dermatomyositis/tyrosine

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Metabolomic profiling for identification of potential biomarkers in patients with dermatomyositis.

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Dermatomyositis (DM) is a rare autoimmune myopathy characterized by skin lesions, proximal muscle weakness and muscle inflammation. The pathogenesis of DM is unclear, and identification of reliable biomarkers for early diagnosis of DM is critical for design of a specific therapy for

Polymyositis and dermatomyositis: no persistence of enterovirus or encephalomyocarditis virus RNA in muscle.

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OBJECTIVE A persistent infection of enteroviruses and cardioviruses has been implicated in polymyositis and dermatomyositis, but conventional hybridisation studies of the presence of enterovirus RNA and encephalomyocarditis (EMC) virus RNA in affected muscle have yielded conflicting results. To

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,

Genome-wide association study of dermatomyositis reveals genetic overlap with other autoimmune disorders.

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OBJECTIVE To identify new genetic associations with juvenile and adult dermatomyositis (DM). METHODS We performed a genome-wide association study (GWAS) of adult and juvenile DM patients of European ancestry (n = 1,178) and controls (n = 4,724). To assess genetic overlap with other autoimmune

GLIS3 and TYK2 Single Nucleotide Polymorphisms Are Not Associated with Dermatomyositis/Polymyositis in Chinese Han Population.

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OBJECTIVE Racial differences and genetic overlap have been shown to be responsible for the difference in susceptibility to dermatomyositis (DM)/polymyositis (PM) in a variety of populations. Single nucleotide polymorphisms (SNPs) in the GLI-similar 3 (GLIS3) and tyrosine kinase 2 (TYK2) genes have

Serum concentrations of Flt-3 ligand in rheumatic diseases.

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Fms-like tyrosine kinase 3 (Flt-3) is a cytokine receptor expressed on the surface of bone-marrow progenitor of hematopoietic cells. Flt-3 ligands are produced by peripheral blood mononuclear cells, and found in various human body fluids. Flt-3 signal is involved in the regulation of vessel

[What's new in dermatological treatment?]

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The therapeutic revolution in the management of inflammatory dermatoses is under way. The therapeutic arsenal is expanding in the field of psoriasis, including biologics (TNF blockers, anti-IL12/IL23, anti-IL17, and anti-IL23 antibodies), new small molecules (tyrosine kinase inhibitor), and a new

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

Search for persistent enterovirus infection of muscle in inflammatory myopathies.

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To investigate the hypothesis that the inflammatory muscle diseases (IMD) polymyositis (PM) and dermatomyositis (DM) may be due to a chronic, persistent enterovirus (EV) infection we sought to determine the prevalence of these viruses in muscle tissue using both nested polymerase chain reaction

Nitric oxide stress in sporadic inclusion body myositis muscle fibres: inhibition of inducible nitric oxide synthase prevents interleukin-1β-induced accumulation of β-amyloid and cell death.

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Sporadic inclusion body myositis is a severely disabling myopathy. The design of effective treatment strategies is hampered by insufficient understanding of the complex disease pathology. Particularly, the nature of interrelationships between inflammatory and degenerative pathomechanisms in sporadic

X-linked agammaglobulinemia. A clinical and molecular analysis.

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X-linked agammaglobulinemia (XLA), characterized by a profound deficiency of B lymphocytes due to an arrest in B lymphocyte development, is caused by mutations in the gene encoding Btk (Bruton tyrosine kinase). The BTK gene has been cloned and the genomic organization determined. BTK codes for 19

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