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I think the answer is NADH
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, electricity is just electrons (sub atomic particles) moving through a conductor. Light is also just subatomic particles moving through a conductor (1.e. transparent medium) and both are part of the electromagnetic spectrum.
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Elastic fibers are made of elastin and microfibrils, that are elastic protein structures. The proteins can be stretched and resume normal shape. These fibers are found in parts of the body such as arteries, skin, lungs, connective tissue and heart that require some stretching. Marfan syndrome affects the elastic connective tissues causing symptoms like dilation of the aorta that doesn't resume normal lumen diameter (aortic aneurysm), and curving of the spine (scoliosis).
The lungs are unable to stretch and resume shape normally and this affects the respiratory system. The subjects will suffer from shortness of breath, wheezing and chest pain.
The sheath/endoneurium of neurons is connective tissue. This part of a neuron allows signals to travel effeciently along the axon of the neuron. This means that a person with Mafran syndrome has a slower response to stimuli that ordinary persons.
Hypothalamus is a part of the brain that links the nervous system to the endocrine system via the pituitary gland. It helps maintain the internal environment constant by regulating major processes in the body such as the heart rate and the body temperature. It is therefore, both a neural and endocrine organ.
The correct answer is the last statement.
If the regulatory serine is mutated to alanine, then acetyl-CoA carboxylase will get activated spontaneously and will produce malonyl-CoA. The increased concentrations of malonyl-CoA will obstruct the oxidation of fatty acids by preventing the entry of fatty acids into the mitochondria.
It is because the AMP-activated protein kinase phosphorylates the serine residues of acetyl-CoA carboxylase to inactivate it. If a mutation occurs in such residues, then the AMPL cannot phosphorylate acetyl-CoA carboxylase and this enzyme will get activated spontaneously.
In such a situation, there will be more than sufficient production of malonyl-CoA, which will inhibit the admittance of more fatty acid getting inside the mitochondria; this will indirectly prevent the oxidation of fatty acids.
