myasthenia gravis/carbohydrate

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Studies of carbohydrate metabolism in myasthenia gravis in conditions of ischaemic exercise.

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Structure of the acetylcholine receptor and specificities of antibodies to it in myasthenia gravis.

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Acetylcholine receptors in skeletal muscle and fish electric organs are intrinsic membrane proteins whose function is to bind acetylcholine released from the nerve ending and trigger the opening of a cation-specific channel in the postsynaptic membrane, thereby facilitating transmission of the nerve

Characterization of a 58- and a 78-kD monocytic membrane protein with affinity to the acetylcholine receptor in myasthenia gravis patients.

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The autoimmune disease myasthenia gravis (MG), caused by the effect of specific antibodies, directed towards the nicotinic acetylcholine receptor, is triggered by autoantigen-specific T cells. In order to investigate cellular parts of the immune response in MG, the authors investigated the binding

Immunosuppressants increase the levels of natural autoantibodies reactive with glycosaminoglycans in myasthenia gravis.

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Increasing number of evidences support the role of glycosylation in the evolution of autoimmunity. We examined carbohydrate-reactive natural autoantibodies systematically for the first time in patients with autoimmune myasthenia gravis. Antibodies reactive to glycosaminoglycans were measured with

Serum metabolomic response of myasthenia gravis patients to chronic prednisone treatment.

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Prednisone is often used for the treatment of autoimmune and inflammatory diseases but they suffer from variable therapeutic responses and significant adverse effects. Serum biological markers that are modulated by chronic corticosteroid use have not been identified. Myasthenia gravis is an

Galectin-1 is expressed by thymic epithelial cells in myasthenia gravis.

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Galectin-1, a member of a family of carbohydrate binding proteins, is synthesized by thymic epithelial cells in normal juvenile thymus, and mediates adhesion of immature T cells to thymic epithelium. Because cell adhesion molecules are proposed to play a role in the thymic hyperplasia and neoplasia

Non-synonymous single nucleotide polymorphisms in genes for immunoregulatory galectins: association of galectin-8 (F19Y) occurrence with autoimmune diseases in a Caucasian population.

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BACKGROUND Galectins are potent immune regulators, with galectin-8 acting as a pro-apoptotic effector on synovial fluid cells and thymocytes and stimulator on T-cells. To set a proof-of-principle example for risk assessment in autoimmunity, and for a mutation affecting physiological galectin sensor

Presynaptic membrane receptor in human brain.

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Myasthenia gravis (MG) is an autoimmune disease that results from antibody mediated damage of Acetylcholine receptor (AChR) at the neuromuscular junction. The autoimmune character of MG and pathogenic role of AChR antibodies have been established by several workers i.e., the demonstration of

Endocrine myopathies.

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The atrophy produced by endocrine disorders is primarily due to alterations in protein and carbohydrate metabolism. Type II muscle fibers are more severely affected than are Type I fibers. Steroid myopathy and the myopathy associated with excess ACTH have a typical pattern of proximal weakness

Heterogeneity of acetylcholine receptors: different forms of receptor distinguished by alpha-bungarotoxin kinetics and by antibody binding properties.

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The interactions of the nicotinic acetylcholine receptor (AChR), extracted from denervated rat hindlimb muscle, with alpha-bungarotoxin, Concanavalin-A (Con-A) and immunoglobulins isolated from the sera of specific patients with Myasthenia Gravis (MG) have been studied. The association and

Therapeutic inhibition of the complement system. Y2K update.

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Activation of complement is an essential part of the mechanism of pathogenesis of a large number of human diseases; its inhibition by pharmacological means is likely to suppress disease processes in complement mediated diseases. From this point of view low molecular weight synthetic inhibitors of

[Pseudo-myasthenic myopathy in a woman with anorexia nervosa].

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Skeletal myopathy, although foreseeable in severe malnutrition, has been rarely reported in patients with anorexia nervosa. We report a case of oculo-oropharyngeal myopathy mimicking myasthenia in a 42-year-old woman with an history of anorexia nervosa, completely reversible after refeeding with

Immunochemical properties of junctional and extrajunctional acetylcholine receptor.

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Immunological assays were performed to compare two distinct forms of the nicotinic acetylcholine receptor (AChR): junctional (JR) and extrajunctional receptor (EJR). Antibodies from myasthenia gravis patients' sera inhibited the binding of [125I]alpha-bungarotoxin (BGT), to EJR more effectively than

[Advances in neuroimmunological laboratory studies on neuromuscular diseases].

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The recent methodological advances in molecular biology, immunology, and genetics have clarified neuroimmunological problems in axonal Guillain-Barré syndrome, seronegative myasthenia gravis, paraneoplastic neurologic syndromes and many others. In addition to clinical and serological studies in

Approach to generalized weakness and peripheral neuromuscular disease.

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A large number of intellectually engaging and potentially serious neuromuscular diseases have been presented. The emergency medicine physician must be able to recognize those entities that have the potential to clinically deterioration. The evaluation of weakness requires a comprehensive,

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