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

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

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.

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

ZNF217 confers resistance to the pro-apoptotic signals of paclitaxel and aberrant expression of Aurora-A in breast cancer cells

<p>Abstract</p> <p>Background</p> <p>ZNF217 is a candidate oncogene located at 20q13, a chromosomal region frequently amplified in breast cancers. The precise mechanisms involved in ZNF217 pro-survival function are currently unknown, and utmost importance is given to deciphering the role of ZNF217 in cancer therapy response.</p> <p>Results</p> <p>We provide evidence that stable overexpression of ZNF217 in MDA-MB-231 breast cancer cells conferred resistance to paclitaxel, stimulated cell proliferation <it>in vitro </it>associated with aberrant expression of several cyclins, and increased tumor growth in mouse xenograft models. Conversely, siRNA-mediated silencing of ZNF217 expression in MCF7 breast cancer cells, which possess high endogenous levels of ZNF217, led to decreased cell proliferation and increased sensitivity to paclitaxel. The paclitaxel resistance developed by ZNF217-overexpressing MDA-MB-231 cells was not mediated by the ABCB1/PgP transporter. However, ZNF217 was able to counteract the apoptotic signals mediated by paclitaxel as a consequence of alterations in the intrinsic apoptotic pathway through constitutive deregulation of the balance of Bcl-2 family proteins. Interestingly, ZNF217 expression levels were correlated with the oncogenic kinase Aurora-A expression levels, as ZNF217 overexpression led to increased expression of the Aurora-A protein, whereas ZNF217 silencing was associated with low Aurora-A expression levels. We showed that a potent Aurora-A kinase inhibitor was able to reverse paclitaxel resistance in the ZNF217-overexpressing cells.</p> <p>Conclusion</p> <p>Altogether, these data suggest that ZNF217 might play an important role in breast neoplastic progression and chemoresistance, and that Aurora-A might be involved in ZNF217-mediated effects.</p

Dynamics and transport in random quantum systems governed by strong-randomness fixed points

We present results on the low-frequency dynamical and transport properties of random quantum systems whose low temperature ($T$), low-energy behavior is controlled by strong disorder fixed points. We obtain the momentum and frequency dependent dynamic structure factor in the Random Singlet (RS) phases of both spin-1/2 and spin-1 random antiferromagnetic chains, as well as in the Random Dimer (RD) and Ising Antiferromagnetic (IAF) phases of spin-1/2 random antiferromagnetic chains. We show that the RS phases are unusual `spin metals' with divergent low-frequency spin conductivity at T=0, and we also follow the conductivity through novel `metal-insulator' transitions tuned by the strength of dimerization or Ising anisotropy in the spin-1/2 case, and by the strength of disorder in the spin-1 case. We work out the average spin and energy autocorrelations in the one-dimensional random transverse field Ising model in the vicinity of its quantum critical point. All of the above calculations are valid in the frequency dominated regime \omega \agt T, and rely on previously available renormalization group schemes that describe these systems in terms of the properties of certain strong-disorder fixed point theories. In addition, we obtain some information about the behavior of the dynamic structure factor and dynamical conductivity in the opposite `hydrodynamic' regime $\omega < T$ for the special case of spin-1/2 chains close to the planar limit (the quantum x-y model) by analyzing the corresponding quantities in an equivalent model of spinless fermions with weak repulsive interactions and particle-hole symmetric disorder.Comment: Long version (with many additional results) of Phys. Rev. Lett. {\bf 84}, 3434 (2000) (available as cond-mat/9904290); two-column format, 33 pages and 8 figure