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  • Chemotherapy  (1)
  • Citric acid  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Metal-hydroxycarboxylate interactions: syntheses and structures of K2[VO2(C6H6O7)]2·4H2O and (NH4)2[VO2(C6H6O7)]2·2H2O (1995)
    Springer
    Journal of chemical crystallography 25 (1995), S. 807-811 
    Details
    ISSN: 1572-8854
    Keywords: Citric acid ; citrate complex ; oxovanadium(V) complex ; vanadate ; molecular structure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geosciences , Physics
    Notes: Abstract Potassium and ammonium dimeric (citrato)dioxovanadium(V) hydrate K2[VO2(H2cit)]2·4H2O1 and (NH4)2[VO2(H2cit)]2·2H2O2 (H4cit=citric acid) have been prepared and characterized by X-ray structure analyses. Vanadate1 crystallizes in the monoclinic space groupP21/n (No. 14) with unit cell parameters:a=9.304(2),b=11.756(2),c=11.911(2)Å, β=111.72(3)°, andD c=1.911 g/cm3,Z=2; Vanadate2 also crystallizes in the monoclinic space groupP21/n with unit cell parameters:a=9.719(2),b=11.111(3),c=11.294(2)Å, β=109.03(2)°, andD c=1.781 g/cm3,Z=2. Each dimer contains a centro-symmetric planar four-member V2O2 ring with two exocyclic citrate entities coordinated by the oxygen atoms of the hydroxy-and α-carboxylate ligands, while the other two β-carboxylate groups remain uncomplexed. Principal dimensions of the V−O bonds are 1.986(4)av (hydroxy) and 1.980(3)Å(α-carboxyl) for vanadate1, 1.988(2)av (hydroxy) and 1.974(3)Å(α-carboxyl) for vanadate2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01671075
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  • 2
    Electronic Resource
    Electronic Resource
    Cellular immunosuppression in children with acute lymphoblastic leukemia: Effect of consolidation chemotherapy (1992)
    Springer
    Cancer immunology immunotherapy 35 (1992), S. 271-276 
    Details
    ISSN: 1432-0851
    Keywords: Immunosuppression ; Chemotherapy ; Acute lymphoblastic leukemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study was designed to evaluate the chemotherapy-induced cellular immunosuppression in 20 children with acute lymphoblastic leukemia (ALL) in remission and receiving maintenance chemotherapy. Peripheral blood was serially obtained from leukemic children during vincristine/cyclophosphamide/6-mercaptopurine/prednisone combined consolidation chemotherapy. The mean absolute number of peripheral blood lymphocytes as well as the mean absolute numbers of lymphocyte subsets (T cells, T cell subsets, B cells, and natural killer cells) from leukemic children before consolidation chemotherapy were all significantly lower than in control subjects; however, the percentages of lymphocyte subsets were similar in both groups. After consolidation chemotherapy, the percentages of CD4+ T lymphocytes and natural killer (NK) cells were significantly decreased and the percentages of monocytes and CD8+ T lymphocytes were significantly increased. Phytohemagglutinin- and 12-O-tetradecanoylphorbol-13-acetate-induced production of interleukin-2 (IL-2) and NK-cell-mediated cytotoxic activity by peripheral blood mononuclear cells (PBMC) were also substantially decreased in the post-therapy groups. NK activity correlated with the percentage of NK cells in PBMC. In contrast, OK432-induced production of tumor necrosis factor α (TNFα) and killer activity against NK-resistant target cells were significantly increased after therapy as compared with the pre-therapy and control groups. TNFα production correlated with the percentage of monocytes in PBMC. These results demonstrate that substantial quantitative and qualitative chemotherapy-induced abnormalities of the cellular immune system are present in the majority of patients treated with ALL. It is also suggested that the increased TNFα production by monocytes and the appearance of potent killing activity against NK-resistant targets might compensate for the defects of IL-2 production and NK activity during intensive consolidation chemotherapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01789334
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