Two-loop self-energy correction in high-Z hydrogen-like ions

A complete evaluation of the two-loop self-energy diagrams to all orders in Z\alpha is presented for the ground state of H-like ions with Z\ge 40.Comment: RevTeX, 5 figures, 1 tabl

Dual kinetic balance approach to basis set expansions for the Dirac equation

A new approach to finite basis sets for the Dirac equation is developed. It solves the problem of spurious states and, as a result, improves the convergence properties of basis set calculations. The efficiency of the method is demonstrated for finite basis sets constructed from B splines by calculating the one-loop self-energy correction for a hydrogenlike ion.Comment: 14 pages, 1 tabl

Evaluation of the self-energy correction to the g-factor of S states in H-like ions

A detailed description of the numerical procedure is presented for the evaluation of the one-loop self-energy correction to the $g$-factor of an electron in the $1s$ and $2s$ states in H-like ions to all orders in $Z\alpha$.Comment: Final version, December 30, 200

Self-energy correction to the hyperfine structure splitting of the 1s and 2s states in hydrogenlike ions

The one-loop self-energy correction to the hyperfine structure splitting of the 1s and 2s states of hydrogenlike ions is calculated both for the point and finite nucleus. The results of the calculation are combined with other corrections to find the ground state hyperfine splitting in lithiumlike ^{209}Bi^{80+} and ^{165}Ho^{64+}.Comment: The table 2 is changed. 6 pages, 1 figure, Late

Differential Regulation of Formyl Peptide and Platelet-Activating Factor Receptors: Role of Phospholipase Cβ3 Phosphorylation by Protein Kinase A

Formylated peptides (e.g. n-formyl-Met-Leu-Phe (fMLP)) and platelet- activating factor (PAF) mediate chemotactic and cytotoxic responses in leukocytes through receptors coupled to G proteins that activate phospholipase C (PLC). In RBL-2H3 cells, fMLP utilizes a pertussis toxin (ptx)-sensitive G protein to activate PLC, whereas PAF utilizes a ptx- insensitive G protein. Here we demonstrate that fMLP, but not PAF, enhanced intracellular cAMP levels via a ptx-sensitive mechanism. Protein kinase A (PKA) inhibition by H-89 enhanced inositol phosphate formation stimulated by fMLP but not PAF. Furthermore, a membrane-permeable cAMP analog 8-(4- chlorophenylthio)-cAMP (cpt-cAMP) inhibited phosphoinositide hydrolysis and secretion stimulated by fMLP but not PAF. Both cpt-cAMP and fMLP stimulated PLCβ3 phosphorylation in intact RBL cells. The purified catalytic subunit of PKA phosphorylated PLCβ3 immunoprecipitated from RBL cell lysate. Pretreatment of intact cells with cpt-cAMP and fMLP, but not PAF, resulted in an inhibition of subsequent PLCβ3 phosphorylation by PKA in vitro. These data demonstrate that fMLP receptor, which couples to a ptx-sensitive G protein, activates both PLC and cAMP production. The resulting PKA activation phosphorylates PLCβ3 and appears to block the ability of G(βγ) to activate PLC. Thus, both fMLP and PAF generate stimulatory signals for PLCβ3, but only fMLP produces a PKA-dependent inhibitory signal. This suggests a novel mechanism for the bidirectional regulation of receptors which activate PLC by ptx-sensitive G proteins

Opiates Transdeactivate Chemokine Receptors: δ and μ Opiate Receptor- Mediated Heterologous Desensitization

An intact chemotactic response is vital for leukocyte trafficking and host defense. Opiates are known to exert a number of immunomodulating effects in vitro and in vivo, and we sought to determine whether they were capable of inhibiting chemokine-induced directional migration of human leukocytes, and if so, to ascertain the mechanism involved. The endogenous opioid met- enkephalin induced monocyte chemotaxis in a pertussis toxin-sensitive manner. Metenkephalin, as well as morphine, inhibited IL-8-induced chemotaxis of human neutrophils and macrophage inflammatory protein (MIP)-1α, regulated upon activation, normal T expressed and secreted (RANTES), and monocyte chemoattractant protein 1, but not MIP-1β-induced chemotaxis of human monocytes. This inhibition of chemotaxis was mediated by δ and μ but not κ G protein-coupled opiate receptors. Calcium flux induced by chemokines was unaffected by met-enkephalin pretreatment. Unlike other opiate-induced changes in leukocyte function, the inhibition of chemotaxis was not mediated by nitric oxide. Opiates induced phosphorylation of the chemokine receptors CXCR1 and CXCR2, but neither induced internalization of chemokine receptors nor perturbed chemokine binding. Thus, inhibition of chemokine-induced chemotaxis by opiates is due to heterologous desensitization through phosphorylation of chemokine receptors. This may contribute to the defects in host defense seen with opiate abuse and has important implications for immunomodulation induced by several endogenous neuropeptides which act through G protein-coupled receptors

Neutron Correlations in Special Nuclear Materials, Experiments and Simulations

Fissile materials emit neutrons with an unmistakable signature that can reveal characteristics of the material. We describe here measurements, simulations, and predicted signals expected and prospects for application of neutron correlation measurement methods to detection of special nuclear materials (SNM). The occurrence of fission chains in SNM can give rise to this distinctive, measurable time correlation signal. The neutron signals can be analyzed to detect the presence and to infer attributes of the SNM and surrounding materials. For instance, it is possible to infer attributes of an assembly containing a few kilograms of uranium, purely passively, using detectors of modest size in a reasonable time. Neutron signals of three radioactive sources are shown to illustrate the neutron correlation and analysis method. Measurements are compared with Monte Carlo calculations of the authenticated sources