ビットコインカジノ オン リージェント ウィニペグ
Causes, ビットコインカジノ オン リージェント ウィニペグ. Most individuals with myasthenia gravis (MG) have no family history of MG and the disorder appears to occur spontaneously (sporadically) for unknown reasons. However, upwards of 5 percent of patients may have family members with MG or other autoimmune disorders. Individuals with MG have an increased frequency of certain genetically determined “human leukocyte antigens” (HLAs), suggesting that genetic predisposition may play some role. (HLAs are proteins that play an important role in the body’s immune system; they influence the outcome of transplantation and appear to affect an individual’s predisposition to certain diseases.) Other autoimmune diseases also appear to occur with increased frequency in individuals with MG, including thyroid disorders and systemic lupus erythematosus. These observations suggest that there is some genetic predisposition to MG which requires a trigger from the environment to cause the disease. Myasthenia gravis is caused by an abnormal immune reaction (antibody-mediated autoimmune response) in which the body’s immune defenses (i.e., antibodies) inappropriately attack certain proteins in muscles that receive nerve impulses. The areas of contact between nerve endings and skeletal muscle fibers are known as neuromuscular junctions. Nerve endings release a chemical (the neurotransmitter acetylcholine) that transmits impulses to muscle fibers, ultimately resulting in their contraction. However, in individuals with myasthenia gravis, antibodies are inappropriately directed against sites (receptors) on the surface of certain muscle cells that bind with the neurotransmitter acetylcholine (acetylcholine receptors). (These antibodies are known as “anti-acetylcholine receptor antibodies [anti-AChR].) The abnormal autoimmune response results in a decreased number of acetylcholine receptors, causing failed nerve transmission at certain neuromuscular junctions and associated deficiency or weakness of muscle contractions. Some patients with anti-AChR have antibodies that attack another protein called the muscle specific kinase protein (MuSK). These anti-MuSK antibodies also lead to a decrease in the number of acetylcholine receptors. Recently, antibodies to LRP-4 (lipoprotein receptor protein 4) were identified in patients without antibodies to MuSK or AChR. In five to eight percent of patients an antibody in the blood cannot be identified but patients have other tests consistent with myasthenia gravis. The specific cause of abnormal autoimmune responses in patients with myasthenia gravis is unknown. However, researchers suggest that the thymus has some role in this process. According to reports in the medical literature, up to approximately 75 percent of individuals with myasthenia gravis have distinctive abnormalities of the thymus. In most cases, there are increased numbers of cells in the thymus (hyperplasia). In addition, in about 10 percent of affected individuals, the thymus contains a tumor (thymoma) that is typically noncancerous (benign). However, some thymomas may be malignant. Researchers suggest that the thymus of MG patients does not appropriately eliminate cells that produce antibodies that attack body tissues. In the case of MG antibodies are produced that react against acetylcholine receptors, triggering the abnormal autoimmune response within the thymus. (A lymphoid tissue organ located behind the breastbone, the thymus plays an important role in the immune system beginning during early fetal development until puberty. It is important in the maturation of certain specialized white blood cells [T lymphocytes] that have several functions, including assisting in the recognition of certain foreign proteins [antigens] or binding to cells invaded by microorganisms and destroying them.) The abnormalities that lead to production of anti-MuSK antibodies is poorly understood and appears not to involve the thymus. OS: http://bitly/dacios Android: http://bit.ly/dacand., ビットコインカジノ オン リージェント ウィニペ