503 research outputs found

    Matrix product state comparison of the numerical renormalization group and the variational formulation of the density matrix renormalization group

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    Wilson's numerical renormalization group (NRG) method for solving quantum impurity models yields a set of energy eigenstates that have the form of matrix product states (MPS). White's density matrix renormalization group (DMRG) for treating quantum lattice problems can likewise be reformulated in terms of MPS. Thus, the latter constitute a common algebraic structure for both approaches. We exploit this fact to compare the NRG approach for the single-impurity Anderson model to a variational matrix product state approach (VMPS), equivalent to single-site DMRG. For the latter, we use an ``unfolded'' Wilson chain, which brings about a significant reduction in numerical costs compared to those of NRG. We show that all NRG eigenstates (kept and discarded) can be reproduced using VMPS, and compare the difference in truncation criteria, sharp vs. smooth in energy space, of the two approaches. Finally, we demonstrate that NRG results can be improved upon systematically by performing a variational optimization in the space of variational matrix product states, using the states produced by NRG as input.Comment: 19 pages, 14 figure

    Non-Fermi liquid behavior in transport through Co doped Au chains

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    We calculate the conductance as a function of temperature G(T)G(T) through Au monoatomic chains containing one Co atom as a magnetic impurity, and connected to two conducting leads with a 4-fold symmetry axis. Using the information derived from {\it ab initio} calculations, we construct an effective model \Heff that hybridizes a 3d7^7 quadruplet at the Co site with two 3d8^8 triplets through the hopping of 5dxz_{xz} and 5dyz_{yz} electrons of Au. The quadruplet is split by spin anisotropy due to spin-orbit coupling. Solving \Heff with the numerical renormalization group (NRG) % Wb: reverted my own change we find that at low temperatures G(T)=abTG(T)=a-b \sqrt{T} and the ground state impurity entropy is ln(2)/2\ln(2)/2, a behavior similar to the two-channel Kondo model. Stretching the chain leads to a non Kondo phase, with the physics of the underscreened Kondo model at the quantum critical point.Comment: Accepted in Physical Review Letter

    Kondo decoherence: finding the right spin model for iron impurities in gold and silver

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    We exploit the decoherence of electrons due to magnetic impurities, studied via weak localization, to resolve a longstanding question concerning the classic Kondo systems of Fe impurities in the noble metals gold and silver: which Kondo-type model yields a realistic description of the relevant multiple bands, spin and orbital degrees of freedom? Previous studies suggest a fully screened spin SS Kondo model, but the value of SS remained ambiguous. We perform density functional theory calculations that suggest S=3/2S = 3/2. We also compare previous and new measurements of both the resistivity and decoherence rate in quasi 1-dimensional wires to numerical renormalization group predictions for S=1/2,1S=1/2,1 and 3/2, finding excellent agreement for S=3/2S=3/2.Comment: 4 pages, 4 figures, shortened for PR

    RAD54 family translocases counter genotoxic effects of RAD51 in human tumor cells.

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    The RAD54 family DNA translocases have several biochemical activities. One activity, demonstrated previously for the budding yeast translocases, is ATPase-dependent disruption of RAD51-dsDNA binding. This activity is thought to promote dissociation of RAD51 from heteroduplex DNA following strand exchange during homologous recombination. In addition, previous experiments in budding yeast have shown that the same activity of Rad54 removes Rad51 from undamaged sites on chromosomes; mutants lacking Rad54 accumulate nonrepair-associated complexes that can block growth and lead to chromosome loss. Here, we show that human RAD54 also promotes the dissociation of RAD51 from dsDNA and not ssDNA. We also show that translocase depletion in tumor cell lines leads to the accumulation of RAD51 on chromosomes, forming complexes that are not associated with markers of DNA damage. We further show that combined depletion of RAD54L and RAD54B and/or artificial induction of RAD51 overexpression blocks replication and promotes chromosome segregation defects. These results support a model in which RAD54L and RAD54B counteract genome-destabilizing effects of direct binding of RAD51 to dsDNA in human tumor cells. Thus, in addition to having genome-stabilizing DNA repair activity, human RAD51 has genome-destabilizing activity when expressed at high levels, as is the case in many human tumors

    Decoherence and relaxation in the interacting quantum dot system

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    In this paper we study the low temperature kinetics of the electrons in the system composed of a quantum dot connected to two leads by solving the equation of motion. The decoherence and the relaxation of the system caused by the gate voltage noise and electron-phonon scattering are investigated. In order to take account of the strong correlation of the electrons in this system, the quasi-exact wave functions are calculated using an improved matrix product states algorithm. This algorithm enables us to calculate the wave functions of the ground state and the low lying excited states with satisfied accuracy and thus enables us to study the kinetics of the system more effectively. It is found that although both of these two mechanisms are proportional to the electron number operator in the dot, the kinetics are quite different. The noise induced decoherence is much more effective than the energy relaxation, while the energy relaxation and decoherence time are of the same order for the electron-phonon scattering. Moreover, the noise induced decoherence increases with the lowering of the dot level, but the relaxation and decoherence due to the electron-phonon scattering decrease.Comment: Minor revision. Add journal referenc

    Correlation density matrices for 1- dimensional quantum chains based on the density matrix renormalization group

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    A useful concept for finding numerically the dominant correlations of a given ground state in an interacting quantum lattice system in an unbiased way is the correlation density matrix. For two disjoint, separated clusters, it is defined to be the density matrix of their union minus the direct product of their individual density matrices and contains all correlations between the two clusters. We show how to extract from the correlation density matrix a general overview of the correlations as well as detailed information on the operators carrying long-range correlations and the spatial dependence of their correlation functions. To determine the correlation density matrix, we calculate the ground state for a class of spinless extended Hubbard models using the density matrix renormalization group. This numerical method is based on matrix product states for which the correlation density matrix can be obtained straightforwardly. In an appendix, we give a detailed tutorial introduction to our variational matrix product state approach for ground state calculations for 1- dimensional quantum chain models. We show in detail how matrix product states overcome the problem of large Hilbert space dimensions in these models and describe all techniques which are needed for handling them in practice.Comment: 50 pages, 34 figures, to be published in New Journal of Physic

    Spatially resolved manipulation of single electrons in quantum dots using a scanned probe

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    The scanning metallic tip of a scanning force microscope was coupled capacitively to electrons confined in a lithographically defined gate-tunable quantum dot at a temperature of 300 mK. Single electrons were made to hop on or off the dot by moving the tip or by changing the tip bias voltage owing to the Coulomb-blockade effect. Spatial images of conductance resonances map the interaction potential between the tip and individual electronic quantum dot states. Under certain conditions this interaction is found to contain a tip-voltage induced and a tip-voltage independent contribution.Comment: 4 pages, 4 figure

    Survivin a radiogenetic promoter for glioblastoma viral gene therapy independently from CArG motifs

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    BACKGROUND: Radiogenetic therapy is a novel approach in the treatment of cancer, which employs genetic modification to alter the sensitivity of tumor cells to the effect of applied radiation. AIM: To select a potent radiation inducible promoter in the context of brain tumors and to investigate if CArG radio responsive motifs or other elements in the promoter nucleotide sequences can correlate to its response to radiation. METHODS: To select initial candidates for promoter inducible elements, the levels of mRNA expression of six different promoters were assessed using Quantitative RTPCR in D54 MG cells before and after radiation exposure. Recombinant Ad/reporter genes driven by five different promoters; CMV, VEGF, FLT-1, DR5 and survivin were constructed. Glioma cell lines were infected with different multiplicity of infection of the (promoter) Ad or CMV Ad. Cells were then exposed to a range of radiation (0–12 Gy) at single fraction. Fluorescent microscopy, Luc assay and X-gal staining was used to detect the level of expression of related genes. Different glioma cell lines and normal astrocytes were infected with Ad survivin and exposed to radiation. The promoters were analyzed for presence of CArG radio-responsive motifs and CCAAT box consensus using NCBI blast bioinformatics software. RESULTS: Radiotherapy increases the expression of gene expression by 1.25–2.5 fold in different promoters other than survivin after 2 h of radiation. RNA analysis was done and has shown an increase in copy number of tenfold for survivin. Most importantly cells treated with RT and Ad Luc driven by survivin promoter showed a fivefold increase in expression after 2 Gy of radiation in comparison to non-irradiated cells. Presence or absence of CArG motifs did not correlate with promoter response to radiation. Survivin with the best response to radiation had the lowest number of CCAAT box. CONCLUSION: Survivin is a selective potent radiation inducible promoter for glioblastoma viral gene therapy and this response to radiation could be independent of CArG motifs
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