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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 7 (1961), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 116 (1964), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 104 (1963), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 85 (1971), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 286 (1980), S. 89-90 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] IN THE introduction to this first volume of the Handbook of Inflammation, the editor, John C. Houck, gives a splendid though brief account of the various steps in the inflammatory process. The book has then been arranged so that the mediators connected with each stage have been discussed. Our old ...
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 254 (1975), S. 308-311 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Corticosteroids as well as non-steroid anti-inflammatory drugs inhibit the prostaglandin-mediated vasodilatation accompanying lipolysis in subcutaneous fat. Whereas the non-steroids produce their effect by inhibition of prostaglandin synthesis, however, corticosteroids inhibit their release. This ...
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 192 (1961), S. 596-599 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] BRADYKININ is a polypeptide discovered in 1949 J3 by Rocha e Silva, Beraldo and Rosenfeld1, who coined the name 'bradykinin' (slow-moving) because, when acting on the guinea pig intestine, it caused a delayed and slow contraction. They showed that it is formed by the action of certain enzymes, such ...
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 188 (1960), S. 999-999 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Since the isolation of natural bradykinin by Elliott, Lewis and Horton1, a nonapeptide has been synthesized2,3 and its structure agrees with that proposed4 for the natural product. The structure is as follows : Arg.Pro.Pro.Gly.Phe.Ser.Pro.Phe.Arg. The reported pharmacological properties of the ...
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A method is described to examine the activity of potential antirheumatic drugs on the release and activity of lymphokines and interleukinsin vitro, using human peripheral blood mononuclear cells and synovial cells. The enhancement of lymphocyte-mediated effects brought about by non-steroid anti-inflammatory drugs has been shown to be the result of inhibition of a prostaglandin negative-feedback mechanism. Since the underlying features of rheumatoid arthritis and related diseases are almost certainly brought about by mononuclear cell activation, their enhancement by non-steroid anti-inflammatory drugs might well have serious clinical implications. The possibility is discussed that aspirin-like drugs, administered in large doses to patients suffering slight joint pain, might well exacerbate, perpetuate or even initiate a chronic arthritic condition. We suggest that, as soon as the disease has been diagnosed, patients should be treated with a disease-modifying drug and, if necessary, an analgesic which does not inhibit cyclo-oxygenase.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 19 (1986), S. 109-115 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Gold salts, auranofin (AF), aurothiomalate (ATM) and aurothioglucose (ATG) displayed immunosuppressive action in a series ofin vitro assays which mimic the cell-cell interactions thought to occur in rheumatoid arthritis. The gold salts inhibited phytohaemagglutinin (PHA)-induced thymidine incorporation and γ-IF production by peripheral blood mononuclear cells, as well as IL-2-induced proliferation of PHA-blasts. The separate addition of IL-2 and γ-IF partly reversed the anti-proliferative effects of ATM and ATG; however, the addition of IL-1 had no effect. ATM and ATG inhibited PHA-stimulated IL-1 production by mononuclear cells but not spontaneous or LPS-induced IL-1 production by adherent monocytes. It was concluded that ATM and ATG inhibited lymphocyte function and lymphocyte-amplification of macrophage function. The anti-proliferative effects of AF were partly reversed by IL-2 but not by γ-IF or IL-1. AF inhibited PHA-stimulated IL-1 production by mononuclear cells as well as spontaneous and LPS-induced production by adherent cells. It appeared that AF inhibited lymphocyte and macrophage function directly. AF also displayed potential anti-inflammatory activity in that it inhibited PGE2 and collagenase production by proteolytically dispersed rheumatoid synovial cells.
    Type of Medium: Electronic Resource
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