1,106 research outputs found

    Low magnetic field reversal of electric polarization in a Y-type hexaferrite

    Full text link
    Magnetoelectric multiferroics in which ferroelectricity and magnetism coexist have attracted extensive attention because they provide great opportunities for the mutual control of electric polarization by magnetic fields and magnetization by electric fields. From a practical point view, the main challenge in this field is to find proper multiferroic materials with a high operating temperature and great magnetoelectric sensitivity. Here we report on the magnetically tunable ferroelectricity and the giant magnetoelectric sensitivity up to 250 K in a Y-type hexaferrite, BaSrCoZnFe11AlO22. Not only the magnitude but also the sign of electric polarization can be effectively controlled by applying low magnetic fields (a few hundreds of Oe) that modifies the spiral magnetic structures. The magnetically induced ferroelectricity is stabilized even in zero magnetic field. Decayless reproducible flipping of electric polarization by oscillating low magnetic fields is shown. The maximum linear magnetoelectric coefficient reaches a high value of ~ 3.0\times10^3 ps/m at 200 K.Comment: 9 pages, 5 figures, a couple of errors are correcte

    Minimal effect of sleep on the risk of age-related macular degeneration: a Mendelian randomization study

    Get PDF
    AimsObservational studies have shown that sleep pattern is associated with age-related macular degeneration (AMD), but whether sleep pattern is a causal factor for AMD remains unclear. This study aims to use Mendelian randomization (MR) analysis to investigate the potential causal relationship between sleep traits and AMD.MethodsThis is a two-sample MR study. The single-nucleotide polymorphisms associated with AMD and early AMD were selected as the outcome from two different genome-wide association studies (GWAS): the early AMD GWAS with 14,034 cases and 91,214 controls, and AMD GWAS with 3,553 cases and 147,089 controls. The datasets of sleep duration, daytime dozing, and sleeplessness were used as exposure, which comprised nearly 0.46 million participants. Inverse-variance weighted method was used as the main result, and comprehensive sensitivity analyses were conducted to estimate the robustness of identified associations and the impact of potential horizontal pleiotropy.ResultsThrough MR analysis, we found that sleep duration was significantly associated with AMD (OR = 0.983, 95% CI = 0.970–0.996, P-value = 0.01). We also found suggestive evidence for the association of genetically predicted sleep duration with early AMD, which showed a consistent direction of effect with a marginal significance (OR = 0.724, 95% CI = 0.503–1.041, P-value = 0.08). Sensitivity analyses further supported the robustness of the causal relationship between sleep duration and AMD. However, we were unable to determine the relationship between daytime dozing or sleeplessness and AMD (including early AMD) (P-value > 0.05).ConclusionSleep duration affects the causal risk for AMD; that is, longer sleep duration reduces the risk of AMD, while shorter sleep duration increases the risk of AMD. Although the influence is minimal, keeping adequate sleep duration is recommended, especially for patients with intermediate or advanced AMD

    Electrical Control of Magnetization in Charge-ordered Multiferroic LuFe2O4

    Full text link
    LuFe2O4 exhibits multiferroicity due to charge order on a frustrated triangular lattice. We find that the magnetization of LuFe2O4 in the multiferroic state can be electrically controlled by applying voltage pulses. Depending on with or without magnetic fields, the magnetization can be electrically switched up or down. We have excluded thermal heating effect and attributed this electrical control of magnetization to an intrinsic magnetoelectric coupling in response to the electrical breakdown of charge ordering. Our findings open up a new route toward electrical control of magnetization.Comment: 14 pages, 5 figure

    Molecular mechanism of ethylene stimulation of latex yield in rubber tree (Hevea brasiliensis) revealed by de novo sequencing and transcriptome analysis

    Get PDF
    Differential expression of unigenes involved in hormone signaling in E8 and E24 compared to C samples of Hevea brasiliensis. Ethylene signalling pathway: ETR1: ETHYLENE RESPONSE 1; CTR1: CONSTITUTIVE TRIPLE RESPONSE 1; EIN2: ETHYLENE INSENSITIVE 2; EIN3: ETHYLENE INSENSITIVE 3; ERF1/2: ETHYLENE RESPONSE FACTOR 1/2; EBF1/2: EIN3 binding F-Box protein 1/2; BR signaling pathway: BRI1: Brassinosteroid-Insensitive 1; BAK1: BRI1-associated kinase 1; BKI1: BRI1 KINASE INHIBITOR 1; BSK: BR SIGNALING KINASE; BSU1: bri1 SUPPRESSOR 1; BIN2: BRASSINOSTEROID-INSENSITIVE 2; BZR1/2: BRASSINAZOLE RESISTANT 1/2; TCH: TOUCH genes; CYCD3: CYCLIN D3; GA signaling pathway: GID1: GIBBERELLIN INSENSITIVE DWARF 1; GID2: GIBBERELLIN INSENSITIVE DWARF 2; DELLAs: DELLA growth inhibitors; TF: transcriptional factor; Auxin signaling pathway: AUX1: AUXIN1; TIR1: TRANSPORT INHIBITOR RESPONSE 1; IAA: INDOLE ACETIC ACID; ARF: AUXIN RESPONSE FACTOR; SAUR: Small Auxin-Up RNA; G10H: geraniol 10-hydroxylase gene; Cytokinin signaling pathway: CRE1: CYTOKININ RESPONSE 1; AHP: histidine phosphotransfer protein; B-ARR: type-B response regulator (ARR); A-ARR: type-A response regulator (ARR); SA signalling pathway: NPR1: Non-expressor of pathogenesis-related genes 1; TGA: the bZIP transcription factors; PR1: pathogenesis related protein 1; JA signaling pathway: JAR1: JASMONATES RESISTANT 1; JA-Ile: jasmonoyl isoleucine; JAZ: Jasmonate ZIM-domain-containing protein; MYC2: a basic helix-loop-helix (bHLH) transcription factor; ORCA3: Octadecanoid-derivative Responsive Catharanthus AP2-domain gene; ABA signalling pathway: PYR1/PYLs: Pyrabactin Resistance Protein1/PYR-Like proteins; PP2Cs: protein phosphatases which fall under the category of type 2C; SnRK2: SNF1 (Sucrose-Nonfermenting Kinase1)-related protein kinase 2: ABF: ABA responsive element (ABRE) binding factors. Cells with gray border lines in the upper rows represent differentially expressed unigenes in E8 compared to C and cells with green border lines in the lower rows represent differentially expressed unigenes in E24 compared to C. Relative levels of expression are showed by a color gradient from low (blue) to high (red). (JPG 249 kb

    Further Study On U(1) Gauge Invariance Restoration

    Full text link
    To further investigate the applicability of the projection scheme for eliminating the unphysical divergence s/me2s/m_e^2 due to U(1) gauge invariance violation, we study the process e+W+e+tˉ+be^-+W^+\to e^-+\bar t+b which possesses advantages of simplicity and clearness. Our study indicates that the projection scheme can indeed eliminate the unphysical divergence s/me2s/m_e^2 caused by the U(1) gauge invariance violation and the scheme can apply to very high energy region.Comment: Latex, 13 pages, 4 EPS fiure

    BCL9 enhances the development of cervical carcinoma by deactivating CPEB3/EGFR axis

    Get PDF
    Purpose: To investigate the differential expression of BCL9 in cervical carcinoma samples, analyze its biological functions in regulating malignant phenotypes of cervical carcinoma cells, and to explore its potential molecular mechanism.Methods: Expression levels of BCL9 in 58 pairs of cervical carcinoma tissues and paracancerous tissues were determined using quantitative real time-polymerase chain reaction (qRT-PCR). Kaplan- Meier curves were used to analyze the prognostic potential of BCL9 in cervical carcinoma. After knockdown using BCL9 by lentivirus transfection, proliferative and migratory changes in Siha and HeLa cells were determined by CCK-8, colony formation and Transwell assays. Cytoplasmic polyadenylation element binding protein 3 (CPEB3), the potential downstream target of BCL9, was confirmed via dualluciferase reporter assay. Western blot analyses were conducted to determine the protein levels of CPEB3, EGFR, AKT and p21 in Siha and HeLa cells with BCL9 knockdown. The co-regulation of BCL9 and CPEB3 on phenotypes of cervical carcinoma cell was investigated.Results: BCL9 was upregulated in cervical carcinoma tissues. The high level of BCL9 was predicted by the tumor size, advanced stage and poor prognosis. The knockdown of BCL9 significantly weakened proliferative and migratory abilities of Siha and HeLa cells (p < 0.05). CPEB3 was the downstream target of BCL9, and was lowly expressed in cervical carcinoma tissues. The knockdown of BCL9 upregulated CPEB3, and downregulated EGFR, AKT and p21 (p < 0.05). The knockdown of CPEB3 also reversed the influence of silenced BCL9 in regulating its proliferative and migratory abilities in cervical carcinoma cells (p < 0.05).Conclusion: BCL9 drives the deterioration of cervical carcinoma by inhibiting the CPEB3/EGFR axis.Thus, BCL9 may be a novel molecular target for cervical carcinoma treatment

    Crystal structure of tubulin folding cofactor A from Arabidopsis thaliana and its β-tubulin binding characterization

    Get PDF
    AbstractMicrotubules are composed of polymerized α/β-tubulin heterodimers. Biogenesis of assembly-competent tubulin dimers is a complex multistep process that requires sequential actions of distinct molecular chaperones and cofactors. Tubulin folding cofactor A (TFCA), which captures β-tubulin during the folding pathway, has been identified in many organisms. Here, we report the crystal structure of Arabidopsis thaliana TFC A (KIESEL, KIS), which forms a monomeric three-helix bundle. The functional binding analysis demonstrated that KIS interacts with β-tubulin in plant. Furthermore, mutagenesis studies indicated that the α-helical regions of KIS participate in β-tubulin binding. Unlike the budding yeast TFC A, the two loop regions of KIS are not required for this interaction suggesting a distinct binding mechanism of TFC A to β-tubulin in plants.Structured summaryMINT-7968902, MINT-7968915, MINT-7968951, MINT-7968966: KIS (uniprotkb:O04350) physically interacts (MI:0915) with Tub9 (uniprotkb:P29517) by anti tag coimmunoprecipitation (MI:0007)MINT-7968928: KIS (uniprotkb:O04350) and Tub9 (uniprotkb:P29517) physically interact (MI:0915) by bimolecular fluorescence complementation (MI:0809
    corecore