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I just happen to read the thread discussing the new moderators' educational backgrounds and after painstaking reading, interpreting/misinterpreting everything in that general field of study....I found a question to make sure you guys never get rusty! p.s I didn't create this question.

organic chemistry......

Given the reaction: C2H2 + 2H2 --> C2H6

This reaction represents:

A. Substitution
B. Addition
C. Esterification
D. Saponification
 
You mentioned supercompensation in terms of bodybuilding contests. Would this be utilized within that brief moment say 24 HRS before stepping onstage and is responsible for that extremely full and hard muscle bellies?

Also one would experience in a typical carb cycle following their days of depletion and subsequent refeeding the swelling sensation...is this effect related to the supercompensation mechanism achieved with precontest dieting, but to a lesser degree?

In terms of glycogen retention limits and the max concentration of glycogen storage one can hold...this variable doesn't share a relation with total carbohydrate consumption, but relies on its own predetermined markers?

^^^when it comes to bodybuilding at a high level, I'm sure the usage of exogenous insulin also alters the level of super compensation and the rate at which the storage takes place. As for the 24hr refeed: I know after being depleted (legit flat, stringy, no real strength) for two weeks and going on a full cheat day, the next day I looked fantastic and had virtually no spillover, muscles were hard and full, veins everywhere as it seemed the newly introduced carbs pulled what little sub q water I had. I have no science, but sharing my experience to maybe spark some thought.

Yes, that's right. You'd usually deplete very hard in the days before, then anything from a day or so before start pushing carbs back in, sometimes fats too. Also you'll likely have been playing around with sodium and water around the same time. Plus you'll add in various compounds in the last days or hours to try to finish off the look (vascularity etc), which might include ethanol, glycerol, PDE5 inhibitors, oxymetholone, halotestin etc. Lots of variables, hence the very hit-and-miss nature of stage condition. Sometimes simpler is better ;)
 
Lol, that's (b) and ethane Grym ;) (I'm pretty sure those are GCSE level questions, thankfully I'm not that rusty!! lol)

What did you study at school? You seem very interested in all this, maybe you should take your interest further.
 
I'm only 22 years old, but have been absolutely fascinated with anything related to science. I'm currently a medical aid and have plans to further myself into the medical world. I'm a little indecisive about what I want to specialize in.... Endocrinology? Gastroenterology? My senior year of high school I took A.P classes (advanced placement) to aid in college credit. It was A.P Genetics, A.P Chemistry, A.P Physics.

I do plan on getting back into college and going for a degree rather than certifications that I got a few years ago to satisfy short term needs.
 
Go for it. Maybe think about what you want at the end of the process, and choose a degree on that basis.
 
Go for it. Maybe think about what you want at the end of the process, and choose a degree on that basis.

I have quite a few irons in the fire in hopes that I can just pay for my college flat out. Hopefully.

On the other hand........ What is the cause of ocular disambiguation such as myodesopsia?

I don't know if you took your MCAT..?
 
LOL, I sat my GAMSAT in 1998, and it had no questions on floaters, which have something to do with degeneration of the vitreous humour (collagen/HA) as you age, though I'm sure you can enlighten me the precise reason ;)

Can't you just take out student loans?
 
I'm looking for scholarships. You were correct on that answer. Degredation of the vitreous humour results in the fluid within the eye becoming more viscous. This eventually leads to collagen precipitating out of solution. I know there is other issues that can also produce the floaters, but you nailed it with the most common issue causing the little squiggles. That is extremely impressive because I really didn't know much about it and had to read up on it and you could produce that answer off the top of your head!

I need to think of something more challenging now......
 
When treated with dilute acid, the compound shown below would change in which of the following ways?

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A. Its water solubility would increase
B. It would lose the ethyl group
C. It would lose one or more double bonds
D. It would gain one or more hydroxyl groups


:)

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LOL. This is becoming like the daily quiz =D

Well it's not C or D, and as its dilute acid its unlikely to be B. If you protonate the amine group (H-N) it should become more soluble... so I'd go with A.
 
Correct again. One day I will get you with something...one day....

Maybe I need to distance the questions from organic chemistry and go towards physics or pharmacology....

It is impressive though. I hope I can one day giggle at these questions.
 
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This shits cracking me up lol. Should make a "stump the mods" thread where we post random obscure shit but still pertains to our subforum.
 
CFC doesn't know what is coming. I'm gonna put down the hammer on this next one......or he will just giggle to himself while mocking me with his intellectual power through the keyboard!
 
I just happen to read the thread discussing the new moderators' educational backgrounds and after painstaking reading, interpreting/misinterpreting everything in that general field of study....I found a question to make sure you guys never get rusty! p.s I didn't create this question.

organic chemistry......

Given the reaction: C2H2 + 2H2 --> C2H6

This reaction represents:

A. Substitution
B. Addition
C. Esterification
D. Saponification

B. Addition

Just seen question, looks like CFC beat me to it...
 
Maybe a little dibble dabble into some genomics...

2. A genotypic male (XY) is born with feminized external genitalia. The testes are retained within the abdominal cavity, and the internal reproductive tracts exhibit the normal male phenotype. Which of the following could account for this abnormal development?
(A) Complete androgen resistance
(B) 5a-reductase deficiency
(C) 17a-hydroxylase deficiency
(D) Sertoli-only syndrome
(E) Testicular dysgenesis


You currently have 3 available life lines. The choice is yours.... *insert obnoxious cliche Inception BWWAAHHHHS*
 
Maybe a little dibble dabble into some genomics...

2. A genotypic male (XY) is born with feminized external genitalia. The testes are retained within the abdominal cavity, and the internal reproductive tracts exhibit the normal male phenotype. Which of the following could account for this abnormal development?
(A) Complete androgen resistance
(B) 5a-reductase deficiency
(C) 17a-hydroxylase deficiency
(D) Sertoli-only syndrome
(E) Testicular dysgenesis

(B) 5a-reductase deficiency

The external genital slit into penis, prostate, & scrotum requires DHT. An absence of 5a-reductase in those tissues will result in feminization.
 
Maybe a little dibble dabble into some genomics...

2. A genotypic male (XY) is born with feminized external genitalia. The testes are retained within the abdominal cavity, and the internal reproductive tracts exhibit the normal male phenotype. Which of the following could account for this abnormal development?
(A) Complete androgen resistance
(B) 5a-reductase deficiency
(C) 17a-hydroxylase deficiency
(D) Sertoli-only syndrome
(E) Testicular dysgenesis


You currently have 3 available life lines. The choice is yours.... *insert obnoxious cliche Inception BWWAAHHHHS*

Testes retained in the abdominal cavity --> TDF deficiency --> absence of the SRY gene on the Y chromosome. All answers are wrong ...?

That, or (A)
 
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