scholarly journals Autoimmune Myasthenia Gravis after Sternal Fracture

2012 ◽  
Vol 4 (1) ◽  
pp. 20-22 ◽  
Author(s):  
Jens A. Petersen ◽  
Hans H. Jung ◽  
Michael Weller ◽  
Michael Linnebank
Keyword(s):  
Myasthenia Gravis ◽  
Sternal Fracture ◽  
Autoimmune Myasthenia

Genetic Factors in Autoimmune Myasthenia Gravis

2008 ◽  
Vol 1132 (1) ◽  
pp. 180-192 ◽  
Author(s):  
Matthieu Giraud ◽  
Claire Vandiedonck ◽  
Henri-Jean Garchon
Keyword(s):  
Myasthenia Gravis ◽  
Genetic Factors ◽  
Autoimmune Myasthenia

scholarly journals Pleiotropic effects of the 8.1 HLA haplotype in patients with autoimmune myasthenia gravis and thymus hyperplasia

2004 ◽  
Vol 101 (43) ◽  
pp. 15464-15469 ◽  
Author(s):  
C. Vandiedonck ◽  
G. Beaurain ◽  
M. Giraud ◽  
C. Hue-Beauvais ◽  
B. Eymard ◽  
...  
Keyword(s):  
Myasthenia Gravis ◽  
Pleiotropic Effects ◽  
Thymus Hyperplasia ◽  
Autoimmune Myasthenia

scholarly journals Clonal expansions of CD4+ B helper T cells in autoimmune myasthenia gravis

2007 ◽  
Vol 37 (3) ◽  
pp. 849-863 ◽  
Author(s):  
Björn Tackenberg ◽  
Jens Kruth ◽  
Johanna E. Bartholomaeus ◽  
Kerstin Schlegel ◽  
Wolfgang H. Oertel ◽  
...  
Keyword(s):  
T Cells ◽  
Myasthenia Gravis ◽  
Helper T Cells ◽  
Autoimmune Myasthenia

Experimental neonatal autoimmune myasthenia gravis: an immunohistochemical, ultrastructural and electrophysiological study of the motor end-plate

1995 ◽  
Vol 132 (2) ◽  
pp. 97-104
Author(s):  
Naoko Tetsuo ◽  
Mitsuhiro Tsujihata ◽  
Akira Satoh ◽  
Toshiro Yoshimura ◽  
Tatsufumi Nakamura ◽  
...  
Keyword(s):  
Myasthenia Gravis ◽  
Electrophysiological Study ◽  
End Plate ◽  
Motor End Plate ◽  
Autoimmune Myasthenia

scholarly journals Pathological mechanisms in experimental autoimmune myasthenia gravis. II. Passive transfer of experimental autoimmune myasthenia gravis in rats with anti-acetylcholine recepotr antibodies.

1976 ◽  
Vol 144 (3) ◽  
pp. 739-753 ◽  
Author(s):  
J M Lindstrom ◽  
A G Engel ◽  
M E Seybold ◽  
V A Lennon ◽  
E H Lambert
Keyword(s):  
Myasthenia Gravis ◽  
Nerve Stimulation ◽  
Neuromuscular Transmission ◽  
Postsynaptic Membrane ◽  
Passive Transfer ◽  
Autoimmune Response ◽  
End Plate ◽  
Experimental Autoimmune Myasthenia Gravis ◽  
Autoimmune Myasthenia ◽  
Experimental Autoimmune

Passive transfer of experimental autoimmune myasthenia gravis (EAMG) was achieved using the gamma globulin fraction and purified IgG from sera of rats immunized with Electrophus electricus (eel) acetylcholine receptor (AChR). This demonstrates the critical role of anti-AChR antibodies in impairing neuromuscular transmission in EAMG. Passive transfer of anti-AChR antibodies from rats with chronic EAMG induced signs of the acute phase of EAMG in normal recipient rats, including invasion of the motor end-plate region by mononuclear inflammatory cells. Clinical, eletrophysiological, histological, and biochemical signs of acute EAMG were observed by 24 h after antibody transfer. Recipient rats developed profound weakness and fatigability, and the posture characteristic of EAMG. Striking weight loss was attributable to dehydration. Recipient rats showed large decreases in amplitude of muscle responses to motor nerve stimulation, and repetitive nerve stimulation induced characteristic decrementing responses. End-plate potentials were not detectable in many muscle fibers, and the amplitudes of miniature end-plate potentials were reduced in the others. Passively transferred EAMG more severely affected the forearm muscles than diaphragm muscles, though neuromuscular transmission was impaired and curare sensitivity was increased in both muscles. Some AChR extracted from the muscles of rats with passively transferred EAMG was found to be complexed with antibody, and the total yield of AChR per rat was decreased. The quantitative decrease in AChR approximately paralleled in time the course of clinical and electrophysiological signs. The amount of AChR increased to normal levels and beyond at the time neuromuscular transmission was improving. The excess of AChR extractable from muscle as the serum antibody level decreased probably represented extrajunctional receptors formed in response to functional denervation caused by phagocytosis of the postsynaptic membrane by macrophages. The amount of antibody required to passively transfer EAMG was less than required to bind all AChR molecules in a rat's musculature. The effectiveness of samll amounts of antibody was probably amplified by the activation of complement and by the destruction of large areas of postsynaptic membrane by phagocytic cells. A self-sustaining autoimmune response to AChR was not provoked in animals with passively transferred EAMG.

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