The USA's "U6" measure is about 17% at the moment (http://www.bls.gov/news.release/empsit.t15.htm). It's what you get if you include part-time workers who say they'd prefer to be full-timers. All the other measures are about 10%. So hesiod's point still stands, sorry:)
How could you possibly make a cogent point about a scientific issue in thirty seconds?
I guess you could talk quickly. "Thereisalargebodyofevidencefrommanysourcessupport ingtheexistenceofevolutiontherealquestionishowtoex plainthatevidencedontyouagreethatDarwinsmodelprovi desa..."
There are some chemical pathways that bacteria cannot abandon.
Triclosan kills bacteria by interfering with an enzyme called FabI. FabI's job can also be done by FabI[G93V], which isn't affected by triclosan very strongly at all. E coli will make FabI[G93V] instead of FabI after a mutation of just a few base pairs.
I don't know about amoxicillin (discussed by TFA), but why is it implausible that bacteria could become resistant to triclosan in this way?
(By the way, my source is R. J. Heath et al., 'Mechanism of triclosan inhibition of bacterial fatty acid synthesis', J. Biol. Chem. 274 (1999) 11110-14.)
Slashdot Mirror
The USA's "U6" measure is about 17% at the moment (http://www.bls.gov/news.release/empsit.t15.htm). :)
It's what you get if you include part-time workers who say they'd prefer to be full-timers. All the other measures are about 10%. So hesiod's point still stands, sorry
...posting here to clear my mods --- sorry, I somehow chose the wrong option from the drop-down...
How could you possibly make a cogent point about a scientific issue in thirty seconds?
I guess you could talk quickly. "Thereisalargebodyofevidencefrommanysourcessupport ingtheexistenceofevolutiontherealquestionishowtoex plainthatevidencedontyouagreethatDarwinsmodelprovi desa..."
As a self-diagnosed genius, I think this is quite right. The education system really failed me.
I console myself by wearing a t-shirt that says "Genius At Work". Man, I love that t-shirt.
Triclosan kills bacteria by interfering with an enzyme called FabI. FabI's job can also be done by FabI[G93V], which isn't affected by triclosan very strongly at all. E coli will make FabI[G93V] instead of FabI after a mutation of just a few base pairs.
I don't know about amoxicillin (discussed by TFA), but why is it implausible that bacteria could become resistant to triclosan in this way?
(By the way, my source is R. J. Heath et al., 'Mechanism of triclosan inhibition of bacterial fatty acid synthesis', J. Biol. Chem. 274 (1999) 11110-14.)
In this particular case, Granger causality might be the term you're looking for.