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multiple sclerosis/phosphatase

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Interferon-beta is a current treatment for multiple sclerosis (MS). Interferon-beta is thought to exert its therapeutic effects on MS by down-modulating the immune response by multiple potential pathways. Here, we document that treatment of MS patients with interferon beta-1a (Rebif) results in a

Protein tyrosine phosphatase receptor-type C exon 4 gene mutation distribution in an Italian multiple sclerosis population.

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In this study, we investigate the role of the C-->G mutation in position 77 of exon 4 of the protein tyrosine phosphatase receptor-type C (PTPRC) gene, coding for the CD45 molecule, for the development of multiple sclerosis (MS) in an Italian continental population. The PTPRC mutated genotype has
Existing techniques have been adapted and it has been possible to demonstrate acid phosphatase (APP) and myelin, lipid or astrocytic fibres in the same histological section. In normal controls APP was demonstrated in neurons, astrocytes, ependyma including choroid plexus epithelium and in pericytes,
In multiple sclerosis there takes place a gradual destruction of most organs and tissues of the sick organism. With progression of the illness changes are noticeable in their functional development. A biochemical mode of assessment of functioning of organs and tissues is analysis of alkaline

Serum alkaline phosphatase in patients with multiple sclerosis.

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Sera from multiple sclerosis patients show a deficit of intestinal alkaline phosphatase (serum type Pp2) by comparison with normal sera. This is not due to variation in ABO frequency, since the specimens from patients and normals are matched for ABO frequency, and it is not due to differences in
Multiple sclerosis (MS) is a common cause of neurological disability in young adults. The disease generally manifests in early to middle adulthood and causes various neurological deficits. Autoreactive T lymphocytes and their associated antigens have long been presumed important features of MS
Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system, and its pathogenesis remains largely unclear. Much attention has been paid to the role of microRNAs (miRs) in regulation of autoimmune disease. Here, we found, for the first time, that miR-448

Evaluating the role of the 620W allele of protein tyrosine phosphatase PTPN22 in Crohn's disease and multiple sclerosis.

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The 620W allele of PTPN22 has been associated with susceptibility to several different forms of chronic inflammatory disease, including Type 1 diabetes (T1D), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and autoimmune thyroiditis (AIT). We set out to explore its possible role in

[Activity of phosphatases of the bone marrow leukocytes in disseminated sclerosis].

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BRAIN ESTERASES AND PHOSPHATASES IN MULTIPLE SCLEROSIS.

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Protein tyrosine phosphatase gene (PTPN22) polymorphism in multiple sclerosis.

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The R620W polymorphism of the protein tyrosine phosphatase PTPN22 is not associated with multiple sclerosis.

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RANKL/RANK/OPG Axis Is Deregulated in the Cerebrospinal Fluid of Multiple Sclerosis Patients at Clinical Onset.

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OBJECTIVE Our study focused on the RANKL (receptor activator of nuclear factor-κB ligand)/RANK/OPG (osteoprotegerin) axis and selected proinflammatory/immunoregulatory upstream mediators in the peripheral blood (PBL) and cerebrospinal fluid (CSF) of multiple sclerosis (MS) patients. METHODS PBL and

High-dose glucocorticoids in multiple sclerosis patients exert direct effects on the kidney and skeleton.

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The effects of acute pharmacologic steroid treatment on skeletal and mineral metabolism were assessed in 56 multiple sclerosis patients who were to receive 1 g intravenous methylprednisolone for 10 days, followed by a 4 day intravenous and 28 day oral glucocorticoid taper. Serum and urine samples

Therapeutic potential of curcumin for multiple sclerosis.

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Multiple sclerosis (MS) is a chronic autoimmune inflammatory disease of the central nervous system (CNS), characterized by demyelination, neuronal injury, and breaching of the blood-brain barrier (BBB). Epidemiological studies have shown that immunological, genetic, and environmental factors
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