8,023 research outputs found

    Confinement induced by fermion damping in three-dimensional QED

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    The three-dimensional non-compact QED is known to exhibit weak confinement when fermions acquire a finite mass via the mechanism of dynamical chiral symmetry breaking. In this paper, we study the effect of fermion damping caused by elastic scattering on the classical potential between fermions. By calculating the vacuum polarization function that incorporates the fermion damping effect, we show that fermion damping can induce a weak confinement even when the fermions are massless and the chiral symmetry is not broken.Comment: 4 pages, no figur

    Field-effect mobility enhanced by tuning the Fermi level into the band gap of Bi2Se3

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    By eliminating normal fabrication processes, we preserve the bulk insulating state of calcium-doped Bi2Se3 single crystals in suspended nanodevices, as indicated by the activated temperature dependence of the resistivity at low temperatures. We perform low-energy electron beam irradiation (<16 keV) and electrostatic gating to control the carrier density and therefore the Fermi level position in the nanodevices. In slightly p-doped Bi2-xCaxSe3 devices, continuous tuning of the Fermi level from the bulk valence band to the band-gap reveals dramatic enhancement (> a factor of 10) in the field-effect mobility, which suggests suppressed backscattering expected for the Dirac fermion surface states in the gap of topological insulators

    Geometric entanglement from matrix product state representations

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    An efficient scheme to compute the geometric entanglement per lattice site for quantum many-body systems on a periodic finite-size chain is proposed in the context of a tensor network algorithm based on the matrix product state representations. It is systematically tested for three prototypical critical quantum spin chains, which belong to the same Ising universality class. The simulation results lend strong support to the previous claim [Q.-Q. Shi, R. Or\'{u}s, J. O. Fj{\ae}restad, and H.-Q. Zhou, New J. Phys \textbf{12}, 025008 (2010); J.-M. St\'{e}phan, G. Misguich, and F. Alet, Phys. Rev. B \textbf{82}, 180406R (2010)] that the leading finite-size correction to the geometric entanglement per lattice site is universal, with its remarkable connection to the celebrated Affleck-Ludwig boundary entropy corresponding to a conformally invariant boundary condition.Comment: 4+ pages, 3 figure

    Drinfel'd Realization of Quantum Affine Superalgebra Uq(gl(11))^U_q\hat{(gl(1|1))}

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    We obtain Drinfel'd's realization of quantum affine superalgebra Uq(gl(11))^U_q\hat{(gl(1|1))} based on the super version of RS construction method and Gauss decomposition

    Inhibition of the Gab2/PI3K/mTOR signaling ameliorates myeloid malignancy caused by Ptpn11 (Shp2) gain-of-function mutations

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    Activating mutations, such as E76K and D61Y, in PTPN11 (SHP2), a protein tyrosine phosphatase implicated in multiple cell signaling processes, are associated with 35% of patients with juvenile myelomonocytic leukemia (JMML), an aggressive childhood myeloproliferative neoplasm (MPN). Here we show that the interaction between leukemia-associated mutant Shp2 and Gab2, a scaffolding protein important for cytokine-induced PI3K/Akt signaling, was enhanced, and that the mTOR pathway was elevated in Ptpn11E76K/+ leukemic cells. Importantly, MPN induced by the Ptpn11E76K/+ mutation was markedly attenuated in Ptpn11E76K/+/Gab2-/- double mutant mice-overproduction of myeloid cells was alleviated, splenomegaly was diminished and myeloid cell infiltration in nonhematopoietic organs was decreased in these double mutants. Excessive myeloid differentiation of stem cells was also normalized by depletion of Gab2. Acute leukemia progression of MPN was reduced in the double mutant mice and, as such, their survival was much prolonged. Furthermore, treatment of Ptpn11E76K/+ mice with Rapamycin, a specific and potent mTOR inhibitor, mitigated MPN phenotypes. Collectively, this study reveals an important role of the Gab2/PI3K/mTOR pathway in mediating the pathogenic signaling of the PTPN11 gain-of-function mutations and a therapeutic potential of Rapamycin for PTPN11 mutation-associated JMML

    A dynamical model reveals gene co-localizations in nucleus

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    Co-localization of networks of genes in the nucleus is thought to play an important role in determining gene expression patterns. Based upon experimental data, we built a dynamical model to test whether pure diffusion could account for the observed co-localization of genes within a defined subnuclear region. A simple standard Brownian motion model in two and three dimensions shows that preferential co-localization is possible for co-regulated genes without any direct interaction, and suggests the occurrence may be due to a limitation in the number of available transcription factors. Experimental data of chromatin movements demonstrates that fractional rather than standard Brownian motion is more appropriate to model gene mobilizations, and we tested our dynamical model against recent static experimental data, using a sub-diffusion process by which the genes tend to colocalize more easily. Moreover, in order to compare our model with recently obtained experimental data, we studied the association level between genes and factors, and presented data supporting the validation of this dynamic model. As further applications of our model, we applied it to test against more biological observations. We found that increasing transcription factor number, rather than factory number and nucleus size, might be the reason for decreasing gene co-localization. In the scenario of frequency-or amplitude-modulation of transcription factors, our model predicted that frequency-modulation may increase the co-localization between its targeted genes
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