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  • autoimmunity  (3)
  • X-ray analysis  (2)
  • apoptosis  (2)
  • 1
    ISSN: 0014-5793
    Keywords: Anionic form ; Extended conformation ; Met-enkephalin analog ; Solid state ; X-ray analysis ; β-Sheet
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/General Subjects 717 (1982), S. 179-181 
    ISSN: 0304-4165
    Keywords: Crystal structure ; Triidothyronine ; X-ray analysis
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Key words Cytomegalovirus ; Epstein ; Barr virus ; polymerase chain reaction ; pancreas biopsy ; autoimmunity ; insulin-dependent diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Viral infection is assumed to trigger or exacerbate autoimmune responses against pancreatic beta cells leading to the development of insulin-dependent diabetes mellitus (IDDM). We therefore examined by polymerase chain reaction the presence of two candidate viruses, cytomegalovirus and Epstein–Barr virus, in IDDM pancreases. Pancreas tissues were obtained by biopsy under laparoscopy from 16 recent-onset IDDM patients: age 17–53 years; disease duration 0–7 months; six had flu-like symptoms before onset. Frozen sections were made and subjected to DNA amplification. DNA samples were prepared from the frozen sections and polymerase chain reaction was performed using primers specific to cytomegalovirus, Epstein–Barr virus and control gene for HLA-DP. Cytomegalovirus- and Epstein–Barr virus-infected cells were used for positive control. Southern blot analysis could detect cytomegalovirus DNA from as few as 2 × 10–1 cytomegalovirus-infected cells and Epstein–Barr virus DNA from two Epstein–Barr virus-infected cells. This highly sensitive analysis, however, could not detect cytomegalovirus or Epstein–Barr virus genomes in pancreases of recent-onset IDDM. A single copy human gene (HLA-DP) was amplified from all IDDM pancreases indicating that DNA amplification was performed without inhibition. We conclude that cytomegalovirus or Epstein–Barr virus genomes are unlikely to exist in pancreas biopsy specimens of recent-onset IDDM patients. [Diabetologia (1995) 38: 667–671]
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Cytomegalovirus ; Epstein-Barr virus ; polymerase chain reaction ; pancreas biopsy ; autoimmunity ; insulin-dependent diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Viral infection is assumed to trigger or exacerbate autoimmune responses against pancreatic beta cells leading to the development of insulin-dependent diabetes mellitus (IDDM). We therefore examined by polymerase chain reaction the presence of two candidate viruses, cytomegalovirus and Epstein-Barr virus, in IDDM pancreases. Pancreas tissues were obtained by biopsy under laparoscopy from 16 recent-onset IDDM patients: age 17–53 years; disease duration 0–7 months; six had flu-like symptoms before onset. Frozen sections were made and subjected to DNA amplification. DNA samples were prepared from the frozen sections and polymerase chain reaction was performed using primers specific to cytomegalovirus, Epstein-Barr virus and control gene for HLA-DP. Cytomegalovirus- and Epstein-Barr virus-infected cells were used for positive control. Southern blot analysis could detect cytomegalovirus DNA from as few as 2×10−1 cytomegalovirus-infected cells and Epstein-Barr virus DNA from two Epstein-Barr virus-infected cells. This highly sensitive analysis, however, could not detect cytomegalovirus or Epstein-Barr virus genomes in pancreases of recent-onset IDDM. A single copy human gene (HLA-DP) was amplified from all IDDM pancreases indicating that DNA amplification was performed without inhibition. We conclude that cytomegalovirus or Epstein-Barr virus genomes are unlikely to exist in pancreas biopsy specimens of recent-onset IDDM patients.
    Type of Medium: Electronic Resource
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  • 5
    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
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  • 6
    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
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  • 7
    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
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