Klauder's coherent states for the radial Coulomb problem in a uniformly curved space and their flat-space limits

First a set of coherent states a la Klauder is formally constructed for the Coulomb problem in a curved space of constant curvature. Then the flat-space limit is taken to reduce the set for the radial Coulomb problem to a set of hydrogen atom coherent states corresponding to both the discrete and the continuous portions of the spectrum for a fixed \ell sector.Comment: 10 pages, no figure

Delocalization and the semiclassical description of molecular rotation

We discuss phase-space delocalization for the rigid rotator within a semiclassical context by recourse to the Husimi distributions of both the linear and the $3D-$anisotropic instances. Our treatment is based upon the concomitant Fisher information measures. The pertinent Wehrl entropy is also investigated in the linear case.Comment: 6 pages, 3 figure

Coherent states for polynomial su(1,1) algebra and a conditionally solvable system

In a previous paper [{\it J. Phys. A: Math. Theor.} {\bf 40} (2007) 11105], we constructed a class of coherent states for a polynomially deformed $su(2)$ algebra. In this paper, we first prepare the discrete representations of the nonlinearly deformed $su(1,1)$ algebra. Then we extend the previous procedure to construct a discrete class of coherent states for a polynomial su(1,1) algebra which contains the Barut-Girardello set and the Perelomov set of the SU(1,1) coherent states as special cases. We also construct coherent states for the cubic algebra related to the conditionally solvable radial oscillator problem.Comment: 2 figure

P1 receptors and cytokine secretion

Evidence has accumulated in the last three decades to suggest tissue protection and regeneration by adenosine in multiple different cell types. Adenosine produced in hypoxic or inflamed environments reduces tissue injury and promotes repair by receptor-mediated mechanisms. Among other actions, regulation of cytokine production and secretion by immune cells, astrocytes and microglia (the brain immunocytes) has emerged as a main mechanism at the basis of adenosine effects in diseases characterized by a marked inflammatory component. Many recent studies have highlighted that signalling through A1 and A2A adenosine receptors can powerfully prevent the release of pro-inflammatory cytokines, thus inhibiting inflammation and reperfusion injury. However, the activation of adenosine receptors is not invariably protective of tissues, as signalling through the A2B adenosine receptor has been linked to pro-inflammatory actions which are, at least in part, mediated by increased release of pro-inflammatory cytokines from epithelial cells, astrocytes and fibroblasts. Here, we discuss the multiple actions of P1 receptors on cytokine secretion, by analyzing, in particular, the role of the various adenosine receptor subtypes, the complex reciprocal interplay between the adenosine and the cytokine systems, their pathophysiological significance and the potential of adenosine receptor ligands as new anti-inflammatory agents

Ion beam radiation effects on InAs semiconductor quantum dots

AbstractSelf-assembled quantum dots (QDs) have attracted significant attention because of their potential applications in novel semiconductor devices. In this work, we investigated radiation effects induced by 1.0 MeV proton ion beams on InAs self-assembled quantum dots. In particular, we emphasized the effects of lattice environments of QDs on their luminescence emission after ion beam irradiation. Photoluminescence (PL) spectroscopy was used to characterize the optical properties of QDs subjected to proton irradiation and post-irradiation annealing. Compared to the single-layer QDs grown in GaAs films, the QDs embedded in an AlAs/GaAs superlattice exhibited much higher PL degradation resistance to proton beam bombardment, e.g., at the highest dose (1.0×1014 cm−2) used in this work, a difference of ~ 20-fold in PL intensity was found between the QDs configured in these two different lattice structures. After thermal annealing of irradiated QD samples, ion beam enhanced blueshift of PL was observed to be much more pronounced for the single-layer QDs. We discuss mechanisms that may result in the differences in optical response to ion beams between QDs with different lattice surroundings.</jats:p

Nitric oxide, atrial natriuretic peptide, and cyclic GMP inhibit the growth-promoting effects of norepinephrine in cardiac myocytes and fibroblasts.

This study tested the hypothesis that nitric oxide (NO) and atrial natriuretic peptide (ANP) can attenuate the effects of adrenergic agonists on the growth of cardiac myocytes and fibroblasts. In ventricular cells cultured from neonatal rat heart, ANP and the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) caused concentration-dependent decreases in the norepinephrine (NE)-stimulated incorporation of [3H]leucine in myocytes and [3H]thymidine in fibroblasts. In myocytes, the NO synthase inhibitor NG-monomethyl-L-arginine potentiated NE-stimulated [3H]leucine incorporation. In both cell types, ANP and SNAP increased intracellular cGMP levels, and their growth-suppressing effects were mimicked by the cGMP analogue 8-bromo-cGMP. Furthermore, in myocytes, 8-bromo-cGMP attenuated the alpha1-adrenergic receptor-stimulated increases in c-fos. Likewise, ANP and 8-bromo-cGMP attenuated the alpha1-adrenergic receptor- stimulated increase in prepro-ANP mRNA and the alpha1-adrenergic receptor-stimulated decrease in sarcoplasmic reticulum calcium ATPase mRNA. The L-type Ca2+ channel blockers verapamil and nifedipine inhibited NE-stimulated incorporation of [3H]leucine in myocytes and [3H]thymidine in fibroblasts, and these effects were not additive with those of ANP, SNAP, or 8-bromo-cGMP. In myocytes, the Ca2+ channel agonist BAY K8644 caused an increase in [3H]leucine incorporation which was inhibited by ANP. These findings indicate that NO and ANP can attenuate the effects of NE on the growth of cardiac myocytes and fibroblasts, most likely by a cGMP-mediated inhibition of NE-stimulated Ca2+ influx