Matter degrees of freedom and string breaking in Abelian projected quenched SU(2) QCD

In the Abelian projection the Yang--Mills theory contains Abelian gauge fields (diagonal degrees of freedom) and the Abelian matter fields (off-diagonal degrees) described by a complicated action. The matter fields are essential for the breaking of the adjoint string. We obtain numerically the effective action of the Abelian gauge and the Abelian matter fields in quenched SU(2) QCD and show that the Abelian matter fields provide an essential contribution to the total action even in the infrared region. We also observe the breaking of an Abelian analog of the adjoint string using Abelian operators. We show that the adjoint string tension is dominated by the Abelian and the monopole contributions similarly to the case of the fundamental particles. We conclude that the adjoint string breaking can successfully be described in the Abelian projection formalism.Comment: 16 pages, 10 figures, 2 table

An Abelian effective action reproducing screening and confinement in quenched SU(2) QCD

In an Abelian projection SU(2) gluodynamics contains Abelian gauge fields (diagonal degrees of freedom) and Abelian matter fields (off-diagonal degrees). The matter fields are essential for the breaking of the adjoint string. We obtain numerically the effective action of the Abelian fields in quenched SU(2) QCD and show that the Abelian matter fields provide an essential contribution to the total action even in the infrared region.Comment: 3 pages, 3 figures, 1 table, uses espcrc2.sty; Lattice2003(topology

Differential expression of ADAMTS -1, -4, -5 and TIMP -3 in rat spinal cord at different stages of acute experimental autoimmune encephalomyelitis

Experimental autoimmune encephalomyelitis (EAE) is an animal model of inflammatory demyelination, a pathological event common to multiple sclerosis (MS). During CNS inflammation there are alterations in the extracellular matrix (ECM). A Disintegrin and Metalloproteinase with Thrombospondin motifs (ADAMTS) -1, -4 and -5 are proteases present in the CNS, which are able to cleave the aggregating chondroitin sulphate proteoglycans, aggrecan, phosphacan, neurocan and brevican. It is therefore important to investigate changes in their expression in different stages of EAE induction. We have investigated expression of ADAMTS-1, -4, -5 and Tissue inhibitor of metalloproteinase (TIMP) -3, by real-time RT-PCR. We have also examined protein expression of ADAMTS-1, -4 and -5 by western blotting and immunocytochemistry in spinal cord from animals at different stages of disease progression. Our study demonstrated a decrease in ADAMTS-4 mRNA and protein expression. TIMP-3 was decreased at the mRNA level although protein levels were increased in diseased animals compared to controls. Our study identifies changes in ADAMTS expression during the course of CNS inflammation which may contribute to ECM degradation and disease progression.</p

ADAMTS -1 and -4 are up-regulated following transient middle cerebral artery occlusion in the rat and their expression is modulated by TNF in cultured astrocytes

ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) enzymes are a recently described group of metalloproteinases. The substrates degraded by ADAMTS-1, -4 and -5 suggests that they play a role in turnover of extracellular matrix in the central nervous system (CNS). ADAMTS-1 is also known to exhibit anti-angiogenic activity. Their main endogenous inhibitor is tissue inhibitor of metalloproteinases (TIMP)-3. The present study was designed to investigate ADAMTS-1, -4 and -5 and TIMP-3 expression after experimental cerebral ischaemia and to examine whether cytokines known to be up-regulated in stroke could alter their expression by astrocytes in vitro. Focal cerebral ischaemia was induced by transient middle cerebral artery occlusion in the rat using the filament method. Our results demonstrate a significant increase in expression of ADAMTS-1 and -4 in the occluded hemisphere but no significant change in TIMP-3. This was accompanied by an increase in mRNA levels for interleukin (IL)-1, IL-1 receptor antagonist (IL-1ra) and tumour necrosis factor (TNF). ADAMTS-4 mRNA and protein was up-regulated by TNF in primary human astrocyte cultures. The increased ADAMTS-1 and -4 in experimental stroke, together with no change in TIMP-3, may promote ECM breakdown after stroke, enabling infiltration of inflammatory cells and contribute to brain injury. In vitro studies suggest that the in vivo modulation of ADAMTS-1 and -4 may be controlled in part by TNF.</p

The Dipion Mass Spectrum In e+e- Annihilation and tau Decay: A Dynamical (rho0, omega, phi) Mixing Approach

We readdress the problem of finding a simultaneous description of the pion form factor data in e+e- annihilations and in tau decays. For this purpose, we work in the framework of the Hidden Local Symmetry (HLS) Lagrangian and modify the vector meson mass term by including the pion and kaon loop contributions. This leads us to define the physical rho, omega and phi fields as linear combinations of their ideal partners, with coefficients being meromorphic functions of s, the square of the 4--momentum flowing into the vector meson lines. This allows us to define a dynamical, i.e. s-dependent, vector meson mixing scheme. The model is overconstrained by extending the framework in order to include the description of all meson radiative (V P gamma and P gamma gamma couplings) and leptonic (Ve+e- couplings) decays and also the isospin breaking (omega/ phi --> pi+ pi-) decay modes. The model provides a simultaneous, consistent and good description of the e+e- and tau dipion spectra. The expression for pion form factor in the latter case is derived from those in the former case by switching off the isospin breaking effects specific to e+e- and switching on those for tau decays. Besides, the model also provides a good account of all decay modes of the form V P gamma, Pgamma gamma as well as the isospin breaking decay modes. It leads us to propose new reference values for the rho^0 --> e+ e- and omega --> pi+ pi- partial widths which are part of our description of the pion form factor. Other topics (phi --> K anti K, the rho meson mass and width parameters) are briefly discussed. Therefore, we confirm the 3.3 sigma discrepancy between the theoretical estimate of a_mu based on e+e- and its direct BNL measurement.Comment: 71 pages, 8 figures. Accepted by EPJ C. Version 3: correct minor typos, minor changes spread out into the text. Extension of Sections 12.2 and 12.3.5 and introduction of the new Appendix

Radiative Decays, Nonet Symmetry and SU(3) Breaking

We re-examine the problem of simultaneously describing in a consistent way all radiative and leptonic decays of light mesons (V -> P gamma, P -> V gamma, P -> gamma gamma, V -> e^+ e^-). For this purpose, we rely on the Hidden Local Symmetry model in both its anomalous and non--anomalous sectors. We show that the SU(3) symmetry breaking scheme proposed by Bando, Kugo and Yamawaki, supplemented with nonet symmetry breaking in the pseudoscalar sector, allows one to reach a nice agreement with all data, except for the K^{*+/-} radiative decay. An extension of this breaking pattern allows one to account for this particular decay mode too. Considered together, the whole set of radiative decays provides a pseudoscalar mixing angle theta_P ~ -11^o and a value for theta_V which is ~ 3^o from that of ideal mixing. We also show that it is impossible, in a practical sense, to disentangle the effects of nonet symmetry breaking and those of glue inside the eta', using only light meson decays.Comment: 36 pages. Published versio

Disrupted endothelial cell heterogeneity and network organization impair vascular function in prediabetic obesity

Background: Obesity is a major risk factor for diabetes and cardiovascular diseases such as hypertension, heart failure, and stroke. Impaired endothelial function occurs in the earliest stages of obesity and underlies vascular alterations that give rise to cardiovascular disease. However, the mechanisms that link weight gain to endothelial dysfunction are ill-defined. Increasing evidence suggests that endothelial cells are not a population of uniform cells but are highly heterogeneous and are organized as a communicating multicellular network that controls vascular function. Purpose: To investigate the hypothesis that disrupted endothelial heterogeneity and network-level organization contribute to impaired vascular reactivity in obesity. Methods and Results: To study obesity-related vascular function without complications associated with diabetes, a state of prediabetic obesity was induced in rats. Small artery diameter recordings confirmed nitric-oxide mediated vasodilator responses were dependent on increases in endothelial calcium levels and were impaired in obese animals. Single-photon imaging revealed a linear relationship between blood vessel relaxation and population-wide calcium responses. Obesity did not alter the slope of this relationship, but impaired calcium responses in the endothelial cell network. The network comprised structural and functional components. The structural architecture, a hexagonal lattice network of connected cells, was unchanged in obesity. The functional network contained sub-populations of clustered specialized agonist-sensing cells from which signals were communicated through the network. In obesity there were fewer but larger clusters of sensory cells and communication path lengths between clusters increased. Communication between neighboring cells was unaltered in obesity. Altered network organization resulted in impaired, population-level calcium signaling and deficient endothelial control of vascular tone. Conclusions: The distribution of cells in the endothelial network is critical in determining overall vascular response. Altered cell heterogeneity and arrangement in obesity decreases endothelial function and provides a novel framework for understanding compromised endothelial function in cardiovascular disease

Effect of ground-state deformation on isoscalar giant resonances in Si 28

Multipole strength distributions for isoscalar L 642 transitions in Si28 have been extracted using 386-MeV inelastic \u3b1 scattering at extremely forward angles, including 0. Observed strength distributions are in good agreement with microscopic calculations for an oblate-deformed ground state. In particular, a large peak at an excitation energy of 17.7 MeV in the isoscalar giant monopole resonance strength is consistent with the calculations