On the Landau Ginzburg theory of MAG projected SU(2) lattice gauge theory

Maximal Abelian gauge fixing and subsequent Abelian projection of SU(2) lattice gauge theory defines closed trajectories of magnetic monopoles. These trajectories can be interpreted in terms of an effective scalar field theory of the MAG monopoles using the worldline representation of the functional determinants. Employing the monopole worldlines detected in the numerical simulation, we show that a scalar bound state exists. The screening mass $m$ of this state properly scales towards the continuum limit. We find m ~ 1.3 $GeV when the string tension sigma = 440 MeV is used as reference scale.Comment: 9 pages, 3 figures, accepted by Phys. Lett.

Fermi-Einstein condensation in dense QCD-like theories

While pure Yang-Mills theory feature the centre symmetry, this symmetry is explicitly broken by the presence of dynamical matter. We study the impact of the centre symmetry in such QCD-like theories. In the analytically solvable Schwinger model, centre transitions take place even under extreme conditions, temperature and/or density, and we show that they are key to the solution of the Silver-Blaze problem. We then develop an effective SU(3) quark model which confines quarks by virtue of centre sector transitions. The phase diagram by confinement is obtained as a function of the temperature and the chemical potential. We show that at low temperatures and intermediate values for the chemical potential the centre dressed quarks undergo condensation due to Bose like statistics. This is the Fermi Einstein condensation. To corroborate the existence of centre sector transitions in gauge theories with matter, we study (at vanishing chemical potential) the interface tension in the three-dimensional Z2 gauge theory with Ising matter, the distribution of the Polyakov line in the four-dimensional SU(2)-Higgs model and devise a new type of order parameter which is designed to detect centre sector transitions. Our analytical and numerical findings lead us to conjecture a new state of cold, but dense matter in the hadronic phase for which Fermi Einstein condensation is realised.Comment: 51 pages, 32 figure

Three-dimensional synaptic ultrastructure in the dentate gyrus and hippocampal area CA3 in the Ts65Dn mouse model of down syndrome

Down syndrome (DS) results from trisomy of human chromosome 21. Ts65Dn mice are an established model for DS and show several phenotypes similar to those in people with DS. However, there is little data on the structural plasticity of synapses in the trisynaptic pathway in the hippocampus. Here we investigate three-dimensional (3D) ultrastructure of synapses in the hippocampus of age-matched control (2N) and Ts65Dn male mice. Serial ultrathin sections and 3D reconstructions characterize synapses in the middle molecular layer (MML) of dentate gyrus and in thorny excrescences (TEs) in proximal portions of apical dendrites of CA3 pyramidal neurons. 3D analysis of synapses shows phenotypes that distinguish Ts65Dn from 2N mice. For the MML, synapse density was reduced by 15% in Ts65Dn vs. 2N mice (P < 0.05). Comparative 3D analyses demonstrate a significant decrease in the number of thorns per TE in CA3 in Ts65Dn vs. 2N mice (by ∼45%, P = 0.01). Individual thorn volume was 3 times smaller in Ts65Dn vs. 2N mice (P = 0.02). A significant decrease in the number of thorn projections per TE in Ts65Dn vs. 2N mice was accompanied by a decrease of filopodium-like protrusions on the surface of TEs (P = 0.02). However, the volume of postsynaptic densities in CA3 Ts65Dn and 2N mice was unchanged (P = 0.78). Our findings suggest that the high degree of plasticity of CA3 thorns may be connected with their filopodial origin. Alterations of 3D synaptic structure in Ts65Dn mice may further contribute to the diminished plasticity in DS

Inhibition of casein kinase 2 enhances the death ligand- and natural kiler cell-induced hepatocellular carcinoma cell death

Recent studies have shown that the inhibition of casein kinase 2 (CK2) sensitizes many cancer cells to Fas ligand- and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. However, it has not been demonstrated directly whether CK2 inhibition can also enhance the cytotoxicity of natural killer (NK) cells, which actually use the death ligands to kill cancer cells in vivo. To address whether NK cell-mediated cancer cell death is affected by the inhibition of CK2, we first checked whether the death ligand-induced apoptosis of hepatocellular carcinoma cells (HCCs) and HeLa were affected by CK2 inhibition. We then investigated the effect of CK2 inhibition on NK cytotoxicity against HCCs and HeLa cells and its mechanistic features. Inhibition of CK2 by emodin increased the apoptotic cell death of HepG2, Hep3B and HeLa when the cancer cell lines were treated with a soluble form of recombinant TRAIL or an agonistic antibody of Fas. This phenomenon appeared to be correlated with the expression level of death receptors on the cancer cell surface. More interestingly, the inhibition of CK2 also greatly increased the NK cell-mediated cancer cell killing. The NK cytotoxicity against the cancer cells increased about twofold when the target cells were pretreated with a specific CK2 inhibitor, emodin or 4,5,6,7-tetrabromobenzotriazole. Furthermore, the increase of the NK cytotoxicity against cancer cells by CK2 inhibition was granule-independent and mediated possibly by the death ligands on the NK cell surface. This suggests that CK2 inhibitors could be used to enhance the cytotoxicity of NK cells and consequently increase host tumour immunity