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polyradiculoneuropathy/carbohydrate

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NesneKlinik denemelerPatentler
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Sera of some patients with acquired sensory neuropathy, chronic inflammatory demyelinating polyradiculoneuropathy and motor neuron disease have high titres of IgG autoantibodies to a minor human peripheral nerve glycoprotein of approximately 36 kDa. This protein cofractionated with PNS myelin and

[Immune-mediated neuropathy and anti-glycolipid antibodies].

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Antibodies to glycolipids likely play a pathogenic role in the development of immune-mediated neuropathy. Guillain-Barre syndrome (GBS), an acute immune-mediated polyradiculoneuropathy, often has IgG antibodies to gangliosides, sialic acid-containing glycolipids. The heterogeneity of ganglioside

Recent studies on the roles of antiglycosphingolipids in the pathogenesis of neurological disorders.

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Evidence is mounting to suggest a causal role of humoral immunity arising from antiglycosphingolipid (GSL) antibodies in a variety of neurological disorders. These disorders include the demyelinating and axonal forms of Guillain-Barre syndrome, multifocal motor neuropathy, chronic inflammatory

Possible mechanism of intravenous immunoglobulin treatment on anti-GM1 antibody-mediated neuropathies.

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Anti-GM1 antibody may function in disease development in some patients with Guillain-Barré syndrome, chronic inflammatory demyelinating polyradiculoneuropathy and multifocal motor neuropathy. Intravenous immunoglobulin (IVIg) therapy is effective in these neuropathies, but the mechanism by which

[Monoclonal IgM autoantibody activity vis-à-vis glycoconjugates of peripheral nerves: apropos of 112 cases].

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Serum IgM and IgG autoantibodies against carbohydrate epitopes on glycolipids and glycoproteins have been determined in a series of 112 neuropathies associated with monoclonal IgM (M-IgM) by different immunological techniques. The M-IgM anti-myelin sheath antibodies were determined by indirect

Antiglycolipid antibodies in Guillain-Barré syndrome and related diseases: review of clinical features and antibody specificities.

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Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy that usually develops following a respiratory or intestinal infection. Although the pathogenic mechanisms of GBS have not been fully established, both humoral and cell-mediated immune factors have been shown to contribute

Antiganglioside antibodies and their pathophysiological effects on Guillain-Barré syndrome and related disorders--a review.

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Guillain-Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy which can cause acute quadriplegia. Infection with micro-organisms, including Campylobacter jejuni (C. jejuni), Haemophilus influenzae, and Cytomegalovirus (CMV), is recognized as a main triggering event for the
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