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  • 1
    Electronic Resource
    Electronic Resource
    Ultrastructural observations on cytotoxic effector cells infiltrating pancreatic islets of low-dose streptozocin treated mice (1992)
    Springer
    Virchows Archiv 420 (1992), S. 5-10 
    Details
    ISSN: 1432-2307
    Keywords: Islets of Langerhans ; Monocytic phagocytes ; Streptozocin ; Type 1 diabetes ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of this study was to observe the ultrastructural events, during the onset of diabetes mellitus in the low-dose streptozocin (LDS)-treated mouse model with emphasis on the infiltrating elements. Forty male C57 BL/6J mice were given 40 mg/streptozocin on 5 consecutive days and killed 5, 6, 7, 8, 9, 10, 15, and 18 days after the first injection. Results demonstrated that islet infiltration occurring in LDS-treated mice is characterized by a very early pre-infiltration state in which mononuclear phagocytes in islet capillary vessels were considerably increased in number. A new histopathological time sequence for the early insulitis is described, in which attraction of blood mononuclear phagocytes into the islet capillary lumen is the first step. During the successive stage, occurring on days 6–8 we observed that mononuclear phagocytes migrate through capillary and venule walls into the islet parenchyma, where they differentiate into tissue macrophages. It was only later (step 3) that these macrophages acquired novel properties, typical of their “activated state” and started to phagocytose islet beta-cell debris. These data suggest that during the pre-infiltration and early insulitis the mononuclear phagocyte system plays a key role in the onset of LDS diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01605977
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The immunosuppressant FK506 inhibits the damage to mouse pancreatic islets induced by low dose streptozocin (1994)
    Springer
    Cell & tissue research 277 (1994), S. 573-578 
    Details
    ISSN: 1432-0878
    Keywords: Pancreatic islet ; B cell ; Streptozocin ; Type 1 diabetes ; Immunosuppression ; FK506 ; Mouse C57BL6
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Diabetes mellitus was induced in 40 male C57BL6 mice by injection of a low dose of streptozocin (45 mg/kg body weight) on 5 consecutive days. Twenty four of the mice were immunosuppressed by administration of 1.5 mg FK506/kg body weight daily for 10, 15, 18 and 24 days. Administration of FK506 almost completely inhibited the streptozocin-induced islet damage, and consequently glycaemia remained normal. In FK506-treated animals any inflammatory infiltrate was very sparse and was limited to the vascular pole of the islets. Immunocytochemical results demonstrated that infiltrating cells were Ia-immunoreactive, but were not activated. Ultrastructural observations confirmed the absence of B cell necrosis and degranulation in FK506-treated mice; the few infiltrating elements encountered did not contain phagocytic vesicles or show other signs of activation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00300231
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    The immunosuppressant FK506 inhibits the damage to mouse pancreatic islets induced by low dose streptozocin (1994)
    Springer
    Cell & tissue research 277 (1994), S. 573-578 
    Details
    ISSN: 1432-0878
    Keywords: Key words: Pancreatic islet ; B cell ; Streptozocin ; Type 1 diabetes ; Immunosuppression ; FK506 ; Mouse C57BL6
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Diabetes mellitus was induced in 40 male C57BL6 mice by injection of a low dose of streptozocin (45 mg/kg body weight) on 5 consecutive days. Twenty four of the mice were immunosuppressed by administration of 1.5 mg FK506/kg body weight daily for 10, 15, 18 and 24 days. Administration of FK506 almost completely inhibited the streptozocin-induced islet damage, and consequently glycaemia remained normal. In FK506-treated animals any inflammatory infiltrate was very sparse and was limited to the vascular pole of the islets. Immunocytochemical results demonstrated that infiltrating cells were Ia-immunoreactive, but were not activated. Ultrastructural observations confirmed the absence of B cell necrosis and degranulation in FK506-treated mice; the few infiltrating elements encountered did not contain phagocytic vesicles or show other signs of activation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00300231
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Macrophages and antioxidant status in the NOD mouse pancreas (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 71 (1998), S. 479-490 
    Details
    ISSN: 0730-2312
    Keywords: macrophages ; antioxidant status ; NOD mice ; immunocytochemistry ; type 1 diabetes ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: This study showed that citiolone (CIT), a free radical scavenger, significantly increased superoxide dismutase (P 〈 0.001 vs. untreated NOD, NMMA-treated, and silica-treated animals), catalase (P 〈 0.01 vs. untreated NOD), and glutathione peroxidase (P 〈 0.001 vs. untreated NOD and C57BL6/J) values. Silica treatment was capable of counteracting the plasma antioxidant capacity (TRAP) decrease observed in untreated NOD mice, although it did not block the blood glucose rise and insulitis progression in type 1 diabetes significantly. Conversely, early silica administration was able to deplete macrophages (as demonstrated by immunocytochemistry) and to block the rise in blood glucose levels and insulitis progression significantly. Silica-treated animals in this study showed the highest TRAP levels, demonstrating that depletion of macrophages also was able to improve the antioxidant status. This study suggested that macrophages are essential for type 1 diabetes development and showed that they also are involved when the antioxidant status is affected. The reported findings are significant in view of previous studies indicating that oxygen and/or nitrogen free radicals contribute to the islet β-cell destruction in type 1 diabetes animal models. J. Cell. Biochem. 71:479-490, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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    Paper (German National Licenses)
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