Surface Plasmonic Core-Shell Nanostructures in Surface Enhanced Raman Scattering and Photocatalysis.

Core-shell nanostructures are a typical material design. Usually, it consists of a core wrapped in a shell. It has attracted much attention due to its tunable structure and composition, high surface area, and high programmability. The properties and resonance frequency of their surface plasmons can be adjusted by regulating the shape, size, and composition of metal core-shell nanostructures. This interaction makes core-shell nanostructures an excellent platform for plasmon-enhanced optical effects. This Perspective explores the categories of core-shell nanostructures, their exchanges with excitons in two-dimensional materials, their spectrum-enhanced aspects, and prospects for future applications of core-shell nanostructures.

Spectral Physics of Stable Cu(III) Produced by Oxidative Addition of an Alkyl Halide.

In this paper, we theoretically investigated spectral physics on Cu(III) complexes formed by the oxidative addition of α-haloacetonitrile to ionic and neutral Cu(I) complexes, stimulated by recent experimental reports. Firstly, the electronic structures of reactants of α-haloacetonitrile and neutral Cu(I) and two kinds of products of Cu(III) complexes are visualized with the density of state (DOS) and orbital energy levels of HOMO and LUMO. The visually manifested static and dynamic polarizability as well as the first hyperpolarizability are employed to reveal the vibrational modes of the normal and resonance Raman spectra of two Cu(III) complexes. The nuclear magnetic resonance (NMR) spectra are not only used to identify the reactants and products but also to distinguish between two Cu(III) complexes. The charge difference density (CDD) reveals intramolecular charge transfer in electronic transitions in optical absorption spectra. The CDDs in fluorescence visually reveal electron-hole recombination. Our results promote a deeper understanding of the physical mechanism of stable Cu(III) produced by the oxidative addition of an alkyl halide.

Effect of the Lipoxin Receptor Agonist BML-111 on Cigarette Smoke Extract-Induced Macrophage Polarization and Inflammation in RAW264.7 Cells.

Background: Macrophages are known to play a crucial role in the chronic inflammation associated with Chronic Obstructive Pulmonary Disease (COPD). BML-111, acting as a lipoxin A4 (LXA4) receptor agonist, has shown to be effective in protecting against COPD. However, the precise mechanism by which BML-111 exerts its protective effect remains unclear. Methods: In order to establish a cell model of inflammation, cigarette smoke extract (CSE) was used on the RAW264.7 cell line. Afterwards, an Enzyme-linked immunosorbent assay (ELISA) kit was employed to measure concentrations of tumor necrosis factor-α (TNF-α), interleukin-1beta (IL-1ß), interleukin-18 (IL-18), and interleukin-10 (IL-10) in the cell supernatants of the RAW264.7 cells.In this study, we examined the markers of macrophage polarization using two methods: quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis. Additionally, we detected the expression of Notch-1 and Hes-1 through Western blotting. Results: BML-111 effectively suppressed the expression of pro-inflammatory cytokines TNF-α, IL-1ß, and IL-18, as well as inflammasome factors NLRP3 and Caspase-1, while simultaneously up-regulating the expression of the anti-inflammatory cytokine IL-10 induced by CSE. Moreover, BML-111 reduced the expression of iNOS, which is associated with M1 macrophage polarization, and increased the expression of Arg-1, which is associated with M2 phenotype. Additionally, BML-111 downregulated the expression of Hes-1 and the ratio of activated Notch-1 to Notch-1 induced by CSE. The effect of BML-111 on inflammation and macrophage polarization was reversed upon administration of the Notch-1 signaling pathway agonist Jagged1. Conclusion: BML-111 has the potential to suppress inflammation and modulate M1/M2 macrophage polarization in RAW264.7 cells. The underlying mechanism may involve the Notch-1 signaling pathway.

Near-Field Imaging and Time-Domain Dynamics of Photonic Topological Edge States in Plasmonic Nanochains.

Time-domain dynamic evolution properties of topological states play an important role in both fundamental physics study and practical applications of topological photonics. However, owing to the absence of available ultrafast time-domain dynamic characterization methods, studies have mostly focused on the frequency-domain-based properties, and there are few reports demonstrating the time-domain-based properties. Here, we measured the dynamic near-field responses of plasmonic topological structures of gold nanochains with the configuration of the Su-Schrieffer-Heeger model by using ultrahigh spatial-temporal resolution photoemission electron microscopy. The dephasing time of plasmonic topological edge states increases with increasing the bulk lattice number that has a threshold requirement and finally reaches saturation. We directly revealed through simulation that there is a transient bulk state in the evolution of topological edge states, that is, the energy undergoes relaxation from oscillation between the bulk lattice and the edge. This work shows a new perspective of time-domain dynamic topological photonics.

Evidence for complex dynamics during U2 snRNP selection of the intron branchpoint.

Splicing of pre-mRNA is initiated by binding of U1 to the 5' splice site and of Msl5-Mud2 heterodimer to the branch site (BS). Subsequent binding of U2 displaces Msl5-Mud2 from the BS to form the prespliceosome, a step governing branchpoint selection and hence 3' splice site choice, and linking splicing to myelodysplasia and many cancers in human. Two DEAD-box proteins, Prp5 and Sub2, are required for this step, but neither is stably associated with the pre-mRNA during the reaction. Using BS-mutated ACT1 pre-mRNA, we previously identified a splicing intermediate complex, FIC, which contains U2 and Prp5, but cannot bind the tri-snRNP. We show here that Msl5 remains associated with the upstream cryptic branch site (CBS) in the FIC, with U2 binding a few bases downstream of the BS. U2 mutants that restore U2-BS base pairing enable dissociation of Prp5 and allows splicing to proceed. The CBS is required for splicing rescue by compensatory U2 mutants, and for formation of FIC, demonstrating a role for Msl5 in directing U2 to the BS, and of U2-BS base pairing for release of Prp5 and Msl5-Mud2 to form the prespliceosome. Our results provide insights into how the prespliceosome may form in normal splicing reaction.

Revealing the Chiroptical Response of Plasmonic Nanostructures at the Nanofemto Scale.

The spatiotemporal origin of plasmonic chiroptical responses in nanostructures remains unexplored and unclear. Here, two orthogonally oriented Au nanorods as a prototype were investigated, with a giant chiroptical response caused by antisymmetric and symmetric mode excitations for obliquely incident left-handed circular polarization (LCP) and right-handed circular polarization (RCP) light. Time-resolved photoemission electron microscopy (PEEM) was employed to measure the near-field spatial distributions, spectra, and spatiotemporal dynamics of plasmonic modes associated with the chiroptical responses at the nanofemto scale, verifying the characteristic near-field distributions at the resonant wavelengths of the two modes and a very large spectral dichroism for LCP and RCP. More importantly, eigenmode excitations and their contributions to the ultrafast plasmonic chiroptical response in the space-time domain were directly revealed, promoting a full understanding of the ultrafast chiral origin in complex nanostructures. These findings open a way to design chiroptical nanophotonic devices for spatiotemporal control of chiral light-matter interactions.

Observer-based state feedback H∞ control for offshore steel jacket structures under denial-of-service attacks.

This article focuses on observer-based state feedback H∞ control for a jacket structure against DoS attacks and external wave loads. First, a networked model of the structure is formulated as a switched delay system, in which DoS attacks and network-induced delays are considered simultaneously. A matching switched observer is developed for estimating states of the networked jacket structure system. Then, some new sufficient conditions are provided for the observer-based networked H∞ controller for the resultant switched system. Finally, it is shown from several case studies that the provided mechanism can maintain desired performance of the jacket structure against attacks and wave loads. In addition, the developed control schemes can save the control cost significantly.

Exciton-plasmon hybrids for surface catalysis detected by SERS.

Surface plasmons (SPs), in which the free electrons are collectively excited on the metal surface, have been successfully used in chemical analysis and signal detection. Generally, SPs possess two types of decay channels. SPs decay either nonradiatively via the generation of hot electrons or radiatively through re-emitted photons, which can trigger surface chemical reactions when the molecules are adsorbed on the surface of metal nanoparticles. An excitation light with a special wavelength is irradiated on the surface of the plasmonic nanostructure, the strong coupling interaction between electrons and light will then occur on this, and this is followed by the development of a series of unique properties. 2D materials have been a hot topic of research for more than a decade, since graphene was found in 2004. Recently, the combination of graphene with metal NPs has been shown to possess many supernormal advantages, such as high stability and catalytic activity, which have been successfully applied in plasmon-exciton co-driven chemical reactions.

Electrically enhanced hot hole driven oxidation catalysis at the interface of a plasmon-exciton hybrid.

In this work, an electro-optical device based on a graphene-Ag nanoparticle hybrid is fabricated as the substrate of graphene mediated surface enhanced Raman scattering (G-SERS) manipulated by the gate and bias voltages. Plasmon-exciton coupling promotes co-driven surface catalytic reactions, where the density of states (DOS) of holes and electrons on graphene is well controlled by the gate voltage, and the kinetic energy of holes and electrons is driven by the bias voltage (or current). Our experimental results reveal that the hot holes on graphene mainly contribute to plasmon-exciton co-driven oxidation reactions. The contribution of hot electrons to oxidation reactions is less important. Our novel electro-optical device can be potentially applied in controlling plasmon-exciton co-driven oxidation or reduction reactions by tuning the gate and bias voltages.

Correction: Recent advances in surface plasmon-driven catalytic reactions.

[This corrects the article DOI: 10.1039/C7RA05346K.].

Surface Plasmon Resonance Sensors on Raman and Fluorescence Spectroscopy.

The performance of chemical reactions has been enhanced immensely with surface plasmon resonance (SPR)-based sensors. In this review, the principle and application of SPR sensors are introduced and summarized thoroughly. We introduce the mechanism of the SPR sensors and present a thorough summary about the optical design, including the substrate and excitation modes of the surface plasmons. Additionally, the applications based on SPR sensors are described by the Raman and fluorescence spectroscopy in plasmon-driven surface catalytic reactions and the measurement of refractive index sensing, especially.

Quantitative CT analysis of pulmonary pure ground-glass nodule predicts histological invasiveness.

OBJECTIVE: To assess whether quantitative computed tomography (CT) can help predict histological invasiveness of pulmonary adenocarcinoma appearing as pure ground glass nodules (pGGNs). METHODS: A total of 110 pulmonary pGGNs were retrospectively evaluated, and pathologically classified as pre-invasive lesions, minimally invasive adenocarcinoma (MIA) and invasive pulmonary adenocarcinoma (IPA). Maximum nodule diameters, largest cross-sectional areas, volumes, mean CT values, weights, and CT attenuation values at the 0th,2th,5th, 25th, 50th,75th, 95th, 98th and100th percentiles on histogram, as well as 2th to 98th, 5th to 95th, 25th to 75th,and 0th to 100thslopes, respectively, were compared among the three groups. RESULTS: Of the 110 pGGNs, 50, 28, and 32 were pre-invasive lesions, MIA, and IPA, respectively. Maximum nodule diameters, largest cross-sectional areas, andmass weights were significantly larger in the IPA group than in pre-invasive lesions. The 95th, 98th, 100th percentiles, and 2th to 98th, 25th to 75th, and 0th to 100thslopes were significantly different between pre-invasive lesions and MIA or IPA. Logistic regression analysis showed that the maximum nodule diameter (OR=1.21, 95%CI: 1.071-1.366, p<0.01) and 100th percentile on histogram (OR=1.02, 95%CI: 1.009-1.032, p<0.001) independently predicted histological invasiveness. CONCLUSIONS: Quantitative analysis of CT imaging can predict histological invasiveness of pGGNs, especiallythe maximum nodule diameter and 100th percentile on CT number histogram; this can instruct the long-term follow-up and selective surgical management.

Intermittent high dose proton pump inhibitor enhances the antitumor effects of chemotherapy in metastatic breast cancer.

BACKGROUND: Acidity is a hallmark of malignant tumor, representing a very efficient mechanism of chemoresistance. Proton pump inhibitors (PPI) at high dosage have been shown to sensitize chemoresistant human tumor cells and tumors to cytotoxic molecules. The aim of this pilot study was to investigate the efficacy of PPI in improving the clinical outcome of docetaxel + cisplatin regimen in patients with metastatic breast cancer (MBC). METHODS: Patients enrolled were randomly assigned to three arms: Arm A, docetaxel 75 mg/m(2) followed by cisplatin 75 mg/m(2) on d4, repeated every 21 days with a maximum of 6 cycles; Arm B, the same chemotherapy preceded by three days esomeprazole (ESOM) 80 mg p.o. bid, beginning on d1 repeated weekly. Weekly intermittent administration of ESOM (3 days on 4 days off) was maintained up to maximum 66 weeks; Arm C, the same as Arm B with the only difference being dose of ESOM at 100 mg p.o. bid. The primary endpoint was response rate. RESULTS: Ninety-four patients were randomly assigned and underwent at least one injection of chemotherapy. Response rates for arm A, B and C were 46.9, 71.0, and 64.5 %, respectively. Median TTP for arm A (n = 32), B (n = 31), C (n = 31) were 8.7, 9.4, and 9.7 months, respectively. A significant difference was observed between patients who had taken PPI and who not with ORR (67.7 % vs. 46.9 %, p = 0.049) and median TTP (9.7 months vs. 8.7 months, p = 0.045) [corrected]. Exploratory analysis showed that among 15 patients with triple negative breast cancer (TNBC), this difference was bigger with median TTP of 10.7 and 5.8 months, respectively (p = 0.011). PPI combination showed a marked effect on OS as well, while with a borderline significance (29.9 vs. 19.2 months, p = 0.090). No additional toxicity was observed with PPI. CONCLUSIONS: The results of this pilot clinical trial showed that intermittent high dose PPI enhance the antitumor effects of chemotherapy in MBC patients without evidence of additional toxicity, which requires urgent validation in a multicenter, randomized, phase III trial. TRIAL REGISTRATION: Clinicaltrials.gov identifier: NCT01069081 .

Telomeric plasmid induces human cancer cell dysfunction depending on ATM activity.

Telomeres are essential for chromosome stability and the regulation of the replicative life-span of somatic cells. Many studies showed that exogenous telomeric repeats could activate p53 protein. It is not known how cell dysfunction is induced by telomeric plasmids. A covalent closed circular (ccc) double-stranded plasmid containing (TTAGGG)(96) repeats (pRST5) was transiently transfected into the human gastric cancer MGC-803 cells. We first confirmed that the cell viabilities decreased by 27%, cell senescence increased by 62% and G2/M cycle arrested in pRST5 plasmid transfected cells. Compared to control groups, cells transfected with telomeric plasmids showed an ATM-dependent increasing of p53, TRF1, and TRF2 expression. Furthermore, telomere dysfunction-induced foci (TIF) were observed. In conclusion, telomeric plasmids can elicit endogenous telomere dysfunction and induce cell senescence by activating ATM-p53 pathway.

Possible roles of a tumor suppressor gene PIG11 in hepatocarcinogenesis and As2O3-induced apoptosis in liver cancer cells.

BACKGROUND: Our previous studies demonstrated that p53-induced gene 11 (PIG11) was involved in arsenic trioxide (As(2)O(3))-induced apoptosis in human gastric cancer MGC-803 cells. Here, we studied further PIG11 expression in human hepatocellular carcinoma (HCC) tissues and cell lines and compared the sensitivity to As(2)O(3)-induced cell apoptosis in HepG2 and L-02 cells. METHODS: PIG11 expression in human normal liver tissues, HCC tissues, and cell lines was determined by immunohistochemistry and immunocytochemistry methods, using an anti-human PIG11 antibody. Cell viability was estimated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diplenyltetrazolium bromide (MTT) assay. Cell apoptosis was determined by flow cytometry. Reverse-transcriptase polymerase chain reaction (RT-PCR) and Western blotting were performed to analyze PIG11 mRNA and protein expression in cells. Protein intensity was calculated by comparison with the intensity of beta-actin, using densitometry. PIG11 was knocked down using small interfering RNA (siRNA). RESULTS: We found that PIG11 expression was significantly downregulated in HCC tissue and the cell lines (Bel-7402, SMMC-7721, HepG2 cells). Further, HepG2 cells were more sensitive to As(2)O(3)-induced apoptosis than L-02 cells. The expression of PIG11 mRNA and protein was upregulated to a greater extent in HepG2 than in L-02 cells. In the presence of actinomycin D or cycloheximide, the amount of PIG11 protein expression did not increase. Likewise, the inhibition of PIG11 by siRNA decreased As(2)O(3)-induced PIG11 protein expression by more than 85% and partially prevented As(2)O(3)-induced apoptosis in both HepG2 and L-02 cells. CONCLUSION: The above results demonstrated that the PIG11 gene may be involved in As(2)O(3)-induced apoptosis in HepG2 cells and suggested that the adaptive response of PIG11 expression is one of the important factors in enhancing cell sensitivity to As(2)O(3)-induced apoptosis.

PIG11 is involved in hepatocellular carcinogenesis and its over-expression promotes Hepg2 cell apoptosis.

PIG11 (p53-induced gene 11) is a p53 target gene and candidate tumour suppressor gene. In this study, the expression of PIG11 protein was detected in human hepatocellular carcinoma (HCC) and normal liver tissues with an immunohistochemical method. Compared with expression in human normal liver tissues, the expression of PIG11 protein was significantly down-regulated in human HCC tissues. In addition, a recombinant pLXSN-PIG11 retroviral vector was constructed and transfected into HepG2 cells (human hepatocellular carcinoma cell line) and the role of PIG11 in apoptosis was analyzed. The percentage (18.60%) of apoptotic cells transfected with pLXSN-PIG11 was higher than that in cells transfected with pLXSN only (6.03%) or the vehicle control (3.81%) (P < 0.01). DNA gel electrophoresis showed a clear DNA ladder in pLXSN-PIG11-infected HepG2 cells. Our results suggested that the PIG11 gene is involved in carcinogenesis and development of hepatocarcinoma. Therefore, PIG11 is considered to be a new candidate liver tumour suppressor gene, and may play an important role in tumour suppression through promotion of cell apoptosis.

Force-induced unfolding of human telomeric G-quadruplex: a steered molecular dynamics simulation study.

We study the unfolding of a parallel G-quadruplex from human telomeric DNA by mechanical stretching using steered molecular dynamics (MD) simulation. We find that the force curves and unfolding processes strongly depend on the pulling sites. With pulling sites located on the sugar-phosphate backbone, the force-extension curve shows a single peak and the unfolding proceeds sequentially. Pulling sites located on the terminal nucleobases lead to a force-extension curve with two peaks and the unfolding is more cooperative. Simulations of the refolding of partially unfolded quadruplexes show very different behavior for the two different pulling modalities. In particular, starting from an unfolded state prepared by nucleobase pulling leads to a long-lived intermediate state whose existence is also corroborated by the free energy profile computed with the Jarzynski equation. Based on this observation, we propose a novel folding pathway for parallel G-quadruplexes with the human telomere sequence.

PIG11 protein binds to DNA in sequence-independent manner in vitro.

PIG11 (p53-induced protein 11), one of early transcriptional targets of tumor suppressor p53, was up-regulated in the induction of apoptosis or cell growth inhibition by multiple chemopreventive agents. However, its biological role remains unclear. Here, we expressed His(6)-tagged PIG11 protein in Escherichia coli and demonstrated the recombinant His(6)-tagged PIG11 protein could bind to supercoiled and relaxed closed circular plasmid DNA or linear DNA with different length using gel retardation assays in vitro. The interaction between DNA and PIG11 protein was sequence-independent and related to charge effect. The reducing thiol group in PIG11 protein was involved in the binding activity of PIG11 to DNA. Furthermore, the images of atomic force microscopy directly confirmed the binding of DNA and PIG11 protein and showed the PIG11-DNA complex formed a beads-on-a-string appearance in which PIG11 protein associated with DNA as polymer. These findings suggest that PIG11 protein may play an important role by interaction with other biological molecules in the regulation of apoptosis and provided us a novel angel of view to explore the possible function of PIG11 in vivo.

Different interactions between the two sides of purple membrane with atomic force microscope tip.

Atomic force microscopy (AFM) is known to be capable of measuring local surface charge density based on the DLVO model. However, it has failed to distinguish charge density difference between the extracellular and cytoplasmic sides of purple membrane (PM) in previous studies. In this paper, tapping-mode AFM with thioglycolate-modified tips was used to image PM in buffers of different salt concentrations. When imaged in 25 mM KCl buffer, the topography of membranes appeared to be of two different types, one flat and the other domelike. Such a difference was not observed in buffers of high salt concentrations. This suggests that the topography variation results from differences in electrostatic interaction between the AFM tip and the different membrane surfaces. With images of papain-digested PM and high-resolution images of membrane surface structure, we proved that the membrane surfaces with flat topography were on the extracellular side while the surfaces with domelike topography were on the cytoplasmic side. Hence, this provides a straightforward method to distinguish the two sides of PM without the requirement of high-resolution imaging. Force-distance curves clearly demonstrated the different tip-sample interactions. The force curves recorded on the extracellular side of PM were consistent with the DLVO model, so its surface charge density can be estimated well. However, the curves recorded on the cytoplasmic side had a much longer decay length, which is supposed to be relevant to the flexibility of the C-terminus of bacteriorhodopsin (bR).