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  • 1985-1989  (3)
  • 1965-1969
  • 1989  (1)
  • 1986  (2)
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  • 1985-1989  (3)
  • 1965-1969
Year
Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Responsiveness of T cells to Mutant Major Histocompatibility Complex Class I Antigen (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 29 (1989), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Mechanisms of the activation of T cells responding to major histocompatibility complex (MHC) class I antigen were investigated with special reference lo interleukin 1 (IL-1) production from stimulator-type accessory cells. For this purpose, we used mainly fractionated Lyt-2+ T cells of C57BL/6 (B6) mice as responder cells and irradiated spleen cells or those deprived of adherent cells of B6. C-H-2bm1 (bm 1) mice as stimulator ceils. Lyt-2+ T cells of B6 mice proliferated in the presence of irradiated whole spleen cells of bm1 mice but did not to Sephadex G-10 column-passed bm1 spleen cells. The unresponsiveness in the latter case was overcome by the supplement of recombinant IL-1 and/or IL-2 in the culture medium. These interleukins were shown to promote the proliferative response of B6 Lyt-2+ T cells in the presence of stimulator-type for B cells. Both interleukins also facilitated the generation of cytotoxic T cells from BA Lyt-2+ cells to H-2Kbm1 antigen in the mixed lymphocyte culture deficient in stimulator-type accessory cells. IL-1 was shown to enhance the expression of IL-2 receptor on the responding Lyt-2+ T cells as assessed by flow cytometry. IL-1 binding to responding T cells were also assayed by means of iodinated IL-1 and was shown to increase significantly on responding Lyt-2+ cells. Overall results indicate that accessory cells might play dual roles in the activation of Lyt-2+ T cells responding to allogeneic MHC class 1 antigen: direct presentation of the antigen to responder T cells and production of IL-1. Both signals are essentially required for Lyt-2+ T cells responding to allogeneic MHC class I antigen to initiate proliferation and also to differentiate into cytotoxic T cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1989.tb01133.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Glucagon-like polypeptide and insulin contents in the brain from acute hepatic failure dogs (1986)
    Springer
    Research in experimental medicine 186 (1986), S. 203-208 
    Details
    ISSN: 1433-8580
    Keywords: Acute hepatic failure ; Insulin ; Glucagon ; Glucagon-like peptides ; Blood-brain barrier ; Thalamus-hypothalamus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin contents in the thalamus-hypothalamus were significantly increased in acute hepatic failure dogs treated with dimethylnitrosamine. Glucagon immunoreactivity (GI) contents also tended to increase in the same portion of the brain. However, insulin and GI contents in the cerebral cortex and midbrain did not rise. Glucagon-like immunoreactivity (GLI) contents were much higher than GI in all the brain regions tested, but the levels were not significantly altered in hepatic failure dogs. A simultaneous infusion of insulin and glucagon to hepatic failure dogs failed to produce an elevation of insulin, GI and GLI contents even in the thalamus-hypothalamus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01852045
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Abstracts of the Twenty-Third Annual Meeting of the Japanese society of Biometeorology, Nagakute, 30 November–1 December 1984 (1986)
    Springer
    International journal of biometeorology 30 (1986), S. 359-385 
    Details
    ISSN: 1432-1254
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geography , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02189374
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    Paper (German National Licenses)
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