text: Yo, check it out, here's the scoop,
  Study's objective: PGHS, let's loop,
  Can it be regulated, pathways new,
  Independent of de novo synthesis, true?
  
  Bovine aortic endothelial cells, BAEC,
  Short incubation, just five minutes, see,
  NaF at 40 mM, it's hot,
  PGHS activity, up by 60%, a lot.
  
  Cycloheximide, actinomycin D, they try,
  No effect on NaF-induced high,
  Aspirin at 25 microM, it's tight,
  Resting PGHS activity, gone, outta sight.
  
  NaF can't stimulate, no further rise,
  NS-398, PGHS-2 inhibitor, no surprise,
  But bFGF, within 30 minutes, it's fly,
  PGHS activity, it amplifies.
  
  Cycloheximide, it can't hold it back,
  bFGF-induced rise, it's on track,
  PGHS-1, PGHS-2, proteins intact,
  Western blots show no impact.
  
  Genistein, tyrosine kinase inhibitor, it's true,
  Attenuates PGHS activity, NaF and bFGF too,
  Sodium orthovanadate, tyrosine phosphatase blocker,
  Raises the response, makes it bolder.
  
  G protein activators, they got the game,
  5'-guanylyl imidodiphosphate, that's the name,
  Guanosine 5'-O-(3-thiotriphosphate) in the mix,
  Resting and NaF-induced PGHS, they fix.
  
  In BAEC, PGHS-1, it's the key,
  Regulated by tyrosine kinase and G proteins, you see,
  Independent of de novo protein synthesis,
  That's the conclusion, no need to analyze.