Answer: tympanic membrane
Answer:
Different flavors of a gene are called alleles
Answer:
Mutations of enzymes involved in nucleotide excision repair.
Explanation:
- Xeroderma pigmentosum is a genetic disorder and the person suffering from this disorder is sensitive to ultraviolet light due to the disability of the enzymes involved in nucleotide excision repair which prevents DNA damage caused by ultraviolet light.
- Thus, the individuals are sensitive to the exposure of UV and suffer severe problems when exposed to sunlight.
- The major cause of the disorder is the inability to repair DNA damage caused by exposure to sunlight due to the mutation in an enzyme involved in nucleotide excision repair.
- Nucleotide excision repair is a DNA repair process that can excise out single-stranded DNA that is damaged by UV.
- UV exposure leads to the addition of bulky adducts in the DNA known as thymine dimers. The enzymes of NER are involved in the removal of these adducts by excising out a segment of DNA that contains such lesions.
- However, in the case of XP, the mutations make this repair system non-functional or partially functional and thus, the individual becomes highly sensitive to UV exposure.
Ch.5: Synaptic Activity
<span>Introduction<span>Otto Loewi studied the heart of the frog, which-like our own hearts- is supplied by two different peripheral nerves. One, the sympathetic nerve, excites the heart and makes it beat more rapidly; the other , the vagus, shows the heart. The problem was to discover the mechanism by which the effects of nerve impulses in either of these nerves are communicated to the heart muscle. Many believed that the electrical nerve impulse spread from the nerve to the muscle as an electrical wave; Loewi thought otherwise.Loewi tested two isolated frog hearts, one with the sympathetic and vagus nerves intact, the other with the nerves removed. A small tube containing salt water was placed in the heart with the nerves attached. When he stimulated the vagus nerve, the heartbeat slowed, as expected. Then he took salt solution that had been in the stimulated heart and placed it inside the heart without nerves. It too immediately slowed- exactly as if its own (missing) vagus nerve had been stimulated.He repeated the same procedure, stimulating the sympathetic nerve instead. The effect was again as if the nerve of the denervated heart itself were stimulated: the denervated heart began beating faster. These results could not be explained electrically; the nerves must have secreted chemicals into the salt solution that directly affect the muscles of the denervated heart.In one simple experiment, Loewi had demonstrated three important findings: (1) that communication at the gap between nerve and heart muscle was chemical, (2) that each nerve released a different transmitter substance, and (3) that it was the characteristics of the different transmitter substances that caused the increase or decrease in heart rate. This was the first direct experimental evidence of the action of chemical neurotransmitters.<span>Like the junction between nerve and heart muscle that Loewi studied, nerve cells communicate with each other at special junctions called synapses. </span></span></span><span><span> thanks and i hope this helps you.....
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The dependent variable would be the heart rates of her classmates.
