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vasculitis/phosphatase

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Página 1 desde 57 resultados

The protein tyrosine phosphatase nonreceptor 22 C1858T polymorphism and vasculitis: a meta-analysis.

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The aim of this study was to determine whether the functional protein tyrosine phosphatase nonreceptor 22 (PTPN22) C1858T polymorphism (rs2476601) confers susceptibility to vasculitis. A meta-analysis was conducted on the PTPN22 C1858T polymorphism across nine comparative studies containing 1,922

Association of alkaline phosphatase with an autoantigen recognised by circulating anti-neutrophil antibodies in systemic vasculitis.

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A solid phase radioimmunoassay has been developed to detect circulating autoantibodies to neutrophil cytoplasmic antigens in systemic vasculitis. After fractionation of these antigens by size, with gel filtration high performance liquid chromatography, sera from patients with clinically different

[Level of nuclease, phosphatase, and cathepsin in the blood serum in children with hemorrhagic vasculitis].

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De Novo PTEN Mutation in a Young Boy with Cutaneous Vasculitis.

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Phosphatase and tensin homolog (PTEN) is the protein encoded by the PTEN gene (10q23.3). PTEN mutations are related to a variety of rare diseases referred to collectively as PTEN hamartoma tumor syndromes (PHTS), which include Cowden Syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus Syndrome, and

Glomerular vascular cell adhesion molecule-1 expression in renal vasculitis.

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OBJECTIVE To study the expression of cell adhesion molecules in the renal biopsy specimens of patients with systemic vasculitis and Henoch-Schönlein purpura (HSP); to correlate this with the severity of glomerular inflammation. METHODS Renal biopsy specimens obtained from eight patients with

[Systemic vasculitis as a cause of fever of unknown origin].

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A prospective clinical study (1974-1988) was carried out in 33 patients with several types of systemic vasculitis (SV) presenting as fever of unknown origin (FUO) according to the 1961 Petersdorf and Beeson's criteria. Histological confirmation, either from biopsy or necropsy, was available in all
An association between mixed cryoglobulinaemia (MC) and hepatotropic viruses, chiefly hepatitis C virus (HCV), has been widely reported. The presence of HCV genomic sequences or HCV-related viral proteins in the serum, purified cryoglobulins, peripheral blood mononuclear cells and into several

Liver involvement in ANCA-associated vasculitis.

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The aim of the study was to investigate the incidence, the clinical course and outcome of liver involvement and autoimmune hepatic diseases in patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Liver function tests (LFT) (i.e. aspartate and alanine

Clinical features of Korean elderly patients with antineutrophil cytoplasmic antibody-associated vasculitis

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Background/aims: We compared the clinical and laboratory data between elderly and non-elderly patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) at diagnosis; further, we investigated the predictors at

Staphylococcal acid phosphatase binds to endothelial cells via charge interaction; a pathogenic role in Wegener's granulomatosis?

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The majority of patients with Wegener's granulomatosis (WG) are chronic nasal carriers of Staphylococcus aureus. Chronic nasal carriage of S. aureus is associated with an increased risk of developing a relapse of the disease. The mechanism by which this occurs is still unknown. We hypothesized that

Development of diabesity in mice with neuronal deletion of Shp2 tyrosine phosphatase.

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Obesity and diabetes, termed "diabesity," are serious health problems that are increasing in frequency. However, the molecular mechanisms and neuronal regulation of these metabolic disorders are not fully understood. We show here that Shp2, a widely expressed Src homology 2-containing Tyr

Distinct HLA and non-HLA associations in different subtypes of ANCA-associated vasculitides in North India.

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Antineutrophil cytoplasmic antibody-associated vasculitis (AAV) is an autoimmune disease characterized by necrotizing small vessel vasculitis that can affect various organs and present multiple symptoms. Susceptibility to AAV is multifactorial and most likely caused by an amalgamation
OBJECTIVE To assess the possible association between the PTPN22 gene 1858C-->T polymorphism and the susceptibility to Henoch-Schönlein purpura (HSP) and determine if this polymorphism is implicated in the severity of this systemic vasculitis. METHODS Fifty-seven unselected patients from Northwest

Spirochetal vasculitis and bile ductular damage in early hepatic syphilis.

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Hepatic involvement in a patient with secondary syphilis was documented by demonstrating spirochetes in the portal tracts. Raised alkaline phosphatase levels in early hepatic syphilis may be explained by involvement of bile ducts and vascular structures.
BACKGROUND To determine whether the PTPN22 (protein tyrosine phosphatase nonreceptor 22)/CSK (c-src tyrosine kinase) pathway is implicated in the susceptibility and clinical heterogeneity of Henoch-Schönlein purpura (HSP) in the largest series of Caucasian HSP patients ever assessed for genetic
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