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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 476-482 
    ISSN: 1432-0428
    Keywords: Key words IDDM, interleukin 2 system, interleukin 4, T helper 1 and 2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The IL-2 system which involves IL-2 production, IL-2 receptor expression, and response to IL-2, is associated with autoimmune phenomena. Immunological abnormalities including autoimmune phenomena are believed to contribute to the pathogenesis of IDDM. In this study, the production of IL-2, the responses to IL-2 and IL-2 receptor expression by peripheral blood T lymphocytes were compared in IDDM and normal non-diabetic children. The percentage of IL-2 receptor-positive circulating T cells was significantly increased in diabetic children, although IL-2 receptor expression induced by con A stimulation did not differ in the diabetic and control children. IL-2 production was significantly decreased in diabetic children compared with the control children. The response of stimulated T cells to IL-2 did not differ in IDDM and control children. In IDDM, IL-2 production by CD4-positive T lymphocytes within the IL-2 system is thought to be selectively defective. On the other hand, IL-4, which is also produced by CD4-positive T lymphocytes, was increased. Since IL-4 did not suppress IL-2 production, it would seem that the IL-2 producing subset in CD4+HLA-DR+ T cells is decreased in IDDM. These results suggest that in recent onset IDDM, IL-2 receptor-positive circulating T cells require an IL-2 supply.[Diabetologia (1994) 37: 476–482]
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Reovirus type 2 ; diabetes ; serum thymic factor ; immunosuppression ; insulitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Reovirus type 2 that had been isolated from a cow with diarrhoea and passaged in bovine kidney cell culture produced a Type 1 (insulin-dependent) diabetes-like syndrome when inoculated into NC mice. The infection resulted in insulitis and destruction of islet cells. Viral antigens were found in islet cells by staining with fluorescein-labelled antibody to reovirus type 2. The destruction of islet cells resulted in abnormalities shown on glucose tolerance testing. Studies on the susceptibility of the host showed that only certain strains of mice had overtly abnormal glucose tolerance tests when infected with reovirus type 2. To assess the immunological role in the pathogenesis of reovirus type 2-induced diabetes, infected mice were subjected to immunosuppressive or thymic hormone treatment. The administration of either anti-thymocyte serum or serum thymic factor reduced or prevented the development of the diabetes-like syndrome, while Arg-Lys-Asp-Val-Try did not show any therapeutic effects.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1106
    Keywords: Key words Nuclear factor-κB ; Kainic acid ; Inflammatory activation ; Microglia ; Astrocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Nuclear factor-κB (NF-κB) is known to play a key role in immune and inflammatory responses. To understand the mechanisms of inflammatory activation that accompany neuronal damage, we determined the cell type in which NF-κB was activated. NF-κB protein was detected in the cytosolic fraction of untreated and vehicle-treated rat hippocampus. After kainic acid (KA) treatment, NF-κB protein was significantly increased in both the cytosolic and particulate fractions. NF-κB immunoreactivity was observed in both brain blood vessels and glial cells after 1 day. Although NF-κB immunoreactivity in brain blood vessels disappeared after 3 days, this activity was maintained in glial cells for up to 7 days. In addition, double immunostaining indicates that NF-κB was activated in glial cells, such as microglia and astrocytes, after 3 days. Thus, NF-κB activation seems to be delayed and to occur continuously in microglia and astrocytes, suggesting that an inflammatory activation in glial cells participates in KA-induced neurodegeneration.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1017
    Keywords: Transferrin ; Metal-binding protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Physics
    Notes: Abstract The kinetics of binding of Cu (II), Tb (III) and Fe(III) to ovotransferrin have been investigated using the stopped-flow technique. Rate constants for the second-order reaction, k +, were determined by monitoring the absorbance change upon formation of the metal-transferrin complex in time range of milliseconds to seconds. The N and C sites appeared to bind a particular metal ion with the same rate; thus, average formation rate constants k + (average) were 2.4 × 104 M−1 s−1 and 8.3 × 104 M−1 S −1 for Cu (II) and Tb (III) respectively. Site preference (N site for Cu (II) and C site for Tb (III)) is then mainly due to the difference in dissociation rate constant for the metals. Fe (III) binding from Fe-nitrilotriacetate complex to apo-ovotransferrin was found to be more rapid, giving an average formation rate constant k + (average) of 5 × 105 M−1 s−1, which was followed by a slow increase in absorbance at 465 nm. This slow process has an apparent rate constant in the range 3 s−1 to 0.5 s−1, depending upon the degree of Fe (III) saturation. The variation in the rate of the second phase is thought to reflect the difference in the rate of a conformational change for monoferric and diferric ovotransferrins. Monoferric ovotransferrin changes its conformation more rapidly (3.4s−1) than diferric ovotransferrin (0.52 s−1). A further absorbance decrease was observed over a period of several minutes; this could be assigned to release of NTA from the complex, as suggested by Honda et al. (1980).
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0942-0940
    Keywords: Cytoskeleton ; delayed neuronal death ; nerve growth factor (NGF) ; neurofilament (NF)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the protective action of nerve growth factor (NGF) on delayed neuronal death, and we also studied the involvement of the 200 kDa neurofilament (NF 200) cytoskeletal proteins. Wistar rats were divided into three groups: Group I, in which transient forebrain ischaemia was produced; Group II, ischaemic group which received intraventricular administration of artificial cerebrospinal fluid (CSF); and Group III, ischaemic group which received intraventricular administration of 2 Μg of 2.5 S NGF. Forebrain ischaemia in these rats was produced by causing transient bilateral occlusion of the common carotid arteries and lowering the mean blood pressure to 50 mmHg for 8 minutes. On the 1st and 7th day after ischaemia we histologically examined neuronal death in the hippocampal CA1 sector. On the 7th day after ischaemia, mean cell death (degenerative cell number/total cell number) was 87±9% in group I (n=7), 51±36% in group II (n=7), and 14±16% in group III (n=8) (p〈0.05 vs. group II). The concentration of NF 200 in the hippocampal homogenate was measured by the Western blotting method on the 1st and 7th day after ischaemia. On the 1st day it was found to be 67±11% of that in the control group in group I (n=6), 73±21% in group II (n=6), and 84±7% in group III (n=6) (p〈0.05 vs. group II). The concentration of NF 200 in all groups remained at the same level until the 7th day after ischaemia (each group, n=6). These results suggest that 1) intraventricular NGF has a protective effect on delayed neuronal death, 2) these protective actions occur within one day after ischaemia, and 3) these effects may be mediated by the suppressed degradation and/or promoted restoration of neuronal cytoskeletal proteins.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Archives of Biochemistry and Biophysics 273 (1989), S. 197-205 
    ISSN: 0003-9861
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 175 (1991), S. 685-689 
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 165 (1989), S. 680-684 
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 170 (1990), S. 259-263 
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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