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  • 1
    Electronic Resource
    Electronic Resource
    Limited T-Cell Receptor V Gene Usage in Inclusion Body Myositis (1996)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 43 (1996), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Inclusion body myositis (IBM) is a chronic, progressive inflammatory myopathy. The inflammatory infiltrates are dominated by T cells, which frequently invade muscle fibres. The present study was performed to characterize the usage of the variable (V)segment of the T-cell receptor of muscle infiltrating cells in IBM. Using the reverse transcriptase polymerase chain reaction (RT-PCR) technique the authors analysed the expression of 22 Vα and 24 Vβ families in muscle tissue from six patientswith IBM displaying intense inflammatory cell infiltration. The following Vα/Vβ families appeared in at least 50% of the patients: Vα1, 5, 7, 15, 16, 17, 20, 21, 22 and Vβ3, 5.2, 8, 12, 14, 22. In all patients Vα7, 16 and Vβ8 wereexpressed in muscle tissue. Furthermore, in two of the patients peripheral blood lymphocytes (PBL) were investigated in parallel. There was a restricted usage of Vα and Vβ families in muscle in comparison to PBL, indicating a selective homing orlocal proliferation of T lymphocytes in the inflammatory lesions in IBM.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1996.d01-10.x
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  • 2
    Electronic Resource
    Electronic Resource
    Local T-Cell Proliferation and Differentiation in Inflammatory Myopathies (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 41 (1995), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Our objective was to investigate the patterns of proliferation and differentiation of infiltrating cells in inflammatory myopathies. Immunohistochemical staining was performed on muscle biopsy specimens from 18 patients with inclusion body myositis, polymyositis and dermatomyositis using monoclonal and polyclonal antibodies.An abundance of cells were TNF-α+ (4–8%), ICAM-1+ (7–65%). IFN-γ+ (3–6%), and Ki-67+ (4–8%). It was shown that 70% of the Ki-67+ cells were Ki-67+CD3+ cells. Very few mononuclear cells were IL-2R+. MHC-I expression was found on nearly all muscle fibres in all cases, while MHC-II expression was found on occasional muscle fibres in 1/3 of cases. Analysis of repeated biopsies from four IBM patients after prednisolone treatment showed no change in the proportions of TNF-α, ICAM-1, IFN-γ or Ki-67 positive cells. In inflammatory myopathies there is an intense proliferation and differentiation of inflammatory cells in situ, indicating a local stimulation of the inflammatory process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1995.tb03587.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Tissue distribution and disease manifestations of the tRNALys A→G(8344) mitochondrial DNA mutation in a case of myoclonus epilepsy and ragged red fibres (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 328-333 
    Details
    ISSN: 1432-0533
    Keywords: Key words Myoclonus epilepsy ; Mitochondrial ; encephalomyopathy ; Mitochondrial DNA ; Mutation ; Neuropathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This man with myoclonus epilepsy and ragged red fibres (MERRF) syndrome due to the tRNALys A→G(8344) mutation of mitochondrial DNA (mtDNA) died of bronchopneumonia at 18 years of age. He had progressive clinical symptoms from 6 months of age manifesting as ataxia, myoclonic seizures, and muscle weakness. A post-mortem examination revealed 91–99% mutated mtDNA in all 32 examined tissue samples, including various organs and different brain regions. The brain appeared without macroscopic changes, but microscopic examination showed degeneration with loss of nerve cells and gliosis affecting the globus pallidus, substantia nigra, red nucleus, dentate nucleus, inferior olivary nucleus, cerebellar cortex, and the spinal cord. Skeletal muscle showed cytochrome c oxidase deficient muscle fibres with proliferation of mitochondria. In addition to pathological changes of muscle and brain there were few morphological changes that could be attributed to his mitochondrial disease. These data support the concept that in patients with the tRNALys A→G(8344) mutation who are manifesting disease there are high levels of mutated mtDNA in all tissues, but only some tissues and brain regions are vulnerable.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296519
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    Paper (German National Licenses)
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