Non separable Werner states in spontaneous parametric down-conversion

The multiphoton states generated by high-gain spontaneous parametric down-conversion (SPDC) in presence of large losses are investigated theoretically and experimentally. The explicit form for the two-photon output state has been found to exhibit a Werner structure very resilient to losses for any value of the gain parameter, g. The theoretical results are found in agreement with the experimental data. The last ones are obtained by quantum tomography of the state generated by a high-gain SPDC.Comment: 16 pages, 6 figure

Entanglement, EPR correlations and mesoscopic quantum superposition by the high-gain quantum injected parametric amplification

We investigate the multiparticle quantum superposition and the persistence of multipartite entanglement of the quantum superposition generated by the quantum injected high-gain optical parametric amplification of a single photon. The physical configuration based on the optimal universal quantum cloning has been adopted to investigate how the entanglement and the quantum coherence of the system persists for large values of the nonlinear parametric gain g.Comment: 9 pages, 5 figure

Laminin-332 (Laminin-5) is the major motility ligand for B cell chronic lymphocytic leukemia

Cell adhesion and motility are central aspects in the pathophysiology of B cell chronic lymphocytic leukemia (B-CLL), but the role of specific extracellular matrix proteins is still to be completely unveiled. Purified peripheral blood neoplastic cells of B-CLL patients migrated poorly on laminins-111,-411,-511, but showed pronounced motility on laminin (LM)-332 in a high percentage of cases. B-CLL cell motility on LM-332 was mediated by the α3β1 integrin and was preferentially observed in cells carrying a mutated IgVH gene profile. Within normal lymph nodes, LM-332 was circumscribed around blood vessels and to areas corresponding to marginal zones, where it was deposited in a pattern reminiscent of reticular fibers. Conversely, in B-CLL involved lymph nodes, a positive LM-332 reticular mesh was diffusely evident, throughout the disrupted nodal architecture. In the present study we identified LM-332 as a crucial motility-promoting factor for B-CLL lymphocytes and as a potential constituent favoring the dissemination of B-CLL lymphocytes through vascular basement membranes and possibly lymph node compartments. © 2007 International Society of Matrix Biology

Bidirectional induction of the cognate receptor-ligand alpha 4/VCAM-1 pair defines a novel mechanism of tumor intravasation

Engagement of cell surface adhesion receptors with extracellular constituents and with cellular counter-receptors is crucial for the extravasation of blood-borne neoplastic cells and their seeding at distant sites; however, the early events of tumor dissemination-ie, the intravasation step(s)-have been largely neglected. A role for the alpha4beta7 integrin was hypothesized to explain the high leukemogenicity exhibited by one (NQ22) among several T-cell lymphomas studied. To clarify the mechanisms of early aggressivity, the behavior of highly and poorly leukemogenic cell lines were compared in vitro. Cocultivation of physically separated leukemic cells with resting endothelial cells resulted in the up-regulation of VCAM-1 expression. NQ22 cells expressed mRNA of different cytokines that up-regulate VCAM-1 and at higher levels than cells of a nonaggressive lymphoma, and they migrated more efficiently through an activated endothelial cell layer. With the use of neutralizing antibodies against interferon-gamma, granulocyte macrophage colony-stimulating factor, and tumor necrosis factor (TNF)-alpha, it was determined that TNF-alpha is one of the soluble factors released by NQ22 cells involved in the up-regulation of VCAM-1. The finding that vascular cells within the early local growth were strongly positive for VCAM-1 indicated that NQ22 cells could activate endothelial cells also in vivo. Finally, cocultivation of preleukemic alpha4(-)NQ22 cells with TNF-alpha-activated endothelial cells induced the expression of alpha4 integrins on the former cells. Reciprocal up-regulation and engagement of alpha4/VCAM-1 pairs determined the sequential transmigration and intravasation steps, and similar mechanisms might affect the aggressivity of human T lymphoblastic lymphomas