polyneuropathies/carbohydrate

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Subclinical beriberi polyneuropathy in the low income group: an investigation with special tools on possible patients with suspected complaints.

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OBJECTIVE To determine the prevalence rate of subclinical beriberi polyneuropathy (PNP) in the low income group and to present new methods for early detection. METHODS We conducted a prospective, randomized observational study on all patients from family members of non-PNP patients presenting to the

Selective loss of myelin-associated glycoprotein from myelin correlates with anti-MAG antibody titre in demyelinating paraproteinaemic polyneuropathy.

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The IgM monoclonal autoantibodies of patients with demyelinating paraproteinaemic polyneuropathy recognize a carbohydrate structure present on both myelin-associated glycoprotein (MAG) and protein zero (P0). These autoantibodies are sufficient to cause the disease but the mechanism of demyelination

Polyneuropathy syndromes associated with serum antibodies to sulfatide and myelin-associated glycoprotein.

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We studied a series of 64 patients with sensory +/- motor peripheral neuropathies by comparing clinical and physiologic features to serum antibody reactivity against compounds containing sulfated carbohydrate moieties. We determined antibody reactivity by an enzyme-linked immunosorbent assay (ELISA)

Heterogeneity of antibody specificity in Taiwanese patients with polyneuropathy and IgM paraproteinemia.

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About half of the Caucasian patients with chronic polyneuropathy and IgM paraproteinemia show serum anti-myelin-associated glycoprotein (MAG) and anti-sulfoglucuronosyl glycosphingolipid (SGGLs) activities. These antibody activities have been demonstrated to react with a carbohydrate epitope known

Serum antibodies to heparan sulfate glycosaminoglycans in Guillain-Barré syndrome and other demyelinating polyneuropathies.

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We tested for serum antibodies to glycosaminoglycans (GAGs), including heparan sulfate, in patients with Guillain-Barré syndrome (GBS) and other disorders. We used ELISA methods that optimize immunoglobulin binding to carbohydrate antigens to measure serum antibodies to heparan sulfate GAGs in GBS,

[Experience with "AFAVIT Diabetes" used in the treatment of diabetic peripheral polyneuropathy in adolescents].

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OBJECTIVE To evaluate the efficiency of using the vitamin and mineral complex (VMC) ALFAVIT Diabetes in the combination therapy of diabetic polyneuropathy (DPNP) in adolescents. METHODS A study group comprised 30 children with diabetic peripheral polyneuropathy, whose combination therapy included

[The carbohydrate deficient glycoprotein syndrome].

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The carbohydrate-deficient glycoprotein syndrome is a newly described hereditary disorder which may be due to a defect in the glycoprotein metabolism. Predominant symptoms are mental retardation, epilepsy, cerebellar ataxia, polyneuropathy, squint, retinitis pigmentosa, retarded growth,

[Paralysis caused by carbohydrate during intensive care].

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In 30 septic, edematous intensive care patients a polyneuropathy occurred during treatment of peritonitis, pancreatitis, adult respiratory distress syndrome, or bronchopneumonia; 28 patients developed a complete tetraplegia. We believe this neuropathy to be an important cause of weaning failure. All

The carbohydrate deficient glycoprotein syndrome in three Japanese children.

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We describe 3 children (from two families) with a multisystemic disorder characterized by mental retardation, nonprogressive ataxia, polyneuropathy, hepatopathy during infancy and growth retardation. Due to the clinical similarities to a recently recognized disorder associated with

[Subclinical diabetes and polyneuropathy (author's transl)].

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By investigation of the carbohydrate metabolism in 357 patients with polyneuropathy observed in hospital in recent years, and by statistical comparison with a control group in the literature, an attempt was made to find out whether subclinical diabetes can cause diabetic polyneuropathy to a greater

Missense mutations in the phosphomannomutase 2 gene of two Japanese siblings with carbohydrate-deficient glycoprotein syndrome type I.

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Carbohydrate-deficient glycoprotein syndrome type I (CDG1) is an autosomal recessive disorder characterized by severe nervous system involvement and a carbohydrate moiety deficiency in N-linked glycoproteins. Clinical symptoms are psychomotor retardation, stroke-like episodes or hemorrhagic

Reactivity with the peripheral myelin glycoprotein P0 in serum from patients with monoclonal IgM gammopathy and polyneuropathy.

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The major glycoprotein P0 from human and bovine peripheral nerves carries the L2/HNK-1 and L3 carbohydrate epitopes and is recognized by serum from patients with IgM gammopathy and polyneuropathy. Only serum from patients with reactivity toward the myelin-associated glycoprotein (MAG) was reactive

Neuroradiological findings in the carbohydrate-deficient glycoprotein syndrome.

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The carbohydrate-deficient glycoprotein syndrome is a newly recognised genetic disorder characterised by mental retardation, liver disfunction during infancy, cerebellar ataxia and atrophy, polyneuropathy, growth retardation, stroke-like episodes, and the appearance of carbohydrate-deficient

The Role of Oxidative Stress, Mitochondrial Function, and Autophagy in Diabetic Polyneuropathy.

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Diabetic polyneuropathy (DPN) is the most frequent and prevalent chronic complication of diabetes mellitus (DM). The state of persistent hyperglycemia leads to an increase in the production of cytosolic and mitochondrial reactive oxygen species (ROS) and favors deregulation of the antioxidant

Shared carbohydrate antigenic determinant between the myelin-associated glycoprotein (MAG) and lung cancers. An immunohistochemical study by an anti-MAG IgM monoclonal antibody.

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An immunochemical study has shown that monoclonal anti-myelin-associated glycoprotein (MAG) antibodies identify some membrane glycoproteins from cell lines of small cell lung cancer. We investigated immunohistochemically 85 specimens of lung cancer from resection and autopsy using one of the

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