Answer:
Blood sugar, also known as blood glucose, comes from the food you eat. Your body creates blood sugar by digesting some food into a sugar that circulates in your bloodstream. Blood sugar is used for energy. The sugar that isn't needed to fuel your body right away gets stored in cells for later use.
Explanation:
It wouldnt survive because it has a different type of soil and it wouldnt be used to it so it would probably die because it couldnt adapt to the different climate in time, as well.
The answer is Klinefelter syndrome.
Nondisjunction disorders are conditions resulting from an unbalanced distribution of chromosomes. In the case of Klinefelter syndrome, the sex chromosomes are affected. Rather than having an XX for female or an XY for male people with Klinefelters have either XXY or XYY.
Non polar molecule move across a membrane through simple diffusion, when moving up their concentration gradient. Simple diffusion involves movement of molecules through a membrane without the help of integral membrane protein. These molecules are driven by the force of diffusion. This is different from facilitated diffusion where molecules only move with the aid of integral protein in the membrane.
<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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