Influence of N-methyl-D-aspartate receptors on ouabain activation of nuclear factor-kappa B in the rat hippocampus

It has been shown that ouabain (OUA) can activate the Na,K-ATPase complex and mediate intracellular signaling in the central nervous system (CNS). Inflammatory stimulus increases glutamatergic transmission, especially at N-methyl-D-aspartate (NMDA) receptors, which are usually coupled to the activation of nitric oxide synthase (NOS). Nuclear factor-kappa B (NF-kappa B) activation modulates the expression of genes involved in development, plasticity, and inflammation. The present work investigated the effects of OUA on NF-kappa B binding activity in rat hippocampus and the influence of this OUA-Na,K-ATPase signaling cascade in NMDA-mediated NF-kappa B activation. The findings presented here are the first report indicating that intrahippocampal administration of OUA, in a concentration that did not alter Na,K-ATPase or NOS activity, induced an activation of NF-kappa B, leading to increases in brain-derived neurotrophic factor (Bdnf), inducible NOS (iNos), tumor necrosis factor-alpha (Tnf-alpha), and B-cell leukemia/lymphoma 2 (Bcl2) mRNA levels. This response was not linked to any significant signs of neurodegeneration as showed via Fluoro-Jade B and Nissl stain. Intrahippocampal administration of NMDA induced NF alpha B activation and increased NOS and alpha 2/3-Na,K-ATPase activities. NMDA treatment further increased OUA-induced NF-kappa B activation, which was partially blocked by MK-801, an antagonist of NMDA receptor. These results suggest that OUA-induced NF-kappa B activation is at least in part dependent on Na,K-ATPase modulatory action of NMDA receptor in hippocampus. The interaction of these signaling pathways could be associated with biological mechanisms that may underlie the basal homeostatic state linked to the inflammatory signaling cascade in the brain. (c) 2011 Wiley Periodicals, Inc.

Measurements of D-0 and D* production in p plus p collisions at root s=200 GeV

We report measurements of charmed-hadron (D-0, D*) production cross sections at midrapidity in p + p collisions at a center-of-mass energy of 200 GeV by the STAR experiment. Charmed hadrons were reconstructed via the hadronic decays D-0 -> K- pi(+), D*(+) -> D-0 pi(+) -> K-pi(+)pi(+) and their charge conjugates, covering the p(T) range of 0.6-2.0 and 2.0-6.0 GeV/c for D-0 and D*(+), respectively. From this analysis, the charm-pair production cross section at midrapidity is d sigma/dy vertical bar(c (c) over bar)(y-0) = 170+/-45(stat)(-59)(+38()sys) mu b. The extracted charm-pair cross section is compared to perturbative QCD calculations. The transverse momentum differential cross section is found to be consistent with the upper bound of a fixed-order next-to-leading logarithm calculation.

QCD sum rules for the 'Z POT + IND C' (3900) state.

We use the QCD sum rules to study the recently observed charmonium-like structure Z+ c (3900) as a tetraquark state. We evaluate the three-point function and extract the coupling constants of the Z+ c J/ψ π+, Z+ c ηc ρ+ and Z+ c D+ ¯D���0 vertices and the corresponding decay widths in these channels. The results obtained are in good agreement with the experimental data and supports to the tetraquark picture of this state.