Color Flux Profiles in SU(2) Lattice Gauge Theory

Results of a high statistics study of chromo field distributions around static sources in pure SU(2) gauge theory on lattices of volumes $16^4$, $32^4$, and $48^3\times 64$ at $\beta=2.5$, $2.635$, and $2.74$ are presented. We establish string formation up to physical distances as large as 2 fm.Comment: Contribution to Lattice '94, 3 pages uu-compressed LaTeX + 3 psfig

SU(2) Colour Fields Around Static Sources

First results of an ongoing high statistics study of the colour flux distribution around static quark sources in SU(2) gauge theory are presented. The flux tube profiles and widths have been investigated for several quark separations at beta=2.5 and beta=2.74. The results are tested against Michael's sum rules.Comment: 3 pages (LaTeX) with 4 epsf incl. PS figs., To be publ. in Proc. of Lattice '9

Microglia Responses to Pro-inflammatory Stimuli (LPS, IFNγ+TNFα) and Reprogramming by Resolving Cytokines (IL-4, IL-10)

Microglia respond to CNS injuries and diseases with complex reactions, often called “activation.” A pro-inflammatory phenotype (also called classical or M1 activation) lies at one extreme of the reactivity spectrum. There were several motivations for this study. First, bacterial endotoxin (lipopolysaccharide, LPS) is the most commonly used pro-inflammatory stimulus for microglia, both in vitro and in vivo; however, pro-inflammatory cytokines (e.g., IFNγ, TNFα) rather than LPS will be encountered with sterile CNS damage and disease. We lack direct comparisons of responses between LPS and such cytokines. Second, while transcriptional profiling is providing substantial data on microglial responses to LPS, these studies mainly use mouse cells and models, and there is increasing evidence that responses of rat microglia can differ. Third, the cytokine milieu is dynamic after acute CNS damage, and an important question in microglial biology is: How malleable are their responses? There are very few studies of effects of resolving cytokines, particularly for rat microglia, and much of the work has focused on pro-inflammatory outcomes. Here, we first exposed primary rat microglia to LPS or to IFNγ+TNFα (I+T) and compared hallmark functional (nitric oxide production, migration) and molecular responses (almost 100 genes), including surface receptors that can be considered part of the sensome. Protein changes for exemplary molecules were also quantified: ARG1, CD206/MRC1, COX-2, iNOS, and PYK2. Despite some similarities, there were notable differences in responses to LPS and I+T. For instance, LPS often evoked higher pro-inflammatory gene expression and also increased several anti-inflammatory genes. Second, we compared the ability of two anti-inflammatory, resolving cytokines (IL-4, IL-10), to counteract responses to LPS and I+T. IL-4 was more effective after I+T than after LPS, and IL-10 was surprisingly ineffective after either stimulus. These results should prove useful in modeling microglial reactivity in vitro; and comparing transcriptional responses to sterile CNS inflammation in vivo

Boundary between the thermal and statistical polarization regimes in a nuclear spin ensemble

As the number of spins in an ensemble is reduced, the statistical uctuations in its polarization eventually exceed the mean thermal polarization. This transition has now been surpassed in a number of recent nuclear magnetic resonance experiments, which achieve nanometer-scale detection volumes. Here, we measure nanometer- scale ensembles of nuclear spins in a KPF6 sample using magnetic resonance force microscopy. In particular, we investigate the transition between regimes dominated by thermal and statistical nuclear polarization. The ratio between the two types of polarization provides a measure of the number of spins in the detected ensemble

Many-spin effects in inelastic neutron scattering and electron paramagnetic resonance of molecular nanomagnets

Many molecular magnetic clusters, such as single-molecule magnets, are characterized by spin ground states with defined total spin S exhibiting zero-field-splittings. In this work, the spectroscopic intensities of the transitions within the ground-state multiplet are analyzed. In particular, the effects of a mixing with higher-lying spin multiplets, which is produced by anisotropic interactions and is neglected in the standard single-spin description, are investigated systematically for the two experimental techniques of inelastic neutron scattering (INS) and electron paramagnetic resonance (EPR), with emphasis on the former technique. The spectroscopic transition intensities are calculated analytically by constructing corresponding effective spin operators perturbationally up to second order and consequently using irreducible tensor operator techniques. Three main effects of spin mixing are observed. Firstly, a pronounced dependence of the INS intensities on the momentum transfer Q, with a typical oscillatory behavior, emerges in first order, signaling the many-spin nature of the wave functions in exchange-coupled clusters. Secondly, as compared to the results of a first-order calculation, the intensities of the transitions within the spin multiplet are affected differently by spin mixing. This allows one, thirdly, to differentiate the higher-order contributions to the cluster magnetic anisotropy which come from the single-ion ligand-field terms and spin mixing, respectively. The analytical results are illustrated by means of the three examples of an antiferromagnetic heteronuclear dimer, the Mn-[3 x 3] grid molecule, and the single-molecule magnet Mn12.Comment: 18 pages, 3 figures, REVTEX4, to appear in PR

The Ca2+ activated SK3 channel is expressed in microglia in the rat striatum and contributes to microglia-mediated neurotoxicity in vitro

<p>Abstract</p> <p>Background</p> <p>Small-conductance Ca²⁺activated K⁺channels are expressed in the CNS, where <it>KCNN2</it>/SK2/KCa2.2 and <it>KCNN3</it>/SK3/KCa2.3 help shape the electrical activity of some neurons. The SK3 channel is considered a potential therapeutic target for diseases and disorders involving neuron hyper-excitability but little is known about its expression and roles in non-neuronal cells in either the healthy or damaged CNS. The purpose of this study was to examine expression of <it>KCNN3</it>/SK3 in CNS microglia <it>in vivo </it>and <it>in vitro</it>, and to use an established <it>in vitro </it>model to determine if this channel contributes to the neurotoxic capacity of activated microglia.</p> <p>Methods</p> <p><it>KCNN3 </it>mRNA (real-time RT-PCR) and SK3 immunoreactivity were examined in rat microglia. Lipopolysaccharide was then used to activate microglia (monitored by iNOS, nitric oxide, activation of NF-κB and p38 MAPK) and transform them to a neurotoxic state. Microglia-mediated neuron damage (TUNEL, activated caspase 3) and nitrotyrosine levels were quantified using a two-chamber system that allowed microglia to be treated with channel blockers, washed and then added to neuron/astrocyte cultures. Contributions of SK3 to these processes were discriminated using a subtractive pharmacological approach with apamin and tamapin. ANOVA and post-hoc tests were used to assess the statistical significance of differences between treatment groups. SK3 immunoreactivity was then compared in the normal and damaged adult rat striatum, by injecting collagenase (a hemorrhagic stroke) or endothelin-1 (a transient ischemic stroke).</p> <p>Results</p> <p><it>KCNN3 </it>mRNA was prevalent in cultured microglia and increased after lipopolysaccharide-induced activation; SK3 channel blockade inhibited microglial activation and reduced their ability to kill neurons. SK3 immunoreactivity was prevalent in cultured microglia and throughout the adult rat striatum (except white matter tracts). After strokes, SK3 was highly expressed in activated microglia/macrophages within the lesions, but reduced in other cells.</p> <p>Conclusions</p> <p>SK3 is expressed in microglia in both the healthy and damaged adult striatum, and mechanistic <it>in vitro </it>studies show it contributes to transformation of microglia to an activated neurotoxic phenotype. Thus, SK3 might be a therapeutic target for reducing inflammation-mediated acute CNS damage. Moreover, its roles in microglia must be considered when targeting this channel for CNS diseases, disorders and reducing neuron hyper-excitability.</p

Szempontok és adatok a szellemi világ néprajzának keresztény értelmezéséhez

A dolgozat állást foglal és érveket sorakoztat fel a keresztény világkép alapján való tudományos elemzés létjogosultsága mellett, s megfogalmaz néhány szempontot az ilyen irányú kutatásokhoz