to snoo-finity ... and beyond!
Welcome to tsl19's page.
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Squamous cell is centrally located and has cavitation, which you can see in the pic. Similar to this one: https://webpath.med.utah.edu/LUNGHTML/LUNG068.html
Thank you for your explanation!
One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated?
I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes.
I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question.
According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up?
could wiki be wrong on phosphorylation being irreversible? according to this article, it is a reversible process: regulation of FoxO transcription factors by reversible phosphorylation and acetylation (https://www.sciencedirect.com/science/article/pii/S0167488911000735#s0010)
some wiki info, however, is helpful : In its un-phosphorylated state, FOXO1 is localized to the nucleus, where it binds to the insulin response sequence located in the promoter for glucose 6-phosphatase and increases its rate of transcription. FOXO1, through increasing transcription of glucose-6-phosphatase, indirectly increases the rate of hepatic glucose production. However, when FOXO1 is phosphorylated by Akt on Thr-24, Ser-256, and Ser-319, it is excluded from the nucleus, where it is then ubiquitinated and degraded. The phosphorylation of FOXO1 by Akt subsequently decreases the hepatic glucose production through a decrease in transcription of glucose 6-phosphatase.
I think it's about adding our opinion and more about seeing what the situation is because a patient contacted you in distress. The others are about contacting management off hearsay; that could also "muddy the waters," I Is this question also addressing quaternary prevention?
I agree with jcrll.
My same thought process but then I changed it to psychiatric consultation in order to first attend the patient's distress and anxiety since it was hindering her decision making.
Besides, the whole ordeal about her treatments and ineffectiveness was emotionally and physically exhausting her.
Referral is NEVER a answer
Going straight to the chair of the ethics committee without having spoken to the other physicians would be inappropriate because it would be jumping a bunch of steps in communication first - like jcrll said, you want to get the picture of what's going on from the other physicians first. Maybe the gynecologic oncologist isn't actually as opposed to palliative measures as the patient perceives him to be and thinks he's doing what the patient wants, etc. It could just be miscommunication, which you could help clear up without getting ethics involved ... better to start there.
This sounds like a case of acute endometritis. In any case, uterus is supplied by uterine artery (branch of internal iliac artery) with collateral flow from ovarian artery (comes right off aorta). I don't think there are any branches of external iliac artery into the pelvis; it becomes femoral artery once it passes under inguinal ligament.
Here's a picture that I found helpful [Female Reproductive Tract arterial supply] (https://teachmeanatomy.info/wp-content/uploads/Blood-Supply-to-Female-Reproductive-Tract.jpg)
FA 2018 - p. 496: ischemia -> pyknosis within 12-24 hours.
yeah the infarct occurring 16 hr ago is key. i zoomed in only on the died 1 hr later