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vasculitis/tyrosine
Koblingen er lagret på utklippstavlen
Side 1 fra 69 resultater
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
[Negative regulatory factor of CAWS (Candida albicans water-soluble fraction) -vasculitis in CBA/J mice as assessed by comparison with Bruton's tyrosine kinase-deficient CBA/N mice].
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Candida albicans water-soluble fraction (CAWS) has microbial pathogen-associated molecular patterns (PAMPs). It is a mannoprotein-β glucan complex obtained from the culture supernatant of Candida albicans NBRC1385 and exhibits vasculitis-inducing activity (CAWS vasculitis) in mice. The sensitivity
Urinary eicosanoid and tyrosine derivative concentrations in patients with vasculitides.
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BACKGROUND
Vasculitides are classified on the basis of the type of cell involved, namely, eosinophilic vasculitides such as Churg-Strauss syndrome (CSS) and noneosinophilic vasculitides. However, knowledge on inflammatory mediators and oxidative tissue damage associated with vasculitides is
IL-10 is a negative regulatory factor of CAWS-vasculitis in CBA/J mice as assessed by comparison with Bruton's tyrosine kinase-deficient CBA/N mice.
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Candida albicans water-soluble fraction (CAWS), a mannoprotein-beta-glucan complex obtained from the culture supernatant of C. albicans NBRC1385, exhibits vasculitis-inducing activity (CAWS-vasculitis) in mice. The sensitivity to CAWS-vasculitis varies greatly among mouse strains. This study
The activation of the neutrophil respiratory burst by anti-neutrophil cytoplasm autoantibody (ANCA) from patients with systemic vasculitis requires tyrosine kinases and protein kinase C activation.
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The ability of antineutrophil cytoplasm autoantibodies (ANCA) from patients with systemic vasculitis to stimulate protein kinase C (PKC) and tyrosine kinases was examined in human neutrophils. Using the superoxide dismutase-inhibitable reduction of ferricytochrome C, the kinetics of ANCA-induced
Spleen tyrosine kinase inhibition is an effective treatment for established vasculitis in a pre-clinical model.
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The anti-neutrophil cytoplasm antibody (ANCA)-associated vasculitides (AAV) are a group of life-threatening multi-system diseases characterized by necrotising inflammation of small blood vessels and crescentic glomerulonephritis. ANCA are thought to play a direct pathogenic role. Previous studies
Leukocytoclastic vasculitis during treatment with the oral EGFR tyrosine kinase inhibitor erlotinib.
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Brain tumors: L-[1-C-11]tyrosine PET for visualization and quantification of protein synthesis rate.
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OBJECTIVE
Positron emission tomography (PET) with the amino acid tracer L-[1-C-11]-tyrosine was evaluated in 27 patients with primary and recurrent brain tumors.
METHODS
Patients underwent either static (n = 14) or dynamic PET (n = 13), with quantification of protein synthesis rate (PSR) and
Recurrent ALK-negative anaplastic large T-cell lymphoma presenting as necrotizing vasculitis.
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Anaplastic large cell lymphoma (ALCL) is a T-cell lymphoma histologically characterized by expression of CD30, a cell surface receptor present on activated T cells and B cells. ALCL may occur in a primary cutaneous form or as systemic ALCL with lymph node involvement. Anaplastic lymphoma kinase
Successful rechallenge with ceritinib after leukocytoclastic vasculitis during ceritinib treatment for non-small cell lung cancer harboring the EML4-ALK fusion protein.
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Anaplastic lymphoma kinase (ALK)-tyrosine kinase inhibitors (TKIs) dramatically improve progression-free survival compared to cytotoxic agents. It is therefore important to manage patients with ALK-TKIs until drug resistance occurs. Leukocytoclastic vasculitis (LCV) is a rare complication during
Imatinib mesylate, a new kid on the block for the treatment of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis?
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Persistent T cell activation is a common finding in anti-neutrophil cytoplasmic autoantibodies (ANCA)-associated systemic vasculitis (AAV) patients. Because imatinib, a selective inhibitor of the ABL, ARG, PDGFR and c-KIT tyrosine kinases, inhibits T cell activation, this study was conducted to
Constitutive tyrosine phosphorylation of the vav proto-oncogene product in MRL/Mp-lpr/lpr mice.
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MRL/Mp-lpr/lpr (lpr) mice develop autoantibodies, vasculitis, and glomerulonephritis, which are similar to human systemic lupus erythematosus, and acquire a generalized, nonmalignant, lymphoproliferative disorder. CD4- CD8- CD3+ TCR alphabeta+ (double-negative, DN) T cells accumulate in spleen and
Feasibility of tumor imaging using L-3-[iodine-123]-iodo-alpha-methyl-tyrosine in extracranial tumors.
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L-3-[123I]-Iodo-alpha-methyl-tyrosine (IMT) is a modified amino acid. It is reported to be avidly taken up in brain tumors, reflecting amino acid transport and is suitable for SPECT.
METHODS
To determine whether tumors outside the brain can also accumulate this tracer, we injected 300-450 MBq IMT
FMS-like tyrosine kinase 3 ligand aggravates the lung inflammatory response to Streptococcus pneumoniae infection in mice: role of dendritic cells.
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Pretreatment of mice with the hemopoietic growth factor, FMS-like tyrosine kinase 3 ligand (Flt3L), has been shown to increase monocyte-derived myeloid dendritic cells (DC) in lung parenchymal tissue, with possible implications for protective immunity to lung bacterial infections. However, whether
FET PET in Primary Central Nervous System Vasculitis.
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Primary central nervous system vasculitis is confined to the brain and spinal cord. While serological markers of inflammation are usually normal, conventional angiography may confirm the diagnosis. The diagnostic method of choice is central nervous system biopsy. A 57-year-old man suffered from a
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