being the most likely candidate. Using array based comparative genomic hybridisation and long range polymerase chain reaction, we have delineated the breakpoints of these nonrecurrent deletions and show that the interstitial genomic rearrangements are likely generated by diverse mechanisms, including the recently described Fork Stalling and Template Switching (FoSTeS)/Microhomology Mediated Break Induced Replication (MMBIR).Conclusions:Microdeletions of chromosome 17p13.3 involving YWHAE present with growth restriction, craniofacial dysmorphisms, structural abnormalities of brain and cognitive impairment. The interstitial deletions are mediated by diverse molecular mechanisms.