Finite Temperature Properties of Quantum Antiferromagnets in a Uniform Magnetic Field in One and Two Dimensions

Consider a $d$-dimensional antiferromagnet with a quantum disordered ground state and a gap to bosonic excitations with non-zero spin. In a finite external magnetic field, this antiferromagnet will undergo a phase transition to a ground state with non-zero magnetization, describable as the condensation of a dilute gas of bosons. The finite temperature properties of the Bose gas in the vicinity of this transition are argued to obey a hypothesis of ZERO SCALE-FACTOR UNIVERSALITY for $d < 2$, with logarithmic violations in $d=2$. Scaling properties of various experimental observables are computed in an expansion in $\epsilon=2-d$, and exactly in $d=1$.Comment: 27 pages, REVTEX 3.0, 8 Postscript figures appended, YCTP-xyz

Long-Time Tails and Anomalous Slowing Down in the Relaxation of Spatially Inhomogeneous Excitations in Quantum Spin Chains

Exact analytic calculations in spin-1/2 XY chains, show the presence of long-time tails in the asymptotic dynamics of spatially inhomogeneous excitations. The decay of inhomogeneities, for $t\to \infty$, is given in the form of a power law $$(t/\tau_{Q}) ^{-\nu_{Q}}$$ where the relaxation time $\tau_{Q}$ and the exponent $\nu_{Q}$ depend on the wave vector $Q$, characterizing the spatial modulation of the initial excitation. We consider several variants of the XY model (dimerized, with staggered magnetic field, with bond alternation, and with isotropic and uniform interactions), that are grouped into two families, whether the energy spectrum has a gap or not. Once the initial condition is given, the non-equilibrium problem for the magnetization is solved in closed form, without any other assumption. The long-time behavior for $t\to \infty$ can be obtained systematically in a form of an asymptotic series through the stationary phase method. We found that gapped models show critical behavior with respect to $Q$, in the sense that there exist critical values $Q_{c}$, where the relaxation time $\tau_{Q}$ diverges and the exponent $\nu_{Q}$ changes discontinuously. At those points, a slowing down of the relaxation process is induced, similarly to phenomena occurring near phase transitions. Long-lived excitations are identified as incommensurate spin density waves that emerge in systems undergoing the Peierls transition. In contrast, gapless models do not present the above anomalies as a function of the wave vector $Q$.Comment: 25 pages, 2 postscript figures. Manuscript submitted to Physical Review

Molecular basis of Lys11-polyubiquitin specificity in the deubiquitinase Cezanne

The post-translational modification of proteins with polyubiquitin regulates virtually all aspects of cell biology. Eight distinct chain linkage types in polyubiquitin co-exist and are independently regulated in cells. This ‘ubiquitin code’ determines the fate of the modified protein1. Deubiquitinating enzymes of the Ovarian Tumour (OTU) family regulate cellular signalling by targeting distinct linkage types within polyubiquitin2, and understanding their mechanisms of linkage specificity gives fundamental insights into the ubiquitin system. We here reveal how the deubiquitinase Cezanne/OTUD7B specifically targets Lys11-linked polyubiquitin. Crystal structures of Cezanne alone and in complex with mono- and Lys11-linked diubiquitin, in combination with hydrogen-deuterium exchange mass spectrometry, enable reconstruction of the enzymatic cycle in exquisite detail. An intricate mechanism of ubiquitin-assisted conformational changes activate the enzyme, and while all chain types interact with the enzymatic S1 site, only Lys11-linked chains can bind productively across the active site and stimulate catalytic turnover. Our work highlights the fascinating plasticity of deubiquitinases, and indicates that new conformational states can occur when a true substrate, such as diubiquitin, is bound at the active site

Vesta, Vestoids, and the howardite, eucrite, diogenite group: Relationships and the origin of spectral differences

Spectra of asteroid 4 Vesta and 21 small (estimated diameters less than 10 km) asteroids with Vesta-like spectral properties (Vestoids) were measured at visible and near-infrared wavelengths (similar to0.44 to similar to1.65 mum). All of the measured small asteroids (except for 2579 Spartacus) have reflectance spectra consistent with surface compositions similar to eucrites and howardites and consistent with all being derived from Vesta. None of the observed asteroids have spectra similar to diogenites. We find no spectral distinction between the 15 objects tabulated as members of the Vesta dynamical family and 6 of the 7 sampled "non-family" members that reside just outside the semi-major axis (a), eccentricity (e), and inclination (i) region of the family. The spectral consistency and close orbital (a-e-i) match of these "non-family" objects to Vesta and the Vesta family imply that the true bounds of the family extend beyond the subjective cut-off for membership. Asteroid 2579 Spartacus has a spectrum consistent with a mixture of eucritic material and olivine. Spartacus could contain olivine-rich material from Vesta's mantle or may be unrelated to Vesta altogether. Laboratory measurements of the spectra of eucrites show that samples having nearly identical compositions can display a wide range of spectral slopes. Finer particle sizes lead to an increase in the slope, which is usually referred to as reddening. This range of spectral variation for the best-known meteoritic analogs to the Vestoids, regardless of whether they are actually related to each other, suggests that the extremely red spectral slopes for some Vestoids can be explained by very fine-grained eucritic material on their surfaces

Exacerbated Pathology of Viral Encephalitis in Mice with Central Nervous System-Specific Autoantibodies

We examine here the outcome of viral encephalomyelitis [mouse hepatitis virus (MHV) A59, Theiler’s encephalomyelitis virus, and Coxsackievirus B3] in mice with autoantibodies to a central nervous system (CNS)-specific antigen, myelin oligodendrocyte glycoprotein, that usually develop no clinical disease. Morbidity and mortality of the acute viral CNS disease was augmented by the presence of the autoantibodies in all three viral infections. Transfer of serum containing the autoantibodies at the time of infection with MHV was sufficient to reproduce the exacerbated disease. The presence of the autoantibodies was found to result in increased infiltration of mononuclear cells into the brain. Early demyelination was severely augmented in brains and spinal cords of MHV-infected mice with CNS-specific autoantibodies. The antibody-mediated exacerbation was shown to be independent of the complement system but to require expression of Fc receptors, because it was observed in C′-3-deficient but not in Fc receptor-deficient mice. Our study illustrates the possibility that infections can lead to much more profound immunopathology in the presence of an otherwise latent autoimmune condition