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familial mediterranean fever/tyrosine
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5 risultati
Lack of the Association of the PTPN22 C1858T Gene Polymorphism With Susceptibility to Familial Mediterranean Fever.
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This study aims to investigate whether the protein tyrosine phosphatase non-receptor type 22 (PTPN22) C1858T gene polymorphism plays a role in the pathogenesis of familial Mediterranean fever (FMF) through T-lymphocyte activation.
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We conducted a case-control study with 180 FMF
Pyrin binds the PSTPIP1/CD2BP1 protein, defining familial Mediterranean fever and PAPA syndrome as disorders in the same pathway.
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Pyrin, the familial Mediterranean fever protein, is found in association with the cytoskeleton in myeloid/monocytic cells and modulates IL-1beta processing, NF-kappaB activation, and apoptosis. These effects are mediated in part through cognate interactions with the adaptor protein ASC, which shares
Colchicine toxicity precipitated by interaction with sunitinib.
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OBJECTIVE
Colchicine is an anti-inflammatory agent used primarily in treatment of gout and familial Mediterranean fever. Toxicity is uncommon, and depends on dose, hepatic or renal impairment, co-administration with P-glycoprotein or CYP3A4 inhibitors and route of administration. In patients taking
[Therapy for systemic metabolic disorders based on the detection of basic corneal landmarks in childhood].
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Many systemic lysosomal storage disorders show basic corneal opacities already in childhood. The lysosome is a cell organelle, produced by Golgi's apparatus, that is surrounded by a membrane and contains hydrolytic enzymes that break down food molecules, especially proteins and other complex
The systemic autoinflammatory diseases: inborn errors of the innate immune system.
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The autoinflammatory syndromes are a newly recognized group of immune disorders that lack the high titers of self-reactive antibodies and T cells characteristic of classic autoimmune disease. Nevertheless, patients with these illnesses experience unprovoked inflammatory disease in the absence of
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