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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Scandinavian journal of immunology 58 (2003), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Inclusion body myositis (IBM) is a chronic inflammatory myopathy. The muscle histology is characterized by infiltration of T cells, which invade and apparently destroy muscle fibres. This study was performed to investigate whether predominant clones of muscle-infiltrating T cells are identical in different muscles and whether they persist over time in IBM. By reverse transcriptase-polymerase chain reaction, 25 T-cell receptor (TCR) variable β (Vβ) chain families and the complementarity-determining region 3 (CDR3) of the TCR were analysed in two different muscle biopsies of four patients with IBM. In two of the patients, the muscle biopsies were obtained from different muscles at one time point, whereas in two patients, the second biopsy was obtained 9 years after the first biopsy. T cells expressing predominant Vβ families were analysed for clonality by fragment length analysis of the CDR3. Predominant Vβ families were analysed by DNA sequencing to identify identical clones. Immunohistochemical staining of Vβ families was performed to study the distribution of T cells expressing identified predominant Vβ families. The muscle-infiltrating lymphocytes showed restricted expression of TCR Vβ families. DNA sequencing proved that clonally expanded T cells were identical in different muscles and persisted 9 years after the first biopsy. Immunohistochemical analysis with Vβ family-specific antibodies demonstrated the endomysial localization of these T cells in inflammatory cell infiltrates. Our results show that in IBM there is clonal restriction of TCR expression in muscle-infiltrating lymphocytes. Identical T-cell clones predominate in different muscles, and these clones persist for many years. These results indicate an important, continuous, antigen-driven inflammatory reaction in IBM.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Lead ; Rat ; Brain ; Blood-brain barrier ; Specific gravity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previous studies on the toxic effects of lead on the brains of young animals have shown damage to the blood-brain barrier (BBB) which in severe forms appears as hemorrhagic encephalopathy. In those studies the doses of lead have been of such magnitude that lead-induced anorexia resulting in growth retardation has contributed to the extent of the injury (Sundström et al. 1984). The growth retardation can be prevented by using low lead doses (Sundström et al. 1983). Consequently, we have examined to which extent the BBB is injured in suckling rats with low dose lead encephalopathy. This was done by a) testing the permeability of the BBB to plasma proteins and b) assessing the possible occurrence of vasogenic edema by measuring the specific gravity of brain tissue. Low dose lead encephalopathy was induced by daily i.p. injections of lead nitrate 10 mg/kg body weight (b.wt.) for the first 15 days. The lead contents of the blood and homogenates of the cerebrum and cerebellum were assayed by atomic absorption spectrophotometry. The brains were examined at 15, 20, or 30 days of age. When Evans blue-albumin (EBA) was injected i.v. 2 h before killing, most 15-day-old rats exposed to lead displayed a bluish discoloration in their cerebellum. Microscopically, red fluorescence of EBA was seen in the blue-stained regions. Immunohistochemically, extravasation of albumin, fibrinogen, and fibronectin was demonstrated as positive staining in the cerebellar cortex, with diffuse spread to the white matter of the corresponding folium. Neither lead-exposed rats aged 20 or 30 days nor any non-exposed rats revealed macroscopic or microscopic leakage of plasma proteins in the brain parenchyma. The specific gravity of the cerebral and cerebellar cortices and the hippocampus of control and lead-exposed rats aged 15 and 20 days was determined using density gradients of Percoll. No increment in the water content was encountered. Rather, the specific gravity of cerebellum of lead-treated rats aged 15 days was slightly higher than that of the controls, though statistical significance for this difference was reached only when nonparametric tests were applied. Our results indicate that low dose lead encephalopathy results in a breakdown of the BBB to plasma proteins without marked vasogenic brain edema. The hypothesis is advanced that the leakage of plasma results in rapid normalization of the tissue water content, whereas proteins remain longer in the parenchyma.
    Type of Medium: Electronic Resource
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