hey everyone
1. I still can't get this one:
Transgenic mice with severe fasting hypoglycemia.
Glucagon -> no effect, epinephrine -> increase in glucose concentration. What's wrong?
I read earlier that the correct answer is "B. defect in glucagon receptor", if I'm not mistaken. But reasonably I could narrow answers only down to these ones: defective adenyl cyclase, G protein, protein kinase A.
First thing: I thought that glicagon doesn't have any specific, its own receptor (???), its receptor is Gs coupled receptor, so that's why I didn't go with B. Choosing among adenyl cyclase, G protein, protein kinase A - I got lost, because all of them are involved in Gs-receptor system and it could be defect in any of them. I decided that the reason why epinephrine worked is because it caused glucogenesis thru a1- Gq-coupled receptor that uses phospholipase C and protein kinase C rather than adenyl cyclase and protein kinase A. So I ended up guessing among adenyl cyclase, G protein, protein kinase A and of course I got this question incorrect.
Could someone be kind and explain me where I went wrong?
2. My "favorite" biostat:
Trial X statistical power is 0.8, Trial Y - 0.9.
What statement is correct regarding the likelihood of a type II error?
Since statist.power = 1 - b, type II error for trial X is 0.2, type II error for trial Y - 0.1. Am I right so far?
So the correct answer should be A. Type II error of trial X > type II error of trial Y ?
3. Again this one:
Patient with metastatic colon ca has maintained remission by taking Bevacizumab as a single agent. The ability to administer this agent despite it being a foreign protein is a result of which? The agent is:
A) Humanized Ab - CORRECT.
B) Variable region of murine Ab directed against VEDGF
C) B cell dysfunction
D) Immune suppression because of previous chemotherapy
E) T cell dysfunction
I found ijn's explanation here: "it's a humanized monoclonal antibody - meaning we recognize the Fc region as self. If it was horse Fc or something, like some antivenoms, then we could end up in anaphylaxis upon repeat administration", but I can't get. I chose D, thought that due to previous immunosuppression therapy there is no reaction on this drug as on foreign agent.
4. And why atrophy of muscles is caused by protein degradation? What initiates this degradation?
Thanks!