GLORIA

GEOMAR Library Ocean Research Information Access

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 36 (1993), S. 1293-1298 
    ISSN: 1432-0428
    Keywords: Genetic risk factors ; retinopathy ; immunoglobulin allotypes ; Gm ; Km ; HLA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetic retinopathy is the leading cause of blindness in adults aged 30 to 65 years. However, 20% of the diabetic population does not develop significant retinopathy. To examine the influence of immune-related genetic factors on the development of diabetic retinopathy, we studied immunoglobulin allotypes in 102 subjects aged 8 to 20 years, who had had Type 1 (insulin-dependent) diabetes mellitus for 4.5 to 11 years (mean 7.3 years). HLA had been previously typed on 59 of these subjects. Retinopathy was assessed by expert review of retinal photographs. Among the 44 patients who had evidence of retinopathy, 33(75%) were G2m(23 +), while among the 58 patients without retinopathy but with similar duration of disease, only 28(48%) were G2m(23 +) (p = 0.006). The HLA-DR types of patients with and without retinopathy were not significantly different. We conclude that there is significant evidence of an association between G2m(23) at the locus encoding IgG2 subclass heavy chains and susceptibility to the development of diabetic retinopathy early in the clinical course of the disease. Our findings provide important independent confirmation of a previous report of association between Gm allotypes and predisposition to diabetic retinopathy. We are unable to determine if the Gm effect on development of retinopathy is due to the G2m(23) allotype itself, or due to genes that are closely linked to, and in linkage disequilibrium with, the locus encoding the G2m(23) allotype.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1432-0428
    Keywords: Cytomegalovirus ; islet cell antibody ; 38 kilodalton antigen ; Autoimmunity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Our previous finding that about 15% of newly diagnosed patients with Type 1 (insulin-dependent) diabetes mellitus had human cytomegalovirus genome in their lymphocytes and islet cell autoantibodies in their sera, suggests that autoimmune Type 1 diabetes is associated with persistent cytomegalovirus infection under certain circumstances. This investigation was initiated to see if cytomegalovirus can induce islet cell autoantibodies and if the autoantibodies react with any specific islet protein(s). Monoclonal antibodies were generated after immunizing Balb/c mice with human cytomegalovirus. When these monoclonal antibodies were tested for the presence of islet cell antibodies, one (MCMVA-51) of 13 monoclonal antibodies reacted strongly with the islets. The titer of islet cell antibodies was 1∶2000. When this monoclonal antibody was reacted with the proteins from the solubilized fraction of human pancreatic islets using the western immunoblotting technique, a band with a molecular weight of 38 kilodalton was detected. The 38 kilodalton band was not observed when the monoclonal antibody was reacted with the proteins prepared from pancreatic islet tissues of rats and mice or from other human organs including stomach, liver, spleen and brain, indicating that the 38 kilodalton protein is human islet cell-specific. It is concluded that human cytomegalovirus can induce islet cell antibodies that react with a 38 kilodalton human islet cell protein and that this protein component may represent islet cell-specific target antigens associated with perinistent cytomegalovirus infection.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1432-0428
    Keywords: Non-obese diabetic (NOD) mice ; streptozotocin ; autoimmunity ; environmental factor ; cumulative insults
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In NOD mice, 50–70% of females and 10–20% of males develop diabetes, although almost all the animals show insulitis. To see if environmental insults could induce diabetes in subjects with pre-clinical anti-Beta cell autoimmunity, non-diabetic NOD mice were selected and injected with a sub-diabetogenic dose of streptozotocin at 6 or 20 weeks of age. The streptozotocin failed to induce diabetes in 16 male and 16 female NOD mice within 4 weeks when they were injected at the age of 6 weeks. In contrast, 6 of 16 male and 10 of 16 female NOD mice developed diabetes within 4 weeks when they were injected at the age of 20 weeks. In untreated age-matched control NOD mice, none of the male and only 2 of 16 female mice became diabetic during the same 4 week period. On histologic examination, the degree of insulitis in streptozotocin-treated NOD mice (at the age of 24 weeks) was not significantly different from that of untreated control NOD mice. However, the streptozotocin-treated animals showed significantly lower pancreatic insulin content than the control mice. These results show that an anti-Beta cell autoimmune process in NOD mice has a predisposing effect on the induction of diabetes by a sub-diabetogenic dose of streptozotocin, and suggest that the precipitation of clinical diabetes by some environmental insults in subjects with pre-existing pre-clinical autoimmune Beta-cell destruction may be one mechanism of disease presentation in human Type 1 (insulin-dependent) diabetes.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...