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drdoom
As Aristotle once quipped, “A ‘single-point in time’ doth not a cross-sectional study make.” The design of a cross-sectional study would not define “ahead of time” two cohorts (two groups); said another way, a cross-sectional design would not “split people into two groups.” In the design of a cross-sectional study there is only “one group”, and then you ask all members of that group some question (“Do you have asthma?”). At the end of a cross-sectional study, the authors will be able to make a statement like this: “We called 10,000 phone numbers with area code 415 at random and asked ‘Do you take Drug X?’ 500 responded ‘I don’t know’, 633 responded ‘Yes’, and 8,867 responded ’No’.”
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castlblack
That is interesting. I think the question is phrased ambiguously. I interpreted the question stem to say that they called random people and sorted them into hemorrhagic stroke pts vs controls after the fact using an ORAL questionnaire. Therefore the question would be " Did you have a stroke?" Yes = 702 or no = 1376. And thus would be a cross-sectional study.
I see now that the questionnaire must be paper and contacted from some unstated list of drug X recipients.
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jatsyuk38
Yea I thought the same thing you did. They could of randomly called people and asked "have you had a stroke" followed by "have you taken drug X" and to me that is cross sectional. Especially when most cohorts (at least in Q stems) have equal numbers of controls and those with disease and in this case they dont. But I think when they explicitly say "control subjects" you know it is cohort, as in cross sectional you get control sort of accidentely when they say "no, I haven't had a stroke" - sorry if this made things more confusing
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pg32
Picked D despite understanding the above ^^ because IL-1 is also known as osteoclast acitivating factor...
+8
plzhelp123
^ I did the same, but it appears that IL-1 activates osteoclasts in multiple myeloma. Which makes sense as that is a neoplasm of immune cells which can produce interleukins.
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caitlyncloy
can anyone explain why this the answer is "PARACRINE" stimulation?? I rule out the correct answer because i was picturing RANK and RANK L binding, which is not paracrine?!
+1
makingstrides
If you can, I Would highly recommend looking at the sketchy pharm for this. It explains this well, in my opinion, and definitely helped me.
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jatsyuk38
Goljan I could've sworn said PTH stimulates osteoblasts to secrete IL-1 to activate osteoclasts. He also said estrogen prevents osteoporosis by inhibiting osteoblast release of IL-1...however there is also a UWorld question where it said RANK-L plays a more important role actor (over IL-1) in PTH mediated bone breakdown
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privatejoker
So is the heavily implied step-wise formation of Syphilis symptoms as presented in FA complete BS then? Why break it down into stages and have us learn it as such if this is not the case in real practice?
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lilmonkey
Exactly, Goljan mentioned this in one of his audio lectures. All kinds of lesions in syphilis caused by vasculitis.
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lovebug
I know it's silly question. but Could anyone give an why answer is lymphocyte and plasma cell not neutorphiles.? bc syphilis is a bacteria, not virus.
+1
trazobone
@lovebug my guess is bc its a spirochete, so it doesn’t act like a normal bacteria. One of the screening test for syphilis is FTA Abs, so a proliferation in plasma cells makes sense. Then by deduction, if its able to affect plasma cells, it can do the same with lymphocytes. But this is me trying to logic everything together so.
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jatsyuk38
May be worth noting that necrotizing granulomas can be found in the gummas of tertiary syphillis. Doesnt change the correct choice as onset was only 2 weeks
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unknown001
lol, i just love trazobone's comment. he's a smart dude
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d_holles
In other words,
Normal enzyme activity = Vmax
Adding more B6 to a mutated enzyme will improve it back to normal (Vmax stays constant, so Km will decreased due to ↑ affinity of the enzyme).
+3
drdoom
@jatsyuk38 the comment or the subcomment?
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drdoom
oh, double caret = bump,bump = the comment (@lamhtu)
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doesn't IFN-gamma upregulate MHCII? Which would activate T lymphocytes to produce cytokines? I do get why macrophages is the better answer, but didn't understand what IL-1 had to do with anything...