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  • 1
    Electronic Resource
    Electronic Resource
    Release of 3,5,3′-triiodothyronine, thyroxine and thyroglobulin from TSH-stimulated mouse thyroids in the perifusion system (1988)
    Springer
    Cellular and molecular life sciences 44 (1988), S. 766-768 
    Details
    ISSN: 1420-9071
    Keywords: Thyroglobulin ; TSH ; T3 ; T4 ; mouse ; thyroid ; perifusion system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary We established a perifusion system using mouse thyroid glands. In this system, TSH increased the release of T3 and T4 significantly, and the response of thyroglobulin to TSH was delayed in comparison with that of T3 and T4.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01959158
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  • 2
    Electronic Resource
    Electronic Resource
    Aspartic acid at position 57 of DQβ chain does not protect against Type 1 (insulin-dependent) diabetes mellitus in Japanese subjects (1989)
    Springer
    Diabetologia 32 (1989), S. 762-764 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes mellitus ; HLA-DR ; HLA-DQ ; polymerase chain reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary HLA DQβ chain, in particular amino acid at position 57, has been reported to contribute to susceptibility and resistance to Type 1 (insulin-dependent) diabetes mellitus in Caucasians. Resistance has been proposed to be conferred by aspartic acid at this position. To ascertain the association of HLA DQβ and DRβ genes with Type 1 diabetes in Japanese subjects, ten Japanese Type 1 diabetic patients were investigated at DNA level. Genomic DNA was amplified by polymerase chain reaction, and dot blot analysis was carried out using the amplified DNA with allele specific oligonucleotide probes. All patients had aspartic acid at position 57 of at least one of their two DQβ chains, and there was no significant difference of amino acids at the same position of DRβ chain in patients compared to control subjects. These data indicate that the protective role of aspartic acid at position 57 of DQβ chain is less significant in Japanese compared with Caucasian subjects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00274539
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  • 3
    Electronic Resource
    Electronic Resource
    Cytokine-induced apoptotic cell death in a mouse pancreatic beta-cell line: inhibition by Bcl-2 (1996)
    Springer
    Diabetologia 39 (1996), S. 530-536 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Pancreatic beta cell ; Bcl-2 ; apoptosis ; cytokine ; interleukin-1 ; tumour necrosis factor ; interferon-γ.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cytokines are thought to contribute to the induction of pancreatic beta-cell destruction in insulin-dependent diabetes mellitus. The molecular mechanisms that underlie beta-cell death were investigated by studying cytokine-induced cell death in beta-cell lines. A combination of three cytokines (interleukin-1β, tumour necrosis factor-α, and interferon-γ) induced apoptotic cell death in the mouse pancreatic beta-cell line βTC1, as judged from the appearance of cells with hypodiploid nuclei and oligonucleosomal DNA fragmentation. The same treatment also induced apoptosis in the mouse pancreatic alpha-cell line αTC1 and the NOD/Lt mouse beta-cell line NIT-1, although to a lesser extent than in βTC1 cells. The abundance of endogenous Bcl-2 in βTC1 cells was lower than that in the other two cell lines. Overexpression of human Bcl-2 in βTC1 cells partially protected them from cytokine-induced cell death. These results suggest that apoptosis may be responsible, at least in part, for cytokine-induced beta-cell destruction and that Bcl-2 prevents apoptosis in pancreatic islet cells. [Diabetologia (1996) 39: 530–536]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403299
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  • 4
    Electronic Resource
    Electronic Resource
    Retrovirus gag protein p30 in the islets of non-obese diabetic mice: relevance for pathogenesis of diabetes mellitus (1992)
    Springer
    Diabetologia 35 (1992), S. 614-618 
    Details
    ISSN: 1432-0428
    Keywords: Non-obese diabetic (NOD) mice ; retrovirus ; gag protein p30 ; autoimmunity ; cyclophosphamide ; pathogenesis ; Western blot analysis ; ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the presence of retroviral protein in the pancreatic islets of non-obese diabetic mice to prove that the virus-like particle observed specifically in the pancreatic Beta cell of these mice was retrovirus. Western blot analysis probed with anti-retrovirus antibody demonstrated the existence of retroviral gag (group specific antigen) protein p30 in the islets of female non-obese diabetic mice. Islets of non-obese diabetic mice which were treated with cyclophosphamide, known to accelerate the development of insulitis and diabetes mellitus, have shown both a significantly increased number of retrovirus-like particles (type C) and enhanced expression of gag protein p30, compared to those of mice not treated with cyclophosphamide. These results confirmed the presence of type C retrovirus in non-obese diabetic mouse Beta cells and suggest a role for retrovirus in the development of insulitis and diabetes in these mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400251
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  • 5
    Electronic Resource
    Electronic Resource
    Three new mutations in the hepatocyte nuclear factor-1α gene in Japanese subjects with diabetes mellitus: clinical features and functional characterization (1999)
    Springer
    Diabetologia 42 (1999), S. 621-626 
    Details
    ISSN: 1432-0428
    Keywords: Keywords MODY ; HNF-1α ; insulin ; arginine ; mutation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Mutations in the hepatocyte nuclear factor-1α gene are a common cause of the type 3 form of maturity-onset diabetes of the young. We examined the clinical features and molecular basis of hepatocyte nuclear factor-1α (HNF-1α) diabetes. Methods. Thirty-seven Japanese subjects with early onset Type II (non-insulin-dependent) diabetes mellitus and 45 with Type I (insulin-dependent) diabetes mellitus were screened for mutations in this gene. Functional properties of mutant HNF-1α were also investigated. Results. Three new mutations [G415R, R272C and A site of the promoter ( + 102G-to-C)] were found. Insulin secretion was impaired in the three subjects. Insulin and glucagon secretory responses to arginine in the subject with the R272C mutation were also diminished. Molecular biological studies indicated that the G415R mutation generated a protein with about 50 % of the activity of wild-type HNF-1α. The R272C mutation had no transactivating or DNA binding activity and acted in a dominant negative manner. The + 102 G-to-C mutation in the A site of the promoter activity was associated with an increase in promoter activity and it had 42–75 % more activity than the wild-type sequence. Conclusion/interpretation. Mutations in the HNF-1α gene may affect the normal islet function by different molecular mechanisms. [Diabetologia (1999) 42: 621–626]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051204
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  • 6
    Electronic Resource
    Electronic Resource
    Examination of islets in the pancreas biopsy specimens from newly diagnosed Type 1 (insulin-dependent) diabetic patients (1990)
    Springer
    Diabetologia 33 (1990), S. 105-111 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes mellitus ; pathology ; pathogenesis ; diagnosis ; pancreas biopsy ; laparoscopy ; immunohistochemistry ; MHC class I antigen ; MHC class II antigen ; immunotherapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We attempted to examine the immunopathological change of the pancreatic islets of newly diagnosed Type 1 (insulin-dependent) diabetic patients and thereby to obtain useful information for the therapy of the patients. For this purpose, pancreas biopsy under laparoscopy was performed 2–4 months after the onset of Type 1 diabetes in seven newly diagnosed patients. All biopsies were performed safely without any complications. Immunohistochemical examination of the biopsy specimens revealed a marked decrease of insulin-containing cells, preservation of glucagon-containing cells, and various degrees of expression of MHC class I and class II antigens in islet cells and in endothelial cells within and around the islets. Signs of active autoimmune phenomena, e. g. lymphocytic infiltration or immunoglobulin deposition in islets, were not detected in any of these patients by light microscopical evaluation. We conclude that pancreas biopsy under laparoscopy has shown various immunological changes in the islets of newly diagnosed Type 1 diabetic patients. Pancreas biopsy, however, may not be suitable under the present protocol for the selection of patients for immunotherapy because of problems including sampling errors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401048
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  • 7
    Electronic Resource
    Electronic Resource
    Cytokine-induced apoptotic cell death in a mouse pancreatic beta-cell line: inhibition by Bcl-2 (1996)
    Springer
    Diabetologia 39 (1996), S. 530-536 
    Details
    ISSN: 1432-0428
    Keywords: Pancreatic beta cell ; Bcl-2 ; apoptosis ; cytokine ; interleukin-1 ; tumour necrosis factor ; interferon-γ
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cytokines are thought to contribute to the induction of pancreatic beta-cell destruction in insulin-dependent diabetes mellitus. The molecular mechanisms that underlie beta-cell death were investigated by studying cytokine-induced cell death in beta-cell lines. A combination of three cytokines (interleukin-1Β, tumour necrosis factor-α, and interferon-γ) induced apoptotic cell death in the mouse pancreatic beta-cell line ΒTC1, as judged from the appearance of cells with hypodiploid nuclei and oligonucleosomal DNA fragmentation. The same treatment also induced apoptosis in the mouse pancreatic alpha-cell line αTC1 and the NOD/Lt mouse beta-cell line NIT-1, although to a lesser extent than in ΒTC1 cells. The abundance of endogenous Bcl-2 in ΒTC1 cells was lower than that in the other two cell lines. Overexpression of human Bcl-2 in ΒTC1 cells partially protected them from cytokine-induced cell death. These results suggest that apoptosis may be responsible, at least in part, for cytokine-induced beta-cell destruction and that Bcl-2 prevents apoptosis in pancreatic islet cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403299
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    Paper (German National Licenses)
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  • 8
    Electronic Resource
    Electronic Resource
    Fas and Fas ligand expression in inflamed islets in pancreas sections of patients with recent-onset Type I diabetes mellitus (1999)
    Springer
    Diabetologia 42 (1999), S. 1332-1340 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Type I diabetes ; Fas ; Fas ligand ; insulitis ; human pancreas ; apoptosis.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Type I (insulin-dependent) diabetes results mainly from T-cell-mediated autoimmune destruction of pancreatic beta cells. Cytotoxic T lymphocytes destroy target cells via a perforin-based or Fas-based mechanism. Our previous study indicated that the Fas-Fas ligand (FasL) pathway is required for the development of autoimmune diabetes in the NOD mouse. We now investigated whether or not the Fas-FasL system is involved in the beta-cell destruction in human Type I diabetes. Methods. We immunohistochemically analysed pancreas biopsy specimens of 13 recent-onset patients. Results. Pancreatic islets were identified but showed various degrees of reduction in beta-cell volume in all patients. Out of 13 patients 6 had insulitis. In these 6 patients Fas was expressed in both the islets and infiltrating cells but not in either cell type in the 7 other patients without insulitis. Double immunostaining showed that Fas was positive in 92.2 to 97.7 % of beta cells but only in 17.6 to 46.7 % of alpha cells in Fas-positive, insulin-remaining islets. We found FasL was expressed exclusively in islet-infiltrating cells in patients with insulitis. Double immunostaining revealed that the most prevalent phenotype of FasL-positive cells was CD8, which was followed by macrophages and CD4. Conclusion/interpretation. The interaction between Fas on beta cells and FasL on infiltrating cells might trigger selective apoptotic beta-cell death in inflamed islets, leading to immune-mediated Type I diabetes. [Diabetologia (1999) 42: 1332–1340]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051446
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  • 9
    Electronic Resource
    Electronic Resource
    R127W-HNF-4α is a loss of function mutation but not a rare polymorphism and causes Type II diabetes in a Japanese family with MODY1 (2000)
    Springer
    Diabetologia 43 (2000), S. 520-524 
    Details
    ISSN: 1432-0428
    Keywords: Keywords MODY, HNF-4α, HNF-1α, L-type pyruvate kinase, insulin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Mutations in the hepatocyte nuclear factor (HNF)-4 α gene cause the type 1 form of maturity-onset diabetes of the young (MODY1). The R127W mutation is a missense mutation located in the T-box region of HNF-4α that was first identified in a Japanese family with MODY. We have examined the functional properties of this mutation in order to clarify the molecular basis of MODY1.¶Methods. The intracellular localisation, DNA binding ability, transactivation activity and functional synergism with the coactivator CREB-binding protein (CBP) of R127W-HNF-4α were investigated.¶Results. The nuclear import and functional synergy with CBP of R127W-HNF-4α were normal. The DNA binding ability of the mutant was decreased as was its transcriptional activation of the HNF-1 α and L-type pyruvate kinase (PKL) genes.¶Conclusion/interpretation. The R127W mutation seems to be a loss-of-function mutation. [Diabetologia (2000) 43: 520–524]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051338
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  • 10
    Electronic Resource
    Electronic Resource
    Immunological abnormalities in islets at diagnosis paralleled further deterioration of glycaemic control in patients with recent-onset Type I (insulin-dependent) diabetes mellitus (1999)
    Springer
    Diabetologia 42 (1999), S. 574-578 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Type I diabetes ; insulitis ; ICA ; GAD ; biopsy ; immunohistochemistry ; HLA typing.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To determine whether the clinical heterogeneity observed in the development of Type I (insulin-dependent) diabetes mellitus correlates with immunohistochemical differences observed at diagnosis. Methods. Patients (n = 17) with recent-onset diabetes clinically considered to be insulin dependent (Type I), underwent pancreatic biopsy for immunohistological analysis. These patients were divided into two groups based on the presence or absence of islet immunological abnormalities (insulitis or hyperexpression of MHC class I antigens or both). The patients were also HLA typed and tested for islet cell antibodies and antibodies to glutamic acid decarboxylase (GAD-Ab). All patients were followed monthly for 2 years and their fasting plasma glucose, haemoglobin A1C and daily insulin doses were recorded. The clinical course of patients with islet immunological abnormalities was compared with that of patients without those abnormalities. Results. Patients with and without islet immunological abnormalities did not differ with regard to HLA type or islet cell antibodies. Antibodies to glutamic acid decarboxylase correlated with the presence of insulitis and MHC class I hyperexpression. These local immunological abnormalities were also associated with higher haemoglobin A1C values (p 〈 0.05) and a trend towards greater insulin requirements. Further, patients with the islet abnormalities had higher fasting plasma glucose concentrations 2 years after the biopsy than at the time of the biopsy (p 〈 0.05). Conclusion/interpretation. The heterogeneous clinical course observed following diagnosis in patients with Type I diabetes correlates with islet immunological abnormalities. Insulitis and hyperexpression of MHC class I correlate with deteriorating glycaemic control. [Diabetologia (1999) 42: 574–578]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051197
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