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The application of NiCuZn ferrites (NCZFs) in high-power communication systems is constrained by their nonlinear excitation. To reduce nonlinear effects, it is essential for ferrite materials to possess a relatively high spin-wave linewidth (ΔHk). Doping with ions such as cobalt and rare-earth (RE) ions with fast relaxation has proven effective in increasing ΔHk of ferrites. However, the regulatory mechanism of doping NCZFs with RE ions with larger ionic radii remains unclear. In this study, Ho3+-substituted NCZFs were synthesized via a solid-state reaction route. The spatial distribution and substitution amount of the Ho3+ ions were carefully investigated via elemental and phase composition analysis, revealing the limited solid solubility of the Ho3+ ions in NCZFs. Some of the Ho3+ ions enter the lattice and occupy the octahedral sites, accelerating relaxation and increasing ΔHk to a maximum value of 2.63 kA·m−1. Insoluble Ho3+ ions combine with Fe3+ ions to form a HoFeO3 heterogeneous phase with Fe3+ ions at the grain boundaries, leading to iron deficiency within NCZF crystals and significantly reducing the dielectric loss tangent at microwave frequencies. These results reveal the great potential of Ho3+-substituted NCZFs for high-power, low-loss microwave applications.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide and presents a significant threat to human health. Despite its prevalence, the underlying regulatory mechanisms of HCC remain unclear. In this study, we integrated RNA-seq datasets, proteome dataset and survival analysis and unveiled Stratifin (SFN) as a potential prognostic biomarker for HCC. SFN knockdown inhibited HCC progression in cell cultures and mouse models. Conversely, ectopic expression of Sfn in primary mouse HCC model accelerated HCC progression. Mechanistically, SFN acted as an adaptor protein, activating AKT1 signaling by fostering the interaction between PDK1 and AKT1, with the R56 and R129 sites on SFN proving to be crucial for this binding. In the syngeneic implantation model, the R56A/R129A mutant of SFN inhibited Akt signaling activation and impeded HCC growth. Additionally, peptide inhibitors designed based on the binding motif of AKT1 to SFN significantly inhibited HCC progression. In summary, our findings establish that SFN promotes HCC progression by activating AKT signaling through the R56 and R129 binding sites. This discovery opens new avenues for a promising therapeutic strategy for the treatment of HCC.

Hepatitis B virus (HBV) chronically infects 296 million people worldwide, posing a major global health threat. Export of HBV RNAs from the nucleus to the cytoplasm is indispensable for viral protein translation and genome replication, however the mechanisms regulating this critical process remain largely elusive. Here, we identify a key host factor embryonic lethal, abnormal vision, Drosophila-like 1 (ELAVL1) that binds HBV RNAs and controls their nuclear export. Using an unbiased quantitative proteomics screen, we demonstrate direct binding of ELAVL1 to the HBV pregenomic RNA (pgRNA). ELAVL1 knockdown inhibits HBV RNAs posttranscriptional regulation and suppresses viral replication. Further mechanistic studies reveal ELAVL1 recruits the nuclear export receptor CRM1 through ANP32A and ANP32B to transport HBV RNAs to the cytoplasm via specific AU-rich elements, which can be targeted by a compound CMLD-2. Moreover, ELAVL1 protects HBV RNAs from DIS3+RRP6+ RNA exosome mediated nuclear RNA degradation. Notably, we find HBV core protein is dispensable for HBV RNA-CRM1 interaction and nuclear export. Our results unveil ELAVL1 as a crucial host factor that regulates HBV RNAs stability and trafficking. By orchestrating viral RNA nuclear export, ELAVL1 is indispensable for the HBV life cycle. Our study highlights a virus-host interaction that may be exploited as a new therapeutic target against chronic hepatitis B.

Hepatitis B virus (HBV) chronically infects 296 million individuals and there is no cure. As an important step of viral life cycle, the mechanisms of HBV egress remain poorly elucidated. With proteomic approach to identify capsid protein (HBc) associated host factors and siRNA screen, we uncovered tumor susceptibility gene 101 (TSG101). Knockdown of TSG101 in HBV-producing cells, HBV-infected cells and HBV transgenic mice suppressed HBV release. Co-immunoprecipitation and site mutagenesis revealed that VFND motif in TSG101 and Lys-96 ubiquitination in HBc were essential for TSG101-HBc interaction. In vitro ubiquitination experiment demonstrated that UbcH6 and NEDD4 were potential E2 ubiquitin-conjugating enzyme and E3 ligase that catalyzed HBc ubiquitination, respectively. PPAY motif in HBc and Cys-867 in NEDD4 were required for HBc ubiquitination, TSG101-HBc interaction and HBV egress. Transmission electron microscopy confirmed that TSG101 or NEDD4 knockdown reduces HBV particles count in multivesicular bodies (MVBs). Our work indicates that TSG101 recognition for NEDD4 ubiquitylated HBc is critical for MVBs mediated HBV egress.

Abstract Voltage source converter‐based high voltage direct current (VSC‐HVDC) transmission system has become the mainstream of power construction and plays an increasingly important role in the power system. However, the DC line fault results in shutting down of the converters, which can greatly endanger the security of the power grid. So it is essential to find a fast fault identification strategy for DC line protection technology. In addition, the existing backup protection scheme has the problems of long delay and strict communication synchronisation requirements. Therefore, this study proposes a novel protection scheme for VSC‐HVDC transmission lines based on the fault current integral autocorrelation coefficient. The fault current and fault current frequency characteristics of VSC‐HVDC transmission lines are analysed first. Second, this study proposes a method to filter out distributed capacitance current by current integration and eliminate the oscillation of fault current. Finally, the difference of the current integral during different faults (internal or external fault) is analysed, and the autocorrelation coefficient is introduced to express the difference. Hence, this study proposes a new principle for identifying faults using the autocorrelation coefficient of the fault current integral. Simulation results show that the protection principle is not affected by the distributed capacitive current and does not require strict communication synchronisation. It has an excellent performance in intolerance to fault resistance and noise interference and can be used as backup protection for VSC‐HVDC transmission system.

MMC-HVdc transmission system has become the mainstream of power construction and plays an increasingly important role in the power system. However, the dc line fault results in shutting down of the converters, which can greatly endanger the security of the power grid. So it is essential to find a fast fault identification strategy for dc line protection technology. Besides, the existing backup protection scheme has the problems of long delay and strict communication synchronization requirements. Therefore, this paper proposes a novel protection scheme for mmc-HVdc transmission lines based on the Cross-Entropy of charge. The fault current oscillation phenomenon and fault current frequency characteristics of mmc-HVdc transmission lines are analyzed first. Secondly, this paper proposes a method to filter out distributed capacitance current by charge and eliminate the current oscillation. Finally, the difference of the charge during different faults (internal fault and external fault) is analyzed, and the Cross-Entropy is introduced to express this difference. Hence, this paper proposes a new principle of identifying faults using the Cross-Entropy of the charge. Simulation results show that the protection principle is not affected by the distributed capacitive current and does not require strict communication synchronization. It has excellent performance in intolerance to fault resistance and noise interference and can be used as backup protection for the mmc-HVdc transmission system.

In cancer, the extracellular matrix is extensively remodeled during chronic inflammation, thus affecting cell transcription, differentiation, migration and cell-cell interactions. Matrix metalloproteinases can degrade the extracellular matrix of tumor tissues and take important roles in disease progression. Numerous efforts to develop cancer treatments targeting matrix metalloproteinases have failed in clinical trials owing to the ineffectiveness and toxicity of the applied inhibitors. In this study, we investigated the potential of targeting matrix metalloproteinases and oncolytic virus combination in cancer therapy. We found that MMP3 expression was upregulated in various cancers and MMP3 expression in the tumor cells, but not in other tissues, was important for tumor growth and metastasis. Single treatment of colon cancer with multiple MMP3 inhibitors was not effective in mice. Nevertheless, the therapeutic effect of MMP3 was greatly improved by combination with an oncolytic virus. A potential mechanism of MMP3 in regulating tumor cell proliferation and invasion was mediated via Erk1/2 an NF-κB signaling. This study reveals that MMP3 is a promising target and the combined treatment with oncolytic virus is a potential strategy for cancer therapy.

This work demonstrates the dependence between magnetic properties and the thickness of NiFe thin films. More importantly, a quantitative study of the surface composition of NiFe thin film exposed to atmospheric conditions has been carried out employing angle-resolved X-ray photoelectron spectroscopy (ARXPS). In this study, we fabricated Ni81Fe19 (NiFe) thin films on Si (100) substrate using electron beam evaporation and investigated their surface morphologies, magnetic properties, and the thickness of the surface oxide layer. The coexistence of metallic and oxidized species on the surface are suggested by the depth profile of ARXPS spectra. The thickness of the oxidized species, including NiO, Ni(OH)2, Fe2O3, and Fe3O4, are also estimated based on the ARXPS results. This work provides an effective approach to clarify the surface composition, as well as the thickness of the oxide layer of the thin films.

pH sensors based on a nanostructured ion-sensitive field-effect transistor have characteristics such as fast response, high sensitivity and miniaturization, and they have been widely used in biomedicine, food detection and disease monitoring. However, their performance is affected by many factors, such as gate dielectric material, channel material and channel thickness. In order to obtain a pH sensor with high sensitivity and fast response, it is necessary to determine the appropriate equipment parameters, which have high processing cost and long production time. In this study, a nanostructured ion-sensitive field-effect transistor was developed based on the SILVACO technology computer-aided design (TCAD) simulator. Through experiments, we analyzed the effects of the gate dielectric material, channel material and channel thickness on the electrical characteristics of the nanostructured field-effect transistor. Based on simulation results, silicon nitride was selected as the gate dielectric layer, while indium oxide was chosen as the channel layer. The structure and parameters of the dual channel ion-sensitive field-effect transistor were determined and discussed in detail. Finally, according to the simulation results, a pH sensor based on the nanostructured ion-sensitive field-effect transistor was fabricated. The accuracy of simulation results was verified by measuring the output, transfer and pH characteristics of the device. The fabricated pH sensor had a subthreshold swing as low as 143.19 mV/dec and obtained an actual sensitivity of 88.125 mV/pH. In addition, we also tested the oxidation reaction of hydrogen peroxide catalyzed by horseradish peroxidase, and the sensitivity was up to 144.26 pA mol−1 L−1, verifying that the ion-sensitive field-effect transistor (ISFET) can be used to detect the pH of micro solution, and then combine the enzyme-linked assay to detect the concentration of protein, DNA, biochemical substances, biomarkers, etc.

Discussed is a novel self-biased hexaferrite gelling system based on a nontoxic and water-soluble copolymer of isobutylene and maleic anhydride. This copolymer simultaneously acts as a dispersant and gelling agent, and recently received much attention from the ceramics community. Herein its effects on the rheological conditions throughout magnetic-field pressing, and consequently, orientation, density and magnetic properties of textured hexaferrites were investigated. Ka-band FMR linewidths were measured, and the crystalline anisotropy and porosity induced linewidth broadening were estimated according to Schlömann’s theory. The copolymer allowed to reduce the friction between micron-sized magnetic particulates, resulting in higher density and degree of crystalline orientation, and lower FMR linewidth.

Co-substituted U-type hexagonal ferrite bulks, with composition of Ba4Ni2−xCoxFe36O60 (x=0.2, 0.4, 0.6, 0.8), were prepared by a conventional ceramic method. Saturation magnetization (4πMs), coercivity (Hc), and Curie temperature (Tc) were investigated. Anisotropy constant (K1) was calculated by fitting the magnetization curve (M-H) according to the law of approach to saturation, and anisotropy field (Ha) was calculated accordingly. The results reveal that all the samples possess the U-type hexagonal crystallographic structure. With increasing cobalt substitution content (x), the lattice parameters (a and c) almost remain the same owing to the similar radii of Ni2+ (0.72 Å) Co2+ (0.74 Å) ions. 4πMs goes up, while Hc Hc shows an opposite trend. K1 and Ha monotonously decrease resulting from that cobalt substitution weakens the c-axis orientation. Additionally, Tc increases from 467 °C to 484 °C.

Transmittance measurements have been performed on La-Co substituted barium hexaferrites in millimeter waves. Broadband millimeter-wave measurements have been carried out using the free space quasi-optical spectrometer, equipped with a set of high power backward wave oscillators covering the frequency range of 30 – 120 GHz. Strong absorption zones have been observed in the millimeter-wave transmittance spectra of all La-Co substituted barium hexaferrites due to the ferromagnetic resonance. Linear shift of ferromagnetic resonance frequency as functions of La-Co substitutions have been found. Real and imaginary parts of dielectric permittivity of La-Co substituted barium hexaferrites have been calculated using the analysis of recorded high precision transmittance spectra. Frequency dependences of magnetic permeability of La-Co substituted barium hexaferrites, as well as saturation magnetization and anisotropy field have been determined based on Schlömann’s theory for partially magnetized ferrites. La-Co substituted barium hexaferrites have been further investigated by DC magnetization to assess magnetic behavior and compare with millimeter wave data. Consistency of saturation magnetization determined independently by both millimeter wave absorption and DC magnetization have been found for all La-Co substituted barium hexaferrites. These materials seem to be quite promising as tunable millimeter wave absorbers, filters, circulators, based on the adjusting of their substitution parameters.

Oncolytic virus (OV) is increasingly being recognized as a novel vector in cancer immunotherapy. Increasing evidence suggests that OV has the ability to change the immune status of tumor microenvironment, so called transformation of 'cold' tumors into 'hot' tumors. The improved anti-tumor immunity can be induced by OV and further enhanced through the combination of various immunomodulators. The Neo-2/15 is a newly de novo synthesized cytokine that functions as both IL-2 and IL-15. However, it specifically lacks the binding site of IL-2 receptor α subunit (CD25), therefore unable to induce the Treg proliferation. In present study, a recombinant vesicular stomatitis virus expressing the Neo-2/15 (VSVM51R-Neo-2/15) was generated. Intratumoral delivery of VSVM51R-Neo-2/15 efficiently inhibited tumor growth in mice without causing the IL-2-related toxicity previously observed in clinic. Moreover, treatment with VSVM51R-Neo-2/15 increased the number of activated CD8+ T cells but not Treg cells in tumors. More tumor-bearing mice were survival with VSVM51R-Neo-2/15 treatment, and the surviving mice displayed enhanced protection against tumor cell rechallenge due to the induced anti-tumor immunity. In addition, combination therapy of OV and anti-PD-L1 immune checkpoint inhibitors further enhanced the anti-tumor immune response. These findings suggest that our novel VSVM51R-Neo-2/15 can effectively inhibit the tumor growth and enhance the sensitivity to immune checkpoint inhibitors, providing promising attempts for further clinical trials. [ABSTRACT FROM AUTHOR]

The global energy demand is increasing due to climate changes and carbon usages. Accumulating evidences showed energy sources using offshore wind from the sea can be added to increase our consumption capacity in long term. In addition, building offshore wind farms can also be environmentally advantageous compared to onshore farms. The assessment of wind energy resources is crucial for the site selection of wind farms. Currently, short-term wind forecast models have been developed to predict the wind power generation. However, methods are needed to improve the forecasting accuracy for ever-changing weather data. So, we try to use deep learning methods to predict long-term wind energy for identifying potential offshore wind farms. The experimental results indicate that PredRNN++ prediction model designed from the spatiotemporal perspective is feasible to evaluate long-term wind energy resources and has better performance than traditional LSTM. [ABSTRACT FROM AUTHOR]

Hepatitis B virus (HBV) infection is a major health burden worldwide, and currently there is no cure. The persistence of HBV covalently closed circular DNA (cccDNA) is the major obstacle for antiviral trement. HBV core protein (HBc) has emerged as a promising antiviral target, as it plays important roles in critical steps of the viral life cycle. However, whether HBc could regulate HBV cccDNA transcription remains under debate. In this study, different approaches were used to address this question. In synthesized HBV cccDNA and HBVcircle transfection assays, lack of HBc showed no effect on transcription of HBV RNA as well as HBV surface antigen (HBsAg) production in a hepatoma cell line and primary human hepatocytes. Reconstitution of HBc did not alter the expression of cccDNA-derived HBV markers. Similar results were obtained from an in vivo mouse model harboring cccDNA. Chromatin immunoprecipitation (ChIP) or ChIP sequencing assays revealed transcription regulation of HBc-deficient cccDNA chromatin similar to that of wild-type cccDNA. Furthermore, treatment with capsid assembly modulators (CAMs) dramatically reduced extracellular HBV DNA but could not alter viral RNA and HBsAg. Our results demonstrate that HBc neither affects histone modifications and transcription factor binding of cccDNA nor directly influences cccDNA transcription. Although CAMs could reduce HBc binding to cccDNA, they do not suppress cccDNA transcriptional activity. Thus, therapeutics targeting capsid or HBc should not be expected to sufficiently reduce cccDNA transcription. [ABSTRACT FROM AUTHOR]