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When a muscle fiber is at rest, the tropomyosin-troponin complexes block the binding sites on the actin molecules and thus prevent the formation of linkages with myosin cross-bridges (fig 9.11a). As the concentration of calcium ions in the cytosol rises, however, the calcium ions bind to the troponin, changing its shape (conformation) and altering the position of the tropomyosin. The movement of the tropomyosin molecules exposes the binding sites

Myasthenia Gravis

In an autoimmune disorder, the immune system attacks part of the body. In myasthenia gravis (MG), that part is the nervous system, particularly receptors for acetylcholine on muscle cells at neuro-muscular junctions, where neuron meets muscle cell. People with MG have one-third the normal number of acetylcholine receptors at these junctions. On a whole-body level, this causes weak and easily fatigued muscles.

MG affect hundreds of thousands of people worldwide, usually women, beginning in their twenties or thirties and men in their sixties and seventies. The specific symptoms depend upon the site of attack. For 85% of patients, the disease causes generalized muscle weakness. Many people develop a characteristic flat smile and nasal voice and have difficulty chewing and swallowing due to affected facial and neck muscles. Many have limb weakness. About 15% of patients experience the illness only in the muscles surrounding their eyes. The disease reaches crisis level when respiratory muscles are affected, requiring a ventilator to support breathing. MG does not affect sensation or reflexes.

Until 1958, MG was a serious threat to health, with a third of patients dying, a third worsening, and only a third maintaining or improving their condition. Today, most people with MG can live near-normal lives, thanks to a combination of the following treatments:

• Drugs that inhibit acetylcholinesterase, which boosts availability of acetylcholine.

• Removing the thymus gland, which oversees much of the immune response.

• Immunosuppressant drugs.

• Intravenous antibodies to bind and inactivate the ones causing the damage.

• Plasma exchange, which rapidly removes the damaging antibodies from the circulation. This helps people in crisis.

on the actin filaments, allowing linkages to form between myosin cross-bridges and actin (fig. 9.11 b).

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