Coherent states for exactly solvable potentials

A general algebraic procedure for constructing coherent states of a wide class of exactly solvable potentials e.g., Morse and P{\"o}schl-Teller, is given. The method, {\it a priori}, is potential independent and connects with earlier developed ones, including the oscillator based approaches for coherent states and their generalizations. This approach can be straightforwardly extended to construct more general coherent states for the quantum mechanical potential problems, like the nonlinear coherent states for the oscillators. The time evolution properties of some of these coherent states, show revival and fractional revival, as manifested in the autocorrelation functions, as well as, in the quantum carpet structures.Comment: 11 pages, 4 eps figures, uses graphicx packag

Multiorder coherent Raman scattering of a quantum probe field

We study the multiorder coherent Raman scattering of a quantum probe field in a far-off-resonance medium with a prepared coherence. Under the conditions of negligible dispersion and limited bandwidth, we derive a Bessel-function solution for the sideband field operators. We analytically and numerically calculate various quantum statistical characteristics of the sideband fields. We show that the multiorder coherent Raman process can replicate the statistical properties of a single-mode quantum probe field into a broad comb of generated Raman sidebands. We also study the mixing and modulation of photon statistical properties in the case of two-mode input. We show that the prepared Raman coherence and the medium length can be used as control parameters to switch a sideband field from one type of photon statistics to another type, or from a non-squeezed state to a squeezed state and vice versa.Comment: 12 pages, 7 figures, to be published in Phys. Rev.

Defective immune response and severe skin damage following UVB irradiation in interleukin-6-deficient mice

Interleukin-6 (IL-6), a multifunctional cytokine, is induced in the acute-phase reaction following ultraviolet (UV) irradiation of humans and mice. Using IL-6-deficient (IL-6−/−) mice, we investigated the role of IL-6 in immunosuppression and inflammatory responses caused by UVB (280–320 nm) radiation. The IL-6−/− mice had a defective contact hypersensitivity (CHS) in response to the sensitizers 2,4-dinitrofluorobenzene and oxazolone. The injection of recombinant IL-6 (rIL-6) into these mice resulted in a marked recovery of the CHS. Serum IL-6 was significantly elevated by UV irradiation of wild-type B6 J/129Sv (IL-6+/+) mice but was not detectable in IL-6−/− mice. Interestingly, there was no induction of serum interleukin-10 (IL-10) by UV irradiation of IL-6−/− mice, whereas UV exposure caused a significant increase in serum IL-10 levels in IL-6+/+ mice. Injection of rIL-6 into IL-6−/− mice increased IL-10 to levels similar to those of IL-6+/+ mice. Being different from IL-6+/+ mice, no epidermal proliferation was found at 48 hr in the IL-6−/− mice, but delayed cell proliferation was observed at 72 hr after UV exposure. Immunohistochemical analysis demonstrated that the epidermis was capable of synthesizing IL-6 at 72 hr after UV irradiation of IL-6+/+ mice. In addition, the IL-6-positive cells appeared to be Langerhans' cells, which were detected with dendritic cell-reactive S-100 antibody. The present study strongly suggests that IL-6 may play a crucial role in the alteration of cutaneous immune responses following UV exposure, and provides evidence that IL-6 is a potent inducer of IL-10. Furthermore, IL-6 production induced by UV radiation appears to be an important early signal for repair of UV-caused skin damage

Protein-kinase-specific inhibitors block Langerhans’ cell migration by inhibiting interleukin-1α release

Previous studies have shown that depletion of Langerhans’ cells (LC) from murine epidermis by the superantigen, staphylococcal enterotoxin A (SEA) involves interleukin-1α (IL-1α) and is inhibitable by agents that block G-protein-associated kinases. The purpose of this study was to determine whether specific kinase inhibitors block LC depletion by inhibiting IL-1α release and to ascertain whether LC depletion by SEA involves cell migration. These goals were addressed by measuring the IL-1α release within whole or LC-depleted epidermal cell suspensions in the presence of SEA and/or H-7 (an inhibitor of protein kinase C) or H-8 (an inhibitor of G-protein-associated kinases) and by examining the migration of cells with LC markers in SEA-treated skin sections. The results suggest that LC depletion by SEA involves migration and that this migration is blocked by protein kinase inhibitors, at least in part, through inhibition of SEA-induced IL-1α release by epidermal cells