<span>There are numerous proteins in muscle. The main two are thin actin filaments and thick myosin filaments. Thin filaments form a scaffold that thick filaments crawl up. There are many regulatory proteins such as troponin I, troponin C, and tropomyosin. There are also proteins that stabilize the cells and anchor the filaments to other cellular structures. A prime example of this is dystrophin. This protein is thought to stabilize the cell membrane during contraction and prevent it from breaking. Those who lack completely lack dystrophin have a disorder known as Duchene muscular dystrophy. This disease is characterized by muscle wasting begininng in at a young age and usually results in death by the mid 20s. The sarcomere is the repeating unit of skeletal muscle. 
Muscle cells contract by interactions of myosin heads on thick filament with actin monomers on thin filament. The myosin heads bind tightly to actin monomers until ATP binds to the myosin. This causes the release of the myosin head, which subsequently swings foward and associates with an actin monomer further up the thin filament. Hydrolysis and of ATP and the release of ADP and a phosphate allows the mysosin head to pull the thick filament up the thin filament. There are roughly 500 myosin heads on each thick filament and when they repeatedly move up the thin filament, the muscle contracts. There are many regulatory proteins of this contraction. For example, troponin I, troponin C, and tropomyosin form a regulatory switch that blocks myosin heads from binding to actin monomers until a nerve impulse stimulates an influx of calcium. This causes the switch to allow the myosin to bind to the actin and allows the muscle to contract. </span><span>
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Mastication is just a fancy way to say chewing. Since nothing chemical is going on and the food is just being chewed, the answer is physical. 
        
             
        
        
        
Fertilization, mitosis, meiosis, birth
        
             
        
        
        
The right answer is A) Trisomy 
Aberrant karyotypes containing an abnormal number of chromosomes are known in the human species. The best-known (and most common) chromosomal abnormality is trisomy 21, which is responsible for Down syndrome (mongolism). There are others such as Turner syndrome (woman with a single X chromosome) or Klinefelter syndrome (man XXY).
These abnormalities originate from the non-disjunction of the chromosomes of a pair of homologues during metaphase I of meiosis. At the end of division I, a daughter cell contains the two chromosomes of the pair considered and the other cell does not contain a chromosome of this pair. A similar result can be obtained during a bad distribution of chromatids during anaphase II.
After fertilization from a gamete of this type, a trisomy or a monosomy is obtained.