Magnetic polarons in weakly doped high-Tc superconductors

We consider a spin Hamiltonian describing $d$-$d$ exchange interactions between localized spins $d$ of a finite antiferromagnet as well as $p$-$d$ interactions between a conducting hole ($p$) and localized spins. The spin Hamiltonian is solved numerically with use of Lanczos method of diagonalization. We conclude that $p$-$d$ exchange interaction leads to localization of magnetic polarons. Quantum fluctuations of the antiferromagnet strengthen this effect and make the formation of polarons localized in one site possible even for weak $p$-$d$ coupling. Total energy calculations, including the kinetic energy, do not change essentially the phase diagram of magnetic polarons formation. For parameters reasonable for high-$T_c$ superconductors either a polaron localized on one lattice cell or a small ferron can form. For reasonable values of the dielectric function and $p$-$d$ coupling, the contributions of magnetic and phonon terms in the formation of a polaron in weakly doped high-$T_c$ materials are comparable.Comment: revised, revtex-4, 12 pages 8 eps figure

Search for single top quark production in ppbar collisions at sqrt(s)=1.96 TeV

We present a search for electroweak production of single top quarks in the s-channel and t-channel using neural networks for signal-background separation. We have analyzed 230 pb$^{-1}$ of data collected with the D0 detector at the Fermilab Tevatron Collider at a center-of-mass energy of 1.96 TeV and find no evidence for a single top quark signal. The resulting 95% confidence level upper limits on the single top quark production cross sections are 6.4 pb in the s-channel and 5.0 pb in the t-channel.Comment: 9 pages, 4 figure

Genome-wide association study of classical Hodgkin lymphoma identifies key regulators of disease susceptibility

Several susceptibility loci for classical Hodgkin lymphoma (cHL) have been reported, however much of the heritable risk is unknown. Here, we perform a meta-analysis of two existing genome-wide association studies (GWAS), a new GWAS, and replication totalling 5,314 cases and 16,749 controls. We identify risk loci for all cHL at 6q22.33 (rs9482849, P=1.52 × 10-8) and for nodular sclerosis HL (NSHL) at 3q28 (rs4459895, P=9.43 × 10-17), 6q23.3 (rs6928977, P=4.62 × 10-55 11), 10p14 (rs3781093, P=9.49 × 10-13), 13q34 (rs112998813, P=4.58 × 10-8) and 16p13.13 (rs34972832, P=2.12 × 10-8). Additionally, independent loci within the HLA region are observed for NSHL (rs9269081, HLA-DPB1*03:01, Val86 in HLA-DRB1) and mixed cellularity HL (rs1633096, rs13196329, Val86 in HLA-DRB1). The new and established risk loci localise to areas of active chromatin and show an over-representation of transcription factor binding for determinants of B-cell development and immune response.In the United Kingdom, Bloodwise (LLR; 10021) provided principal funding for the study. Support from Cancer Research UK (C1298/A8362 supported by the Bobby Moore Fund) and the Lymphoma Research Trust is also acknowledged. A.S. is supported by a clinical fellowship from Cancer Research UK. For the UK-GWAS, sample and data acquisition were supported by Breast Cancer Now, the European Union and the Lymphoma Research Trust. The UK-GWAS made use of control genotyping data generated by the WTCCC. For further information, please visit the publishr's website