89 research outputs found
Making confining strings out of mesons
The light mesons such as pi, rho, omega, f0, and a0 are possible candidates
of magnetic degrees of freedom, if a magnetic dual picture of QCD exists. We
construct a linear sigma model to describe spontaneous breaking of the magnetic
gauge group, in which there is a stable vortex configuration of vector and
scalar mesons. We numerically examine whether such a string can be interpreted
as the confining string. By using meson masses and couplings as inputs, we
calculate the tension of the string as well as the strength of the Coulomb
force between static quarks. They are found to be consistent with those
inferred from the quarkonium spectrum and the Regge trajectories of hadrons. By
using the same Lagrangian, the critical temperature of the QCD phase transition
is estimated, and a non-trivial flavor dependence is predicted. We also discuss
a possible connection between the Seiberg duality and the magnetic model we
studied.Comment: 22 pages, 2 figures, 3 tables, typos corrected, references adde
Berry phase in Magnetic Superconductors
In magnetic systems, electronic bands often acquire nontrivial topological
structure characterized by gauge flux distribution in momentum (k)-space. It
sometimes follows that the phase of the wavefunctions cannot be defined
uniquely over the whole Brillouin zone. In this Letter we develop a theory of
superconductivity in the presence of this gauge flux both in two- and
three-dimensional systems. It is found that the superconducting gap has "nodes"
as a function of k where the Fermi surface is penetrated by a gauge string.Comment: 4 pages, 3 figures, substantial changes in the presentation, to be
published in Phys. Rev. Let
Effects of Zirconium Doping Into a Monoclinic Scheelite BiVO4 Crystal on Its Structural, Photocatalytic, and Photoelectrochemical Properties
Effects of zirconium (Zr) doping into BiVO4 powder on its structural properties and photocatalytic activity for O2 evolution were examined. The formation of BiVO4 powder crystallized in a monoclinic scheelite structure (ms-BiVO4) was achieved when the sample was doped with a relatively small amount of Zr. The photocatalytic activity of Zr-doped ms-BiVO4 powder was much higher than that of non-doped ms-BiVO4. However, further doping caused a reduction of photocatalytic activity for O2 evolution due to the occurrence of structural alterations into tetragonal scheelite and tetragonal zircon structures. Similar effects of Zr doping were also observed for the photoelectrochemical (PEC) system based on BiVO4 thin films doped with various amounts of Zr. Thus, Zr doping was confirmed to be effective for improvements of photocatalytic and PEC functions of BiVO4 for water oxidation
Extracellular nanovesicles for packaging of CRISPR-Cas9 protein and sgRNA to induce therapeutic exon skipping
Prolonged expression of the CRISPR-Cas9 nuclease and gRNA from viral vectors may cause off-target mutagenesis and immunogenicity. Thus, a transient delivery system is needed for therapeutic genome editing applications. Here, we develop an extracellular nanovesicle-based ribonucleoprotein delivery system named NanoMEDIC by utilizing two distinct homing mechanisms. Chemical induced dimerization recruits Cas9 protein into extracellular nanovesicles, and then a viral RNA packaging signal and two self-cleaving riboswitches tether and release sgRNA into nanovesicles. We demonstrate efficient genome editing in various hard-to-transfect cell types, including human induced pluripotent stem (iPS) cells, neurons, and myoblasts. NanoMEDIC also achieves over 90% exon skipping efficiencies in skeletal muscle cells derived from Duchenne muscular dystrophy (DMD) patient iPS cells. Finally, single intramuscular injection of NanoMEDIC induces permanent genomic exon skipping in a luciferase reporter mouse and in mdx mice, indicating its utility for in vivo genome editing therapy of DMD and beyond
A liver-derived secretory protein, selenoprotein P, causes insulin resistance
金沢大学医薬保健研究域医学系The liver may regulate glucose homeostasis by modulating the sensitivity/resistance of peripheral tissues to insulin, by way of the production of secretory proteins, termed hepatokines. Here, we demonstrate that selenoprotein P (SeP), a liver-derived secretory protein, causes insulin resistance. Using serial analysis of gene expression (SAGE) and DNA chip methods, we found that hepatic SeP mRNA levels correlated with insulin resistance in humans. Administration of purified SeP impaired insulin signaling and dysregulated glucose metabolism in both hepatocytes and myocytes. Conversely, both genetic deletion and RNA interference-mediated knockdown of SeP improved systemic insulin sensitivity and glucose tolerance in mice. The metabolic actions of SeP were mediated, at least partly, by inactivation of adenosine monophosphate-activated protein kinase (AMPK). In summary, these results demonstrate a role of SeP in the regulation of glucose metabolism and insulin sensitivity and suggest that SeP may be a therapeutic target for type 2 diabetes. © 2010 Elsevier Inc
Selenoprotein P as a diabetes-associated hepatokine that impairs angiogenesis by inducing VEGF resistance in vascular endothelial cells
Aims/hypothesis Impaired angiogenesis induced by vascular endothelial growth factor (VEGF) resistance is a hallmark of vascular complications in type 2 diabetes; however, its molecular mechanism is not fully understood. We have previously identified selenoprotein P (SeP, encoded by the SEPP1 gene in humans) as a liver-derived secretory protein that induces insulin resistance. Levels of serum SeP and hepatic expression of SEPP1 are elevated in type 2 diabetes. Here, we investigated the effects of SeP on VEGF signalling and angiogenesis. Methods We assessed the action of glucose on Sepp1 expression in cultured hepatocytes. We examined the actions of SeP on VEGF signalling and VEGF-induced angiogenesis in HUVECs. We assessed wound healing in mice with hepatic SeP overexpression or SeP deletion. The blood flow recovery after ischaemia was also examined by using hindlimb ischaemia model with Sepp1-heterozygous-knockout mice. Results Treatment with glucose increased gene expression and transcriptional activity for Sepp1 in H4IIEC hepatocytes. Physiological concentrations of SeP inhibited VEGF-stimulated cell proliferation, tubule formation and migration in HUVECs. SeP suppressed VEGF-induced reactive oxygen species (ROS) generation and phosphorylation of VEGF receptor 2 (VEGFR2) and extracellular signal-regulated kinase 1/2 (ERK1/2) in HUVECs. Wound closure was impaired in the mice overexpressing Sepp1, whereas it was improved in SeP-/-mice. SeP+/-mice showed an increase in blood flow recovery and vascular endothelial cells after hindlimb ischaemia. Conclusions/interpretation The hepatokine SeP may be a novel therapeutic target for impaired angiogenesis in type 2 diabetes. © 2014 Springer-Verlag Berlin Heidelberg
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