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  • 1
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature America Inc.
    Nature medicine 5 (1999), S. 877-879 
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Tumor necrosis factor, an essential mediator of inflammation, inhibits degradation of the molecular switch RGS7 and may lead to the neurological changes that occur during inflammation (page ...
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature medicine 3 (1997), S. 1193-1195 
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] SEPSIS, A FREQUENT cause of death in intensive care units, remains a major public health problem1. Although potent antibiotics and drugs to treat cardiopulmonary failure are available, new therapeutic approaches that can be taken during the early stages of sepsis regardless of the causative ...
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 381 (1996), S. 75-77 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] FIG. 1 Highly increased mortality of mast-cell-deficient W/WV mice after CLP, compared to identically treated age- and sex-matched normal litter-mates (+/+) (12 mice per group) (P 〈 0.0001 for +/+ versus W/WV; log rank statistic). W/WV and +/+ mice were generated from heterozygous breeding pairs ...
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cancer immunology immunotherapy 33 (1991), S. 177-182 
    ISSN: 1432-0851
    Keywords: Tumour necrosis factor ; Viscum album ; Lectin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A purified lectin (MLI) fromViscum album was used to test whether peripheral monocytes from human blood can be activated for the production of tumour necrosis factor (TNF). Cytotoxic activity was detected in the supernatant of MLI-stimulated monocyte cultures. This cytotoxic activity was completely inhibited by monoclonal antibodies to TNFα. Small amounts of soluble TNF protein were measured in a TNFα-specific enzyme-linked immunospecific assay system. Strong expression of TNFα mRNA was induced in human monocytes as well as in macrophage cultures from C3H/HeJ mice having a low response to endotoxin after 2 h of stimulation. Both chains of the MLI were found to induce TNF mRNA equally well in human monocytes. In macrophages of endotoxin-low-responder mice the toxic A chain was a better inducer of TNF mRNA than the galactose-specific lectin B chain. Thus, MLI has immunomodulating effects in activating monocytes/macrophages for inflammatory responses.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0851
    Keywords: Key words Tumor necrosis factor α ; Interferon γ ; NK cell activity ; Soluble TNF receptors ; Malignant ascites
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Tumor necrosis factor α (TNFα) and interferon γ (IFNγ) are important immunomodulators. They are capable of acting in a synergistic manner on tumor cells in vitro and in vivo. In a clinical phase I study 13 patients with malignant ascites due to abdominal spread of different primary tumors received intraperitoneally (i. p.) TNFα and IFNγ once weekly over 3 – 8 weeks in order to evaluate the effect of locoregionally administered TNFα/IFNγ on ascites formation. Therefore some peripheral and local immunological functional parameters of peripheral blood and malignant ascites were investigated. Mononuclear lymphocytes and natural killer (NK) cell activity of peripheral blood and ascites, TNF-inhibitory activity, soluble p55 and p75 TNF receptors, and prostaglandin E2 values in ascites were measured immediately before and 24 h after each TNFα/IFNγ infusion. Peripheral mononuclear lymphocytes and NK activity decreased significantly 24 h after i. p. TNFα/IFNγ application. However, over the entire treatment schedule, peripheral NK activity in all responders showed a continuous increase, when compared to pre TNFα/IFNγ treatment levels. In contrast, NK activity in non-responders constantly decreased. In contrast to non-responders, TNF-inhibitory activity and soluble p55 TNF receptor levels, determined in ascites, decreased in responders. Taken together, our findings suggest, that successful locoregional i. p. TNFα/IFNγ therapy induces systemic immunological reactions possibly after saturation of soluble p55 TNF receptors in ascites, which leads to an increase of peripheral NK activity.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 752-753 
    ISSN: 1432-1440
    Keywords: Cytotoxic Factor ; Lymphokines ; Host Resistance ; Tumor-cytotoxicity ; Lipopolysaccharides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Macrophages activated in a variety of ways in vivo as well as in vitro release a cytotoxic factor upon LPS stimulation. Physicochemical characterization revealed a heat-stable 60,000 D protein with an isoelectric point at pH 4.8. This cytotoxin is one of the effector molecules in tumor cell killing by activated macrophages since cytolysis can be inhibited by antibodies directed against the cytotoxic factor.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1831
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To investigate a possible role of cytokines in parvovirus-mediated suppression of tumorigenesis, we tested in cell culture whether parvoviruses are able to induce interferon (IFN)-β, tumor necrosis factor (TNF)-α or interleukin-6 (IL-6). Infection of rodent or human cells with the parvoviruses minute virus of mice (MVM), H-1 or adeno-associated virus (AAV) types 2 or 5 failed to induce expression of the luciferase or β-galactosidase reporter genes transfected into these cells as constructs containing an IFN-β promoter. Parvoviruses did weakly induce synthesis of TNF-α and of IL-6 in cell culture and could slightly enhance synthesis of these cytokines when induced by other agents. These in vitro data suggest that the rather unspecific tumor-suppressive properties of parvoviruses are unlikely to be attributable to stimulation of the synthesis of IFN, TNF or IL-6.
    Type of Medium: Electronic Resource
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