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Due to the demand for temporary rapid grid connection in renewable energy power plants, the topology structure of T-connected power lines has been widely used in the power grid. In this three-terminal system, fault localization is difficult because of traditional impedance-based or traveling wave-based fault localization methods; the three-terminal data should be synchronized and communicated. Since different terminal assets belong to different enterprises, it is actually difficult to maintain good synchronization between them. Therefore, in practical applications, the fault location of T-connected power lines often fails. This article proposes a single terminal fault location method for a T-connection power line to address this issue. It is based on the fact that the local topology of the T-connected power line in the healthy phase remains unchanged during the fault-clearing process. It utilizes the sequential current and voltage data changes generated by the sequential tripping ping emitted by the circuit breaker from different terminals to describe the constant topology of the healthy phase as an equation and calculates the accurate fault location after solving the equation. The Levenberg–Marquardt algorithm was used to calculate fault distance and transition resistance, and the effectiveness of this method was verified through simulation. [ABSTRACT FROM AUTHOR]

Circuit breakers on the filter bank branches in converter stations are vulnerable to contact wear and mechanical deterioration caused by frequent operations, which can lead to circuit breaker breakdowns and explosions. It is imperative to conduct research on the early detection of abnormal states in circuit breakers. Existing electrical quantity-based detection methods are constrained by a priori assumptions, and their measurement methods are susceptible to interference, leading to misjudgments. To address this issue, this paper examines the influence of changes in critical breakdown field strength and contact spacing on circuit breaker operation states. It also proposes a technical scheme that employs breakdown current values to comprehensively characterize circuit breaker operation states, replacing the use of critical breakdown field strength and contact spacing. An early detection method for abnormal circuit breaker states based on a sequence of breakdown current ratios at different times is proposed, and its effectiveness is verified through simulation and field recording data. [ABSTRACT FROM AUTHOR]

Barrier membranes play a prominent role in guided bone regeneration (GBR), and polycaprolactone (PCL) is an attractive biomaterial for the fabrication of barrier membranes. However, these nanofiber membranes (NFMs) require modification to improve their biological activity. PCL-NFMs incorporating with laponite (LAP) achieve biofunctional modification. Decellularized extracellular matrix (dECM) could modulate cell behaviour. The present study combined dECM with PCL/LAP-NFMs to generate a promising strategy for bone tissue regeneration. Bone marrow mesenchymal stem cells (BMSCs) were cultured on NFMs and deposited with an abundant extracellular matrix (ECM), which was subsequently decellularized to obtain dECM-modified PCL/LAP-NFMs (PCL/LAP-dECM-NFMs). The biological functions of the membranes were evaluated by reseeding MC3T3-E1 cells in vitro and transplanting them into rat calvarial defects in vivo. These results indicate that PCL/LAP-dECM-NFMs were successfully constructed. The presence of dECM slightly improved the mechanical properties of the NFMs, which exhibited a Young's modulus of 0.269 MPa, ultimate tensile strength of 2.04 MPa and elongation at break of 51.62 %. In vitro , the PCL/LAP-dECM-NFMs had favourable cytocompatibility, and the enhanced hydrophilicity was conducive to cell adhesion, proliferation, and osteoblast differentiation. PCL/LAP-dECM-NFMs exhibited an excellent bone repair capacity in vivo. Overall, dECM-modified PCL/LAP-NFMs should be promising biomimetic barrier membranes for GBR. • LAP incorporated into PCL stimulated more extracellular matrix formation in bone marrow mesenchymal stem cells. • PCL/LAP-dECM-NFMs were constructed with highly hydrophilicity and cytocompatibility. • PCL/LAP-dECM-NFMs enhanced osteogenic differentiation and accelerated bone defect repair. • PCL/LAP-dECM-NFMs can be promising biomimetic barrier membranes for bone regeneration. [ABSTRACT FROM AUTHOR]

The hydraulic turbine governing system (HTGS) is a complex nonlinear system that regulates the rotational speed and power of a hydro-generator set. In this work, an incremental form of an HTGS nonlinear model was established and the Takagi–Sugeno (T-S) fuzzy linearization and mixed H2/H∞ robust control theory was applied to the design of an HTGS controller. A T-S fuzzy H2/H∞ controller for an HTGS based on modified hybrid particle swarm optimization and gravitational search algorithm integrated with chaotic maps (CPSOGSA) is proposed in this paper. The T-S fuzzy model of an HTGS that integrates multiple-state space equations was established by linearizing numerous equilibrium points. The linear matrix inequality (LMI) toolbox in MATLAB was used to solve the mixed H2/H∞ feedback coefficients using the CPSOGSA intelligent algorithm to optimize the weighting matrix in the process so that each mixed H2/H∞ feedback coefficients in the fuzzy control were optimized under the constraints to improve the performance of the controller. The simulation results show that this method allows the HTGS to perform well in suppressing system frequency deviations. In addition, the robustness of the method to system parameter variations is also verified. [ABSTRACT FROM AUTHOR]

Previous studies have verified that teacher-student relationship quality has a positive effect on students' academic engagement. Few studies, however, have examined whether school psychological capital mediates the linkage between teacher-student relationship and academic engagement. The present study aimed to examine the mediated role of school PsyCap between teacher-student relationship and academic engagement in a sample of 986 Chinese college students in their English as a foreign language (EFL) learning. Having controlled for gender and family resources, structural equation modelling (SEM) analysis was conducted to explore the predictive effect of the teacher-student relationship on academic engagement via mediator of school PsyCap. Results showed that the teacher-student relationship predicted school PsyCap. School PsyCap, in turn, predicted EFL learners' academic engagement. The present study provides evidence for the linkage between teacher-student relationship and academic engagement and contributes to the literature by uncovering the mediator mechanism between these two constructs. Both theoretical and practical implications are discussed. [ABSTRACT FROM AUTHOR]

Surging multi-service heterogeneous data offloading in new type distribution grid places new demands on latency. Cloud-edge collaboration enables low-latency data offloading through sufficient information sharing and resource allocation. However, there exist transmission and computing uncertainty on data offloading such as emergent task and burst interference in distribution grid. The conflicts of resource competition bring another challenge to multi-service data offloading with different priorities. In this paper, we address the cloud-edge multi-service data offloading problem which aims to minimize the weighted total data offloading delay based on the priorities. Then, the optimization problem is transformed as two-dimensional matching problem. We propose the uncertainty and priority awareness based low-latency multi-service data offloading optimization algorithm which achieves uncertainty and priority awareness and solves the resource competition among devices through price rising matching. Simulation results indicate that the proposed algorithm outperforms existing algorithms in total data offloading delay. [ABSTRACT FROM AUTHOR]

Highlights: [•] 4,4′-Bipyridyl was used to increase the ordering of the porphyrin π-system. [•] The ordered structure was confirmed by morphology studies, absorption spectra and XRD. [•] A significantly enhanced charge mobility and solar cell performance were obtained. [•] The results demonstrated a new efficient strategy to develop high efficiency OSCs. [Copyright &y& Elsevier]

Four new donor-acceptor (donor) [D-A(D)], PBDT-PTQ, PBDT-PTTQ, PBDT-TQ, and PBDT-TTQ, bearing the same backbone of alternative benzodithiophene (BDT) and quinoxaline units but with phenylene thienyl, phenylene di-thienyl, thienyl and di-thienyl groups (other donors), respectively, at the acceptor quinoxaline units, were designed and synthesized to investigate the impacts of the conjugated side chains at the acceptor units on the photovoltaic properties of polymers. The power conversion efficiencies (PCEs) of the polymer solar cells (PSCs) based on PBDT-TQ:[6,6]-phenyl-C-70-butyric acid methyl ester (PC70BM) and PBDT-PTQ:PC70BM reach to 4.39 and 3.58%, respectively, which are 43 and 17% higher, respectively, than that of a reported alkylphenyl substituted polymer with the same main chain. However, the PCEs based on PBDT-TTQ and PBDT-PTTQ, in which an additional thiophene is added at a side chain of PBDT-TQ and PBDT-PTQ, respectively, decline. The mechanism how the conjugated side chains affect the performance of the PSCs is also discussed. © 2013 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem, 2013 [ABSTRACT FROM AUTHOR]

Abstract: Alternating low bandgap π-conjugated polymers consisting of 5,7-dithien-2-yl-thieno[3-4-b]pyrazine and phenylene linked directly (PP-DTTP) and by ethynylene linkages (PPE-DTTP) have been prepared in high yields by Suzuki coupling polymerization and Sonogashira condensation, respectively. Thin films of PPE-DTTP and PP-DTTP exhibit an optical bandgap of 1.55 and 1.36eV, respectively, and the devices provide estimated power conversion efficiencies (PCE) of 0.82% and 0.30%, respectively, in bulk heterojunction solar cells with [6,6]-phenyl C61 butyric acid methyl ester (PCBM) as the acceptor. Preliminary optimizations of the devices based on PPE-DTTP gave 1.20% PCE, which ranks in one of the best PCEs of thieno[3-4-b]pyrazines based solar cells. After the introduction of ethynylene linkages in PPE-DTTP, a higher open circuit voltage and a higher short circuit current were obtained with no loss of the fill factor though PPE-DTTP has a higher bandgap, therefore PPE-DTTP shows better performance, which was contributed by the more efficient intramolecular electron transport in PPE-DTTP demonstrated by the hole mobility results and quantum chemistry calculations. [Copyright &y& Elsevier]

Necroptosis is a form of regulated cell death that has been implicated in multiple diseases. TNF-induced necroptosis is regulated by necrosomes, complexes consisting of RIPK1, RIPK3 and MLKL. In this study, by screening of a small-compound library, we identified dozens of compounds that inhibited TNF-induced necroptosis. According to the mechanisms by which they inhibited necroptosis, these compounds were classified into different groups. We then identified Ibrutinib as an inhibitor of RIPK3 and found that Quizartinib protected against the TNF-induced systemic inflammatory response syndrome in mice by inhibiting the activation of RIPK1. Altogether, our work revealed dozens of necroptosis inhibitors, suggesting new potential approaches for treating necroptosis-related diseases. Screening a library of compounds identifies several inhibitors of TNF-induced necroptosis, including Ibrutinib as an inhibitor of RIPK3 and Quizartinib as an indirect RIPK1 kinase activity inhibitor. [ABSTRACT FROM AUTHOR]

Vascular smooth muscle cells (VSMCs) proliferation is a critical event that contributes to the pathogenesis of vascular remodeling such as hypertension, restenosis, and pulmonary hypertension. Increasing evidences have revealed that VSMCs proliferation is associated with the activation of receptor tyrosine kinases (RTKs) by their ligands, including the insulin-like growth factor receptor (IGFR), fibroblast growth factor receptor (FGFR), epidermal growth factor receptor (EGFR), vascular endothelial growth factor receptor (VEGFR), and platelet-derived growth factor receptor (PDGFR). Moreover, some receptor tyrosinase inhibitors (TKIs) have been found and can prevent VSMCs proliferation to attenuate vascular remodeling. Therefore, this review will describe recent research progress on the role of RTKs and their inhibitors in controlling VSMCs proliferation, which helps to better understand the function of VSMCs proliferation in cardiovascular events and is beneficial for the prevention and treatment of vascular disease. [ABSTRACT FROM AUTHOR]

The primary control goals of a wind turbine (WT) are structural load shedding, maximum wind energy capture in the underpowered situation, and consistent power production in the full power condition. A crucial component of the control problem for wind turbines with varying speeds is maximum power tracking control. Conventional maximum power tracking control tracks the ideal blade tip speed ratio to provide the most wind power at the specified wind speeds. However, because of the wind turbine's great nonlinearity and the significant external disturbances it encounters, it is difficult to react quickly to variations in wind speed, and the tracking speed is sluggish, which lowers the amount of electricity produced annually. In light of this, this work develops a novel preset performance controller for a wind power system maximum power tracking control. With this technique, the convergence rate and tracking precision may be set. In particular, based on the concept of time-varying feedback, a time-varying function, known as the preset performance function, is first created to allow the convergence speed and accuracy to be predetermined; then this time-varying function is used to transform the actual specified time problem of the original system into a bounded time problem of the new system; finally, a direct robust controller design strategy with pre-defined performance is suggested based on the design concept of the backstepping technique. The plan may maximize the rotor power coefficient by altering the wind turbine speed, track the ideal blade tip speed ratio for a given tracking accuracy and speed, and get the most wind power to produce the most power with the strongest robustness. The simulation results show that the recommended control technique works. [ABSTRACT FROM AUTHOR]

Pulmonary arterial hypertension (PAH) is a chronic and fatal disease characterized by pulmonary vascular remodeling, similar to the 'Warburg effect' observed in cancer, which is caused by reprogramming of glucose metabolism. Oroxylin A (OA), an active compound derived from Scutellaria baicalensis, which can inhibit glycolytic enzymes [hexokinase 2 (HK2), Lactate dehydrogenase (LDH), and pyruvate dehydrogenase kinase 1 (PDK1) by downregulating aerobic glycolysis to achieve the treatment of liver cancer. To the best of our knowledge, however, the impact of OA on PAH has not been addressed. Consequently, the present study aimed to evaluate the potential protective role and mechanism of OA against PAH induced by monocrotaline (MCT; 55 mg/kg). The mean pulmonary artery pressure (mPAP) was measured using the central venous catheter method; HE and Masson staining were used to observe pulmonary artery remodeling. Non-targeted metabolomics was used to analyze the metabolic pathways and pathway metabolites in MCT-PAH rats. Western Blot analysis was employed to assess the levels of glucose transporter 1 (Glut1), HK2), pyruvate kinase (PK), isocitrate dehydrogenase 2 (IDH2), pyruvate dehydrogenase kinase 1(PDK1), and lactate dehydrogenase (LDH) protein expression in both lung tissue samples from MCT-PAH rats. The results demonstrated that intragastric administration of OA (40 and 80 mg/kg) significantly decreased mPAP from 43.61±1.88 mmHg in PAH model rats to 26.51±1.53 mmHg and relieve pulmonary artery remodeling. Untargeted metabolomic analysis and multivariate analysis indicated abnormal glucose metabolic pattern in PAH model rats, consistent with the Warburg effect. OA administration decreased this effect on the abnormal glucose metabolism. The protein levels of key enzymes involved in glucose metabolism were evaluated by western blotting, which demonstrated that OA could improve aerobic glycolysis and inhibit PAH by decreasing the protein levels of Glut1, HK2, LDH, PDK1 and increasing the protein levels of PK and IDH2. In conclusion, OA decreased MCT-induced PAH in rats by reducing the Warburg effect. [ABSTRACT FROM AUTHOR]

The auto-phosphorylation of murine receptor-interacting protein 3 (Rip3) on Thr 231 and Ser 232 in the necrosome is required to trigger necroptosis. However, how Rip3 phosphorylation is regulated is still largely unknown. Here we identified protein phosphatase 1B (Ppm1b) as a Rip3 phosphatase and found that Ppm1b restricts necroptosis in two settings: spontaneous necroptosis caused by Rip3 auto-phosphorylation in resting cells, and tumour necrosis factor-α (TNF)-induced necroptosis in cultured cells. We revealed that Ppm1b selectively suppresses necroptosis through the dephosphorylation of Rip3, which then prevents the recruitment of mixed lineage kinase domain-like protein (Mlkl) to the necrosome. We further showed that Ppm1b deficiency (Ppm1bd/d) in mice enhanced TNF-induced death in a Rip3-dependent manner, and the role of Ppm1b in inhibiting necroptosis was evidenced by elevated Rip3 phosphorylation and tissue damage in the caecum of TNF-treated Ppm1bd/d mice. These data indicate that Ppm1b negatively regulates necroptosis through dephosphorylating Rip3 in vitro and in vivo. [ABSTRACT FROM AUTHOR]

Mixed lineage kinase domain-like protein (MLKL) is identified as the terminal executor of necroptosis. However, its role in acute alcoholic liver injury remains unclear. This study elucidates that MLKL can contribute to acute alcoholic liver injury independently of necroptosis. Although the expression of MLKL was upregulated, no significant increase in its phosphorylation or membrane translocation was observed in the liver tissues of mice treated with ethanol. This finding confirms that alcohol intake does not induce necroptosis in mouse liver tissue. Additionally, the deletion of Mlkl resulted in the downregulation of NLRP3 expression, which subsequently inhibited the activation of the NLRP3 inflammasome and the ensuing inflammatory response, thereby effectively mitigating liver injury induced by acute alcohol consumption. The knockout of Nlrp3 did not affect the expression of MLKL, further confirming that MLKL acts upstream of NLRP3. Mechanistically, inhibiting the nuclear translocation of MLKL reduced the nuclear entry of p65, the principal transcriptional regulator of NLRP3, thereby limiting the transcription of Nlrp3 mRNA and subsequent NLRP3 expression. Overall, this study unveils a novel mechanism of MLKL regulates the activation of NLRP3 inflammasomes in a necroptosis independent way in acute alcoholic liver injury [Display omitted] • Acute alcohol increased MLKL and RIPK3 without MLKL phosphorylation/translocation. • Mlkl deficiency can alleviate acute alcoholic liver injury". • Mlkl deficiency can limit NLRP3 inflammasome activation. • Nlrp3 -/- mice were resistant to alcoholic liver injury and inflammatory responses. • Loss of MLKL limits NLRP3 by decreasing NF-κB p65's nuclear entry. [ABSTRACT FROM AUTHOR]

Survivin is the key component of the chromosomal passenger complex and plays important roles in the regulation of cell division. Survivin has also been implicated in the regulation of apoptosis and tumorigenesis. Although the survivin protein has been reported to be degraded by a ubiquitin/proteasome-dependent mechanism, whether there is a DUB that is involved in the regulation of its protein stability is largely unknown. Using an expression library containing 68 deubiquitinating enzymes, we found that ubiquitin-specific-processing protease 35 (USP35) regulates survivin protein stability in an enzymatic activity-dependent manner. USP35 interacted with and promoted the deubiquitination of the survivin protein. USP38, an ortholog of USP35 encoded by the human genome, is also able to regulate survivin protein stability. Moreover, we found that the deubiquitinating enzyme DUBAI, the Drosophila homolog of human USP35, is able to regulate the protein stability of Deterin, the Drosophila homolog of survivin. Interestingly, USP35 also regulated the protein stability of Aurora B and Borealin which are also the component of the chromosomal passenger complex. By regulating protein stabilities of chromosomal passenger complex components, USP35 regulated cancer cell proliferation. Taken together, our work uncovered an evolutionarily conserved relationship between USP35 and survivin that might play an important role in cell proliferation. • USP35 regulates the stability of survivin protein. • USP35 interacts with survivin and promotes survivin deubiquitination. • The regulation of survivin protein stability by DUBs is evolutionarily conserved. • USP35 regulates the protein levels of components of the CPC and cell proliferation. [ABSTRACT FROM AUTHOR]

• Six ion channel genes were continuous differentially expressed in the tumorigenesis and progression of LUAD. • LUAD patients with overexpression of GJB2 or underexpression of SCNN1B had shorter overall survival. • Hypomethylation of GJB2 and hypermethylation of SCNN1B in the promoter region may contribute to the aberrant expressions. • The prognostic model with GJB2 and SCNN1B could stratify all LUAD patients into two groups with significantly different overall survival. • GJB2 and SCNN1B might have potential indicative therapeutic value for LUAD patients. Abnormal expressions of ion channel genes are associated with the occurrence and progression of tumors. At present, their roles in the carcinogenesis of lung adenocarcinoma (LUAD) are not clear. Differentially expressed (DE) genes in the tumorigenesis were identified from 328 ion channel genes in 102 LUAD and paired adjacent normal samples. Similar analyses were performed between 177 metastatic and 286 non-metastatic LUAD samples to identify DE ion channel genes in the progression of LUAD. Independent prognostic factors selected from DE ion channel genes were used to construct a prognostic model. Correlation analysis and drugs-drug targets interaction network were used to screen the potential drugs for LUAD patients stratified by GJB2 or SCNN1B. Six ion channel genes (GJB2 , CACNA1D , KCNQ1 , SCNN1B , SCNN1G and TRPV6) were continuous differentially expressed in the tumorigenesis and progression of LUAD. The survival analysis in four datasets with 522 LUAD samples showed that GJB2 and SCNN1B were independent prognostic biomarkers. Patients with overexpression of GJB2 or underexpression of SCNN1B had shorter overall survival. Moreover, multi-omics analysis showed that hypomethylation of GJB2 and hypermethylation of SCNN1B in the promoter region may contribute to their aberrant expressions. KEGG enrichment analysis showed that the overexpressed genes in the group with high GJB2 or low SCNN1B were enriched in cancer-related pathways, while the underexpressed genes were enriched in metabolism-related pathways. The prognostic model with GJB2 and SCNN1B can stratify all LUAD patients into two groups with significantly different survival. Correlation analysis and drugs-drug targets interaction network suggested that GJB2 and SCNN1B expression might have indicative therapeutic values for LUAD patients. Finally, pan-cancer analysis in other eight cancer types showed that GJB2 and SCNN1B might be also potential prognostic factors for KIRC. GJB2 and SCNN1B were identified as prognostic biomarkers and therapeutic targets for LUAD. [ABSTRACT FROM AUTHOR]

Deubiquitinating enzymes (DUBs) play important roles in many physiological and pathological processes by modulating the ubiquitination of their substrates. DUBs undergo post-translational modifications including ubiquitination. However, whether DUBs can reverse their own ubiquitination and regulate their own protein stability requires further investigation. To answer this question, we screened an expression library of DUBs and their enzymatic activity mutants and found that some DUBs regulated their own protein stability in an enzymatic activity- and homomeric interaction-dependent manner. Taking Ubiquitin-specific-processing protease 29 (USP29) as an example, we found that USP29 deubiquitinates itself and protects itself from proteasomal degradation. We also revealed that the N-terminal region of USP29 is critical for its protein stability. Taken together, our work demonstrates that at least some DUBs regulate their own ubiquitination and protein stability. Our findings provide novel molecular insight into the diverse regulation of DUBs. • Deubiquitinating enzymes regulate their protein level in an enzymatic activity dependent manner; • USP26/USP29/USP37 subfamily members regulate the protein stability and ubiquitination of themselves; • N terminal region of USP29 is a degron that targets USP29 to be degraded. [ABSTRACT FROM AUTHOR]

Necroptosis is a form of regulated cell death that depends on the receptor-interacting serine-threonine kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL). The molecular mechanisms underlying distinct instances of necroptosis have only recently begun to emerge. In the present study, we characterized RABGEF1 as a positive regulator of RIPK1/RIPK3 activation in vitro. Based on the overexpression and knockdown experiments, we determined that RABGEF1 accelerated the phosphorylation of RIPK1 and promoted necrosome formation in L929 cells. The pro-necrotic effect of RABGEF1 is associated with its E3 ubiquitin ligase activity and guanine nucleotide exchange factor (GEF) activity. We further confirmed that RABGEF1 interacts with cIAP1 protein by inhibiting its function and plays a regulatory role in necroptosis, which can be abolished by treatment with the antagonist Smac mimetic (SM)-164. In conclusion, our study highlights a potential and novel role of RABGEF1 in promoting TNF-induced cell necrosis. • RABGEF1 promotes the phosphorylation of RIPK1 and formation of complex Ⅱb in L929 cells. • RABGEF1 does not affect TNF-induced activation of NF-kB and MAPK signaling pathways. • Knockdown of RABGEF1 levels inhibits TNF-induced necroptosis and necrosome formation. • The pro-necrotic effect of RABGEF1 is associated with the A20-type zinc finger and Vps9 domains. • RABGEF1 interacts with cIAP1 but does not affect cIAP1 protein levels. [ABSTRACT FROM AUTHOR]

Metal ion etching is an important pretreatment before the deposition of PVD coatings, which has a crucial effect on the bonding force. In this paper, Cr ion etching with different target current intensities was used to treat cemented carbide substrates, and then TiAlN was deposited on them. By studying the morphology and elements on the substrate surface after etching, it was found that the bombardment and deposition effects of the etching process are controlled by the target current intensity, and the bombardment will preferentially sputter Co while deposition will preferentially be on W. It would form droplet defects and greater roughness on the substrate surface, while transforming the residual stress to tensile. TiAlN grows in a different way because etching changes the morphology of the substrate surface and leaves Cr residues. 150 A etching results in a very rough surface, the substrate surface integrity was destroyed, and the final coating bond was unchanged. 200 A etching removes mainly the Co phase from the substrate and the coating bond is significantly improved due to the increased effective mechanical occlusion. The 250 A etching has a less efficient bombardment, mainly depositing Cr layers, which induced the competitive growth of TiAlN in multiple directions, causing the bonding force to be not effectively enhanced. In addition, the etched coatings were less subjected to adhesive wear in the ball-disk friction test, due to the high bonding force and roughness. • TiAlN coatings were deposited on cemented carbide etched with various currents. • Cr ion etching with different target currents treat substrates in different ways. • Cr ion etching changes the substrate surface, significantly increasing roughness. • After a proper Cr ion etching, adhesive strength was improved by 52.92%. • Cr ion etching with appropriate current can greatly reduce the wear rate of TiAlN. [ABSTRACT FROM AUTHOR]

Inorganic pyrophosphatase (PPase) plays an essential role in energy conservation and provides energy for many biosynthetic pathways. Here, we present two three-dimensional structures of PPase from Homo sapiens (Hu-PPase) at 2.38 Å and 3.40 Å in different crystallization conditions. One of the Hu-PPase structures complex of two magnesium metal ions was determined to be a monomer (Hu-PPase-mono) here, while the other one to be a dimer-dimer (Hu-PPase-dd). In each asymmetric unit of Hu-PPase-mono, there are four α-helices and ten β-strands and folds as a barrel structure, and the active site contains two magnesium ions. Like PPases from many species, we found that Hu-PPase was able to undergo self-assembly. To our surprise, disruption of the self-assembly of Hu-PPase did not influence its enzymatic activity or the ability to promote cell growth. Our work uncovered that different structure forms of Hu-PPase and found that the pyrophosphatase activity of Hu-PPase is independent of its self-assembly. • Two different structure forms of PPase from Homo sapiens (Hu-PPase) were described. • The pyrophosphatase activity of Hu-PPase is independent of its self-assembly. • The ability of promotion the proliferation of cancer cells of Hu-PPase is independent of its self-assembly. [ABSTRACT FROM AUTHOR]

While an increasing literature on multilingualism addresses the key role of language in access to social resources, including crisis communication, little attention has been paid to practices of English-mediated multilingualism. Based on semi-structured interviews with 10 international students from South Asia and Southeast Asia receiving their higher education in China, the study reveals what language-related challenges international students encounter, how they mobilize their multilingual resources to enhance their access to crisis communication and build a shared community, and how their multilingual competences are valorized and enacted in the shifting paradigm of the China-oriented new economy addressing mutual accountability in South-South cooperation. The study suggests that English-mediated multilingualism in China fails to bridge the needs of international students of diverse backgrounds. The study also calls attention to the shifting paradigm of multilingual studies and the necessity of addressing the real world problems of health communication in a diverse context. [ABSTRACT FROM AUTHOR]

Rhubarb is commonly used to treat constipation in China for its function of promoting intestinal movement and optimum water content in feces. However, its mechanism of mucus secretion is vague. The aim of the study is to investigate the role of mast cells and enteric neurons in rhubarb extract (RE)-induced mucus secretion in the rat colon. Immunofluorescence was used to detect histamine receptors. Western blotting and 3,3′-diaminobenzidine (DAB) were applied to explore the content changes of mast cells activation. The changes in colonic goblet cells (GCs) were determined by means of PAS/AB staining. An intestinal perfusion system with a Bradford protein assay kit was directly to estimate in vitro secretion. And the cytokines were investigated with ELISA. The longitudinal aspect of this study indicate that the number and water content of faecal pellets were enhanced after the administration of different doses of RE accompanied by mast cells accumulated and increased the content of interferon (IFN) -γ or decreased the levels of interleukin (IL) −10 at doses of 3 and 6 g/kg. Pretreatment with ketotifen, mast cell stabilizer, had partially inhibited on RE-induced mucus secretion. Furthermore, RE induced the release of acetylcholine and mucin-2 in the colonic tissue and the histamine levels from the faeces. The results suggest that RE induced colonic mucus secretion involves mast cell activation and some cytokine. [ABSTRACT FROM AUTHOR]

Vascular restenosis has been proved as the major drawback of percutaneous coronary interventions, which is characterized by neointimal hyperplasia. Naringenin is a kind of natural dihydroflavonoid with a variety of beneficial effects, including anti-oxidative, anti-microbial, anti-cancer and anti-inflammatory properties. However, the effects of naringenin on vascular restenosis remain unclear. This study aimed at investigating the effect and the mechanisms of naringenin on balloon injury (BI)-induced neointimal hyperplasia in the common carotid artery (CCA). BI model of CCA was induced by a 2F Forgarty catheter balloon, and the pathological process of neointimal hyperplasia was noted at 1, 3, 7 and 14 days. Neointimal hyperplasia in CCA increased significantly, especially on day 14 after BI. Subsequently, naringenin (25, 50, 100 mg/kg/d) or volume-matched vehicle were administered to the rats by gavage daily for 14 days. Ultrasound detection and histopathological examination showed that naringenin dose-dependently inhibited BI-induced intimal hyperplasia, as evidenced by reducing imima-media thickness (IMT), neointimal area (NIA), neointimal area/media area (NIA/MA) and neointimal area/internal elastic area (NIA/IELA). Immunohistochemistry revealed that naringenin decreased the expression of proliferating cell nuclear antigen (PCNA) and the cluster of differentiation 163 (CD163). ELISA indicated naringenin significantly reduced the overproduction of IL-1β and TNF-α. By detecting the activity of superoxide dismutase and the level of malondialdehyde and glutathione, we found that naringenin attenuated BI-induced oxidative stress. Additionally, RT-qPCR demonstrated that receptor-interacting protein 1 (RIP1), RIP3 and mixed lineage kinase domain-like (MLKL) mRNA expression were further down-regulated by naringenin treatment. These results suggested that naringenin can suppress BI-induced vascular neointimal hyperplasia through anti-inflammation and anti-oxidative stress, which may be related to the regulation of RIP1-RIP3-MLKL signaling pathway. Image 1 [ABSTRACT FROM AUTHOR]

Graphical abstract Highlights • TSG inhibited intimal hyperplasia in rat common carotid artery balloon injury. • TSG reduced the expression of SCF/c-kit, SDF-1α/CXCR4 and FKN/CX3CR1 axes. • TSG enhanced re-endothelialization through increasing VEGF levels and CD34 cells. Abstract Background Intimal hyperplasia is the major therapeutic concern after percutaneous coronary intervention. The aim of this study is to investigate effects of 2,3,4′,5-tetrahydroxystilbene-2-O-β-D glucoside (TSG) on intimal hyperplasia and the underling mechanisms through attenuating the expressions of stromal cell-derived factor-1α (SDF-1α)/CXCR4, stem cell factor (SCF)/c-kit and fractalkine (FKN)/CX3CR1, and through promoting re-endothelialization with vascular endothelial growth factor (VEGF). Method Rats were operated with carotid artery balloon injury. The treatment groups were gavaged with 50 and 100 mg/kg/d of TSG. After 10 days of treatment, carotid artery pathological changes were evaluated by histology. Serum levels of SDF-1α, SCF, FKN and VEGF were detected by enzyme linked immunosorbent assay. The protein expressions of the receptors c-kit, CXCR4, CX3CR1, as well as CD34 and proliferating cell nuclear antigen (PCNA) were detected by immunochemistry. Results TSG dose-dependently inhibited balloon injury-induced intimal hyperplasia, as evidenced by reducing neointima area (NIA), neointima area/media area (NIA/MA), neointima area/internal elastic area (NIA/IELA), and by decreasing the protein expression of PCNA. TSG reduced serum levels of SDF-1α, SCF and FKN, and it also decreased the expressions of the corresponding receptors c-kit, CXCR4, CX3CR1 in neointima. Importantly, the level of VEGF in peripheral blood and the expression of CD34 in vascular walls were increased to promote re-endothelialization. Conclusions This study clearly demonstrated that TSG was effective in inhibiting intimal hyperplasia, and this effect was mediated, at least in part, through the SCF/c-kit, SDF-1α/CXCR4 and FKN/CX3CR1 axes. Importantly, TSG could increase VEGF and CD34 to promote endothelial repair. [ABSTRACT FROM AUTHOR]

In this paper, YG8 cemented carbide substrate was treated with Cr ion etching at different bias voltages followed by deposition of TiAlN coating on it based on the cathodic arc technique. The effects of Cr ion etching at different bias voltages on morphology, roughness, elemental composition of the surface of substrate and residual stress, as well as on the growth, microstructure, adhesion and frictional properties of the coating were investigated. After Cr ion etching, the roughness of cemented carbide surface was improved with a significant reduction of residual stresses. At a − 200 V bias voltage, a Cr interlayer was formed on substrate surface, which increased the roughness and improved the match of mechanical properties between substrate and coating, resulting in an increase in adhesion between coating and substrate from 50 N to 73 N. At an etching bias voltage of −800 V, etching effectively refined the coating grains and improved the hardness of the coating. The TEM cross section images of the coating showed that TiAlN coating was epitaxially grown on the etched substrate, which benefited adhesion of coatings to substrate. With increment of etching bias voltage, wear resistance of the coated cemented carbide tends to increase, and its major wear mechanisms are abrasive wear and adhesive wear. • Etching cemented carbide using Cr ions at different bias voltages. • Cr ion etching changes substrate morphology and dramatically improves roughness. • Deposition of TiAlN coating on cemented carbide after pre-etching treatment. • After proper Cr ion etching, the adhesion of coating is increased from 50 N to 73 N. [ABSTRACT FROM AUTHOR]

Osthole (Ost) is a coumarin that exhibits wide pharmacological effects in the cardiovascular system. However, whether Ost can inhibit apoptosis and inflammation in right ventricle (RV) cardiomyocytes and prevent RV remodeling is not clear. This study was designed to investigate the effect of Ost on RV remodeling and the underlying mechanism. By applying a monocrotaline (MCT)-induced rat model, the effect of Ost on RV remodeling was investigated. Rats were given a single dose of MCT (50 mg/kg) subcutaneously (s.c.) to establish the RV remodeling model, followed by treatment with 10 or 20 mg/kg Ost via daily gavage for 28 days. The RV pressure was measured, and a histological analysis was performed. The results suggested that Ost remarkably decreased RV pressure and improved myocardial hypertrophy and mitochondrial swelling, vacuolization, and sarcoplasmic reticulum enlargement when compared with the model group. To further investigate the roles of apoptosis and inflammation in the effects of Ost on MCT-induced RV remodeling, apoptosis-related factors and inflammatory-associated factors were examined by western blot. Ost was found to inhibit myocardial apoptosis and inflammation in the RV. Overall, the present results indicate that Ost suppresses the RV remodeling process induced by MCT in rats, which may be at least partially mediated through the reduction of myocardial apoptosis and inflammation. [ABSTRACT FROM AUTHOR]

Calcium-sensing receptor (CaSR) is a G protein-coupled receptor, widely distributed in various tissues, including vascular endothelial cells and smooth muscle cells, which plays an important role in the migration and homing of stem/progenitor cells and the proliferation of tissue cells. Restenosis after Percutaneous coronary intervention (PCI) seriously affects its prognosis and application. Our previous research has found that ginsenoside Rg1 (GS-Rg1) can inhibit the occurrence of restenosis after balloon injury of the common carotid artery in rats, but the mechanism is still unclear. In this study, it was found that GS-Rg1 (4, 8, 16 mg/kg) inhibited vascular restenosis caused by balloon injury, and mobilize endothelial progenitor cells (EPCs) to promote reendothelialization and inhibit intimal hyperplasia, which significantly reduced after administration of CaSR antagonist NPS 2143. Interestingly, CaSR and its downstream JNK, P38 were highly expressed in the proliferative intima and participated in the abnormal proliferation of vascular smooth muscle cells mediated by smooth muscle progenitor cells (SMPCs). GS-Rg1 inhibited intimal hyperplasia, while it decreased the expression of CaSR, JNK, and P38. This might relate to the distribution of CaSR and the facilitation of GS-Rg1 on the vascular endothelial repair. It is concluded that CaSR plays a key role in GS-Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon Injury. [Display omitted] • GS-Rg1 mobilizes EPCs to promote reendothelialization after balloon injury. • CaSR inhibitor reduces the effects of Rg1. • The expression of CaSR is decreased in hyperplastic intimal after GS-Rg1 treatment. • Contradiction of CaSR involves its distribution and endothelial repair effect of Rg1. [ABSTRACT FROM AUTHOR]

Introducing ethynylene linkages in a conjugated molecule can deepen the HOMO level, decrease the steric constraints and better delocalize the π electrons and so on, which are beneficial for organic solar cells. Furthermore, the typical method of introducing acetylene linkages by Sonogashira reactions can avoid the usage of toxic stannyl intermediates and potentially dangerous lithiation reactions. In this study, two simple small molecules BEDPP and NEDPP are designed and synthesized, in which two diketopyrrolopyrrole units are symmetrically connected to benzene and naphthalene cores, respectively, via acetylene linkages. And the BHJ (Bulk Heterojunction) solar cells based on BEDPP and NEDPP without using solvent additive and without any post-treatment for the active layers provide us power conversion efficiencies of 1.48% and 2.31% with remarkably high open circuit voltages up to 0.90 and 0.98 V, respectively. [ABSTRACT FROM AUTHOR]

The unique properties of boron dipyrromethene (BODIPY) dyes including facile synthesis, high absorption coefficients, and delocalized molecular orbitals as well as excellent photochemical and thermal stability, make them promising as materials for organic solar cells. Accordingly, in this study three A- D-A structural small molecules of BDTT-BODIPY, FL-BODIPY, and TT-BODIPY have been synthesized, in which two BODIPY acceptor units are symmetrically conjugated to 4,8-bis(5-(2-ethylhexyl) thiophen-2-yl)benzo[1,2-b:4,5-b]dithiophene (BDTT), 9,9-dioctyl-9H-fluorene (FL), and thieno[3,2-b]thiophene (TT) donor cores, respectively. The manipulation of the structural parameters significantly improves the performances of the BHJ OSCs, which show power conversion efficiencies of 4.75 %, 1.51 %, and 1.67 % based on [6,6]-phenyl C71-butyric acid methyl ester (PC71BM) as the acceptor material and BDTT-BODIPY, FL-BODIPY, and TT-BODIPY as the donor materials, respectively. [ABSTRACT FROM AUTHOR]

Viruses hijack host factors for their high speed protein synthesis, but information about these factors is largely unknown. In searching for genes that are involved in viral replication, we carried out a forward genetic screen for Drosophila mutants that are more resistant or sensitive to Drosophila C virus (DCV) infection-caused death, and found a virus-resistant line in which the expression of pelo gene was deficient. Our mechanistic studies excluded the viral resistance of pelo deficient flies resulting from the known Drosophila anti-viral pathways, and revealed that pelo deficiency limits the high level synthesis of the DCV capsid proteins but has no or very little effect on the expression of some other viral proteins, bulk cellular proteins, and transfected exogenous genes. The restriction of replication of other types of viruses in pelo deficient flies was also observed, suggesting pelo is required for high level production of capsids of all kinds of viruses. We show that both pelo deficiency and high level DCV protein synthesis increase aberrant 80S ribosomes, and propose that the preferential requirement of pelo for high level synthesis of viral capsids is at least partly due to the role of pelo in dissociation of stalled 80S ribosomes and clearance of aberrant viral RNA and proteins. Our data demonstrated that pelo is a host factor that is required for high efficiency translation of viral capsids and targeting pelo could be a strategy for general inhibition of viral infection. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality among all types of diseases in the world, affecting many millions of individuals every year. CVD includes hypertension, atherosclerosis, pulmonary hypertension, heart failure, cardiomyopathy, coronary heart disease, etc., which are involved in complex etiology, pathogenesis and many risk factors. Modern pharmacological studies have revealed that Epimedium possesses a variety of beneficial effects in regulating cardiovascular inflammation and other biological activities, which provides a therapeutic value for the prevention and treatment of these cardiovascular diseases. In this review, we discuss the cardiovascular protective effects of icariin, an active component from Epimedium, and its metabolites. We summarize a range of studies showing that the modes of action of icariin on CVD relate to its inhibition of myocardial apoptosis and prevention of inflammation on endothelial cell injury, emphasizing the multiple effects of icariin and its metabolites in the repair of common heart failure and myocardial infarction, as well as the formation of neointima. In particular, an emphasis is placed on the discussion of the action mechanism of icariin in combination with new advances in the understanding of the pathology of CVD with potential application of icariin in the treatment of this human disorder. [ABSTRACT FROM AUTHOR]

• PAH induced by MCT is a progressive disease with persistent inflammation. • The inflammation in MCT-PAH model includes acute (the first 6 days after MCT injection) and chronic stages (after acute inflammation stage). • Acute inflammation stage may be the time window of anti-inflammatory treatment in PAH induced by MCT. A growing evidence demonstrates that inflammation is a major contributor to the pathogenesis of pulmonary arterial hypertension (PAH). However, blocking inflammation has only been shown to be of minor clinical benefit due to a lack of understanding of the precise inflammation present in PAH. Thus, the present study aimed to investigate characteristics of inflammatory process in PAH induced by monocrotaline (MCT) in rats. Adult male Sprague-Dawley rats received a single dose of MCT (50 mg/kg, ip), and the occurrence of PAH and inflammation biomarkers were measured at 3, 6, 9, 12, 15, 18, 21, 24, 27 and 30 days after MCT injection. From the 6th day after the injection of MCT, the mean pulmonary artery pressure gradually increased and doubled on the 30th day, accompanied by right ventricular hypertrophy and pulmonary arterial remodeling in a time-dependent manner. In the first 6 days after MCT treatment, only pro-inflammatory cytokines TNF-α, IL-1β increased, which was defined as acute inflammatory phase, after that, both pro-inflammatory factors TNF-α, IL-1β, IL-6, IL-12 and anti-inflammatory factors Arg1, IL-10, TGF-β increased, which was defined as chronic inflammatory phase. The M1/M2 macrophage ratios in lung and alveolar lavage fluid were elevated on the 6th and 30th day, moreover, which were higher on the 6th than 30th day, and the PI3K/Akt signaling pathway increased along with the progression of PAH and correlated with pro-inflammatory proteins, which revealed also to some extent the characteristics of inflammation of PAH induced by MCT. The course of PAH induced by MCT injection is progressive with persistent inflammation, which is defined as acute inflammatory phase within 6 days after MCT treatment, after that, is defined as chronic inflammatory phase. [ABSTRACT FROM AUTHOR]

Panax ginseng C. A. Mey. is a traditional tonic that has been used for thousands of years, and has positive effects on vascular diseases. Ginsenoside Rg1 (GS-Rg1) is one of the active ingredients of Panax ginseng C. A. Mey. and has been shown to have beneficial effects against ischemia/reperfusion injury. Our previously study has found that GS-Rg1 can mobilize bone marrow stem cells and inhibit vascular smooth muscle proliferation and phenotype transformation. However, pharmacological effects and mechanism of GS-Rg1 in inhibiting intimal hyperplasia is still unknown. This study was aimed to investigate whether GS-Rg1 prevented vascular intimal hyperplasia, and the involvement of stromal cell-derived factor-1α (SDF-1α)/CXCR4, stem cell factor (SCF)/c-kit and fractalkine (FKN)/CX3CR1 axes. Rats were operated with carotid artery balloon injury. The treatment groups were injected with 4, 8 and 16 mg/kg of GS-Rg1 for 14 days. The degree of intimal hyperplasia was evaluated by histopathological examination. The expression of α-SMA (α-smooth muscle actin) and CD133 were detected by double-label immunofluorescence. Serum levels of SDF-1α, SCF and soluble FKN (sFKN) were detected by enzyme linked immunosorbent assay (ELISA). The protein expressions of SCF, SDF-1α and FKN, as well as the receptors c-kit, CXC chemokine receptor type 4 (CXCR4) and CX3C chemokine receptor type 1 (CX3CR1) were detected by immunochemistry. GS-Rg1 reduced intimal hyperplasia by evidence of the values of NIA, the ratio of NIA/MA, and the ratio of NIA/IELA and the ratio of NIA/LA, especially in 16 mg/kg group. Furthermore, GS-Rg1 8 mg/kg group and 16 mg/kg group decreased the protein expressions of the SDF-1α/CXCR4, SCF/c-kit and FKN/CX3CR1 axes in neointima, meanwhile GS-Rg1 8 mg/kg group and 16 mg/kg group also attenuated the expressions of SDF-1α, SCF and sFKN in serum. In addition, the expression of α-SMA and CD133 marked smooth muscle progenitor cells (SMPCs) was decreased after GS-Rg1 treatment. GS-Rg1 has a positive effect on inhibiting vascular intimal hyperplasia, and the underlying mechanism is related to inhibitory expression of SDF-1α/CXCR4, SCF/c-kit and FKN/CX3CR1 axes. [ Image 1 ] • GS-Rg1 reduced the degree of intimal hyperplasia induced by balloon injury. • SDF-1α/CXCR4, SCF/c-kit and FKN/CX3CR1 axes were involved in the effect of GS-Rg1. • SMPCs might be related to the effect of GS-Rg1 on inhibiting intimal hyperplasia. [ABSTRACT FROM AUTHOR]

Background: Myeloid cell leukaemia 1 (MCL1) is a pro-survival Bcl-2 family protein that plays important roles in cell survival, proliferation, differentiation and tumourigenesis. MCL1 is a fast-turnover protein that is degraded via an ubiquitination/proteasome-dependent mechanism. Although several E3 ligases have been discovered to promote the ubiquitination of MCL1, the deubiquitinating enzyme (DUB) that regulates its stability requires further investigation. Methods: The immunoprecipitation was used to determine the interaction between OTUD1 and MCL1. The ubiquitination assays was performed to determine the regulation of MCL1 by OTUD1. The cell viability was used to determine the regulation of BH3-mimetic inhibitor induced cell death by OTUD1. The survival analysis was used to determine the relationship between OTUD1 expression levels and the survival rate of cancer patients. Results: By screening a DUB expression library, we determined that the deubiquitinating enzyme OTUD1 regulates MCL1 protein stability in an enzymatic-activity dependent manner. OTUD1 interacts with MCL1 and promotes its deubiquitination. Knockdown of OTUD1 increases the sensitivity of tumour cells to the BH3-mimetic inhibitor ABT-263, while overexpression of OTUD1 increases tumour cell tolerance of ABT-263. Furthermore, bioinformatics analysis data reveal that OTUD1 is a negative prognostic factor for liver cancer, ovarian cancer and specific subtypes of breast and cervical cancer. Conclusions: The deubiquitinating enzyme OTUD1 antagonizes BH3-mimetic inhibitor induced cell death through regulating the stability of the MCL1 protein. Thus, OTUD1 could be considered as a therapeutic target for curing these cancers. [ABSTRACT FROM AUTHOR]

The cover page of the journal "Chinese Journal of Chemistry" is presented.