Less freshwater! Good luck!
Answer:
The correct answer is ''loss of acetylcholine receptors in the end-plate membrane.''
Explanation:
Myasthenia gravis represents a human autoimmune disease. The neuromuscular junction abnormalities that occur in this disease are due to antibody-mediated processes. A reduction in the number of functional acetylcholine receptors on the postsynaptic membrane was established to contribute to the physiological abnormalities of myasthenia gravis. The reduction in receptors is due to immunological alterations directed against the acetylcholine receptor. Normally, when acetylcholine binds to its receptor, it opens allowing the rapid entry of cations, especially sodium. With this, the depolarization of the postsynaptic region of the muscle fiber occurs. Although acetylcholine is normally released in myasthenia gravis, it is not capable of causing an action potential in the muscle sufficient to initiate or weaken contraction. In patients with myasthenia gravis, failure to activate muscles is responsible for myasthenic fatigue. Most patients have elevated serum titers of antireceptor antibodies, which in turn accelerate receptor degradation.
The scrotum reacts to temperature. When it is cold, the scrotum shrinks, pulling the testes against the body to keep them warm. When it is hot, the scrotum relaxes, lowering the testes away from the body. This contractile ability of the scrotum can either raise or lower the temperature of the testes by a few degrees, ensuring that the optimum temperature for sperm production is maintained.
You didn’t list any statements but the answer should include his contributions to being the father of genetics.
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