Religion or not? (split from science thread)

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knobren
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Postby knobren » Fri Jul 27, 2007 2:57 pm

http://www.sciencemag.org/cgi/content/a ... /5782/1944

Science 30 June 2006:
Vol. 312. no. 5782, pp. 1944 - 1946
DOI: 10.1126/science.1124410
Prev | Table of Contents | Next

Reports
The Competitive Cost of Antibiotic Resistance in Mycobacterium tuberculosis
Sebastien Gagneux,1,4* Clara Davis Long,2* Peter M. Small,4,5 Tran Van,1 Gary K. Schoolnik,1,3 Brendan J. M. Bohannan2

Mathematical models predict that the future of the multidrug-resistant tuberculosis epidemic will depend on the fitness cost of drug resistance. We show that in laboratory-derived mutants of Mycobacterium tuberculosis, rifampin resistance is universally associated with a competitive fitness cost and that this cost is determined by the specific resistance mutation and strain genetic background. In contrast, we demonstrate that prolonged patient treatment can result in multidrug-resistant strains with no fitness defect and that strains with low- or no-cost resistance mutations are also the most frequent among clinical isolates.

(I added the italics and bold type for emphasis. Note: no fitness defects in multi-drug resistant clinical isolates. That means they don't grow any slower, etc.)

1 Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, CA 94305, USA.
2 Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA.
3 Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305, USA.
4 Institute for Systems Biology, Seattle, WA 98103, USA.
5 Bill and Melinda Gates Foundation, Seattle, WA 98102, USA.

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Postby knobren » Fri Jul 27, 2007 3:18 pm

http://jac.oxfordjournals.org/cgi/conte ... t/56/3/544


JAC Advance Access originally published online on July 22, 2005
Journal of Antimicrobial Chemotherapy 2005 56(3):544-551; doi:10.1093/jac/dki255


Assessment of the fitness impacts on Escherichia coli of acquisition of antibiotic resistance genes encoded by different types of genetic element
V. I. Enne1,*, A. A. Delsol2, G. R. Davis1, S. L. Hayward1, J. M. Roe2 and P. M. Bennett1
1 Bristol Centre for Antimicrobial Research, Department of Pathology and Microbiology, University of Bristol, Medical Sciences Building, University Walk, Bristol BS8 1TD, UK; 2 Division of Animal Health and Husbandry, Department of Clinical Veterinary Science, University of Bristol, Langford BS40 5DU, UK

Received 4 March 2005; returned 27 April 2005; revised 3 June 2005; accepted 23 June 2005



--------------------------------------------------------------------------------
* Corresponding author. Tel: +44-117-9287522; Fax: +44-117-9287896; E-mail: v.i.enne@bristol.ac.uk
Objectives: Little is known of the fitness cost that antibiotic resistance exerts on wild-type bacteria, especially in their natural environments. We therefore examined the fitness costs that several antibiotic resistance elements imposed on a wild-type Escherichia coli isolate, both in the laboratory and in a pig gut colonization model.

Methods: Plasmid R46, Tn1 and Tn7 and a K42R RpsL substitution were separately introduced into E. coli 345-2 RifC, a rifampicin-resistant derivative of a recent porcine isolate. The insertion site of Tn1 was determined by DNA sequencing. The fitness cost of each resistance element was assessed in vitro by pairwise growth competition and in vivo by regularly monitoring the recovery of strains from faeces for 21 days following oral inoculation of organic piglets. Each derivative of 345-2 RifC carrying a resistance element was grown in antibiotic-free broth for 200 generations and the experiments to assess fitness were repeated.

Results: RpsL K42R was found to impose a small fitness cost on E. coli 345-2 RifC in vitro but did not compromise survival in vivo. R46 imposed a cost both before and after laboratory passage in vitro, but only the pre-passage strain was at a disadvantage in vivo. The post-passage isolate had an advantage in pigs. Acquisition of Tn7 had no impact on the fitness of E. coli 345-2 RifC. Two derivatives containing Tn1 were isolated and, in both cases, the transposon inserted into the same cryptic chromosomal sequence. Acquisition of Tn1 improved fitness of E. coli 345-2 RifC in vitro and in vivo in the case of the first derivative, but in the case of a second, independent derivative, Tn1 had a neutral effect on fitness.

Conclusions: The fitness impact imposed on E. coli 345-2 RifC by carriage of antibiotic resistance elements was generally low or non-existent, suggesting that once established, resistance may be difficult to eliminate through reduction in prescribing alone.


(I added the bold type for emphasis. Resistant strains may be at a disadvantage in the lab, but not in the host animal or human. Also note that the paper says it may be difficult to get rid of the resistant strains once they are established, so contrary to what you might believe, they aren't reverting quickly to non-resistant strains even when the antibiotic use stops.)

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Postby Theodore » Fri Jul 27, 2007 6:08 pm

Hmm, the antibiotic resistance article is exactly what I asked for. I imagine it's flawed in its methodology somehow, since the study was done by the Antimicrobial Chemotherapy lobby, but until I can figure out how, you win this particular point. However...

Is Bacterial Resistance to Antibiotics an Appropriate Example of Evolutionary Change?

EDIT: Perhaps the resistant forms also provide a resistance to something else found in the pig's system? Hence, increased survival advantage even when the specific antiobiotic / antibody being tested for isn't present.

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Postby knobren » Fri Jul 27, 2007 6:21 pm

Last edited by knobren on Fri Jul 27, 2007 7:01 pm, edited 1 time in total.

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Postby knobren » Fri Jul 27, 2007 7:00 pm


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Postby knobren » Fri Jul 27, 2007 7:02 pm


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Postby Theodore » Sat Jul 28, 2007 4:28 am

By "Antimicrobial Chemotherapy lobby", I just mean that they are obviously going to be in favor of antibiotic use, and an experiment that shows that bacteria don't easily lose their resistance in animals means that reducing antiobiotic use won't get rid of the resistant strains, and that new antibiotics are even more necessary. There will be bias, though whether or not that seriously impacts their science, I do not know. It all depends on where their funding comes from.

In any case, even if I give you this point, the article I linked to brings up an interesting question - if the bacteria are just "evolving" by acquiring genes that are already in existence, rather than creating new ones, then how can this be proof for macroevolution? You can shuffle a deck of cards all you want, and you'll never draw a 14 of Truffles. Also, this was animal testing on single animals, not animal testing on populations, and the bacteria also have to show a survival advantage for the host, since if the host dies, so do the bacteria. Weaponized biological agents do not survive long in real life, since the host dies at a much greater rate. 10 or 20 iterations at most and the large majority of their effectiveness is gone (albeit, having killed millions by then). A stronger bacteria won't necessarily survive longer than a weaker one.

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Postby momo3boys » Sat Jul 28, 2007 8:09 am

Phi 4:13 I can do all things through Christ which strengtheneth me.

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Postby knobren » Sat Jul 28, 2007 5:08 pm


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Postby knobren » Sat Jul 28, 2007 5:29 pm


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Postby knobren » Sat Jul 28, 2007 5:51 pm

http://jb.asm.org/cgi/content/full/188/7/2297

"With the report in 1985 (3) of a community-based outbreak of penicillin-resistant gonorrhea due to a strain not producing a beta-lactamase, the final blow to penicillin therapy for treatment of this sexually transmitted infection was, unfortunately, realized. The culprit strain (FA6140 [3]) from this outbreak contained (12) a number of chromosomal mutations (penA, penB, ponA, and mtr) that are known to alter cell envelope structure and/or function. In general terms, these mutations impact penicillin's accumulation in gonococci (penB and mtr) or affinity (penA and ponA) for penicillin-binding proteins; this commentary will be restricted to issues related to penB and mtr. The penB mutation was originally linked (7) to production of an altered major outer membrane protein (termed POMP or protein I) and was found to confer two- to fourfold increases in MIC levels of penicillin and tetracycline. Curiously, phenotypic expression of penB required the presence of the mtr mutation, which was found to confer single-step resistance to structurally diverse hydrophobic antimicrobial agents (10) and was presumed to decrease cell envelope permeability to such agents (6). "

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Postby momo3boys » Sun Aug 19, 2007 6:15 pm

Hey guys, we've been on vacation for a while and I was reading something in the news that made me think of this debate.

The story of two different groups of people that until now were thought to have lived thousands of years apart. One was primarily agricultural and that other was a hunter gatherer.

http://www.thestar.com/sciencetech/article/244399

http://news.bbc.co.uk/1/hi/sci/tech/6937476.stm

here are two of the articles I've read.

This is an amazing example of two different views from the same evidence. Creationists will automatically thinking Cain and Abel's descendants. I'm not sure what evolutionists are thinking. That is why I bring it up.
Phi 4:13 I can do all things through Christ which strengtheneth me.

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Postby Theodore » Sun Aug 19, 2007 11:15 pm

That's how science is supposed to work, anyhow. It's been known for some time that you can get thicker jaws and even different jaw structures from eating a coarse diet, and arthritis can give the rounded, hunched skeletons normally associated with "missing links". The only difference between "ancient man" and "modern man" is the supposed age of the skeletons. There are natives living now in various parts of the world whose skeletons are indistinguishable from those of "ancient man", so are we to assume that they are lower forms of humanity and that we are higher forms? Evolution leads inescapably to racism.

Also, as I stated elsewhere, there are known cases of scientists actually dislocating the jaws of their skeletons so they can make them jut an inch or two more for photos. The skeletons may be real, but the photos are complete frabrications, and anyone who looks at the original skulls can easily see that they're identical to modern skulls. Regardless of whether you believe in evolution or not, stuff like this needs to stop. It makes science into a mockery and a fraud, though I suppose it's good snake oil for the masses.

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Postby seekingmyLord » Mon Aug 20, 2007 5:11 am

As I have said before, I will not argue the finer points of creationism vs. evolution, but I will point out how the minds of scientists work to fit everything into the evolution model, which can lead to erroneous conclusions.

I just watched a documentary about scientist retrieving a complete mammoth frozen in ice. The position of the mammoth, they agreed, suggested that the mammoth was in a pool of water when it froze. As they were carefully digging around it to free it from the surrounding ice, they found frozen vegetation, still green.

Then they said because of the depth of the aquatic vegetation they concluded it was thousands of years older than the mammoth. Now, it was just a foot or two under the mammoth's feet, so why is it assumed because it is under the mammoth that it is older rather than it was at the bottom of the pool when the mammoth froze? Would it be because scientists are programmed to think depth means age? I mean, I would imagine that a mammoth struggling to get out of the water would have stirred up the mud at the bottom of a pond, right?

I still cannot get around that, even if I did believe in evolution. Here is a mammoth swimming, according to the positioning of its body, and it gets frozen in ice. Maybe fell through the ice and was struggling to get out, but the scientists stated that the mammoths lived there, in Siberia, at a time when it was green--not covered with ice. So, they assume it when into the water and got stuck in the mud. Okay, but what about the green plant? If it was layers down from the mammoth buried in mud, instead of ice when the mammoth entered the pond, why would it be still green?

Sometimes scientists are so eager to prove their theories based on the evolutionary model that they don't see how the facts don't fit--they simply must fit so they make theories to make them fit. :roll: Circular reasoning.


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