Blueprint Diagnostic Bio/BioChem Passage 1

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MP 275: Blueprint Diagnostic Bio/BioChem Passage 1

Session 275

Come listen to our breakdown of the first Bio/Biochem MCAT diagnostic passage. We’re joined by Evan from Blueprint MCAT. He also shares some things you need to think about when highlighting science sections as well as some tips to get better on the MCAT.

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Listen to this podcast episode with the player above, or keep reading for the highlights and takeaway points.

[01:37] Preparing Yourself for the Bio/Biochem Section

After the CARS section, Bio/Biochem comes next which typically happens after lunch. Evan says it can be very quick and restful, and it will allow you to come back in with a lot of energy. But it can also be tempting to overthink and go back and think about what you could have done in the last section. And this is not helpful at all.

Make sure that you’re always forward thinking. Be conservative with what you’re eating. Eat something you’ve had several times before. Don’t try out some new recipe on the day of the test and risk some GI issues.

Go to your space of solace before you go back to the storm. It’s okay to take a slightly shorter lunch. And then maybe you have a couple of minutes left on your lunch break where you’re just sitting at the desk where it’s quiet. There’s no one else rustling or nervously chatting and you can just have a second yourself.

[04:32] Highlighting the Science Sections

While the cadence is pretty similar in terms of going paragraph by paragraph, Evan recommends you focus your highlighting a little differently.

'In CARS, there's absolutely no outside knowledge that's tested on. In the science sections, in the bio/biochem, thre are lots of outside science knowledge that you're tested in.'Click To Tweet

And so, you still want to incorporate the key ideas. If there’s an experimental style passage, including the results and the hypothesis can be helpful.

You may also highlight the things that you know are MCAT-testable. They’re not going to ask something that’s not required knowledge. But if they draw a connection between this new passage information and amino acid composition, or this passage information and enzyme kinetics – these are possible things for them to test on.

[05:53] Passage 1 (Questions 1 – 5)

Paragraph 1

Cataract generation triggered by lens injury is considered to be driven by the action of the proliferation and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) as a complication of injury and inflammation. The epithelium quickly expands, creating a hundredfold increase in the number of cells. In response to trauma, irritation or surgery, cytokines and growth factors increase in the aqueous humor and stimulate LECs to proliferate and undergo EMT. This response is significantly diminished in organisms where EMT is inhibited by the inactivation of transforming growth factor β (TGFβ), especially TGFβ2, the major isoform in the aqueous humor.


Evan says we don’t need to have a deep anatomical or physiological understanding of what lens epithelial cells do. And so, the beginning part tells us what happens – what’s causing this cataract generation and the definition of that. Then there’s a part that focuses the inactivation of this TGF beta, and specifically beta two that that’s going to help.

[09:00] Paragraph 2

During the process of EMT, LECs undergo cytoskeletal rearrangement, with the addition of a large amount of extracellular matrix proteins, such as collagen and fibronectin. In anterior cataracts, the proliferation and EMT of LECs in situ leads to the formation of opaque plaques just beneath the lens anterior capsule.


Things worth highlighting here are “extracellular matrix proteins” as well as the insight to formation of plaques.

[10:31] Paragraph 3

The production of TGFβ is catalyzed by histone deacetylase-1 (HDAC1). HDAC1 removes acetyl groups from N-acetyl lysine groups on histone. Once synthesized, TGFβ is secreted by activated monocytes in the aqueous humor. Since monocytes mediate almost 80 percent of the local TGFβ, scientists tested the theory that TGFβ is responsible for the monocytes’ impact on LEC production. The number of LECs expressing MIB1, a nuclear protein, was utilized as a measure of LEC proliferation and expected EMT.


We can find any cause and effect relationships or any hypotheses they’re making here.

[12:47] Paragraph 4

Experiment 1

After simulated injury, monocyte/LEC cultures were treated with an antibody that lyses all but a negligible fraction of available monocytes; a division of these cultures was also treated with a TGFβ agonist. A second set of cell cultures was treated with antagonists of epithelial cell TGFβ receptors TGFBR1 and TGFBR2 (Table 1).

Table 1 Results of the study on monocyte lysis, TGF agonist, and TGF receptor antagonists


It’s telling us in words, what we’re seeing in the table. And for a lot of students, dissecting these tables and figures can be really difficult.

Sometimes, you won’t get any questions about some of the tables or figures. For that reason, Evan usually spends just five or 10 seconds glancing at each table. 

And so, we look at what’s happening when we have either the antibody present that’s an anti monocyte antibody when it’s present, or it’s not present. We’re also looking to see what happens when we have the antagonist present, or when we have the antagonist present or absent.

[16:15] Paragraph 5

Experiment 2

In an effort to determine whether MIB1 is associated with LEC regulation, LEC density was assessed during the course of epithelial growth in wild-type and MIB1-null cell cultures (Figure 1).

Figure 1 Growth of LECs after an injury in both wild-type and MIB1-null strains


Here, we’re looking at the LEC density.

[18:12] Question 1

The catalyst for TGFβ production most likely plays a direct role in:

A.gene silencing.

B.ribosomal inactivation.

C.transfer of an acetyl group from acetyl-CoA.

D.gene activation.

Thought Process:

First, figure out what is a catalyst for TGFβ production. Paragraph 3 in the passage mentions that the production of TGFβ is catalyzed by histone deacetylase-1 (HDAC1).

The second thing they tell us is that it’s doing some of these chemical modifications to histones. Histones are protein complexes, which are important for is this DNA packet. There are modifications on these histones and this is where a little bit of that outside knowledge does come into play here.

Lysine is one of our amino acids that we want to be familiar with. When it is acetylated, lysine is neutrally charged, it doesn’t have any charge at all. When we deacetylate lysine, it gets a positive charge. DNA is negatively charged.

And so, once that lysine gets deacetylated, lysine and DNA come together since positive and negative opposites attract. After we deacetylate that lysine group, the DNA gets stuck to the histone which makes it inaccessible to our transcription machinery or RNA polymerase, that ends up causing this gene silencing.

If the RNA polymerase can’t get there to that gene anymore, we have no way to transcribe it, and therefore, it’s going to turn off transcription.

Correct Answer: A

[24:20] Question 2

Monocytes, in conjunction with epithelium-derived factors, can act to facilitate which biological process?

A.Fatty acid oxidation


C.Lipid synthesis

D.Host immune response

Thought Process:

Monocytes are white blood cells that has to do with immune response. And so this question has little to `do with the passage.

Correct Answer: D

[25:38] Question 3

After injury-induced cataract formation has begun, which of the following are LEAST likely to be found in nearby monocytes?

A.TGFβ transporters

B.TGFβ receptors

C.Tight junctions


Thought Process:

White blood cells are important for our immune system. They’re zipping around the circulatory system around our blood until the lymph system deals with infection. So if we’re talking about just normal monocytes, they’re probably unlikely to have tight junctions. Tight junctions make them anchored down in place, so they can’t move and they’re stuck. And that’s the opposite of the function of monocytes.

Correct Answer: C

[29:55] Question 4

The structure of lysine is shown below.

This molecule is best described as:


B.polar and basic.

C.nonpolar and not aromatic.


Thought Process:

B and C are two opposites, saying one thing polar and one saying nonpolar. Polar molecule is one where you have a lot of electrons in one part of the molecule, and not a lot of electrons and other parts. There’s a difference in that electron distribution. There are some atoms that get a lot of electrons and some get very few, Whereas nonpolar, they’re very evenly spread out.

It’s not evenly distributed, which means that it’s true that it’s polar. Therefore, we can definitely rule out C nonpolar here.

Hydrophobic things have really long chains. But it has to be a chain that’s made up of carbons and hydrogens since carbon and hydrogen are very nonpolar. This thing has a lot of polar groups, which are not hydrophobic. And this is why B ends up being an answer.

Correct Answer: B

[34:24] Question 5

Given the findings in the passage, which additional result most strongly indicates that the TGFBR1 and TGFBR2 receptors regulate TGFβ-dependent epithelial proliferation?

A.Treatment with TGFBR1 receptor agonist resulted in reduced MIB1 detection.

B.Expression of TGFBR1 and TGFBR2 was observed to increase during intervals of heightened epithelial cell proliferation.

C.Genes for several different receptor subtypes were found in untreated epithelium.

D.Treatment with new TGFBR3 receptor antagonists decreased the number of MIB1-positive cells.

Thought Process:

If we rephrase this question, it would be: what result would most strongly indicate that these two receptors TGFBR1 and TGFBR2 regulate TGFβ-dependent epithelial proliferation And so, you want to look at the result indicating that when we change the receptors and the receptors are there, the proliferation happens. And when the receptors are gone, no proliferation happens.

A – We actually never mentioned the receptor agonist. It never makes any mention of the receptors or proliferation. So A is out because it’s not even answering the question.

B – You could see that it’s got the right stuff with TGFBR1 and TGFBR2 and proliferation. And so, answer choice B is the only one that even attempts to answer the question by using these three pieces of information. Now, we want something that’s making some type of comparison between the three of them, and B is the only one that actually does that for us.

Correct Answer: B

[40:29] Final Thoughts

Finally, Evan can’t stress enough the importance of doing practice tests and getting used to doing this practice and very comfortable doing that.

'What matters is that you're learning from any mistakes you make.'Click To Tweet

If you do 10 practice tests before test day, Evan guarantees you will come across passages in the past that are just as difficult, if not more difficult than this one.

Just like any other skill that you’re trying to develop, just practicing it and trying to get incrementally better before test day is the best way to avoid a bad outcome.


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