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The man whose brain injury sparked new interest in brain research was:
Phineas Gage
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~
an Antibody!
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~Just a girl in love with Shawn Mendes
B.False
Because starch is the storage form of glucose in plants, and glycogen as the storage carbohydrate in animals
Answer:
systemic lupus erythematosus
Explanation:
Systemic lupus erythematosus (SLE or just lupus) is a chronic inflammatory disease of autoimmune origin, the symptoms of which may appear in various organs slowly and progressively (in months) or more rapidly (in weeks) and vary with phases of activity and remission. Because it is a disease of the immune system, which is responsible for producing antibodies and organizing inflammation mechanisms in all organs, when a person has SLE they may have different types symptoms and various body locations. Some symptoms are general such as fever, weight loss, loss of appetite, weakness and discouragement. Others, specific to each organ such as joint pain, skin blemishes, pleural inflammation, hypertension, and / or kidney problems.
The main cause of this disease is the imbalance in the production of antibodies that react with proteins in the body itself and cause inflammation in various organs such as the skin, mucous membranes, pleura and lungs, joints, kidneys, etc.). Thus, we understand that the type of symptom a person develops depends on the type of autoantibody the person has, and that as the development of each antibody relates to the genetic characteristics of each person, each person with lupus tends to have clinical manifestations. specific and very personal (symptoms).
Autoantibodies are antibodies directed to the body's own cells and tissues. Normally, the immune system differentiates the body's own proteins from foreign proteins, forming antibodies only against those identified as potentially dangerous.
Answer and Explanation:
In rest, attraction strengths between myosin and actin filaments are inhibited by the tropomyosin. When the muscle fiber membrane depolarizes, the action potential caused by this depolarization enters the t-tubules depolarizing the inner portion of the muscle fiber. This activates calcium channels in the T tubules membrane and releases calcium into the sarcolemma. At this point, tropomyosin is obstructing binding sites for myosin on the thin filament. When calcium binds to the troponin C, the troponin T alters the tropomyosin by moving it and then unblocks the binding sites. Myosin heads bind to the uncovered actin-binding sites forming cross-bridges, and while doing it ATP is transformed into ADP and inorganic phosphate which is released. Myofilaments slide impulsed by chemical energy collected in myosin heads, producing a power stroke. The power stroke initiates when the myosin cross-bridge binds to actin. As they slide, ADP molecules are released. A new ATP links to myosin heads and breaks the bindings to the actin filament. Then ATP splits into ADP and phosphate, and the energy produced is accumulated in the myosin heads, which starts a new binding cycle to actin. Z-bands are then pulled toward each other, thus shortening the sarcomere and the I-band, and producing muscle fiber contraction.
