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  • 1
    Electronic Resource
    Electronic Resource
    (1R,2R)-(−)-N,N'-Bis(3,5-di-tert-butylsalicylidene)-1,2-cyclohexanediamine: a Salen Ligand of Jacobsen's Catalyst (1997)
    Oxford [u.a.] : International Union of Crystallography (IUCr)
    Acta crystallographica 53 (1997), S. 1685-1687 
    Details
    ISSN: 1600-5759
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1107/S0108270197006379
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  • 2
    Electronic Resource
    Electronic Resource
    (1R,2R)-(–)-[Bis(3,5-di-tert-butylsalicylidene)-1,2-cyclohexanediamine]chloromanganese(III), an (R,R)-Jacobsen catalyst (1999)
    Oxford [u.a.] : International Union of Crystallography (IUCr)
    Acta crystallographica 55 (1999), S. 1766-1769 
    Details
    ISSN: 1600-5759
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1107/S0108270199009397
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  • 3
    Electronic Resource
    Electronic Resource
    The initial step in the developement of organ specific autoimmune disease in BB rats (1988)
    Springer
    Diabetologia 31 (1988), S. 779-780 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00274787
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  • 4
    Electronic Resource
    Electronic Resource
    Prevention of lymphocytic thyroiditis and insulitis in diabetes-prone BB rats by the depletion of macrophages (1988)
    Springer
    Diabetologia 31 (1988), S. 400-402 
    Details
    ISSN: 1432-0428
    Keywords: Autoimmunity ; BB rats ; Type 1 (insulin-dependent) diabetes ; lymphocytic thyroiditis ; insulitis ; silica ; macrophage ; antigen-presenting cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetes-prone biobreeding (BB) rats often develop lymphocytic thyroiditis. Intraperitoneal administration of silica to young BB rats (40-days-old) nearly completely prevented the development of lymphocytic thyroiditis as well as insulitis. Since silica is known to be toxic to macrophages, these data suggest that the presentation of autoantigen(s) on the specific target cells such as thyroid and pancreatic B cells by antigen-presenting cells (e.g., macrophages) would be the initial step in the development of organ-specific autoimmune diseases in diabetes-prone BB rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02341511
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  • 5
    Electronic Resource
    Electronic Resource
    Studies on autoimmunity for initiation of Beta-cell destruction VIII. Pancreatic Beta-cell dependent autoantibody to a 38 kilodalton protein precedes the clinical onset of diabetes in BB rats (1991)
    Springer
    Diabetologia 34 (1991), S. 548-554 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes-prone BB rats ; 38 kD islet cell autoantibody ; prediction of Type 1 (insulin-dependent) diabetes mellitus ; immunoprecipitation ; differential Western blotting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Autoantibody to a rat islet cell-protein of 38 kilodalton was detectable at around 30 days of age in the sera of diabetes-prone Biobreeding (DP-BB) rats by both immunoprecipitation and differential Western blotting methods. Anti-38 kilodalton islet cell autoantibody was not, however, observed in the sera from 5- to 20-day-old DP-BB rats. Over 90% of DP-BB rats in which the antibody was detected, eventually developed Type 1 (insulin-dependent) diabetes mellitus. The antibody disappeared within 2 weeks after diabetes onset. However, it was preserved in the sera of DP-BB rats which had been treated with silica to prevent insulitis. The anti-38 kilodalton islet cell autoantibody was not detected in sera from control Wistar Furth (WF) rats. The autoantibody also cross-reacted with a rat insulinoma (RINm5F) cell protein of 38 kilodalton, but did not react with protein from mouse fibroblast (L-929 cells), rat pituitary cells (GH3 cells), or normal rat lymphocytes. The production of the autoantibody appears to be pancreatic Beta-cell dependent, since the autoantibody disappears after almost complete depletion of Beta cells, but is consistently present as long as Beta cells remain. Identification of the Beta-cell dependent anti-38 kilodalton islet cell autoantibody, which cross-reacts with a rat insulinoma cell protein of 38 kilodalton and precedes the onset of Type 1 diabetes in BB rats, will be invaluable for study of the molecular nature of a target islet cell autoantigen associated with the induction of autoimmunity in DP-BB rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400271
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  • 6
    Electronic Resource
    Electronic Resource
    Virus-induced diabetes in mice: A quantitative evaluation of islet cell population by immunofluorescence technique (1978)
    Springer
    Diabetologia 15 (1978), S. 395-401 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes ; EMC-virus ; islet cells ; immunofluorescence ; morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The endocrine cell populations of pancreatic islets in encephalomyocarditis (EMC)-virus infected mice were assessed quantitatively by immunofluorescence using specific antisera against 4 islet hormones. A marked reduction of the volume of insulin-containing (B-) cells (up to one tenth of control values) was observed at all stages studied in the hyperglycaemic mice. This was accompanied by the inversion of the normal ratio between B- and non B-cells. The volume of the latter cell types was also modified at different time points after infection: glucagon-cells were augmented 14 days after infection; PP-cells were decreased 2–3 days and 21 days after infection; somatostatin-cells decreased to one-fourth of control values in hyperglycaemic animals 21 days after infection. The latter results suggest that non B-cells are also involved in islet reaction to virus infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01219649
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  • 7
    Electronic Resource
    Electronic Resource
    Human pancreatic islet cell specific 38 kilodalton autoantigen identified by cytomegalovirus-induced monoclonal islet cell autoantibody (1990)
    Springer
    Diabetologia 33 (1990), S. 569-572 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00404146
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  • 8
    Electronic Resource
    Electronic Resource
    Low incidence of autoimmune type I diabetes in BB rats fed a hydrolysed casein-based diet associated with early inhibition of non-macrophage-dependent hyperexpression of MHC class I molecules on beta cells (1995)
    Springer
    Diabetologia 38 (1995), S. 1138-1147 
    Details
    ISSN: 1432-0428
    Keywords: Key words Pathogenesis ; major histocompatibility complex ; BioBreeding rat ; autoimmunity.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetes-prone BioBreeding (DPBB) rats were fed a diabetogenic, mainly plant-based rodent diet, Purina Chow 5001, or a diabetes-retardant, hydrolysed casein-based diet. The expression of MHC class I antigens on pancreatic beta cells occurred at around 25 days of age in Purina Chow-fed rats, and progressively increased with the length of time of feeding with the Purina diet. Most of the Purina Chow-fed DPBB rats revealed hyperexpression of MHC class I antigens on their pancreatic beta cells by 50 days of age. Approximately 92 % of the hyperexpressed Purina Chow-fed DPBB rats developed severe insulitis and diabetes. In contrast, the majority of hydrolysed casein-fed DPBB rats did not show MHC class I antigen hyperexpression and these rats failed to develop insulitis or diabetes. Purina Chow-fed Wistar-Furth rats and diabetes-resistant BioBreeding (DRBB) rats showed only very weak background staining for MHC class I antigens on their beta cells. When Purina Chow-fed DPBB rats were treated with silica to inhibit macrophage infiltration into the pancreatic islets, the hyperexpression of MHC class I antigens was seen even more clearly, as beta cells remained intact. MHC class II antigens were not detected on pancreatic beta cells from DPBB, DRBB or Wistar-Furth rats, regardless of their diet. On the basis of these observations, we concluded that hyperexpression of MHC class I antigens on pancreatic beta cells was mainly restricted to Purina Chow-fed DPBB rats and that suppression of non-macrophage-dependent MHC class I antigen hyperexpression on pancreatic beta cells by a hydrolysed casein-based diet resulted in the prevention of insulitis and diabetes. [Diabetologia (1995) 38: 1138–1147]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00422362
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  • 9
    Electronic Resource
    Electronic Resource
    Predisposing effect of anti-Beta cell autoimmune process in NOD mice on the induction of diabetes by environmental insults (1990)
    Springer
    Diabetologia 33 (1990), S. 709-712 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00400339
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  • 10
    Electronic Resource
    Electronic Resource
    Studies on autoimmunity for initiation of beta-cell destruction X. Delayed expression of a membrane-bound islet cell-specific 38 kDa autoantigen that precedes insulitis and diabetes in the diabetes-prone BB rat (1994)
    Springer
    Diabetologia 37 (1994), S. 460-465 
    Details
    ISSN: 1432-0428
    Keywords: Key words Islet cell-specific 38 kDa autoantigen, immunological effectors, BB rat, autoimmune IDDM.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The diabetic syndrome in the DP-BB rat results from progressive beta-cell destruction by autoimmune responses. However, the initial events causing the autoimmune destruction of beta cells remain largely unknown. Our recent experimental results suggest that the delayed expression of a beta-cell-specific autoantigen may result in the initiation of beta-cell-specific autoimmunity. The present investigation was initiated to identify such an autoantigen. Islets were isolated from DP-BB rats of several different ages, and protein extracts from the membrane fraction of the islet preparations were immunoprecipitated with sera from diabetic DP-BB rats. We have found that a membrane-bound islet cell-specific 38 kDa autoantigen is not expressed early in the life of DP-BB rats, but is delayed-expressed by approximately 30 days of age, the time at which immunological effectors begin to recognize beta cells. In contrast, a 64 kDa islet cell protein is expressed from birth in DP-BB rats. On the basis of these observations, we suggest that delayed expression of a gene encoding for the membrane-bound islet cell-specific 38 kDa autoantigen may result in a breakdown of self-tolerance, leading to beta-cell-specific autoimmune IDDM in the BB rat. [Diabetologia (1994) 37: 460–465]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050132
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