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To further unravel the basic immunoregulatory defect present in myasthenia gravis, we undertook to study nicotinic acetylcholine receptor (AchR) activity on human peripheral blood leukocytes. A biphasic suppressive effect of nicotine was observed on lymphocyte proliferative responses to
The aim of the present study was to further characterize the site of action of nicotine-induced hypothalamo-hypophyseal-adrenal (HHA) activation. A systemic injection of nicotine in concentrations of 65-2,100 micrograms/kg elevated serum corticosterone (CS) concentrations in a time and
We report a case of myasthenia gravis worsened by a nicotine transdermal system, in a man who usually was smoking fourty cigarettes per day without any worsening of his symptomatology. He noted an increased bilateral ptosis, total ophtalmoplegia, difficulty in chewing and generalized weakness two
Myasthenia gravis (MG) is a chronic autoimmune disease caused by autoantigen against the nicotine acetylcholine receptor at the neuromuscular junction. With modern treatment facilities, the treatment effect and outcome for MG has been greatly improved with MG and non-MG patients enjoying the same
15% of myasthenia gravis (MG) patients do not have antibodies against the acetylcholine receptor (AChR). Some of these "seronegative" MG patients have antibodies against muscle specific kinase (MuSK), and many have a non-IgG factor that acutely inhibits AChR function in a muscle-like cell line,
A patient with myasthenia gravis developed nephrotic syndrome 3 years after thymectomy. The kidney biopsy specimen revealed mesangial proliferative glomerulonephritis with immune deposits. The glomerular mesangial cells and tubular epithelial cells were sensitive to alpha-bungarotoxin (alpha-BT), a
Clinical and immunological changes in patients with myasthenia gravis (MG) who had extended thymectomy (Tx) and/or corticosteroid therapy were examined to elucidate the mechanisms of improvement following the treatments. The changes found were: 1) After Tx and steroid therapy, in patients with MG
Auto-antibodies to the nicotine acetylcholine receptor (AChR) cause the disease myasthenia gravis (MG). Animals immunized with AChR or receiving anti-AChR antibodies acquire MG symptoms. The majority of the monoclonal antibodies (mAbs) raised in rats against intact AChR bind to a region on the
Overwhelming evidence now supports Simpson's concept, originally proposed in 1960, that acquired myasthenia gravis (MG) is an autoimmune disease in which antibodies are directed against the nicotine postsynaptic acetylcholine receptor (AChR).1 An autoimmune pathogenesis of acquired MG implies that
Anti-muscle nicotinic acetylcholine receptor (nAR) antibodies were sought in epileptic patients without clinical signs of myasthenia gravis. Low titers of such antibodies were found in 3 cases characterized by primary generalized seizures, IgA deficiency and HLA A1 and B8 antigens. These three
Serotherapy, an approach currently used to protect humans against animal bites or stings, is often too specific. To broaden antiserum paraspecificity, use of antibodies directed against areas shared by all members of a toxin family was previously proposed. MST2 is a mAb that recognizes all
This meeting, the tenth in a series of conferences that was established in Stockholm in 1970, focused on fundamental and applied aspects of processes involving acetylcholine (ACh) as a neurotransmitter. The role of cholinergic mechanisms in central and peripheral nervous systems, sensory organs and