Solitons in finite droplets of noncommutative Maxwell-Chern-Simons theory

We find soliton solutions of the noncommutative Maxwell-Chern-Simons theory confined to a finite quantum Hall droplet. The solitons are exactly as hypothesized in \cite{Manu}. We also find new variations on these solitons. We compute their flux and their energies. The model we consider is directly related to the model proposed by Polychronakos\cite{Poly} and studied by Hellerman and Van Raamsdonk\cite{HvR} where it was shown that it is equivalent to the quantum Hall effect.Comment: 18 pages, 7 figures, minor corrections, version accepted for publication, this time really

Automorphic Equivalence within Gapped Phases of Quantum Lattice Systems

Gapped ground states of quantum spin systems have been referred to in the physics literature as being `in the same phase' if there exists a family of Hamiltonians H(s), with finite range interactions depending continuously on $s \in [0,1]$, such that for each $s$, H(s) has a non-vanishing gap above its ground state and with the two initial states being the ground states of H(0) and H(1), respectively. In this work, we give precise conditions under which any two gapped ground states of a given quantum spin system that 'belong to the same phase' are automorphically equivalent and show that this equivalence can be implemented as a flow generated by an $s$-dependent interaction which decays faster than any power law (in fact, almost exponentially). The flow is constructed using Hastings' 'quasi-adiabatic evolution' technique, of which we give a proof extended to infinite-dimensional Hilbert spaces. In addition, we derive a general result about the locality properties of the effect of perturbations of the dynamics for quantum systems with a quasi-local structure and prove that the flow, which we call the {\em spectral flow}, connecting the gapped ground states in the same phase, satisfies a Lieb-Robinson bound. As a result, we obtain that, in the thermodynamic limit, the spectral flow converges to a co-cycle of automorphisms of the algebra of quasi-local observables of the infinite spin system. This proves that the ground state phase structure is preserved along the curve of models $H(s), 0\leq s\leq 1$.Comment: Updated acknowledgments and new email address of S

Sudden switch of generalized Lieb-Robinson velocity in a transverse field Ising spin chain

The Lieb-Robinson theorem states that the speed at which the correlations between two distant nodes in a spin network can be built through local interactions has an upper bound, which is called the Lieb-Robinson velocity. Our central aim is to demonstrate how to observe the Lieb-Robinson velocity in an Ising spin chain with a strong transverse field. We adopt and compare four correlation measures for characterizing different types of correlations, which include correlation function, mutual information, quantum discord, and entanglement of formation. We prove that one of correlation functions shows a special behavior depending on the parity of the spin number. All the information-theoretical correlation measures demonstrate the existence of the Lieb-Robinson velocity. In particular, we find that there is a sudden switch of the Lieb-Robinson speed with the increasing of the number of spin

Lieb-Robinson Bounds for the Toda Lattice

We establish locality estimates, known as Lieb-Robinson bounds, for the Toda lattice. In contrast to harmonic models, the Lieb-Robinson velocity for these systems do depend on the initial condition. Our results also apply to the entire Toda as well as the Kac-van Moerbeke hierarchy. Under suitable assumptions, our methods also yield a finite velocity for certain perturbations of these systems

Pharmacological characterization of six trkB antibodies reveals a novel class of functional agents for the study of the BDNF receptor

International audienceBACKGROUND AND PURPOSE:By interacting with trkB receptors, brain-derived neurotrophic factor (BDNF) triggers various signalling pathways responsible for neurone survival, differentiation and modulation of synaptic transmission. Numerous reports have implicated BDNF and trkB in the pathogenesis of various central nervous system affections and in cancer, thus representing trkB as a promising therapeutic target. In this study, we used an antibody-based approach to search for trkB-selective functional reagents.EXPERIMENTAL APPROACH:Six commercially available polyclonal and monoclonal antibodies were tested on recombinant and native, human and rodent trkB receptors. Functional and pharmacological characterization was performed using a modified version of the KIRA-elisa method and radioligand binding studies. Western blot analyses and neurite outgrowth assays were carried out to determine the specificity and selectivity of antibody effects. The survival properties of one antibody were further assessed on cultured neurones in a serum-deprived paradigm.KEY RESULTS:The functional trkB-selective antibodies showed distinct pharmacological profiles, ranging from partial agonists to antagonists, acting on trkB receptors through allosteric modulations. The same diversity of effects was observed on the mitogen-activated protein kinase signalling pathway downstream of trkB and on the subsequent neurite outgrowth. One antibody with partial agonist activity demonstrated cell survival properties by activating the Akt pathway. Finally, these antibodies were functionally validated as true trkB-selective ligands because they failed activating trkA or trkC, and contrary to BDNF, none of them bind to p75(NTR).CONCLUSIONS AND IMPLICATIONS:These trkB-selective antibodies represent a novel class of pharmacological tools to explore the pathophysiological roles of trkB and its potential therapeutic relevance for the treatment of various disorders

Interleukin-1 enhances the ATP-evoked release of arachidonic acid from mouse astrocytes.

During neuropathological states associated with inflammation, the levels of cytokines such as interleukin-1beta (IL-1beta) are increased. Several studies have suggested that the neuronal damage observed in pathogenesis implicating IL-1beta are caused by an alteration in the neurochemical interactions between neurons and astrocytes. We report here that treating striatal astrocytes in primary culture with IL-1beta for 22-24 hr enhances the ATP-evoked release of arachidonic acid (AA) with no effect on the ATP-induced accumulation of inositol phosphates. The molecular mechanism responsible for this effect involves the expression of P2Y2 receptors (a subtype of purinoceptor activated by ATP) and cytosolic phospholipase A2 (cPLA2, an enzyme that mediates AA release). Indeed, P2Y2 antisense oligonucleotides reduce the ATP-evoked release of AA only from IL-1beta-treated astrocytes. Further, both the amount of cPLA2 (as assessed by Western blotting) and the release of AA resulting from direct activation of cPLA2 increased fourfold in cells treated with IL-1beta. We also report evidence indicating that the coupling of newly expressed P2Y2 receptors to cPLA2 is dependent on PKC activity. These results suggest that during inflammatory conditions, IL-1beta reveals a functional P2Y2 signaling pathway in astrocytes that results in a dramatic increase in the levels of free AA. This pathway may thus contribute to the neuronal loss associated with cerebral ischemia or traumatic brain injury

Interleukin-1 enhances the ATP-evoked release of arachidonic acid from mouse astrocytes.

During neuropathological states associated with inflammation, the levels of cytokines such as interleukin-1beta (IL-1beta) are increased. Several studies have suggested that the neuronal damage observed in pathogenesis implicating IL-1beta are caused by an alteration in the neurochemical interactions between neurons and astrocytes. We report here that treating striatal astrocytes in primary culture with IL-1beta for 22-24 hr enhances the ATP-evoked release of arachidonic acid (AA) with no effect on the ATP-induced accumulation of inositol phosphates. The molecular mechanism responsible for this effect involves the expression of P2Y2 receptors (a subtype of purinoceptor activated by ATP) and cytosolic phospholipase A2 (cPLA2, an enzyme that mediates AA release). Indeed, P2Y2 antisense oligonucleotides reduce the ATP-evoked release of AA only from IL-1beta-treated astrocytes. Further, both the amount of cPLA2 (as assessed by Western blotting) and the release of AA resulting from direct activation of cPLA2 increased fourfold in cells treated with IL-1beta. We also report evidence indicating that the coupling of newly expressed P2Y2 receptors to cPLA2 is dependent on PKC activity. These results suggest that during inflammatory conditions, IL-1beta reveals a functional P2Y2 signaling pathway in astrocytes that results in a dramatic increase in the levels of free AA. This pathway may thus contribute to the neuronal loss associated with cerebral ischemia or traumatic brain injury