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So we are told in the passage that an ulcer causing bacteria produces a highly efficient urease, located on the outer portion of its cell wall, that converts urea to ammonia and carbon dioxide, and that this is the basis of a medical test in which the patient is given a drink of radioactive urea and then tested for the exhalation of radioactive CO2.
The question then asks : "Which of the following experiments would test the hypothesis that urease is necessary for the colonization of the bacteria in the stomach?"
I narrowed it down to these two responses:
A) Exposing ulcer patients to antibodies to urease
B) Exposing uninfected animals to a strain of the bacteria that lacks urease
I picked A, but the answer is B. Here is my issue: In B, we are told that the strain of bacteria "lacks urease". We are not told that it lacks the GENE for urease, therefore we can assume that it might be the case that the strain has the capacity to produce urease but it has simply not expressed the gene for whatever reason. Perhaps it only expresses it once it enters its host. Therefore, if you injected uninfected animals with a strain that "lacks urease", it is liable to turn on the expression of the latent urease gene that it may have, thus causing a false negative. In other words, you would conclude that urease was not necessary for colonization when, in reality, it was.
Answer choice A can be a legitimate test, however. It you successfully get antibodies onto the viral ureases in ulcer patients, you have effectively knocked out the effect of the urease while keeping everything else constant. Therefore, if the patient's ulcers subsided after the administration of these bacterial urease antibodies, then you could say without a doubt that the urease was in fact involved in the colonization of the stomach.
The only issue is that antibodies are made out of protein, which is digestible in the stomach. But if we can make the assumption that answer choice B implied that the strain lacked the gene for urease when it wasn't explicitly stated, then why can't we make the assumption that the antibody of answer choice A was modified or administered in such a way (perhaps as part of a drug cocktail that included pepsin inhibitors) that prevents it from being degraded?
I rest my case.
The question then asks : "Which of the following experiments would test the hypothesis that urease is necessary for the colonization of the bacteria in the stomach?"
I narrowed it down to these two responses:
A) Exposing ulcer patients to antibodies to urease
B) Exposing uninfected animals to a strain of the bacteria that lacks urease
I picked A, but the answer is B. Here is my issue: In B, we are told that the strain of bacteria "lacks urease". We are not told that it lacks the GENE for urease, therefore we can assume that it might be the case that the strain has the capacity to produce urease but it has simply not expressed the gene for whatever reason. Perhaps it only expresses it once it enters its host. Therefore, if you injected uninfected animals with a strain that "lacks urease", it is liable to turn on the expression of the latent urease gene that it may have, thus causing a false negative. In other words, you would conclude that urease was not necessary for colonization when, in reality, it was.
Answer choice A can be a legitimate test, however. It you successfully get antibodies onto the viral ureases in ulcer patients, you have effectively knocked out the effect of the urease while keeping everything else constant. Therefore, if the patient's ulcers subsided after the administration of these bacterial urease antibodies, then you could say without a doubt that the urease was in fact involved in the colonization of the stomach.
The only issue is that antibodies are made out of protein, which is digestible in the stomach. But if we can make the assumption that answer choice B implied that the strain lacked the gene for urease when it wasn't explicitly stated, then why can't we make the assumption that the antibody of answer choice A was modified or administered in such a way (perhaps as part of a drug cocktail that included pepsin inhibitors) that prevents it from being degraded?
I rest my case.
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