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myositis/phosphatase
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MAP kinase phosphatase-1 is induced in abnormal fibers in inclusion body myositis.
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OBJECTIVE
To investigate alterations in protein kinases and phosphatases that regulate the activity of mitogen activated protein kinase (MAPK) in sporadic inclusion body myositis (IBM).
BACKGROUND
In vacuolated fibers in IBM, several studies reported upregulation of the extracellular regulated
Tartrate-resistant acid phosphatase containing cells in nodular fasciitis, proliferative fasciitis, and proliferative myositis.
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Five cases of nodular fasciitis, three cases of proliferative fasciitis, and one case of proliferative myositis were investigated by tartrate-resistant acid phosphatase (TRAP) histochemistry on conventional paraffin-embedded material. In all cases varying numbers of enzyme-positive cells were
The protein tyrosine phosphatase N22 gene is associated with juvenile and adult idiopathic inflammatory myopathy independent of the HLA 8.1 haplotype in British Caucasian patients.
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OBJECTIVE
To examine single-nucleotide polymorphisms (SNPs) of the protein tyrosine phosphatase N22 gene (PTPN22) and to study the relationship between PTPN22 and the HLA region in patients with idiopathic inflammatory myopathies (IIMs).
METHODS
PTPN22 SNPs were assessed in a large, cross-sectional,
[Phosphatase studies in progressive myositis ossificans].
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MyoD expression restores defective myogenic differentiation of human mesoangioblasts from inclusion-body myositis muscle.
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Inflammatory myopathies (IM) are acquired diseases of skeletal muscle comprising dermatomyositis (DM), polymyositis (PM), and inclusion-body myositis (IBM). Immunosuppressive therapies, usually beneficial for DM and PM, are poorly effective in IBM. We report the isolation and characterization of
The PTPN22 gene is associated with idiopathic inflammatory myopathy.
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The aim of this study was to determine whether a single-nucleotide polymorphism (SNP; 1858CT, R620W) in the protein tyrosine phosphatase N22 (PTPN22) gene confers susceptibility to idiopathic inflammatory myopathy (IIM) in South Australian patients with IIM.
Genotyping was performed on stored DNA
[Idiopathic Inflammatory Myopathy and Anti-aminoacyl-tRNA Synthetase Antibody].
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Anti-aminoacyl-tRNA synthetase (ARS) antibodies (anti-Jo-1, anti-PL-7, anti-PL-12, anti-EJ, anti-KS, anti-OJ, anti-Ha, and anti-Zo antibodies) are found in 25 to 40% of myositis patients. The patients with these antibodies have anti-synthetase syndrome with one or more of the following clinical
An update on the immunogenetics of idiopathic inflammatory myopathies: major histocompatibility complex and beyond.
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OBJECTIVE
To update the reader on immunogenetic advances in idiopathic inflammatory myopathy (IIM) over the past 18 months.
RESULTS
In Caucasian IIM, despite a shared association with the human leukocyte antigen (HLA) 8.1 ancestral haplotype (HLA-DRB1*03-DQA1*05-DQB1*02), anti-Jo-1 and anti-PM-Scl
SHP-1-dependent macrophage differentiation exacerbates virus-induced myositis.
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Virus-induced myositis is an emerging global affliction that remains poorly characterized with few treatment options. Moreover, muscle-tropic viruses often spread to the CNS, causing dramatically increased morbidity. Therefore, there is an urgent need to explore genetic factors involved in this
Experimental allergic myositis: ultrastructural, histochemical, immunological and immunohistochemical studies.
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The quadriceps femoris muscles of experimental allergic myositis, in strain 13 guinea pigs immunised with rabbit myosin B fraction, were subjected to histochemical, immunohistochemical and electron microscopic studies. They demonstrated a variety of degenerative changes of muscle fibres,
[Immunocytochemical study of the inflammatory forms of facioscapulohumeral myopathies and correlation with other types of myositis].
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The inflammatory forms of facioscapulohumeral myopathies are rare. In a series of 52 cases, six patients had these types. Only four cases could be investigated with immunochemical staining (immunoperoxidase). Monoclonal antibodies reactive for B cells, T4 cells, T8 cells, natural killer cells were
Rimmed vacuoles with beta-amyloid and ubiquitinated filamentous deposits in the muscles of patients with long-standing denervation (postpoliomyelitis muscular atrophy): similarities with inclusion body myositis.
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In the chronically denervated muscles of patients with prior paralytic poliomyelitis, there are secondary myopathic features, including endomysial inflammation and rare vacuolated fibers. To assess the frequency and characteristics of the vacuoles and their similarities with those seen in inclusion
[Inclusion body myositis, Paget's disease of the bone and frontotemporal dementia: early involvement of the heart and respiratory muscles].
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Since valosin-containing protein mutations were reported as a cause of hereditary inclusion body myositis associated with Paget's disease of the bone and frontotemporal dementia, many new mutations have been described in the last decade. We report on a 46-year-old German male with a progressive
[Myositis ossificans progressiva].
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The case of a 19-year-old female patient with myositis ossificans progressiva is reported. This disease is a rare hereditary disorder with a dominant autosomal genotype. The patient had typical ossifications of the humeral and dorsal muscles, as well as of those of the left thigh and upper arm, and
Mixed connective tissue disease presenting as a peculiar myositis with poor muscle regeneration.
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Mixed connective tissue disease (MCTD) is a rheumatological disease which has to be distinguished from other entities causing inflammatory myopathy. The usual clinical presentation of inflammatory myopathy associated with connective tissue disease is not different from isolated polymyositis or
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