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Sökning: WFRF:(Jansson Johan) > (1990-1994) > Tidskriftsartikel

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1.
  • Brabant, G, et al. (författare)
  • E-cadherin: a differentiation marker in thyroid malignancies.
  • 1993
  • Ingår i: Cancer research. - 0008-5472. ; 53:20, s. 4987-93
  • Tidskriftsartikel (refereegranskat)abstract
    • Loss of E-cadherin (uvomorulin), a Ca(2+)-dependent cell adhesion molecule required for normal epithelial function, has been attributed a pathogenetic role in tumor invasion. The expression of E-cadherin was studied in normal and neoplastic follicular epithelium of the human thyroid by Northern blot analysis and immunofluorescence on frozen tissue sections. In the normal thyroid (n = 10) and in benign thyroid disorders (n = 21; toxic diffuse goitre; multinodular goitre; follicular adenomas), E-cadherin mRNA levels were equally high and the follicles were generally stained, mainly along the lateral surface of the epithelial cells, by the anti-E-cadherin monoclonal antibody. In anaplastic thyroid carcinomas (n = 6) E-cadherin expression was very low or lacking. In papillary carcinomas (n = 23), E-cadherin mRNA levels varied from nearly normal to highly reduced, which roughly correlated with the overall immunofluorescence intensity. However, the immunostaining also revealed a heterogeneous "all-or-nothing" expression of E-cadherin among adjacent cells in the same tumor. In the follicular carcinomas (n = 9), E-cadherin mRNA levels were in general rather high but the immunostaining varied considerably. A few papillary and follicular tumors lacked immunoreactive E-cadherin in spite of high mRNA levels. In oxyphilic (Hürthle) cell tumors, comprising both adenomas (n = 4) and carcinomas (n = 2), E-cadherin immunoreactivity was reduced and distributed intracellularly rather than at the cell surface. The expression of E-cadherin in relapsing thyroid carcinomas and in tumors with metastatic spreading was, irrespective of the histiotype, low or lacking. Sequential Northern analysis revealed a close correlation between the expression levels of E-cadherin and the thyrotropin receptor. Together, the data suggest that in human thyroid malignancies both gene expression and posttranscriptional control of E-cadherin may be impaired.
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2.
  • Fu, Michael, 1963, et al. (författare)
  • Increase in functional activity rather than in amount of Gi-alpha in failing human heart with dilated cardiomyopathy.
  • 1992
  • Ingår i: Cardiovascular research. - 0008-6363. ; 26:10, s. 950-5
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: The aim was to investigate whether or not increased pertussis toxin catalysed ADP ribosylation correlates with increased amount of Gi-alpha in failing human heart. DESIGN: Antisera raised against unique synthetic peptides corresponding to alpha subunits of Gs and Gi 1-3 were used in immunoblotting and ELISA to determine amounts of various G proteins. Adenylyl cyclase activity, beta adrenoceptors, and muscarinic receptors were then measured in cardiomyopathic hearts (n = 6) obtained at transplant in order to study whether or not an altered expression of G proteins has relevance to the integrity and function of the receptor--adenylyl cyclase system. Six non-failing control hearts were also studied. RESULTS: No significant differences in the peptide equivalent amounts of either Gs or Gi were found in the failing human heart as compared to the non-failing heart. However, functional activity of Gi was shown to increase significantly since there was a decrease in basal (57%), isoprenaline stimulated (60%), and guanyliminodiphosphate stimulated (52%) adenylyl cyclase activity. In contrast the density of beta adrenoceptors was markedly decreased (51%) in failing human heart in comparison to non-failing hearts. Neither the density nor the affinity of muscarinic receptors changed in the failing human heart. CONCLUSION: These results suggest that in the failing human heart, there is an increase in functional activity rather than in amount of Gi, and an important part of functional expression of Gi-alpha may be regulated at the post-translational level.
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3.
  • Mölne, Johan, 1958, et al. (författare)
  • Adherence of RFD-1 positive dendritic cells to the basal surface of thyroid follicular cells in Graves' disease.
  • 1994
  • Ingår i: Autoimmunity. - 0891-6934. ; 17:1, s. 59-71
  • Tidskriftsartikel (refereegranskat)abstract
    • HLA-DR positive cells infiltrating Graves' thyroid tissue were examined for their expression of cell-specific immunological markers using light and electron microscopic immunostaining of frozen sections and isolated open thyroid follicles. Graves' glands (n = 21) were enriched of CD68 and Leu-M5/CD11c positive monocytes/macrophages as well as CD4 and CD8 lymphocytes. These cell types were distributed juxta-follicular as well as in other tissue areas. Only the RFD-1 antibody, considered to label antigen-presenting cells including dendritic cells, identified cells invariably located close to the interstitial follicular surface. After follicle isolation, RFD-1 cells were enriched compared to Leu-M5 cells and exclusively adherent to the follicular epithelium. The plasma membrane of RFD-1 positive cells were in intimate contact with the basolateral membrane of the thyrocytes, sometimes extending deeply into the intercellular space of the epithelium. Parallel labelling experiments suggested that the follicle-adhering RFD-1 cells also expressed HLA-DR. Our findings show that in human thyroid glands with Graves' disease RFD-1 positive cells with a dendritic morphology establish direct contact with the follicular epithelium. In view of the fact that both HLA-DR and RFD-1 are associated with antigen-presenting functions it is suggested that a direct interaction of dendritic cells with thyrocytes might be an important component of the autoimmune reaction in Graves' disease.
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4.
  • Mölne, Johan, 1958, et al. (författare)
  • Non-polarized cell surface expression of HLA-A,B,C and HLA-DR antigens in Graves' thyroid follicle cells.
  • 1991
  • Ingår i: Autoimmunity. - 0891-6934. ; 10:3, s. 189-99
  • Tidskriftsartikel (refereegranskat)abstract
    • The intrathyroidal distribution and cell surface location of HLA-A,B,C and HLA-DR antigens was studied in polarized thyroid follicle cells from Graves' (n = 11) and normal (n = 3) thyroid tissue, using light and electron microscopy. Cryosections and isolated, open follicle segments were incubated with monoclonal antibodies against HLA-A,B,C and HLA-DR antigens and with patient sera containing autoantibodies against the microsomal antigen/thyroperoxidase. Immunoreactivity for HLA-A,B,C and HLA-DR on isolated thyroid follicle cells was frequently detected in Graves' disease, but absent in normal glands. There was a large variation in the immunolabelling between follicles as well as between different glands. Both HLA-A,B,C and HLA-DR immunoreactivity were detected on the apical and the basal surface of the follicle cells. Microsomal antigen/thyroperoxidase immunoreactivity was restricted to the apical cell surface. In contrast to normal tissue, HLA-DR positive cells with a dendritic or macrophage-like morphology were frequent in Graves' tissue. These cells adhered directly to the basal surface of isolated follicle segments. We conclude that HLA antigens are, unlike thyroid-specific plasma membrane constituents, expressed in a non-polarized manner at the surface of the follicular epithelium. These observations might have implications on the immune recognition of thyroidal autoantigens in Graves' disease.
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