Measuring the Decorrelation Times of Fourier Modes in Simulations

We describe a method to study the rate at which modes decorrelate in numerical simulations. We study the XY model updated with the Metropolis and Wolff dynamics respectively and compute the rate at which each eigenvector of the dynamics decorrelates. Our method allows us to identify the decorrelation time for each mode separately. We find that the autocorrelation function of the various modes is markedly different for the `local' Metropolis compared to the `non-local' Wolff dynamics. Equipped with this new insight, it may be possible to devise highly efficient algorithms.Comment: 16 pp (LaTeX), PUPT-1378 , IASSNS-HEP-93/

Multigrid Monte Carlo Algorithms for SU(2) Lattice Gauge Theory: Two versus Four Dimensions

We study a multigrid method for nonabelian lattice gauge theory, the time slice blocking, in two and four dimensions. For SU(2) gauge fields in two dimensions, critical slowing down is almost completely eliminated by this method. This result is in accordance with theoretical arguments based on the analysis of the scale dependence of acceptance rates for nonlocal Metropolis updates. The generalization of the time slice blocking to SU(2) in four dimensions is investigated analytically and by numerical simulations. Compared to two dimensions, the local disorder in the four dimensional gauge field leads to kinematical problems.Comment: 24 pages, PostScript file (compressed and uuencoded), preprint MS-TPI-94-

Theoretical Analysis of Acceptance Rates in Multigrid Monte Carlo

We analyze the kinematics of multigrid Monte Carlo algorithms by investigating acceptance rates for nonlocal Metropolis updates. With the help of a simple criterion we can decide whether or not a multigrid algorithm will have a chance to overcome critial slowing down for a given model. Our method is introduced in the context of spin models. A multigrid Monte Carlo procedure for nonabelian lattice gauge theory is described, and its kinematics is analyzed in detail.Comment: 7 pages, no figures, (talk at LATTICE 92 in Amsterdam

Effective Field Theories

Effective field theories encode the predictions of a quantum field theory at low energy. The effective theory has a fairly low ultraviolet cutoff. As a result, loop corrections are small, at least if the effective action contains a term which is quadratic in the fields, and physical predictions can be read straight from the effective Lagrangean. Methods will be discussed how to compute an effective low energy action from a given fundamental action, either analytically or numerically, or by a combination of both methods. Basically,the idea is to integrate out the high frequency components of fields. This requires the choice of a "blockspin",i.e. the specification of a low frequency field as a function of the fundamental fields. These blockspins will be the fields of the effective field theory. The blockspin need not be a field of the same type as one of the fundamental fields, and it may be composite. Special features of blockspins in nonabelian gauge theories will be discussed in some detail. In analytical work and in multigrid updating schemes one needs interpolation kernels \A from coarse to fine grid in addition to the averaging kernels $C$ which determines the blockspin. A neural net strategy for finding optimal kernels is presented. Numerical methods are applicable to obtain actions of effective theories on lattices of finite volume. The constraint effective potential) is of particular interest. In a Higgs model it yields the free energy, considered as a function of a gauge covariant magnetization. Its shape determines the phase structure of the theory. Its loop expansion with and without gauge fields can be used to determine finite size corrections to numerical data.Comment: 45 pages, 9 figs., preprint DESY 92-070 (figs. 3-9 added in ps format

Quenched Hadrons using Wilson and O(a)-Improved Fermion Actions at beta=6.2

We present the first study of the light hadron spectrum and decay constants for quenched QCD using an O(a)-improved nearest-neighbour Wilson fermion action at \beta=6.2. We compare the results with those obtained using the standard Wilson fermion action, on the same set of 18 gauge field configurations of a 24^3 times 48 lattice. For pseudoscalar meson masses in the range 330-800 MeV, we find no significant difference between the results for the two actions. The scales obtained from the string tension and mesonic sector are consistent, but differ from that derived from baryon masses. The ratio of the pseudoscalar decay constant to the vector meson mass is roughly independent of quark mass as observed experimentally, and in approximate agreement with the measured value.Comment: 11 page

Multi-Grid Monte Carlo. IV. One-Dimensional O(4)O(4)-Symmetric Nonlinear σ\sigma-Model

We study the dynamic critical behavior of the multi-grid Monte Carlo (MGMC) algorithm with piecewise-constant interpolation and a W-cycle, applied to the one-dimensional $O(4)$-symmetric nonlinear $\sigma$-model [= $SU(2)$ principal chiral model], on lattices from $L=128$ to $L=16384$. Our data for the integrated autocorrelation time $\tau_{int,{\cal M}^2}$ are well fit by a logarithmic growth. We have no idea why the critical slowing-down is not completely eliminated.Comment: 377866 bytes Postscript, 16 pages, includes figure

Multi-Grid Monte Carlo via XYXY Embedding. II. Two-Dimensional SU(3)SU(3) Principal Chiral Model

We carry out a high-precision simulation of the two-dimensional $SU(3)$ principal chiral model at correlation lengths $\xi$ up to $\sim 4 \times 10^5$, using a multi-grid Monte Carlo (MGMC) algorithm and approximately one year of Cray C-90 CPU time. We extrapolate the finite-volume Monte Carlo data to infinite volume using finite-size-scaling theory, and we discuss carefully the systematic and statistical errors in this extrapolation. We then compare the extrapolated data to the renormalization-group predictions. The deviation from asymptotic scaling, which is $\approx 12$ at $\xi \sim 25$, decreases to $\approx 2$ at $\xi \sim 4 \times 10^5$. We also analyze the dynamic critical behavior of the MGMC algorithm using lattices up to $256 \times 256$, finding the dynamic critical exponent $z_{int,{\cal M}^2} \approx 0.45 \pm 0.02$ (subjective 68% confidence interval). Thus, for this asymptotically free model, critical slowing-down is greatly reduced compared to local algorithms, but not completely eliminated.Comment: self-unpacking archive including .tex, .sty and .ps files; 126 pages including all figure

Establishment of a new human osteosarcoma cell line, UTOS-1: cytogenetic characterization by array comparative genomic hybridization

The cytogenetic characteristics of osteosarcoma (OS) remain controversial. The establishment of a new human OS cell line may improve the characterization. We report the establishment of a new human osteosarcoma cell line, UTOS-1, from a typical osteoblastic OS of an 18-year-old man. Cultured UTOS-1 cells are spindle-shaped, and have been maintained in vitro for over 50 passages in more than 2 years. Xenografted UTOS-1 cells exhibit features typical of OS, such as production of osteoid or immature bone matrix, and proliferation potency in vivo. UTOS-1 also exhibit morphological and immunohistochemical characteristics typical of osteoblastic OS. Chromosomal analysis by G-band show 73~85 chromosomes with complicated translocations. Array CGH show frequent gains at locus DAB2 at chromosome 5q13, CCND2 at 12p13, MDM2 at 12q14.3-q15, FLI and TOP3A at 17p11.2-p12 and OCRL1 at Xq25, and show frequent losses at HTR1B at 6q13, D6S268 at 6q16.3-q21, SHGC17327 at 18ptel, and STK6 at 20q13.2-q13.3. The UTOS-1 cell line may prove useful for biologic and molecular pathogenetic investigations of human OS

Quantitative Assessment of Whole-Body Tumor Burden in Adult Patients with Neurofibromatosis

Patients with neurofibromatosis 1 (NF1), NF2, and schwannomatosis are at risk for multiple nerve sheath tumors and premature mortality. Traditional magnetic resonance imaging (MRI) has limited ability to assess disease burden accurately. The aim of this study was to establish an international cohort of patients with quantified whole-body internal tumor burden and to correlate tumor burden with clinical features of disease.We determined the number, volume, and distribution of internal nerve sheath tumors in patients using whole-body MRI (WBMRI) and three-dimensional computerized volumetry. We quantified the distribution of tumor volume across body regions and used unsupervised cluster analysis to group patients based on tumor distribution. We correlated the presence and volume of internal tumors with disease-related and demographic factors.WBMRI identified 1286 tumors in 145/247 patients (59%). Schwannomatosis patients had the highest prevalence of tumors (P = 0.03), but NF1 patients had the highest median tumor volume (P = 0.02). Tumor volume was unevenly distributed across body regions with overrepresentation of the head/neck and pelvis. Risk factors for internal nerve sheath tumors included decreasing numbers of café-au-lait macules in NF1 patients (P = 0.003) and history of skeletal abnormalities in NF2 patients (P = 0.09). Risk factors for higher tumor volume included female gender (P = 0.05) and increasing subcutaneous neurofibromas (P = 0.03) in NF1 patients, absence of cutaneous schwannomas in NF2 patients (P = 0.06), and increasing age in schwannomatosis patients (p = 0.10).WBMRI provides a comprehensive phenotype of neurofibromatosis patients, identifies distinct anatomic subgroups, and provides the basis for investigating molecular biomarkers that correlate with unique disease manifestations

Imprinted CDKN1C Is a Tumor Suppressor in Rhabdoid Tumor and Activated by Restoration of SMARCB1 and Histone Deacetylase Inhibitors

SMARCB1 is deleted in rhabdoid tumor, an aggressive paediatric malignancy affecting the kidney and CNS. We hypothesized that the oncogenic pathway in rhabdoid tumors involved epigenetic silencing of key cell cycle regulators as a consequence of altered chromatin-remodelling, attributable to loss of SMARCB1, and that this hypothesis if proven could provide a biological rationale for testing epigenetic therapies in this disease. We used an inducible expression system to show that the imprinted cell cycle inhibitor CDKN1C is a downstream target for SMARCB1 and is transcriptionally activated by increased histone H3 and H4 acetylation at the promoter. We also show that CDKN1C expression induces cell cycle arrest, CDKN1C knockdown with siRNA is associated with increased proliferation, and is able to compete against the anti-proliferative effect of restored SMARCB1 expression. The histone deacetylase inhibitor (HDACi), Romidepsin, specifically restored CDKN1C expression in rhabdoid tumor cells through promoter histone H3 and H4 acetylation, recapitulating the effect of SMARCB1 on CDKNIC allelic expression, and induced cell cycle arrest in G401 and STM91-01 rhabdoid tumor cell lines. CDKN1C expression was also shown to be generally absent in clinical specimens of rhabdoid tumor, however CDKN1A and CDKN1B expression persisted. Our observations suggest that maintenance of CDKN1C expression plays a critical role in preventing rhabdoid tumor growth. Significantly, we report for the first time, parallels between the molecular pathways of SMARCB1 restoration and Romidepsin treatment, and demonstrate a biological basis for the further exploration of histone deacetylase inhibitors as relevant therapeutic reagents in the treatment of rhabdoid tumor