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Tutor profile: Farah A.

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Farah A.
Teaching Assistant at UC Berkeley for 2 years
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Questions

Subject: R Programming

TutorMe
Question:

How do I make a beautiful, publishable table in R?

Inactive
Farah A.
Answer:

My favorite tool is kable() from the knitr package and kable_styling() from the kableExtra package. They take your regular base R table and upgrade it so it's truly beautiful and customizable. There are a TON of options I won't list, but below is my go-to code for any table I'm trying to make beautiful. # Install the packages if you don't already have them install.packages("knitr") install.packages("kableExtra") # Calling libraries library(knitr) library(kableExtra) # Upgrading your table kable(regular_table, booktabs = TRUE) %>% # this takes your regular base R table and is the first step in upgrading it. My regular_table has its own row and column names, but you can also add row and column names in kable() kable_styling(latex_options = "striped") %>% # kable_styling() is the key to global customization of your table. I always use "striped" for my latex_options, but there are MANY different choices add_indent(c(3, 4, 6, 7, 9, 10, 11)) %>% # add indentation to row names to make your table more readable add_header_above(c(" " = 2, "Model 1" = 1, "Model 2" = 1)) %>% # add headers above columns row_spec(0, bold = TRUE) %>% # bold, underline, or italicize rows add_footnote("Look at this beautiful table!") # add footnotes to your table The code above is just the tip of the iceberg. With kableExtra, you can color, add links, change fonts, specify table location, and so much more. Here's a great article that goes more into depth with all the different things you can do in kableExtra: https://cran.r-project.org/web/packages/kableExtra/vignettes/awesome_table_in_html.html

Subject: Biology

TutorMe
Question:

Glycogen storage disease type 0 (GSD-0) is a rare disease caused by an inactive glycogen synthase enzyme. Type II diabetes is a more common disease (1 in 10 people in the US) causing “insulin resistance”, where the body’s insulin receptors don’t respond to insulin normally. Both diseases cause high glucose levels after feeding. How would you differentiate between the two diseases? A. GSD-0 would cause dysregulation of homeostasis, but type II diabetes would not. B. GSD-0 would cause a depletion in stored glycogen, but type II diabetes would not. C. GSD-0 would cause excess glucose to be secreted into the urine, but type II diabetes would not. D. GSD-0 would have normal RTK activity, but type II diabetes would not. E. People with GSD-0 would have suppression of appetite after feeding, but type II diabetes would not.

Inactive
Farah A.
Answer:

This seems like a long, complicated question! But as with all multiple-choice questions, let's take it step by step. Let's start with the question: "Glycogen storage disease type 0 (GSD-0) is a rare disease caused by an inactive glycogen synthase enzyme. Type II diabetes is a more common disease (1 in 10 people in the US) causing “insulin resistance”, where the body’s insulin receptors don’t respond to insulin normally. Both diseases cause high glucose levels after feeding. How would you differentiate between the two diseases?" Ok, let's look at the first disease: GSD-0 causes an inactive glycogen synthase enzyme. Remember that glycogen is the storage molecule of glucose in the body, so all the extra glucose we get from our food is converted into glycogen that we can use later. This disease causes an inactive glycogen synthase enzyme. Let's try to deduce what the function of this enzyme is: well, it's a "synthase", which should remind you of the word "synthesizing" which means making something. So here, this enzyme likely makes glycogen from glucose. This disease causes an inactive glycogen synthase enzyme, so we likely have a bunch of excess glucose floating around the blood in this disease. Now, let's look at the second disease: Type II diabetes causes the insulin receptor to be unresponsive to insulin. Remember that insulin is the hormone released after meals, and its goal is to lower the level of glucose in the blood. Incidentally, it lowers the level of glucose in the blood by making glycogen through glycogen synthase. This means that in this disease, we also have a bunch of excess glucose floating around in the blood. But notice the difference, this disease has an active glycogen synthase enzyme, but the signal (insulin + insulin receptor) that activates the glycogen synthase enzyme is faulty. Also, remember that the insulin receptor is a "receptor tyrosine kinase" or RTK, an important class of receptors in the body. Ok, now that we've understood both diseases, let's go through the answers one by one. "A. GSD-0 would cause dysregulation of homeostasis, but type II diabetes would not." Homeostasis is a dynamic balance in the body for specific functions like body temperature, pH, and blood glucose. Here, both diseases will cause high levels of glucose in the blood, so they will both disrupt homeostasis. So, this answer is incorrect. "B. GSD-0 would cause a depletion in stored glycogen, but type II diabetes would not." Usually, the body depletes glycogen stores (i.e. breaks down glycogen to glucose) when the level of glucose is LOW in the blood, for example after fasting. Here, both diseases will cause high levels of glucose in the blood, so they will definitely NOT deplete glycogen stores. "C. GSD-0 would cause excess glucose to be secreted into the urine, but type II diabetes would not." As a response to high levels of glucose in the blood, our body often dumps excess glucose into the urine. So for both diseases, we are likely to find glucose in the urine. Fun fact: before we had tests for GSD-0 and diabetes, doctors used to taste patients' urine to see if it was sweet to determine whether the patient had a disorder of glucose regulation. That's REAL dedication! "D. GSD-0 would have normal RTK activity, but type II diabetes would not." As we mentioned, the insulin receptor is a receptor tyrosine kinase or RTK. We know that type II diabetes has a faulty insulin receptor, but GSD-0 has a faulty glycogen synthase, so we would expect RTK activity to be normal in GSD-0, but abnormal (likely reduced) in type II diabetes. This is starting to look like the right answer! But let's read the last choice to be sure. "E. People with GSD-0 would have suppression of appetite after feeding, but type II diabetes would not." This doesn't seem relevant to anything we talked about, so it's not the right answer. That gives us the correct answer choice of D!

Subject: Statistics

TutorMe
Question:

Five students, Adnan, Beth, Chao, Dan, and Edmund are to be arranged in a line. How many arrangements are possible if Beth is not allowed to stand next to Dan?

Inactive
Farah A.
Answer:

First, let's figure out the possible recombinations if we had no restrictions. We have 5 spaces, and 5 people to fill them: _ _ _ _ _ For the first space, we have 5 possibilities of students to pick: 5 _ _ _ _ For the second space, we have 4 possibilities, since we already took out one student for the first space: 5 4 _ _ _ You may have already spotted the pattern for the remaining spots: 5 4 3 2 1 This represents the number of possibilities for each space working from the left. Now what do we do with all these numbers? Well, think about what we are saying writing down these numbers: "There are 5 possibilities for the first space AND 4 possibilities for the second space AND 3 possibilities for the third space..." With that, we recall the cardinal rule of statistics: AND means multiply; OR means add. So here, we're going to multiply all these numbers to get: 5 x 4 x 3 x 2 x 1 = 5! = 120 possible arrangements. We would have stopped here if there were no additional restrictions, but we're told that Beth is not allowed to stand next to Dan. So, let's subtract all the different arrangements where Beth IS standing next to Dan, to get the number of arrangements where Beth is NOT standing next to Dan. To find out the number of arrangements where Beth is standing next to Dan, let's consider Beth and Dan as one unit, which means we have 4 possible spaces now: __ _ _ _ Using the principles from before, we realize that this is just 4 x 3 x 2 x 1 = 4! = 24. But wait! There are 2 possibilities within this arrangement: Beth first then Dan OR Dan first then Beth. Notice that we used OR here, so the number of arrangements where Beth is standing next to Dan is 24 + 24 = 24 x 2 = 48. Finally, we subtract the total possible arrangements (120) by the total possible arrangements where Beth is standing next to Dan (48) to get our answer: 120 - 48 = 72 possible arrangements where Beth is NOT standing next to Dan.

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