Evidence of quantum criticality in the doped Haldane system Y2BaNiO5

Experimental bulk susceptibility X(T) and magnetization M(H,T) of the S=1-Haldane chain system doped with nonmagnetic impurities, Y2BaNi1-xZnxO5 (x=0.04,0.06,0.08), are analyzed. A numerical calculation for the low-energy spectrum of non-interacting open segments describes very well experimental data above 4 K. Below 4 K, we observe power-law behaviors, X(T)=T^-alpha and M(H,T)/T^(1-alpha)=f(alpha,(H/T)), with alpha (<1) depending on the doping concentration x.This observation suggests the appearance of a gapless quantum phase due to a broad distribution of effective couplings between the dilution-induced moments.Comment: 4 pages, 3 figure

Random interactions and spin-glass thermodynamic transition in the hole-doped Haldane system Y2−x_{2-x}Cax_xBaNiO5_5

Magnetization, DC and AC bulk susceptibility of the $S$=1 Haldane chain system doped with electronic holes, Y$_{2-x}$Ca$_x$BaNiO$_5$ (0$\leq$x$\leq$0.20), have been measured and analyzed. The most striking results are (i) a sub-Curie power law behavior of the linear susceptibility, $\chi (T)$$\sim$ $T$$^{-\alpha}$, for temperature lower than the Haldane gap of the undoped compound (x=0) (ii) the existence of a spin-glass thermodynamic transition at $T$$_g$ = 2-3 K. These findings are consistent with (i) random couplings within the chains between the spin degrees of freedom induced by hole doping, (ii) the existence of ferromagnetic bonds that induce magnetic frustration when interchain interactions come into play at low temperature.Comment: 4 pages, 4 figures, to appear in Phys. Rev.

Evidence for local lattice distortions in giant magnetocapacitive CdCr2S4

Raman scattering experiments on CdCr2S4 single crystals show pronounced anomalies in intensity and frequency of optical phonon modes with an onset temperature T*=130 K that coincides with the regime of giant magnetocapacitive effects. A loss of inversion symmetry and Cr off-centering are deduced from the observation of longitudinal optical and formerly infrared active modes for T<T_c=84 K. The intensity anomalies are attributed to the enhanced electronic polarizability of displacements that modulate the Cr-S distance and respective hybridization. Photo doping leads to an annihilation of the symmetry reduction. Our scenario of multiferroic effects is based on the near degeneracy of polar and nonpolar modes and the additional low energy scale due to hybridization.Comment: 4 pages, 6 figure

Gauge Invariant Factorisation and Canonical Quantisation of Topologically Massive Gauge Theories in Any Dimension

Abelian topologically massive gauge theories (TMGT) provide a topological mechanism to generate mass for a bosonic p-tensor field in any spacetime dimension. These theories include the 2+1 dimensional Maxwell-Chern-Simons and 3+1 dimensional Cremmer-Scherk actions as particular cases. Within the Hamiltonian formulation, the embedded topological field theory (TFT) sector related to the topological mass term is not manifest in the original phase space. However through an appropriate canonical transformation, a gauge invariant factorisation of phase space into two orthogonal sectors is feasible. The first of these sectors includes canonically conjugate gauge invariant variables with free massive excitations. The second sector, which decouples from the total Hamiltonian, is equivalent to the phase space description of the associated non dynamical pure TFT. Within canonical quantisation, a likewise factorisation of quantum states thus arises for the full spectrum of TMGT in any dimension. This new factorisation scheme also enables a definition of the usual projection from TMGT onto topological quantum field theories in a most natural and transparent way. None of these results rely on any gauge fixing procedure whatsoever.Comment: 1+25 pages, no figure

Exposure to Maternal Diabetes Is Associated With Early Abnormal Vascular Structure in Offspring

Aim/hypothesis: In utero exposure to maternal diabetes increases the risk of developing hypertension and cardiovascular disorders during adulthood. We have previously shown that this is associated with changes in vascular tone in favor of a vasoconstrictor profile, which is involved in the development of hypertension. This excessive constrictor tone has also a strong impact on vascular structure. Our objective was to study the impact of in utero exposure to maternal diabetes on vascular structure and remodeling induced by chronic changes in hemodynamic parameters. Methods and Results: We used an animal model of rats exposed in utero to maternal hyperglycemia (DMO), which developed hypertension at 6 months of age. At a pre-hypertensive stage (3 months of age), we observed deep structural modifications of the vascular wall without any hemodynamic perturbations. Indeed, in basal conditions, resistance arteries of DMO rats are smaller than those of control mother offspring (CMO) rats; in addition, large arteries like thoracic aorta of DMO rats have an increase of smooth muscle cell attachments to elastic lamellae. In an isolated perfused kidney, we also observed a leftward shift of the flow/pressure relationship, suggesting a rise in renal peripheral vascular resistance in DMO compared to CMO rats. In this context, we studied vascular remodeling in response to reduced blood flow by in vivo mesenteric arteries ligation. In DMO rats, inward remodeling induced by a chronic reduction in blood flow (1 or 3 weeks after ligation) did not occur by contrast to CMO rats in which arterial diameter decreased from 428 ± 17 μm to 331 ± 20 μm (at 125 mmHg, p = 0.001). In these animals, the transglutaminase 2 (TG2) pathway, essential for inward remodeling development in case of flow perturbations, was not activated in low-flow (LF) mesenteric arteries. Finally, in old hypertensive DMO rats (18 months of age), we were not able to detect a pressure-induced remodeling in thoracic aorta. Conclusions: Our results demonstrate for the first time that in utero exposure to maternal diabetes induces deep changes in the vascular structure. Indeed, the early narrowing of the microvasculature and the structural modifications of conductance arteries could be a pre-emptive adaptation to fetal programming of hypertension