to snoo-finity ... and beyond!
Welcome to sklawpirt's page.
Contributor score: 19
pg. 47 on FA got the good visuals!
COPII* proteins are needed to coat vesicles from the RER to Golgi. "Two(COPII) steps forward; one(COPI) step back."
Anterograde goes RER -> Golgi -> Lysosomes/Secretory Vesicles -> Plasma membrane
and I thought large lysosomes due to lack of enzymes to degrade
The size of the lysosome is not affected by the presence or absence of protein, but its function is compromised (eg. protein is getting stuck in the RER)
I hope this helps to whomever was lost like me
Null mutation: A mutation (a change) in a gene that leads to its not being transcribed into RNA and/or translated into a functional protein product. For example, a null mutation in a gene that usually encodes a specific enzyme leads to the production of a nonfunctional enzyme or no enzyme at all.
Exactly, it has to do with where in the kidney renin is released and requires a bit of knowledge of the artery branches that give rise to the afferent arteriole in the first place and where this branch point is located. http://anatomyforme.blogspot.com/2008/05/histology-of-kidney-lot-to-process.html
Where renin production occurs in JGA cells, EPO production occurs in the renal peritubular interstitium (especially the proximal renal tubule, corext and some of the outer medulla.) Thus with the same questions stem it might ask where is concentration of EPO the highest? [And it would still be the cortex, with lower concentrations in the outer medulla, lowest concentration in the inner medulla, and none found in the papilla or renal pelvis.
Actually, the renal medulla receives significantly less blood flow than renal cortex. So the medulla is the one that's very sensitive to hypoxia and vulnerable to ischemic damage. I don't think this question is related to "what area is the most poorly perfused."
It's just knowing that renal artery stenosis is going to decrease blood flow to the kidney. JG cells sense the decrease in perfusion pressure and secrete renin. Knowing that renin is produced by the JG cells and that JG cells are in the cortex should be enough to answer this question.
I thought all the renin would collect in the pelvis where the arteries whould drain into a common vein and changed my answer to pelvis ._.
I think its just that the patient is CONSCIOUSLY experiencing chest pain. Because he is consciously feeling the pain and would be able to directly point to it (and that it is not referred visceral pain) it has to be a somatic afferent nerve fiber. This narrows it down exclusively to the intercostal nerve exc;usively. https://en.wikipedia.org/wiki/Intercostal_nerves
IMportant to the patients "right sided chest pain" is his history of MVA and x-ray confirming multiple rib fractures.
I think this is correct? Does that make sense ? All of the other choices do not carry SA fibers in that area