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Página 1 a partir de 44 resultados
Multiple viral determinants mediate myopathogenicity in coxsackievirus B1-induced chronic inflammatory myopathy.
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Mice infected with myopathic coxsackievirus B1 Tucson (CVB1(T)) develop chronic inflammatory myopathy (CIM) consisting of hind limb weakness and inflammation. Amyopathic virus variants are infectious but attenuated for CIM. In this report, viral clones, chimeras, and sequencing were used to identify
Conspicuous accumulation of a single-stranded DNA binding protein in skeletal muscle fibers in inclusion body myositis.
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In muscle biopsies from patients with inclusion body myositis (IBM), multiple sites were found in many muscle fibers that bound single-stranded but not double-stranded DNA without sequence specificity, as exemplified by several different cDNA probes. This activity was attributable to a protein,
ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease.
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The "A disintegrin and metalloprotease" (ADAM) family is thought to play an important role in tissue destruction and inflammatory reactions. ADAM-17 was first described as the protease responsible for tumor necrosis factor (TNF)-α shedding. Here, we have shown the expression of ADAM-17 in
Chemokine-like factor expression in the idiopathic inflammatory myopathies.
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OBJECTIVE
We evaluated the expression of chemokine-like factor (CKLF) in biopsied muscle fibers in inflammatory myopathies, non-inflammatory myopathies and neurologically diseased controls.
METHODS
We studied the expression of CKLF in 15 polymyositis (PM), five dermatomyositis (DM), 15
Cystatin C colocalizes with amyloid-beta and coimmunoprecipitates with amyloid-beta precursor protein in sporadic inclusion-body myositis muscles.
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Cystatin C (CC), an endogenous cysteine protease inhibitor, is accumulated within amyloid-beta (A beta) amyloid deposits in Alzheimer's disease (AD) brain and was proposed to play a role in the AD pathogenesis. Because the chemo-morphologic muscle phenotype of sporadic inclusion-body myositis
Development of autoantibodies against muscle-specific FHL1 in severe inflammatory myopathies.
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Mutations of the gene encoding four-and-a-half LIM domain 1 (FHL1) are the causative factor of several X-linked hereditary myopathies that are collectively termed FHL1-related myopathies. These disorders are characterized by severe muscle dysfunction and damage. Here, we have shown that patients
Zoonotic necrotizing myositis caused by Streptococcus equi subsp. zooepidemicus in a farmer.
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Streptococcus equi subsp. zooepidemicus is a beta-hemolytic group C streptococcus mainly causing infections in domesticated animals. Here we describe the first case of zoonotic necrotizing myositis caused by this bacterium.
The patient was a 73-year-old, previously healthy farmer with two
Necrotizing fasciitis and myositis caused by group A streptococci. Epidemiology, diagnosis, and treatment of "flesh-eating bacteria".
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Despite the absence of conclusive proof, the incidence of necrotizing fasciitis and myositis due to GAS may be increasing, possibly related to shifts in the proportion of GAS isolates of M-Types 1 and 3. These M-types (or the production of exotoxins and proteases associated with them) may lead to
Protease nexin I expression is up-regulated in human skeletal muscle by injury-related factors.
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Protease nexin I is a 43-50 kDa glycoprotein capable of inhibiting a number of serine proteases. In cultured differentiated human skeletal muscle (myotubes), we previously found that protease nexin I was localized in patches at their surface where it was active and able to inhibit thrombin. To
beta-Amyloid precursor protein mRNA is increased in inclusion-body myositis muscle.
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Vacuolated muscle fibers in muscle biopsies of 8 out of 8 inclusion body myositis (IBM) patients, including 2 hereditary patients, manifested increased mRNA for the beta-amyloid precursor protein (beta APP) that contains Kunitz-type protease inhibitor motif. In affected fibers, increased beta
Presence of BACE1 and BACE2 in muscle fibres of patients with sporadic inclusion-body myositis.
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Sporadic inclusion-body myositis (IBM) is the most common, progressive muscle disease of older individuals. We investigated the presence of BACE1 and BACE2-two beta secretases that cleave amyloid-beta-precursor protein-in muscle-biopsy samples from patients with IBM and from controls. On
Calcium dysregulation, functional calpainopathy, and endoplasmic reticulum stress in sporadic inclusion body myositis.
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Sporadic inclusion body myositis (IBM) is the most common primary myopathy in the elderly, but its pathoetiology is still unclear. Perturbed myocellular calcium (Ca2+) homeostasis can exacerbate many of the factors proposed to mediate muscle degeneration in IBM, such as mitochondrial dysfunction,
Cysteine proteases as disease markers.
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This review comprises issues concerning cysteine cathepsins (CCs): human peptidases belonging to papain family (C1) of clan CA of cysteine proteases: cathepsins B, L, H, S, K, F, V, X, W, O and C. The involvement of these enzymes in physiological and pathological processes is described, especially
The DNA mismatch repair enzyme PMS1 is a myositis-specific autoantigen.
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OBJECTIVE
The specificity of the autoantibody response in different autoimmune diseases makes autoantibodies useful for diagnostic purposes. It also focuses attention on tissue- and event-specific circumstances that may select unique molecules for an autoimmune response in specific diseases.
Antigen processing and presentation in human muscle: cathepsin S is critical for MHC class II expression and upregulated in inflammatory myopathies.
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The immunological properties of muscle cells are of critical importance for both the pathogenesis of inflammatory muscle disorders as well as for understanding and controlling novel therapeutic strategies. Muscle cells can present antigens to both CD4 and CD8 cells. However, the cellular
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