Fixed-Node Monte Carlo Calculations for the 1d Kondo Lattice Model

The effectiveness of the recently developed Fixed-Node Quantum Monte Carlo method for lattice fermions, developed by van Leeuwen and co-workers, is tested by applying it to the 1D Kondo lattice, an example of a one-dimensional model with a sign problem. The principles of this method and its implementation for the Kondo Lattice Model are discussed in detail. We compare the fixed-node upper bound for the ground state energy at half filling with exact-diagonalization results from the literature, and determine several spin correlation functions. Our `best estimates' for the ground state correlation functions do not depend sensitively on the input trial wave function of the fixed-node projection, and are reasonably close to the exact values. We also calculate the spin gap of the model with the Fixed-Node Monte Carlo method. For this it is necessary to use a many-Slater-determinant trial state. The lowest-energy spin excitation is a running spin soliton with wave number pi, in agreement with earlier calculations.Comment: 19 pages, revtex, contribution to Festschrift for Hans van Leeuwe

Green Function Monte Carlo with Stochastic Reconfiguration

A new method for the stabilization of the sign problem in the Green Function Monte Carlo technique is proposed. The method is devised for real lattice Hamiltonians and is based on an iterative ''stochastic reconfiguration'' scheme which introduces some bias but allows a stable simulation with constant sign. The systematic reduction of this bias is in principle possible. The method is applied to the frustrated J1-J2 Heisenberg model, and tested against exact diagonalization data. Evidence of a finite spin gap for J2/J1 >~ 0.4 is found in the thermodynamic limit.Comment: 13 pages, RevTeX + 3 encapsulated postscript figure

Direct magneto-optical compression of an effusive atomic beam for high-resolution focused ion beam application

An atomic rubidium beam formed in a 70 mm long two-dimensional magneto-optical trap (2D MOT), directly loaded from a collimated Knudsen source, is analyzed using laser-induced fluorescence. The longitudinal velocity distribution, the transverse temperature and the flux of the atomic beam are reported. The equivalent transverse reduced brightness of an ion beam with similar properties as the atomic beam is calculated because the beam is developed to be photoionized and applied in a focused ion beam. In a single two-dimensional magneto-optical trapping step an equivalent transverse reduced brightness of $(1.0\substack{+0.8-0.4})$ $\times 10^6$ A/(m$^2$ sr eV) was achieved with a beam flux equivalent to $(0.6\substack{+0.3-0.2})$ nA. The temperature of the beam is further reduced with an optical molasses after the 2D MOT. This increased the equivalent brightness to $(6\substack{+5-2})$$\times 10^6$ A/(m$^2$ sr eV). For currents below 10 pA, for which disorder-induced heating can be suppressed, this number is also a good estimate of the ion beam brightness that can be expected. Such an ion beam brightness would be a six times improvement over the liquid metal ion source and could improve the resolution in focused ion beam nanofabrication.Comment: 10 pages, 8 figures, 1 tabl

Optimization of Gutzwiller Wavefunctions in Quantum Monte Carlo

Gutzwiller functions are popular variational wavefunctions for correlated electrons in Hubbard models. Following the variational principle, we are interested in the Gutzwiller parameters that minimize e.g. the expectation value of the energy. Rewriting the expectation value as a rational function in the Gutzwiller parameters, we find a very efficient way for performing that minimization. The method can be used to optimize general Gutzwiller-type wavefunctions both, in variational and in fixed-node diffusion Monte Carlo.Comment: 9 pages RevTeX with 10 eps figure

Unbalanced segregation of a paternal t(9;11)(p24.3;p15.4) translocation causing familial Beckwith-Wiedemann syndrome: a case report.

BACKGROUND: The vast majority of cases with Beckwith-Wiedemann syndrome (BWS) are caused by a molecular defect in the imprinted chromosome region 11p15.5. The underlying mechanisms include epimutations, uniparental disomy, copy number variations, and structural rearrangements. In addition, maternal loss-of-function mutations in CDKN1C are found. Despite growing knowledge on BWS pathogenesis, up to 20% of patients with BWS phenotype remain without molecular diagnosis. CASE PRESENTATION: Herein, we report an Iranian family with two females affected with BWS in different generations. Bisulfite pyrosequencing revealed hypermethylation of the H19/IGF2: intergenic differentially methylated region (IG DMR), also known as imprinting center 1 (IC1) and hypomethylation of the KCNQ1OT1: transcriptional start site (TSS) DMR (IC2). Array CGH demonstrated an 8 Mb duplication on chromosome 11p15.5p15.4 (205,827-8,150,933) and a 1 Mb deletion on chromosome 9p24.3 (209,020-1,288,114). Chromosome painting revealed that this duplication-deficiency in both patients is due to unbalanced segregation of a paternal reciprocal t(9;11)(p24.3;p15.4) translocation. CONCLUSIONS: This is the first report of a paternally inherited unbalanced translocation between the chromosome 9 and 11 short arms underlying familial BWS. Copy number variations involving the 11p15.5 region are detected by the consensus diagnostic algorithm. However, in complex cases which do not only affect the BWS region itself, characterization of submicroscopic chromosome rearrangements can assist to estimate the recurrence risk and possible phenotypic outcomes