809 research outputs found

    Electrical Control of Magnetization in Charge-ordered Multiferroic LuFe2O4

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    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

    Expressions and clinic significance of miRNA-143, miRNA- 34A, miRNA-944, miRNA-101 and miRNA-218 in cervical cancer tissues

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    Purpose: To search for novel biomarkers for early diagnosis of cervical cancer, as well as novel therapeutic target for cervical cancer.Methods: A total of 96 cervical tissue specimens were collected from patients in the Second Affiliated Hospital of Zhengzhou University, out of which 10 were normal control. The remaining specimens (86) were cervical cancer specimens and were divided into 4 groups (A - D) based on tumor-biomarker levels of CA125 and SCC. Quantitative real-time polymerase chain reaction technology (qRT-PCR) was used to detect the expressions of miRNA-143, miRNA-34A, miRNA-944, miRNA-101 and miRNA-218 in the cervical cancer tissues.Results: The levels of CA125 (U/mL) and SCC (ug/L) expressed in normal control group and groups A - D were 11.75 and 0.73 (n = 10), 382 and 2.72 (n = 25), 912.9 and 3.93 (n = 21), 1675 and 5.87 (n = 29), and 2120 and 6.66 (n = 11), respectively. Furthermore, qRT-PCR results showed that the expressions of miRNA-944 and miRNA-218 in cervical cancer tissues were markedly up-regulated compared to normal control tissues (p < 0.01). In contrast, the expression level of miRNA-143, miRNA-34A, and miRNA-101 were significantly decreased (p < 0.01).Conclusion: The biomarkers, miRNA-143, miRNA-34A, miRNA-944, miRNA-101 and miRNA-218, can be considered novel for early diagnosis of cervical cancer.Keywords: Cervical cancer, Biomarkers, miRNA-143, miRNA-34A, miRNA-944, miRNA-101, miRNA- 21

    6-Mercaptopurine attenuates tumor necrosis factor-Ī± production in microglia through Nur77-mediated transrepression and PI3K/Akt/mTOR signaling-mediated translational regulation

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    Physical interaction between Nur77 and p65. BV-2 cells were pretreated with 6-MP (50Ā Ī¼M) for 16Ā h followed by exposure to LPS (100Ā ng/ml) for 60Ā min. Nuclear extracts were harvested for immunoprecipitation (IP) experiments using anti-Nur77 and anti-p65 antibodies. Immunoblot (IB) analyses of the immunoprecipitates were performed using these antibodies. The immunoblots are representative of three independent experiments. (TIF 280 kb

    Glycogen synthase kinase-3Ī² inactivation inhibits tumor necrosis factor-Ī± production in microglia by modulating nuclear factor ĪŗB and MLK3/JNK signaling cascades

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    <p>Abstract</p> <p>Background</p> <p>Deciphering the mechanisms that modulate the inflammatory response induced by microglial activation not only improves our insight into neuroinflammation but also provides avenues for designing novel therapies that could halt inflammation-induced neuronal degeneration. Decreasing glycogen synthase kinase-3Ī² (GSK-3Ī²) activity has therapeutic benefits in inflammatory diseases. However, the exact molecular mechanisms underlying GSK-3Ī² inactivation-mediated suppression of the inflammatory response induced by microglial activation have not been completely clarified. Tumor necrosis factor-Ī± (TNF-Ī±) plays a central role in injury caused by neuroinflammation. We investigated the regulatory effect of GSK-3Ī² on TNF-Ī± production by microglia to discern the molecular mechanisms of this modulation.</p> <p>Methods</p> <p>Lipopolysaccharide (LPS) was used to induce an inflammatory response in cultured primary microglia or murine BV-2 microglial cells. Release of TNF-Ī± was measured by ELISA. Signaling molecules were analyzed by western blotting, and activation of NF-ĪŗB and AP-1 was measured by ELISA-based DNA binding analysis and luciferase reporter assay. Protein interaction was examined by coimmunoprecipitation.</p> <p>Results</p> <p>Inhibition of GSK-3Ī² by selective GSK-3Ī² inhibitors or by RNA interference attenuated LPS-induced TNF-Ī± production in cultured microglia. Exploration of the mechanisms by which GSK-3Ī² positively regulates inflammatory response showed that LPS-induced IĪŗB-Ī± degradation, NF-ĪŗBp65 nuclear translocation, and p65 DNA binding activity were not affected by inhibition of GSK-3Ī² activity. However, GSK-3Ī² inactivation inhibited transactivation activity of p65 by deacetylating p65 at lysine 310. Furthermore, we also demonstrated a functional interaction between mixed lineage kinase 3 (MLK3) and GSK-3Ī² during LPS-induced TNF-Ī± production in microglia. The phosphorylated levels of MLK3, MKK4, and JNK were increased upon LPS treatment. Decreasing GSK-3Ī² activity blocked MLK3 signaling cascades through disruption of MLK3 dimerization-induced autophosphorylation, ultimately leading to a decrease in TNF-Ī± secretion.</p> <p>Conclusion</p> <p>These results suggest that inactivation of GSK-3Ī² might represent a potential strategy to downregulate microglia-mediated inflammatory processes.</p

    Hydrogen sulfide inhibits the renal fibrosis of obstructive nephropathy

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    Hydrogen sulfide has recently been found decreased in chronic kidney disease. Here we determined the effect and underlying mechanisms of hydrogen sulfide on a rat model of unilateral ureteral obstruction. Compared with normal rats, obstructive injury decreased the plasma hydrogen sulfide level. Cystathionine-Ī²-synthase, a hydrogen sulfide-producing enzyme, was dramatically reduced in the ureteral obstructed kidney, but another enzyme cystathionine-Ī³-lyase was increased. A hydrogen sulfide donor (sodium hydrogen sulfide) inhibited renal fibrosis by attenuating the production of collagen, extracellular matrix, and the expression of Ī±-smooth muscle actin. Meanwhile, the infiltration of macrophages and the expression of inflammatory cytokines including interleukin-1Ī², tumor necrosis factor-Ī±, and monocyte chemoattractant protein-1 in the kidney were also decreased. In cultured kidney fibroblasts, a hydrogen sulfide donor inhibited the cell proliferation by reducing DNA synthesis and downregulating the expressions of proliferation-related proteins including proliferating cell nuclear antigen and c-Myc. Further, the hydrogen sulfide donor blocked the differentiation of quiescent renal fibroblasts to myofibroblasts by inhibiting the transforming growth factor-Ī²1-Smad and mitogen-activated protein kinase signaling pathways. Thus, low doses of hydrogen sulfide or its releasing compounds may have therapeutic potentials in treating chronic kidney disease

    Electronic Structures of Graphene Layers on Metal Foil: Effect of Point Defects

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    Here we report a facile method to generate a high density of point defects in graphene on metal foil and show how the point defects affect the electronic structures of graphene layers. Our scanning tunneling microscopy (STM) measurements, complemented by first principle calculations, reveal that the point defects result in both the intervalley and intravalley scattering of graphene. The Fermi velocity is reduced in the vicinity area of the defect due to the enhanced scattering. Additionally, our analysis further points out that periodic point defects can tailor the electronic properties of graphene by introducing a significant bandgap, which opens an avenue towards all-graphene electronics.Comment: 4 figure

    Arbitrarily primed sequence-related amplified polymorphism (AP-SRAP)

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    Sequence-related amplified polymorphism (SRAP) is a new-type molecular technique that targets coding sequences in the genome and results in a moderate number of co-dominant markers. Based on the SRAP program, the random primer combinations of SRAP, amplified fragment length polymorphism (AFLP) and simple sequence repeat (SSR) were used as new primers in marker analysis. We defined this technique as arbitrarily primed sequence-related amplified polymorphism (AP-SRAP). Of 256 tested AP-SRAP primers, 37.6% primers produced polymorphic patterns from the DNA of one or more species, which showed that AP-SRAP is an effective method to screen markers. Additionally, 80 SRAP primers were used to screen markers in seven plant species (Chinese cabbage, Chinese kale, eggplant, pepper, cucumber, rose and lily), which indicated obvious polymorphism. The primers of AP-SRAP combine simply and reliably. It can overcome the limitation of the number of standard SRAP primers, make greater use of the supply of alternative primers, and potentially reduce laboratory costs. We expect that AP-SRAP may be of wide application in identity testing, population studies, linkage analysis and genome mapping.Keywords: Arbitrarily primed amplification, DNA markers, plantsAfrican Journal of Biotechnology Vol. 12(29), pp. 4588-459
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