Search

Your search keyword '"Kenneth A. Stauderman"' showing total 2 results
Start Over Author "Kenneth A. Stauderman" Journal annals of the new york academy of sciences
2 results on '"Kenneth A. Stauderman"'

1. Differential Effect of Lambert-Eaton Myasthenic Syndrome Immunoglobulin on Cloned Neuronal Voltage-gated Calcium Channelsa

Author

Mark Williams, Bethan Lang, John Boot, Kenneth A. Stauderman, Fraser J. Moss, John Newsom-Davis, Ashwin Pinto, Paul Brust, and Michael M. Harpold

Subjects
medicine.medical_specialty, Protein subunit, chemistry.chemical_element, Calcium, Transfection, General Biochemistry, Genetics and Molecular Biology, Neuromuscular junction, Cell Line, chemistry.chemical_compound, History and Philosophy of Science, Internal medicine, Calcium flux, medicine, Humans, Cloning, Molecular, Neurotransmitter, Autoantibodies, Neurons, Voltage-gated ion channel, Voltage-dependent calcium channel, General Neuroscience, medicine.disease, Recombinant Proteins, Kinetics, Lambert-Eaton Myasthenic Syndrome, Endocrinology, medicine.anatomical_structure, chemistry, Immunoglobulin G, Potassium, Calcium Channels, Lambert-Eaton myasthenic syndrome
Abstract

Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder in which antibodies to presynaptic calcium channels at the neuromuscular junction lead to muscle weakness. Around 60% of patients with LEMS have an associated small cell lung carcinoma (SCLC), which is known to express voltage-gated calcium channels (VGCCs). Immunoglobulin (IgG) from patients with LEMS causes inhibition of calcium flux in an SCLC cell line.1 This inhibition has been shown to correlate with disease severity.1 Neuronal VGCCs can be classified into P-, Q-, N-, L-, and R-type according to their electrophysiological and pharmacological properties. Around 92% of LEMS patients have antibodies that immunoprecipitate P/Q-type (125I-CTx-MVIIC labeled) VGCCs and around 30% have antibodies to N-type (125I-CTx-GVIA labeled) VGCCs.2 In addition, antibodies from LEMS patients have been shown to abolish the component of neurotransmitter release subserved by both P-type and Q-type VGCCs in sympathetic and parasympathetic neurons of mice injected with LEMS IgG.3 Neuronal VGCCs consist of an 1 subunit with and 2 subunits. Several of the human genes encoding the different types of VGCC have now been cloned and sequenced, including the 1A, 1B, 1D, 1E, 1–4, and 2 subunits. Human embryonic

Published
1998
Full Text
View/download PDF

2. The role of autoantibodies in Lambert-Eaton myasthenic syndrome

Author

Fraser J. Moss, Dominic Jones, Paul Brust, Bethan Lang, John Newsom-Davis, Angela Vincent, Masakatsu Motomura, Michael M. Harpold, Ashwin Pinto, Kenneth A. Stauderman, J. Moll, Sally Waterman, John Boot, and Mark E. Williams

Subjects
medicine.medical_specialty, Paraneoplastic Syndromes, Neuromuscular transmission, Motor nerve, Autonomic Nervous System, General Biochemistry, Genetics and Molecular Biology, Mice, History and Philosophy of Science, Downregulation and upregulation, Reference Values, omega-Conotoxin GVIA, Internal medicine, Medicine, Animals, Humans, Autoantibodies, biology, business.industry, General Neuroscience, Autoantibody, Immunization, Passive, Muscle weakness, Cancer, medicine.disease, Calcium Channel Blockers, Lambert-Eaton Myasthenic Syndrome, Endocrinology, biology.protein, Calcium Channels, medicine.symptom, Antibody, business, Peptides, Acetylcholine, medicine.drug
Abstract

The Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder of neuromuscular transmission that causes fatigable muscle weakness, loss of tendon reflexes, and autonomic dysfunction.1–3 LEMS antibodies bind to and induce a downregulation of voltage-gated channels (VGCCs),4,5 resulting in a reduction in the nerve-evoked, Ca2+-dependent release of acetylcholine from motor nerve terminals. Approximately 60% of patients have an associated small cell lung carcinoma (SCLC),6 a tumor that is thought to be neuroendocrine in origin. This strong association with cancer makes LEMS a member of the group of paraneoplastic disorders. SCLC cells have been shown to express functional VGCCs,7,8 and preincubation in LEMS sera or IgG reduces the K+-stimulated 45Ca2+ flux into these cells.8–10

Published
1998

Catalog

Books, media, physical & digital resources
See catalog results