6 research outputs found

    Turismo e Turismi dell\u2019Adriatico

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    1.Adriapolis . 2. La regione delle vacanze? I flussi turistici internazionali e domestici. 3.La Riviera Adriatica. 4.La Riviera Romagnola: il pi\uf9 grande distretto turistico dell\u2019Europa.5. Le politiche regionali dell\u2019Emilia-Romagna: un modello di turismi per l\u2019Adriatico? 6. Conclusione: I turismi e l\u2019identit\ue0 adriatic

    Proton-Transfer Reactions on Hexanuclear Platinum Clusters: Reversible Heterolytic Cleavage of H2 and C-H Activation Affording a Linear, Cluster-Containing Polymer

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    The hexanuclear cluster {Pt6}H2 (2) contains a sterically hindered and chemically stable {Pt6}=Pt 6-(\u3bc-PtBu2)4(CO)4 core, with the six metals forming an edge-bridged tetrahedron. The two hydrides are the reactive sites of the cluster and lie on opposite sides of the cluster, terminally bonded to the two "apical" edge-bridging platinum centres. Indeed, cluster 2 reacts with acids of different acidity (HA=CF 3SO3H, HBF4, p-CH3-C 6H4-SO3H, CF3COOH, PhCOOH and CH3COOH), affording, after evolution of two equivalents of dihydrogen, the corresponding anion-substituted clusters {Pt6}A 2 (4). We suggest that the reaction proceeds through a mechanism similar to the one generally accepted for the analogous protonation of mononuclear hydrides, with some of the intermediates partially characterised at low temperature. Interestingly, the reverse reaction, the heterolytic splitting of H2 by clusters 4, occurs readily under mild conditions. The anions in clusters 4a and 4b (4a: A=CF3SO3, 4b: A=BF 4) are bonded in the solid state but very easily dissociate in solution and may be substituted under mild conditions by weak ligands, such as CH2Cl2 or CH3CN. With dialkyl ethers, the reaction proceeds further with the heterolytic splitting of a C-H bond of the ethereal ligand. This process allowed us to isolate the polymer [{Pt 6}(CH2OCH2CH2OCH2)]x (8), in which the {Pt6} cluster units are connected by insulating spacers arising from dimethoxyethane. The results of single-crystal X-ray diffraction studies on 4a and 8 are also reported

    Antilymphocyte globulin, cyclosporine, prednisolone, and granulocyte colony-stimulating factor for severe aplastic anemia: an update of the GITMO/EBMT study on 100 patients

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    One hundred consecutive patients with severe aplastic anemia (SAA) received horse antilymphocyte globulin (ALG), cyclosporin A (CyA), 6-methylprednisolone (6Mpred), and granulocyte colony-stimulating factor (G-CSF) as first-line therapy. The median age was 16 years (range, 1-72 years) and median neutrophil count was 0.2 x 10(9)/L (range, 0-0.5 x 10(9)/L). Trilineage hematologic recovery (at a median interval of 96 days from treatment) was seen in 77 patients (48 complete, 29 partial) after 1 (n = 50) or more courses of ALG (n = 27). Of the 23 nonresponders, 11 patients died at a median interval of 83 days (range, 16-1132 days), 6 were considered treatment failures and underwent transplantation, and 6 were pancytopenic. Cytogenetic abnormalities were seen in 11% of patients, clonal hematologic disease in 8%, and relapse of marrow aplasia in 9%. The actuarial survival at 5 years was 87% (median follow-up 1424 days): 76% versus 98% for patients with neutrophil counts less than versus greater than 0.2 x 10(9)/L (P =.001) and 88% versus 87% for patients aged less than versus more than 16 years (P =.8). The actuarial probability of discontinuing CyA was 38%. Patients who did not achieve a white blood cell (WBC) count of 5 x 10(9)/L during G-CSF treatment have a low probability of responding (37%) and a high mortality rate (42%). This update confirms a high probability for SAA patients of becoming transfusion independent and of surviving after treatment with ALG, CyA, 6Mpred, and G-CSF, with a significant effect of neutrophil counts on outcome. Problems still remain, such as absent or incomplete responses, clonal evolution, relapse of the original disease, and cyclosporine dependence. Early transplantation, also from alternative donors, may be warranted in patients with poor WBC response to G-CSF
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