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Long-term hepatitis C virus (HCV) infection is strongly associated with hepatocellular carcinoma (HCC), yet the mechanisms of the progression process remain unclear. The research is aiming to establish a crucial prognostic model that indicates the risk of HCV-associated cirrhosis evolving into HCC.Differentially expressed microRNAs (DE-miRNAs) and differentially expressed genes (DEGs) between HCV-associated cirrhosis and HCC were screened from the GSE40744 and GSE6764 datasets, respectively. Downstream target genes of DE-miRNAs were predicted by the miRNet tool and then overlapped with the DEGs to select intersection genes. The GSE15654 was downloaded to establish a prognostic model. Expression levels of risk genes and their corresponding miRNAs were measured in liver tissues of clinical patients. HCC cell lines with UHRF1 knockdown or overexpression were assayed for cell proliferation and migration.Thirty-nine DE-miRNAs and 796 DEGs are identified between HCV-associated cirrhosis and HCC. Main intersection genes and their corresponding miRNAs constitute a miRNA-mRNA regulatory network. PABPC1 (Polyadenylate-binding protein 1), SLC2A9 (solute carrier gene family 2, member 9), and UHRF1 (ubiquitin-like with PHD and ring finger domains 1) form a prognostic model indicating the risk of HCC development among HCV-associated cirrhosis. The genetic mutations of PABPC1, SLC2A9, and UHRF1 in HCC patients are 9%, 0.8%, and 0.6%, respectively. Compared to that in HCV-associated cirrhosis, the expression levels of PABPC1 and UHRF1 are higher while the expression level of SLC2A9 is lower in clinical HCV-associated HCC samples. UHRF1 enhances the proliferation and migration ability of HCC cells.PABPC1, SLC2A9, and UHRF1 and their corresponding miRNAs are involved in the evolution process of HCV-associated cirrhosis into malignant HCC. UHRF1 serves as an oncogene that promotes the proliferation and migration of HCC cells.

The salt overly sensitive (SOS) pathway is essential for maintaining sodium ion homeostasis in plants. This conserved pathway is activated by a calcium signaling-dependent phosphorylation cascade. However, the identity of the phosphatases and their regulatory mechanisms that would deactivate the SOS pathway remain unclear. In this study, we demonstrate that PP2C.D6 and PP2C.D7, which belong to clade D of the protein phosphatase 2C (PP2C) subfamily in Arabidopsis thaliana, directly interact with SOS1 and inhibit its Na+/H+ antiporter activity under non-salt-stress conditions. Upon salt stress, SOS3-LIKE CALCIUM-BINDING PROTEIN8 (SCaBP8), a member of the SOS pathway, interacts with the PP2Cs and suppresses their phosphatase activity; simultaneously, SCaBP8 regulates the subcellular localization of PP2C.D6 by releasing it from the plasma membrane. Thus, we identified two negative regulators of the SOS pathway that repress SOS1 activity under nonstress conditions. These processes set the stage for the activation of SOS1 by the kinase SOS2 to achieve plant salt tolerance. Our results suggest that reversible phosphorylation/dephosphorylation is crucial for the regulation of the SOS pathway, and that calcium sensors play dual roles in activating/deactivating SOS2 and PP2C phosphatases under salt stress.

Macroautophagy (autophagy) utilizes a serial of receptors to specifically recognize and degrade autophagy cargoes, including damaged organelles, to maintain cellular homeostasis. Upstream signals spatiotemporally regulate the biological functions of selective autophagy receptors through protein post-translational modifications (PTM) such as phosphorylation. However, it is unclear how acetylation directly controls autophagy receptors in selective autophagy. Here, we report that an ER-phagy receptor FAM134B is acetylated by CBP acetyltransferase, eliciting intense ER-phagy. Furthermore, FAM134B acetylation promoted CAMKII-mediated phosphorylation to sustain a mode of milder ER-phagy. Conversely, SIRT7 deacetylated FAM134B to temper its activities in ER-phagy to avoid excessive ER degradation. Together, this work provides further mechanistic insights into how ER-phagy receptor perceives environmental signals for fine-tuning of ER homeostasis and demonstrates how nucleus-derived factors are programmed to control ER stress by modulating ER-phagy.

Although two Enhancer of Polycomb-like proteins, EPL1A and EPL1B (EPL1A/B), are known to be conserved and characteristic subunits of the NuA4-type histone acetyltransferase complex in Arabidopsis thaliana, the biological function of EPL1A/B and the mechanism by which EPL1A/B function in the complex remain unknown. Here, we report that EPL1A/B are required for the histone acetyltransferase activity of the NuA4 complex on the nucleosomal histone H4 in vitro and for the enrichment of histone H4K5 acetylation at thousands of protein-coding genes in vivo. Our results suggest that EPL1A/B are required for linking the NuA4 catalytic subunits HISTONE ACETYLTRANSFERASE OF THE MYST FAMILY 1（HAM1) and HAM2 with accessory subunits in the NuA4 complex. EPL1A/B function redundantly in regulating plant development especially in chlorophyll biosynthesis and de-etiolation. The EPL1A/B-dependent transcription and H4K5Ac are enriched at genes involved in chlorophyll biosynthesis and photosynthesis. We also find that EAF6, another characteristic subunit of the NuA4 complex, contributes to de-etiolation. These results suggest that the Arabidopsis NuA4 complex components function as a whole to mediate histone acetylation and transcriptional activation specifically at light-responsive genes and are critical for photomorphogenesis.

Methanobactins (Mbns) are a family of copper-binding peptides involved in copper uptake by methanotrophs, and are potential therapeutic agents for treating diseases characterized by disordered copper accumulation. Mbns are produced via modification of MbnA precursor peptides at cysteine residues catalyzed by the core biosynthetic machinery containing MbnB, an iron-dependent enzyme, and MbnC. However, mechanistic details underlying the catalysis of the MbnBC holoenzyme remain unclear. Here, we present crystal structures of MbnABC complexes from two distinct species, revealing that the leader peptide of the substrate MbnA binds MbnC for recruitment of the MbnBC holoenzyme, while the core peptide of MbnA resides in the catalytic cavity created by the MbnB–MbnC interaction which harbors a unique tri-iron cluster. Ligation of the substrate sulfhydryl group to the tri-iron center achieves a dioxygen-dependent reaction for oxazolone-thioamide installation. Structural analysis of the MbnABC complexes together with functional investigation of MbnB variants identified a conserved catalytic aspartate residue as a general base required for MbnBC-mediated MbnA modification. Together, our study reveals the similar architecture and function of MbnBC complexes from different species, demonstrating an evolutionarily conserved catalytic mechanism of the MbnBC holoenzymes.

Mixed lineage leukemia 1 (MLL1) is a histone methyltransferase. Kaposi's sarcoma-associated herpesvirus (KSHV) is a leading cause of malignancy in AIDS. KSHV latently infects tumor cells and its genome is decorated with epigenetic marks. Here, we show that KSHV latency-associated nuclear antigen (LANA) recruits MLL1 to viral DNA where it establishes H3K4me3 modifications at the extensive KSHV terminal repeat elements during primary infection. LANA interacts with MLL1 complex members, including WDR5, integrates into the MLL1 complex, and regulates MLL1 activity. We describe the 1.5-Å crystal structure of N-terminal LANA peptide complexed with MLL1 complex member WDR5, which reveals a potential regulatory mechanism. Disruption of MLL1 expression rendered KSHV latency establishment highly deficient. This deficiency was rescued by MLL1 but not by catalytically inactive MLL1. Therefore, MLL1 is LANA regulable and exerts a central role in virus infection. These results suggest broad potential for MLL1 regulation, including by non-host factors.

SUMMARYMitophagy is a fundamental quality control mechanism of mitochondria. Its regulatory mechanisms and pathological implications remain poorly understood. Here via a mitochondria-targeted screen, we found that knockout (KO) of FBXL4, a mitochondrial disease gene, hyperactivates mitophagy at basal conditions. Subsequent counter screen revealed that FBXL4-KO hyperactivates mitophagy via two mitophagy receptors BNIP3 and NIX. We determined that FBXL4 functions as an integral outer-membrane protein that forms an SCF-FBXL4 ubiquitin E3 ligase complex. SCF-FBXL4 ubiquitinates BNIP3 and NIX to target them for degradation. Pathogenic FBXL4 mutations disrupt SCF-FBXL4 assembly and impair substrate degradation.Fbxl4−/−mice exhibit elevated BNIP3 and NIX proteins, hyperactive mitophagy, and perinatal lethality. Importantly, knockout of eitherBnip3orNixrescues metabolic derangements and viability of theFbxl4−/−mice. Together, beyond identifying SCF-FBXL4 as a novel mitochondrial ubiquitin E3 ligase restraining basal mitophagy, our results reveal hyperactivated mitophagy as a cause of mitochondrial disease and suggest therapeutic strategies.

Necroptosis is a form of programmed cell death. Mixed lineage kinase domain-like protein (MLKL) is the necroptosis executor, and it is involved in various diseases such as tissue damage and neurodegeneration-related diseases. Here, we report the development of novel MLKL inhibitors with a uracil nucleus through scaffold morphing from our previously reported xanthine MLKL inhibitor TC13172. After a rational structure-activity relationship study, we obtained the highly potent compounds

Human enterovirus A71 (EV-A71), a member of the Picornaviridae family, is one of the main etiological viruses that lead to hand, foot, and mouth disease (HFMD). We utilized a multiplex tandem mass tag-based quantitative proteomic technique to monitor the alternation of the whole cell proteome and phosphoproteome of human rhabdomyosarcoma cells over the course of EV-A71 infection. We successfully quantified more than 7000 host proteins and 17,000 phosphosites, of which 80 proteins and nearly 1700 phosphosites were significantly regulated upon viral infection. We found that Myc proto-oncogene protein level decreased significantly, benefiting EV-A71 replication. Multiple signaling pathways were regulated in phosphorylation events that converge for protein translation, cell cycle control, and cell survival. Numerous host factors targeted by virus proteins are phosphoproteins. These factors are involved in host translational initiation, unfolded protein response, endoplasmic reticulum stress, and stress granule formation, and their phosphorylation may play key roles in the virus life cycle. Notably, we identified three conserved phosphorylation sites on viral polyproteins that have not been previously reported. Our study provides valuable resources for a systematic understanding of the interaction between the host cells and the EV-A71 at the protein and the post-translational level.

In the INO80 chromatin remodeling complex, all of the accessory subunits are assembled on the following three domains of INO80: N-terminal domain (NTD), HSA domain, and ATPase domain. Although the ATPase and HSA domains and their interacting accessory subunits are known to be responsible for chromatin remodeling, it is largely unknown how the accessory subunits that interact with the INO80 NTD regulate chromatin status. Here, we identify both conserved and nonconserved accessory subunits that interact with the three domains in the INO80 complex in Arabidopsis thaliana. While the accessory subunits that interact with all the three INO80 domains can mediate transcriptional repression, the INO80 NTD and the accessory subunits interact with it can contribute to transcriptional activation even when the ATPase domain is absent, suggesting that INO80 has an ATPase-independent role. A subclass of the COMPASS histone H3K4 methyltransferase complexes interact with the INO80 NTD in the INO80 complex and function together with the other accessory subunits that interact with the INO80 NTD, thereby facilitating H3K4 trimethylation and transcriptional activation. This study suggests that the opposite effects of the INO80 complex on transcription are required for the balance between vegetative growth and flowering under diverse environmental conditions.

Due to the greenhouse effect of SF6, the search for new environmentally friendly substitute gases has become an urgent task for the electrical industry. In this article, we have employed a 2-D fluid model to study the characteristic of streamer discharges in the C4F7N-N2 mixture. The discharge process and insulation performance of the C4F7N-N2 mixture with different C4F7N content are compared under the same conditions. In a5.07% C4F7N-N2 mixture, the streamer expands continuously and reaches the top boundary quickly. In 7% and 13.1% C4F7N-N2 mixture, the streamer is gradually stagnated in the simulation domain. The streamer radius shows a decreasing trend, and a low electron density area appears behind the streamer head as the streamer moves forward. The streamer discharge simulation in 50% SF6–50% N2 is also performed to compare its insulation performance to the C4F7N-N2 mixture. The results show that the discharge is suppressed more heavily in 13.1% C4F7N-N2 than in 50% SF6–50% N2. The influence of buffer gas is studied by comparing the discharge process in C4F7N-N2 and C4F7N-CO2 with 13.1% C4F7N content. It is found that the discharge is more easily to a breakdown in C4F7N-CO2 than that in C4F7N-N2 in our simulation configuration. The simulation provides a way to optimizing the buffer gas ratio of new environmentally friendly gases from a microscopic perspective.

The extended grading capacitor (EGC) is a cost‐effective technique to suppress secondary arc. However, whether the use of EGC would weaken the interrupting capability of circuit breakers (CB) or not is still undetermined. In this work, an equivalent circuit model for ultra‐high voltage transmission line was established. The expressions of transient recovery voltage (TRV) across the contact gap of CB are derived, and hence the rate of rise of recovery voltage (RRRV). Then, a series of simulations have been performed, including the long‐line fault, the short‐line fault (SLF) and the terminal fault. It is found that the RRRV had approximately linear downward trend with the increase of the capacitance of EGC under long‐line fault but had approximately index downward trend under SLF. The SLF poses the strictest requirements to the CB. In addition to suppressing secondary arc current, the use of EGC would mitigate the interrupting severity and enhancing the interrupting performance of CB.

Loss of polarity protein Par3 promotes breast cancer tumorigenesis and metastasis. The underlying molecular mechanisms of Par3 down-regulation and related prognostic significance in breast cancer remain unclear. Here, we discovered that Par3 down-regulation was associated with shorter relapse-free survival in Luminal A subtype of breast cancer. Par3 knockdown promoted breast cancer cells migration and invasion. Importantly, we identified that transcription factor Sp1 bound to PARD3 promoter region and induced Par3 expression. Breast cancer patients with low Sp1 showed significantly worse RFS and low expression level of Par3. Par3 over-expression partially reversed Sp1 knockdown induced migration and invasion. Together, decreased Sp1 level mediates Par3 down-regulation, which correlated with poor prognosis of ER + breast cancer patients, via reduced binding with PARD3 promoter.

The effect of the position and amount of surface charges on cylindrical polytetrafluoroethylene (PTFE) insulators with different surface conductivities is studied. The surface potential decay property with time is investigated subjected to different electric fields. A simulation model for charge transport is established. The results show that the surface potential decays exponentially after surface treatment. The decay rate of surface charges increases with the surface conductivity. At $t = 180$ seconds, the decay rates of surface potentials for different surface conductivity are 2%, 42%, 60% and 84%, respectively. For samples with the same surface conductivity, the decay rates of surface potentials under different initial values are about 57%, and the decay rates at different accumulated locations are about 62%. It is demonstrated that the surface charge decay rate has little difference when initial charges with different amount and positions are introduced. However, the dissipation of surface charges can be promoted by applying a voltage of the same polarity. When the surface conductivity is increased to 5.1 × 10−16 S, the potential decay rate under the applied voltage increases to 76%. Furthermore, the flashover voltage decreases with the increase of surface conductivity. As a result, the effect of homopolar surface charges on the flashover voltage is reduced.

The histone chaperone facilitates chromatin transactions (FACT) functions in various DNA transactions. How FACT performs these multiple functions remains largely unknown. Here, we found, for the first time, that the N-terminal domain of its Spt16 subunit interacts with the Set3 histone deacetylase complex (Set3C) and that FACT and Set3C function in the same pathway to regulate gene expression in some settings. We observed that Spt16-G132D mutant proteins show defects in binding to Set3C but not other reported FACT interactors. At the permissive temperature, induction of the GAL1 and GAL10 genes is reduced in both spt16-G132D and set3Δ cells, whereas transient upregulation of GAL10 noncoding RNA (ncRNA), which is transcribed from the 3′ end of the GAL10 gene, is elevated. Mutations that inhibit GAL10 ncRNA transcription reverse the GAL1 and GAL10 induction defects in spt16-G132D and set3Δ mutant cells. Mechanistically, set3Δ and FACT (spt16-G132D) mutants show reduced histone acetylation and increased nucleosome occupancy at the GAL1 promoter under inducing conditions and inhibition of GAL10 ncRNA transcription also partially reverses these chromatin changes. These results indicate that FACT interacts with Set3C, which in turn prevents uncontrolled GAL10 ncRNA expression and fine-tunes the expression of GAL genes upon a change in carbon source.

Bladder cancer (BLCA) remains the leading cause of cancer‐related mortality among genitourinary malignancies worldwide. BLCA metastasis represents the primary reason for its poor prognosis. In this study, we report that decreased expression of partitioning defective 3 (Par3), a polarity protein (encoded by PARD3), is associated with tumor aggressive phenotypes and poor prognosis in BLCA patients. Consistently, ablation of Par3 promotes the metastasis and invasion of BLCA cells in vitro and in vivo. Further studies reveal that zinc finger protein Snail represses the expression of Par3 by binding to E2‐box (CAGGTG) of PARD3 promoter‐proximal. Inhibition of GSK‐3β promotes the expression and nuclear localization of Snail and then reduces the expression of Par3, resulting in the metastasis and invasion of BLCA cells. Moreover, we detected the interaction between Par3 (936‐1356 aa) and ZO‐1 (1372‐1748 aa), which is involved in the maintenance of tight junction. Together, our results demonstrate that the GSK‐3β/Snail/Par3/ZO‐1 axis regulates BLCA metastasis, and Snail is a major regulator for Par3 protein expression in BLCA., We report here that (a) polarity protein Par3 is frequently lost in BLCA patients and is associated with muscle‐invasive phenotypes and poor prognosis; (b) Par3 deficiency is required for BLCA invasion and metastasis in vitro and in vivo; (c) Snail suppresses Par3 expression through its binding to PARD3 E2‐box; and (d) overexpression of Par3 abolishes LiCl‐ or Snail‐induced BLCA metastatic behaviors, suggesting a role of the GSK‐3β/Snail/Par3 axis in regulating BLCA metastasis.

Although previous studies have identified several autonomous pathway components that are required for the promotion of flowering, little is known about how these components cooperate. Here, we identified an autonomous pathway complex (AuPC) containing both known components (FLD, LD and SDG26) and previously unknown components (EFL2, EFL4 and APRF1). Loss-of-function mutations of all of these components result in increased FLC expression and delayed flowering. The delayed-flowering phenotype is independent of photoperiod and can be overcome by vernalization, confirming that the complex specifically functions in the autonomous pathway. Chromatin immunoprecipitation combined with sequencing indicated that, in the AuPC mutants, the histone modifications (H3Ac, H3K4me3 and H3K36me3) associated with transcriptional activation are increased, and the histone modification (H3K27me3) associated with transcriptional repression is reduced, suggesting that the AuPC suppresses FLC expression at least partially by regulating these histone modifications. Moreover, we found that the AuPC component SDG26 associates with FLC chromatin via a previously uncharacterized DNA-binding domain and regulates FLC expression and flowering time independently of its histone methyltransferase activity. Together, these results provide a framework for understanding the molecular mechanism by which the autonomous pathway regulates flowering time.

The demand for DC gas-insulated switchgear/gas-insulated transmission line (GIS/GIL) becomes more and more urgent in recent years owing to the rapid development of high voltage direct current (HVDC) transmission systems. Insulators in DC GIS/GIL could easily accumulate a large number of charges on its surface during long-term operation, which might lead to overstressing of polymeric insulation or surface flashover. Therefore, it is of great significance to propose an effective method for dissipating extra surface charges. However, achieving charge dissipation without opening the tank is still a great challenge to SF 6 -insulated equipment for a long time. In this paper, a novel method, which is named X-ray based non-contact charge dissipation method (XNCDM) for insulators in SF 6 -insulated equipment, is proposed. The effects of X-ray irradiation on the charges dissipation and the influences of irradiation dose were experimentally investigated in SF 6 . The mechanisms underlying are discussed in detail. Results show that surface charges on the insulator can be almost completely dissipated after short-time X-ray irradiation with enough dose, owing to the significant enhancement of electric conduction along the insulator surface and charge neutralization by gas ions near the gas-solid interface. This paper provides a novel technique for realizing rapid surface charge dissipation on the insulator, which is of great significance for a variety of engineering applications of DC GIS/GIL.

Background Sphingomyelin (SM) is an essential component of biological lipid rafts, and it plays an indispensable role in maintaining plasma membrane stability and in mediating signal transduction. The ultimate biosynthesis of SM is catalyzed by two sphingomyelin synthases (SMSs) namely SMS1 and SMS2, which are selectively distributed in the trans-Golgi apparatus and the plasma membrane. It has been demonstrated that SMS2 acts as an irreplaceable molecule in the regulation of transmembrane signaling, and loss of SMS2 has been reported to worsen atherosclerosis and liver steatosis. However, the function of SMS2 in platelet activation and its association with the pathological process of thrombosis in acute coronary syndrome (ACS) and portal hypertension (PH) remain unclear. Methods In this study, we tested the role of SMS2 in platelet activation and thrombosis using SMS2 knockout (SMS2 –/–) mice and SMS2-specific inhibitor, D609. Furthermore, we detected SMS2 expression in patients with ACS and PH. Results SMS2 –/– platelets showed significant reduction in platelet aggregation, spreading, clot retraction and in vivo thrombosis. Similar inhibitory effects on platelet activation were detected in D609-treated wild-type platelets. PLCγ/PI3K/Akt signaling pathway was inhibited in SMS2 –/– platelets and D609-treated wild-type platelets. In addition, we discovered that platelet SMS2 expression was remarkably increased in patients with ACS and PH, compared with healthy subjects. Conclusions Our study indicates that SMS2 acts as a positive regulator of platelet activation and thrombosis, and provides a theoretical basis for the potential use of D609 in anti-thrombosis treatment.

In eukaryotes, MEDIATOR is a conserved multi-subunit complex that links transcription factors and RNA polymerase II and that thereby facilitates transcriptional initiation. Although the composition of MEDIATOR has been well studied in yeast and mammals, relatively little is known about the composition of MEDIATOR in plants. By affinity purification followed by mass spectrometry, we identified 28 conserved MEDIATOR subunits in Arabidopsis thaliana, including putative MEDIATOR subunits that were not previously validated. Our results indicated that MED34, MED35, MED36, and MED37 are not Arabidopsis MEDIATOR subunits, as previously proposed. Our results also revealed that two homologous CBP/p300 histone acetyltransferases, HAC1 and HAC5 (HAC1/5) are in fact plant-specific MEDIATOR subunits. The MEDIATOR subunits MED8 and MED25 (MED8/25) are partially responsible for the association of MEDIATOR with HAC1/5, MED8/25 and HAC1/5 co-regulate gene expression and thereby affect flowering time and floral development. Our in vitro observations indicated that MED8 and HAC1 form liquid-like droplets by phase separation, and our in vivo observations indicated that these droplets co-localize in the nuclear bodies at a subset of nuclei. The formation of liquid-like droplets is required for MED8 to interact with RNA polymerase II. In summary, we have identified all of the components of Arabidopsis MEDIATOR and revealed the mechanism underlying the link of histone acetylation and transcriptional regulation.

Trimethylated histone H3 lysine 27 (H3K27me3) is a repressive histone marker that regulates a variety of developmental processes, including those that determine flowering time. However, relatively little is known about the mechanism of how H3K27me3 is recognized to regulate transcription. Here, we identified BAH domain-containing transcriptional regulator 1 (BDT1) as an H3K27me3 reader. BDT1 is responsible for preventing flowering by suppressing the expression of flowering genes. Mutation of the H3K27me3 recognition sites in the BAH domain disrupted the binding of BDT1 to H3K27me3, leading to de-repression of H3K27me3-enriched flowering genes and an early-flowering phenotype. We also found that BDT1 interacts with a family of PHD finger-containing proteins, which we named PHD1-6, and with CPL2, a Pol II carboxyl terminal domain (CTD) phosphatase responsible for transcriptional repression. Pull-down assays showed that the PHD finger-containing proteins can enhance the binding of BDT1 to the H3K27me3 peptide. Mutations in all of the PHD genes caused increased expression of flowering genes and an early-flowering phenotype. This study suggests that the binding of BDT1 to the H3K27me3 peptide, which is enhanced by PHD proteins, is critical for preventing early flowering.

In this paper, a model of the Kelvin probe is established in COMSOL Multiphysics based on electrostatic field theory, and it is verified by measuring the surface potentials. The influence of the probe is also investigated. An improved charge inversion method based on surface potentials measured online is proposed. The surface charge density is directly obtained by the Gauss's theorem to avoid the calculation of the inversion matrix. The improved method is verified by comparing the surface charge density calculated by the analytical method. When considering the effect of the probe, the maximum difference in surface charge density is 0.3 µC/m2 comparing to that when ignoring its effect, and the percentage of the difference is as high as 41%. The results indicate that the effects of the voltage of the probe under online measurement conditions must be considered.

We investigate the onset of detwinning in magnesium alloy Mg-3Al-1Zn under continuous loading with real-time in situ synchrotron X-ray diffraction. Detwinning of the { 10 1 ¯ 2 } extension twins activated both by tension parallel to and compression perpendicular to the c-axis fibers is explored. The experimental results reveal that detwinning of the { 10 1 ¯ 2 } extension twins occurs immediately upon unloading, regardless of whether the twins are activated by tension parallel to or compression perpendicular to the c-axis fibers.

An improved model for the motion dynamics of a metallic particle located in the non-uniform electric field area in the gas insulated system is proposed. To represent the special area, a diverging conducting electrode is used in this study. Based on the fluid mechanics theory, the forces imposed on metallic particle are first developed. The motion process is then divided into two modes, i.e. the particle rolls on the electrode surface and moves in the gap. The collision and reflection processes between the particle and the electrode are crucial to the motion, and they are fully considered in the proposed model. The trajectory of the particle under different voltages is obtained. The evolution of metallic particle is divided into four stages, and it is featured by four quantities, i.e. the critical jumping point, the minimum horizontal position, the falling point, and the motion time. The characteristics for each stage are analysed, and the sensitivity analysis of the quantities are performed. The impacts of the applied voltage, the particle radius, the initial position etc. are discussed. The results provide guidance for particle trap design.