Crossover and self-averaging in the two-dimensional site-diluted Ising model

Using the newly proposed probability-changing cluster (PCC) Monte Carlo algorithm, we simulate the two-dimensional (2D) site-diluted Ising model. Since we can tune the critical point of each random sample automatically with the PCC algorithm, we succeed in studying the sample-dependent $T_c(L)$ and the sample average of physical quantities at each $T_c(L)$ systematically. Using the finite-size scaling (FSS) analysis for $T_c(L)$, we discuss the importance of corrections to FSS both in the strong-dilution and weak-dilution regions. The critical phenomena of the 2D site-diluted Ising model are shown to be controlled by the pure fixed point. The crossover from the percolation fixed point to the pure Ising fixed point with the system size is explicitly demonstrated by the study of the Binder parameter. We also study the distribution of critical temperature $T_c(L)$. Its variance shows the power-law $L$ dependence, $L^{-n}$, and the estimate of the exponent $n$ is consistent with the prediction of Aharony and Harris [Phys. Rev. Lett. {\bf 77}, 3700 (1996)]. Calculating the relative variance of critical magnetization at the sample-dependent $T_c(L)$, we show that the 2D site-diluted Ising model exhibits weak self-averaging.Comment: 6 pages including 6 eps figures, RevTeX, to appear in Phys. Rev.

Scaling and finte-size-scaling in the two dimensional random-coupling Ising ferromagnet

It is shown by Monte Carlo method that the finite size scaling (FSS) holds in the two dimensional random-coupled Ising ferromagnet. It is also demonstrated that the form of universal FSS function constructed via novel FSS scheme depends on the strength of the random coupling for strongly disordered cases. Monte Carlo measurements of thermodynamic (infinite volume limit) data of the correlation length ($\xi$) up to $\xi \simeq 200$ along with measurements of the fourth order cumulant ratio (Binder's ratio) at criticality are reported and analyzed in view of two competing scenarios. It is demonstrated that the data are almost exclusively consistent with the scenario of weak universality.Comment: 9 pages, 4figuer

Properties of the Top Quark

The top quark was discoverd at the CDF and D0 experiments in 1995. As the partner of the bottom quark its properties within the Standard Model are fully defined. Only the mass is a free parameter. The measurement of the top quark mass and the verification of the expected properties have been an important topic of experimental top quark physics since. In this review the recent results on top quark properties obtained by the Tevatron experiments CDF and D0 are summarised. At the advent of the LHC special emphasis is given to the basic measurement methods and the dominating systematic uncertainties.Comment: Habilitation thesis, revised and updated for publication in EPJ

Generating conditional knockout mice.

Gene targeting in ES cells is extensively used to generate designed mouse mutants and to study gene function in vivo. Knockout mice that harbor a null allele in their germline provide appropriate genetic models of inherited diseases and often exhibit embryonic or early postnatal lethality. To study gene function in adult mice and in selected cell types, a refined strategy for conditional gene inactivation has been developed that relies on the DNA recombinase Cre and its recognition (loxP) sites. For conditional mutagenesis, a target gene is modified by the insertion of two loxP sites that enable to excise the flanked (floxed) gene segment through Cre-mediated recombination. Conditional mutant mice are obtained by crossing the floxed strain with a Cre transgenic line such that the target gene becomes inactivated in vivo within the expression domain of Cre. A large collection of Cre transgenic lines has been generated over time and can be used in a combinatorial manner to achieve gene inactivation in many different cell types. A growing number of CreER(T2) transgenic mice further allows for inducible inactivation of floxed alleles in adult mice upon administration of tamoxifen. This chapter covers the design and construction of loxP flanked alleles and refers to the vectors, ES cells, and mice generated by the European conditional mouse mutagenesis (EUCOMM) project. We further describe the design and use of Cre and CreER(T2) transgenic mice and a convenient breeding strategy to raise conditional mutants and controls for phenotype analysis

Using Metamodels and Ontologies for Enterprise Model Reconciliation

Part 8: Ontology-Based InteroperabilityInternational audienceModeling the enterprise from different views, at different levels of abstraction, and in different modeling languages yields a variety of models. Oftentimes the models referring to the same subject exist independently of each other and their semantic relations are hard to discover or to analyze. This fact hinders the effective exploitation of enterprise models for the purpose of integration and interoperability. The method proposed in this paper is based on semantic annotations and aims for the externalization and machine readability of the model contained information. This assures the accessibility for further automatic processing and facilitates the discovery and analysis of inter-model relations

Neuronal Sodium-Channel α1-Subunit Mutations in Generalized Epilepsy with Febrile Seizures Plus

Generalized epilepsy with febrile seizures plus (GEFS+) is a familial epilepsy syndrome characterized by the presence of febrile and afebrile seizures. The first gene, GEFS1, was mapped to chromosome 19q and was identified as the sodium-channel β1-subunit, SCN1B. A second locus on chromosome 2q, GEFS2, was recently identified as the sodium-channel α1-subunit, SCN1A. Single-stranded conformation analysis (SSCA) of SCN1A was performed in 53 unrelated index cases to estimate the frequency of mutations in patients with GEFS+. No mutations were found in 17 isolated cases of GEFS+. Three novel SCN1A mutations—D188V, V1353L, and I1656M—were found in 36 familial cases; of the remaining 33 families, 3 had mutations in SCN1B. On the basis of SSCA, the combined frequency of SCN1A and SCN1B mutations in familial cases of GEFS+ was found to be 17%