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The transition metal dichalcogenides (TMDs) have drawn great research attention, motivated by the derived remarkable optoelectronic properties and the potentials for high-efficient excitonic devices. The plasmonic nanocavity, integrating deep-sub wavelength confinement of optical mode with dramatic localized field enhancement, provides a practical platform to manipulate light–matter interaction. In order to obtain strong exciton–plasmon coupling effects, it’s crucial to match the vibration direction of exciton to the available strong localized in-plane electric field. Herein, we demonstrate the coupling effect of in-plane exciton in monolayer tungsten diselenide (WSe2) to deterministic gap-plasmon field which is produced by nanometrically gapped collapsed nanofingers. The gap-plasmon field which is completely parallel to the in-plane excitons in WSe2 will drive a strong exciton–plasmon coupling at room temperature. More interestingly, it is experimentally observed that the luminescence of exciton–polariton cannot be influenced by the temperature in the range from 77 K to 300 K due to the presence of nanofingers. According to the theoretical analysis results, we attribute this finding to the dielectric screening effect arising from the extremely strong localized electric field of plasmonic nanofingers. This work proposes a feasible way to harness and manipulate the exciton of low-dimensional semiconductor, which might be potential for quantum optoelectronics.

The combination of higher-order topological insulators and valley photonic crystals has recently aroused extensive attentions due to the great potential in flexible and efficient optical field manipulations. Here, we computationally propose a photonic device for the 1550 nm communication band, in which the topologically protected electromagnetic modes with high quality can be selectively triggered and modulated on demand. Through introducing two valley photonic crystal units without any structural alteration, we successfully achieve multi-dimensional coupled topological states thanks to the diverse electromagnetic characteristics of two valley edge states. According to the simulations, the constructed topological photonic devices can realize Fano lines on the spectrum and show high-quality localized modes by tuning the coupling strength between the zero-dimensional valley corner states and the one-dimensional valley edge states. Furthermore, we extend the valley-locked properties of edge states to higher-order valley topological insulators, where the selected corner states can be directionally excited by chiral source. More interestingly, we find that the modulation of multi-dimensional coupled photonic topological states with pseudospin dependence become more efficient compared with those uncoupled modes. This work presents a valuable approach for multi-dimensional optical field manipulation, which may support potential applications in on-chip integrated nanophotonic devices. [ABSTRACT FROM AUTHOR]

Higher-order topological insulators have drawn great research attention in nanophotonics due to their ability to both support robust edge states and lower dimensional corner states. In this work, we present a theoretical proposal for achieving topologically switchable and valley-selective corner states based on two-dimensional C3-symmetric photonic crystals (PCs), with breaking of inversion symmetry. Through the concatenation of two valley PCs with contrasting topological indices, we demonstrate the emergence of two types of valley-locked chiral topological edge states resulting from the valley–valley interaction. More importantly, we find that the system exhibits two distinct types of corner states, characterized by strong robustness and high localization, when the PCs are spliced at a 60° angle. However, the corner states are absent when the splicing angle is set as 120°. According to the theoretical analysis, the selective activation of topological valley corner states is related to the sign flip of valley Chern number at the corner. Based on this feature, we further propose a topological photonic switching device, in which the corner can be lighted up or off selectively. By combining the benefits of higher-order topology and valley degree of freedom, our work provides an efficient and flexible method for light manipulation. [ABSTRACT FROM AUTHOR]

Higher‐order topological (HOT) insulators have been extensively studied for their unique multidimensional boundary states such as hinge states and corner states. However, most of the recent studies are limited to static excitation of topological boundary states, restricting the development of their practical devices that possess the capability of diverse and programmable dynamic control of states. Here, a facile approach to achieve flexible control of light‐steering based on the symmetrized wave profiles of topological corner states is introduced. Specifically, multiple coherent sources are imported at symmetrical positions in higher‐order topological photonic crystals. By engineering phase differences among the sources, a controllable spatial‐resolved excitation of topological corner states is realized and a coding technique via controllable excitation of topological corner states is raised conceptually. Furthermore, an effective way to achieve direction‐selective excitation of topological edge states without the requirement of circularly polarized sources is proposed. The result provides a reliable active technique to modulate HOT boundary states while keeping the photonic structure invariable, which might be a practical alternative to manipulate light flexibly in integrated topological photonic devices with fixed configuration. [ABSTRACT FROM AUTHOR]

All‐inorganic perovskites have recently drawn considerable attention due to their excellent optoelectronic properties. With the help of gap‐plasmon nanostructures, the optical properties of perovskites can be tuned through the coupled near‐field. Here, the optical coupling between CsPbBr3 quantum dots (QDs) and gap‐plasmon through placing QDs in a 2‐nm tetrahedral amorphous carbon gap region of collapsible Ag nanofingers is demonstrated. Compared to the CsPbBr3 QDs on SiO2, the photoluminescence (PL) of CsPbBr3 QDs on collapsed nanofinger is enhanced by 4 times and the lifetime decreases from 11.04 to 3.8 ns. A Purcell‐enhanced emission can be achieved by combining QDs and plasmonic nanofingers. In addition, the intensity of PL can be manipulated by the polarization of incident light because of the different polarization responses of dimer nanofingers. More importantly, PL intensity shows a quadric dependence on the incident power and lasing‐like PL spectra can be observed at room temperature by continuous‐wave laser excitation. Such observations can be ascribed to the strong coupling between CsPbBr3 QDs and surrounding Ag nanofingers. This finding indicates that it is possible to achieve lasing‐like PL through coupling CsPbBr3 QDs to the near‐field of plasmonic nanostructures, which can enrich the applications of CsPbBr3 QDs in nanolasing devices. [ABSTRACT FROM AUTHOR]

Surface‐enhanced Raman spectroscopy (SERS) is known as a powerful technique to provide label‐free analyses for chemical sensing. While the sensitivity of SERS is heavily dependent on the prepared SERS functional substrates, finding appropriate substrates is critical to achieve sufficient signal enhancement. Meanwhile, the capture of targets to such effective enhancing region becomes challenging especially for low concentration. Here, we report a coupled Au/DNAs/Au gap plasmon platform that provides remarkable SERS enhancement and sensitivity for mercury ion sensing. Through nanoimprint lithography, large area of Au nanofingers can be fabricated with excellent uniformity and flexibility. These Au nanofingers can be further modified by DNA aptamers to construct Au/DNAs/Au gap plasmon nanostructures with well‐defined gap sizes. Due to the subnanometer gap size, strong interaction between collapsed Au nanofingers can be induced to create extremely enhanced near‐field with nanoscale mode volume. When Hg2+ ions exist around the platform, they can specially bind to thymine (T) bases of DNA and form T‐Hg2+‐T pairs between adjacent single strand DNAs. As a result, DNAs that initially lie on the Au surface are forced to stand in rigid duplex‐structures. This morphology change can be directly indicated by the ratio between adenine (A) and guanine (G) SERS signals to reveal the Hg2+ concentration. Given the strong field enhancement as well as the close distance between DNA and hotspot, ultralow Hg2+ concentration down to 10−9 M is successfully detected. This work demonstrates a SERS platform with high selectivity and sensitivity, which exhibits significant potential for molecule sensing applications. [ABSTRACT FROM AUTHOR]

The transition metal dichalcogenides (TMDs) have drawn great research attention, motivated by the derived remarkable optoelectronic properties and the potentials for high-efficient excitonic devices. The plasmonic nanocavity, integrating deep-sub wavelength confinement of optical mode with dramatic localized field enhancement, provides a practical platform to manipulate light–matter interaction. In order to obtain strong exciton–plasmon coupling effects, it's crucial to match the vibration direction of exciton to the available strong localized in-plane electric field. Herein, we demonstrate the coupling effect of in-plane exciton in monolayer tungsten diselenide (WSe2) to deterministic gap-plasmon field which is produced by nanometrically gapped collapsed nanofingers. The gap-plasmon field which is completely parallel to the in-plane excitons in WSe2 will drive a strong exciton–plasmon coupling at room temperature. More interestingly, it is experimentally observed that the luminescence of exciton–polariton cannot be influenced by the temperature in the range from 77 K to 300 K due to the presence of nanofingers. According to the theoretical analysis results, we attribute this finding to the dielectric screening effect arising from the extremely strong localized electric field of plasmonic nanofingers. This work proposes a feasible way to harness and manipulate the exciton of low-dimensional semiconductor, which might be potential for quantum optoelectronics. [ABSTRACT FROM AUTHOR]

ABSTRACT: To evaluate the effects of intraarticular injections of autologous platelet‐rich plasma (PRP) or bone marrow concentrate (BMC) on osteoarthritis (OA), 24 adult goats were equally divided into control (Ctrl), saline (NS), PRP, and BMC groups, and OA was induced by surgery in NS, PRP, and BMC groups. Autologous PRP and BMC were obtained from whole blood and bone marrow aspirates, respectively. The data revealed, platelets were increased in BMC by 1.8‐fold, monocytes by 5.6‐fold, TGF‐β1 by 7.7‐fold, and IGF‐1 by 3.6‐fold (p < 0.05), and platelets were increased in PRP by 2.9‐fold, and TGF‐β1 by 3.3‐fold (p < 0.05). From the sixth week post‐operation, saline, PRP, and BMC were administered by intraarticular injection once every 4 weeks, three consecutive times. After the animals were sacrificed, inflammatory cytokines in the synovial fluid was measured, and bone and cartilage degeneration progression was observed by macroscopy, histology, and immunohistochemistry. Compared with the NS group, the level of inflammatory cytokines was reduced in the PRP and BMC groups (p < 0.05). Histologically, delayed cartilage degeneration and higher levels of extracellular matrix (ECM) were observed in both PRP and BMC treated groups (p < 0.05). Furthermore, the BMC group showed greater cartilage protection and less ECM loss than the PRP group (p < 0.05). In summary, this study showed that intraarticular injection of autologous PRP and BMC has therapeutic efficacy in a goat osteoarthritis model, with the greater benefit in terms of cartilage protection being observed in the BMC‐treated group than PRP. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:2140–2146, 2018. [ABSTRACT FROM AUTHOR]

• We aimed to reveal pathogenesis of RA in peptidomic perspective. • Bioinformatics analyses disclosed the roles of differentially peptides in RA. • A galectin-1 derived peptide inhibited abnormal proliferation of synovial cells. Rheumatoid arthritis (RA) is an autoimmune disease that leads to small joints irreversible destruction. Despite intense efforts, the pathophysiology of RA currently remains unclear. We aimed to gain insight into the pathophysiology process in peptidomic perspective and to identify bioactive peptides for RA treatment. The endogenous peptides in synovial tissue between control and rheumatoid arthritis group were identified by liquid chromatography-mass spectrometry (LC-MS/MS). Since the biological function of peptides were always associated with precursor proteins, the potential function of the differentially peptides were predicted by GO and pathway analysis of their precursors. Besides, peptides located in the domains of their precursors were identified. Finally, we determined the impact of galectin-1 derived peptide by administration on the damage to MH7A cells caused by TNF-α. Totally, 141 down-regulated peptides and 10 up-regulated peptides were identified (Fold change > 1.5 and P < 0.05). It indicated that these differentially peptides were tightly involved in the pathophysiology process of RA preliminarily. Finally, we identified a peptide derived from the domain of galectin-1 could inhibit the abnormal proliferation induced by TNF-α and promoted apoptosis of MH7A. In summary, our study provided a better understanding of endogenous peptides in RA. We found a peptide that might be used in anti-RA treatment. [ABSTRACT FROM AUTHOR]

Plasmonic nanostructures exhibit intriguing optical properties due to spectrally selective plasmon resonance and thus have broad applications, including biochemical sensing and photoelectric detections. However, excited plasmons are often strongly influenced by the substrates supporting the metallic nanostructures, which not only weakens the intrinsic plasmon coupling effect, but also results in a great reduction of optical near‐field enhancement. Here, a plasmonic nanostructure combining collapsible Au‐nanofingers with selective‐etching that enables Au to be suspended is demonstrated, thus avoiding the undesirable influence of the substrates on the local near‐field distribution and forming symmetric electromagnetic‐field enhancements at both the top and bottom surfaces. The polymer support of the Au‐nanofingers is selectively etched by oxygen plasma, while the Au‐cap retains its original size. After an ultrathin dielectric coating is applied on the Au‐nanofingers, suspended Au‐caps with extremely small dielectric gaps are formed via the collapse of neighboring Au‐nanofingers by exposing them to ethanol. These nanostructures can provide a surface‐enhanced Raman scattering (SERS) enhancement of up to ≈109, which is nearly twice that in the nonsuspended system. As a highly active SERS substrate, the label‐free detection of low‐concentration harmful plastic phthalates in a child's urine without any pretreatment is successfully demonstrated, which suggests that this method is suitable for medical prediagnosis. [ABSTRACT FROM AUTHOR]

Circular RNA (circRNA) dysregulation has been linked to osteoarthritis (OA). The present study investigated the involvement of hsa&#95;circ&#95;0072568 (circ0072568) in OA. The expression of circ0072568 was detected in OA tissues and interleukin (IL)-1β-stimulated human chondrocytes. After performing dual-luciferase reporter and RNA immunoprecipitation assays, MTT, enzyme-linked immunosorbent assay and western blot analysis were used to assess the functions of circ0072568 in IL-1β-induced inflammation in chondrocytes in vitro . Circ0072568 was inhibited in OA tissues and the cell model in vitro . Circ0072568 overexpression protected the chondrocytes against IL-1β-induced inflammation and extracellular matrix (ECM) breakdown. Circ0072568 directly attached to microRNA (miR)-382-5p and enhanced the production of topoisomerase 1 (TOP1). Furthermore, miR-382-5p overexpression or TOP1 knockdown attenuated the effects of circ0072568 in IL-1β-stimulated human chondrocytes. On the whole, the present study demonstrates that the Circ0072568/miR-382-5p/TOP1 axis is involved in inflammation and ECM degradation in OA. These findings may contribute to the development of potential therapeutic strategies for OA., Competing Interests: The authors declare that they have no competing interests., (Copyright: © Chang et al.)

Backgrounds: Rheumatoid arthritis synovial fibroblasts (RASFs) are the primary cells responsible for destruction of marginal cartilage in rheumatoid arthritis (RA). G1dP3, a bioactive peptide derived from galectin-1 domain, possesses potent anti-inflammatory and anti-proliferation properties in RASFs. This study aimed to determine the effects of G1dP3 ferroptosis induction in RASFs and to further clarify the possible mechanisms. Methods: TNF-α was used to establish a RA model in MH7A cells. Cell Counting Kit-8 assays were employed to detect MH7A cell viability with different treatments. The occurrence of ferroptosis was examined by Lipid ROS assay, cellular labile iron pool measurement, reduced glutathione/oxidized glutathione activity, Gpx4 expression and transmission electron microscopy (TEM) morphology observation. Lentiviral-mediated siRNA interference was used to determine the downstream pathway. Results: G1dP3 markedly suppressed MH7A cell viability induced by TNF-α. G1dP3-treated MH7A cells presented the morphological features of ferroptosis. Moreover, G1dP3 triggered ferroptosis in MH7A cells by promoting the accumulation of lipid peroxides as well as iron deposition. Inhibition of ferroptosis alleviated G1dP3-mediated suppression of MH7A cell viability. Furthermore, G1dP3 increased p53 expression, which in turn transcriptionally suppressed SLC7A11, a key component of system X c - essential for ferroptosis. Knockdown of p53 abrogated the ferroptotic effects of G1dP3 on MH7A cells. Conclusion: Our findings reveal that the bioactive peptide G1dP3 promotes RASFs ferroptosis cell death via a p53/SLC7A11 axis-dependent mechanism, suggesting its potential role in the treatment of RA., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Hu, Zhang, Chang, Ji, Zhang, Geng, Li and Wang.)

To evaluate the effects of intraarticular injections of autologous platelet-rich plasma (PRP) or bone marrow concentrate (BMC) on osteoarthritis (OA), 24 adult goats were equally divided into control (Ctrl), saline (NS), PRP, and BMC groups, and OA was induced by surgery in NS, PRP, and BMC groups. Autologous PRP and BMC were obtained from whole blood and bone marrow aspirates, respectively. The data revealed, platelets were increased in BMC by 1.8-fold, monocytes by 5.6-fold, TGF-β1 by 7.7-fold, and IGF-1 by 3.6-fold (p < 0.05), and platelets were increased in PRP by 2.9-fold, and TGF-β1 by 3.3-fold (p < 0.05). From the sixth week post-operation, saline, PRP, and BMC were administered by intraarticular injection once every 4 weeks, three consecutive times. After the animals were sacrificed, inflammatory cytokines in the synovial fluid was measured, and bone and cartilage degeneration progression was observed by macroscopy, histology, and immunohistochemistry. Compared with the NS group, the level of inflammatory cytokines was reduced in the PRP and BMC groups (p < 0.05). Histologically, delayed cartilage degeneration and higher levels of extracellular matrix (ECM) were observed in both PRP and BMC treated groups (p < 0.05). Furthermore, the BMC group showed greater cartilage protection and less ECM loss than the PRP group (p < 0.05). In summary, this study showed that intraarticular injection of autologous PRP and BMC has therapeutic efficacy in a goat osteoarthritis model, with the greater benefit in terms of cartilage protection being observed in the BMC-treated group than PRP. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res., (© 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.)

Background/aims: Chondrocyte apoptosis is closely related to the development and progression of osteoarthritis. Global adiponectin (gAPN), secreted from adipose tissue, possesses potent anti-inflammatory and antiapoptotic properties in various cell types. This study aimed to investigate the role of autophagy induced by gAPN in the suppression of H2O2-induced apoptosis and the potential mechanism of gAPN-induced autophagy in chondrocytes., Methods: H2O2 was used to induce apoptotic injury in rat chondrocytes. CCK-8 assay was performed to determine the viability of cells treated with different concentrations of gAPN with or without H2O2. Cell apoptosis was detected by flow cytometry and TUNEL staining. Mitochondrial membrane potential was examined using JC-1 fluorescence staining assay. The autophagy inhibitors 3-MA and Bafilomycin A1 were used to treat cells and then evaluate the effect of gAPN-induced autophagy. To determine the downstream pathway, chondrocytes were preincubated with the AMPK inhibitor Compound C. Beclin-1, LC3B, P62 and apoptosis-related proteins were identified by Western blot analysis., Results: H2O2 (400 µM)-induced chondrocytes apoptosis and caspase-3 activation were attenuated by gAPN (0.5 µg/mL). gAPN increased Bcl-2 expression and decreased Bax expression. The loss of mitochondrial membrane potential induced by H2O2 was also abolished by gAPN. Furthermore, the antiapoptotic effect of gAPN was related to gAPN-induced autophagy by increased formation of Beclin-1 and LC3B and P62 degradation. In particular, the inhibition of gAPN-induced autophagy by 3-MA prevented the protective effect of gAPN on apoptosis induced by H2O2. Moreover, gAPN increased p-AMPK expression and decreased p-mTOR expression. Compound C partly suppressed the expression of autophagy-related proteins and restored the expression of p-mTOR suppressed by gAPN. Thus, the AMPK/mTOR pathway played an important role in the induction of autophagy and protection of H2O2-induced chondrocytes apoptosis by gAPN., Conclusions: gAPN protected chondrocytes from H2O2-induced apoptosis by inducing autophagy possibly associated with AMPK/mTOR signal-pathway activation., (© 2017 The Author(s). Published by S. Karger AG, Basel.)

The aim of the present study was to investigate the protective mechanism of ginsenoside Rg1 against the apoptosis of rat bone marrow stem cells (rBMSCs) under oxidative stress, and to determine the association with the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway. H2O2 was used to induce oxidative injury in rBMSCs. The cells in the H2O2 model group were treated with 800 µM H2O2 for 6 h to induce oxidative injury. The cells in the ginsenoside Rg1 group were treated with 10 µM ginsenoside Rg1 for 24 h, followed by H2O2 treatment. The cells in the Akt pathway blockage group were treated with 25 µM LY294002 for 1 h, followed by ginsenoside Rg1 + H2O2 treatment. The cell counting kit-8 assay was performed to determine cell viability. Cell apoptosis was detected by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The results of flow cytometry and TUNEL staining indicated that the apoptotic rate of the H2O2 model group was significantly higher compared with that of the control group. Following the ginsenoside Rg1 pretreatment, the apoptotic rate was significantly reduced. In the Akt pathway blockage group, no significant alterations in the levels of cell apoptosis were observed compared with the H2O2 model group. Western blot analysis demonstrated that the ginsenoside Rg1 group had a significant downregulation of Bax and cleaved caspase‑3 and an upregulation of Bcl‑2 and phosphorylated Akt protein expression levels compared with the H2O2 model group and the Akt pathway blockage group. In conclusion, ginsenoside Rg1 had a protective effect against the H2O2‑induced oxidative stress of rBMSCs, and the specific mechanism may be associated with the activation of the PI3K/Akt pathway by ginsenoside Rg1.