Posted on 03/28/2006 2:37:59 PM PST by Conservative Coulter Fan
PING..
This seems more like a cracker jack box science degree holder.
The spread of resisting bacteria is beause the non-resistent ones are dead and thus not around to spread their dna like the resistant dna.
This gobldy gook is basically trying to rehash the "spontaneous generation" pseudo science of the pre evolution era. (see the maggot experiments etc.)
It is "survival of the fittest" not the spontaneous appearance of the fittest.
Hello Creation lovers!
Piled much higher and Deeper. Is this PhD, or OP, familiar with Popper's falsifiability? If PhD must recapitulate the whole argument then he's hiding something from a naive audience.
No.
It's a real degree if this site is to be believed:
http://www.christiananswers.net/creation/people/anderson-k.html
...which doesn't make his science one bit better.
Muleteam1
I think that's the whole point of the article. Evolution implies both the spontaneous appearance of beneficial mutations, thus spontaneous appearance of the fitness as well as survival of the fittest.
But we don't see spontaneous appearance of beneficial mutations except when the mutation results in a loss of functionality and that loss of functionality is somehow beneficial as in the case of sickle cell anemia.
Bacterial resistance has been offered as spontaneous appearance of beneficial mutations. But this article examines that and rejects bacterial resistance as being the result of a beneficial mutation except for loss of functionality.
Yep. Two words: Intellectual dishonesty.
Well I would call it an example of natural selection. Nothing has changed really, except the proportion of resistant bacteria.
See my post #12. You won't see the spontaneous appearance of beneficial mutations if you close your eyes. . .
placemarker.
I'd rather be a creation lover than a "I-go-to-the-zoo-to worship-the-Sabbath Lover."
Biologists mimic evolution in the lab?
"This is evolution? The gene that produces ‘penicillin killer’ enzymes (TEM-1 ß-lactamase) easily mutates into different forms that break down a variety of antibiotic molecules. Hall was able to get eight bacterial cultures in his laboratory to ‘develop’ resistance to various antibiotics. In seven cases, bacteria in nature already had this resistance, and in one case, the laboratory bacteria actually developed resistance to an antibiotic (cefepime) that bacteria in nature are not known to be resistant to. In two other cases, the laboratory bacteria did not develop resistance, although bacteria in nature have apparently done so."
The beta-lactamases are evolved from a class of beta-lactamases.
MRSA is derived from a novel gene which originated in 1987 from splicing together a gene from S. aureus and E. coli. This novel gene has since undergone mutation to give several variants.
The vancomycin resistance family originated from co-opting genes that had nothing to do with antibiotic resistance. These genes were either duplicated or stolen and then underwent mutation and selection to produce the complicated vancomycin resistance system we have now, and it is continuing evolving with some interesting variants.
You are incorrect in your statement about MRSA. For staph aureus
most of the resistance mechanisms are due to plasmid transmission
of already existing genes, or tranposons, or mutation of
a gene alreay present. There may be two "novel" chromosomal
areas which have been acquired from an unknown source. Most
of the resistance is therefore due to already existing genes.
At least two are of unknown origin.
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