Answer:
B) FADH2 -- FMN of Complex I -- Fe-S of Complex II -- Q -- Fe-S of Complex III -- Cyt c -- Cyt a of Complex IV -- O2
Explanation:
FADH2 and NADH give their high energy electrons to the terminal electron acceptor molecular oxygen via an electron transport chain. As the electrons move through electron carriers of the electron transport chain, they lose their free energy. Part of the free energy of the electrons is used to pump the protons from the matrix into the intermembrane space. Therefore, part of the energy of electrons is temporarily stored in the form of a proton concentration gradient.
NADH gives its electrons to FMN of complex I while FADH2 gives its electrons to the Fe-S center of complex II. Both the complexes are oxidized by coenzyme (Q) which in turn reduces Fe-S centers of complex III. Cyt c of complex IV obtains electrons from complex III and passes them to CuA center, to heme "a" to heme "a3-CuB center" and finally to the molecular oxygen.
So, the compounds arranged with respect to the energy content of electrons in descending order are as follows: FADH2 -- FMN of Complex I -- Fe-S of Complex II -- Q -- Fe-S of Complex III -- Cyt c -- Cyt a of Complex IV -- O2.
In competition, males use feather color to warn potential rivals that they occupy a piece of territory.
C, because it protects the cell from the outside environment
0B)21% that’s your answer
Answer:
The correct answer is a. absent spinal reflexes below the level of injury.
Explanation:
Spinal shock strictly refers to the neurological condition that occurs immediately after a spinal cord injury, in which the loss of not only motor and sensory functions occurs, but also the abolition of all reflexes below the injury (reflexes of muscular or myotatic stretching and cutaneous reflexes). There is also flaccidity, loss of reflexes. It is characterized by hypotension associated with cervical or upper thoracic spinal injuries. This characteristic shock results from the lesion of the descending sympathetic pathway in the spinal cord, producing a loss of vasomotor tone and sympathetic innervation of the heart. This causes vasodilation of the affected area with accumulation of blood and a decrease in venous return to the heart as well as cardiac output.
