PT141.S4.Q20 > Question

SECTION 1 · rc

PASSAGE 1

Question 1 Question 2 Question 3 Question 4 Question 5 Question 6 Question 7

PASSAGE 2

Question 8 Question 9 Question 10 Question 11 Question 12 Question 13 Question 14 Question 15

PASSAGE 3

Question 16 Question 17 Question 18 Question 19 Question 20 Question 21

PASSAGE 4

Question 22 Question 23 Question 24 Question 25 Question 26 Question 27

SECTION 2 · lr

Question 1 Question 2 Question 3 Question 4 Question 5 Question 6 Question 7 Question 8 Question 9 Question 10 Question 11 Question 12 Question 13 Question 14 Question 15 Question 16 Question 17 Question 18 Question 19 Question 20 Question 21 Question 22 Question 23 Question 24 Question 25

SECTION 3 · rc

PASSAGE 1

Question 1 Question 2 Question 3 Question 4 Question 5 Question 6 Question 7

PASSAGE 2

Question 8 Question 9 Question 10 Question 11 Question 12 Question 13 Question 14

PASSAGE 3

Question 15 Question 16 Question 17 Question 18 Question 19 Question 20

PASSAGE 4

Question 21 Question 22 Question 23 Question 24 Question 25 Question 26 Question 27

SECTION 4 · lr

The author concludes that glutamate leaking from damaged or oxygen-starved nerve cells is a cause of long-term brain damage resulting from strokes. This is based on the fact that in a study of stroke patients, those who showed deterioration of nerve cells in the brain also exhibited the highest levels of glutamate in the blood. In addition, glutamate can kill surrounding nerve cells if it leaks from damaged or oxygen-starved nerve cells.

The author assumes that the glutamate observed in the blood leaked from damaged or oxygen-starved nerve cells (as opposed to originating from another source). The author assumes there’s no other explanation for the continued deterioration of nerve cells in the patients observed.

If anything, this might undermine the argument by raising the possibility that some other neurotransmitter besides glutamate might be the cause of damaged nerve cells in stroke patients.

The presence of other chemicals in blood does not help establish a connection between glutamate and the damaged brain nerve cells in stroke patients. We want to know that the glutamate leaked from damaged/oxygen-starved nerve cells. (B) doesn’t establish this.

We care about where the glutamate in the blood came from, not whether there are other kinds of chemicals that could come from damaged/oxygen-starved cells.

This strengthens by establishing that the glutamate observed in the blood of stroke patients must come from damaged/oxygen-starved nerve cells. This makes the premise concerning damage/oxygen-starved nerve cells more supportive of the conclusion.

We want to know that the glutamate leaked from damaged/oxygen-starved nerve cells. (E) doesn’t establish this. It simply tells us that nerve cells can leak glutamate without destroying themselves. But did the glutamate leak from damaged cells? We don’t know.

PrepTest 141 - Section 4 - Question 20

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