- Joined
- Jun 23, 2010
- Messages
- 11,808
- Reaction score
- 2,807
This thread shall serve as the site for discussion of questions from the AAMC Self-Assessment in MCAT Biological Sciences.
More Hb means more O2 can bind. Fully oxygenated blood is HbO8. Btw,,,,I got that acholinesterace blocker question wrong too and my ans was same as yours.Biology #59: http://puu.sh/cg05J.png
Can someone explain why Hb is involved to regulate oxygen perfusion?
Ahh so I guess in this question, Hb refers to the perfusion aspect. Didn't occur to me at the time.More Hb means more O2 can bind. Fully oxygenated blood is HbO8. Btw,,,,I got that acholinesterace blocker question wrong too and my ans was same as yours.
View attachment 184901 View attachment 184902 View attachment 184903 someone please explain why it is B? it says NaOH will make a salt COO- group but it says the IR has no peak at 1700. unless it's because the carbonyl oxygen in COOH is more around 1720? that would be very specific though considering there's a range or IR measurements for ketones and COOH
http://www.chem.ucla.edu/~webspectra/irtable.html
I'm also curious about Oh-Gee's question (# 56 in the organic chemistry self-assessment). How can compound C be the result of NaOH hydrolysis of an ester when that would yield a carboxylate ion, which has a C=O bond and DOES have a peak around 1700, even though figure 1 indicates there was no peak found at 1700.
View attachment 186680
Looks like this was never answered but I'm wondering the same thing. Anyone have any ideas on this?Biology #45:
Does acceptance of the mechanism of self-tolerance described in Hypothesis 1 rule out acceptance of the mechanism described in Hypothesis 2?
C. No; suppressor T cell formation can only occur after clonal deletion has occurred
D. No; clones of self-reactive lymphocytes not destroyed by clonal deletion may e controlled by suppressor T cells
Why is C correct and not D?
thanks for replying to me on the jan 10th threadLooks like this was never answered but I'm wondering the same thing. Anyone have any ideas on this?
Here's the relevant passage info:
Hypothesis 2
In addition to effector lymphocytes (such as helper T cells and cytotoxic T cells) that selectively attack and destroy antigens, the body contains other lymphocytes (suppressor T cells) that prevent this destruction by selectively limiting the action of the effector cells. Normally, a regulatory balance is maintained between effector and suppressor T cells. However, when this balance is disturbed (for example, by loss or inactivation of suppressor-cell clones), an autoimmune disease may result.
What does your question 26 and 27 say? I have the paper version that seems to have different questions than some of the posts here.and my question is about Bio self assessment question 26 and 27 >.< anyone help me with that please?
Thanks for your reply. I see what you are saying, it seems pretty straight forward. But I'm still wondering why can't suppressor T cells act as a check on clonal deletion, regulating those self-reactive clones that should have been destroyed but somehow "slipped through"?thanks for replying to me on the jan 10th thread
as for #45 I think the answer is C because "Normally, a regulatory balance is maintained between effector and suppressor T cells. However, when this balance is disturbed (for example, by loss or inactivation of suppressor-cell clones), an autoimmune disease may result"
which tells that suppressor T cells forms only when ( clonal deletion has occured) ... which matches hypotheses 1 because " During this time, the process of clonal deletion destroys any newly formed groups of lymphocytes that might attack the body's own tissues. If clonal deletion of such lymphocytes does not occur or is hindered, these lymphocytes will incorrectly recognize a specific body tissue as foreign or non-self, and begin to destroy it."
Thanks for your reply. I see what you are saying, it seems pretty straight forward. But I'm still wondering why can't suppressor T cells act as a check on clonal deletion, regulating those self-reactive clones that should have been destroyed but somehow "slipped through"?
No problem ... I got 26 but 27 still do not get it ... it is the same questions u haveWell I guess the key I have to the paper version is wrong then, thanks!
Did you ever figure out #26 and #27? If not let me know if your #26 and #27 are the same as mine:
View attachment 187940
I got them right so can explain if needed.
thank you so much that really helped! i get it nowLast paragraph of the passage states, "Dietary restriction [aka fasting]... increases the maximum life span of rats from 125 to 185 weeks." So the fasting group should have the longer survivorship curve with a maximum point around 185 weeks. C is the only plot that reflects this info given in the passage.
View attachment 187942
Anyone understand 41?
I get how B is plausible (its what I originally thought) but the passage doesn't indicate that, and I didn't know how to rule out D either so I went conservative and picked A.
View attachment 187952
The passage states the test strain needs histidine in the culture medium to survive. So when the test strain is placed on a histidine-deficient culture they should not grow. If they do grow it means they have mutated, likely due to mutagen exposure. This is basically how the Ames test works. See this article for more.Anyone understand 41?
I get how B is plausible (its what I originally thought) but the passage doesn't indicate that, and I didn't know how to rule out D either so I went conservative and picked A.
View attachment 187952
A assumes that w/o carcinogen, the bacterium is there but not visible; however, the passage specifically says that the "test strains do not survive" in His- medium (also ignore wild-type part since Ames test uses test strains according to passage). hence a is false
B is true because before/after carcinogen, medium is still same but bacterial growth increases - hence a previous disability is corrected
The passage states the test strain needs histidine in the culture medium to survive. So when the test strain is placed on a histidine-deficient culture they should not grow. If they do grow it means they have mutated, likely due to mutagen exposure. This is basically how the Ames test works. See this article for more.