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Author Topic:   Evolutionary Biology as a Science
Coragyps
Member
Posts: 5377
From: Snyder, Texas, USA
Joined: 11-12-2002


Message 31 of 34 (501579)
03-06-2009 7:14 PM
Reply to: Message 29 by Kelly
03-06-2009 7:00 PM


Re: Oops, so sorry it took me so long
Mutations do not explain drug-resistant bacteria.

Source for this assertion, please? "My imagination" or "I heard that once" do not qualify as sources. A article from Science or PNAS might - they're free and online for most of the last century. I'll match any citations you find supporting your claim with fifty showing the opposite, Kelly. Deal?

http://www.sciencemag.org/magazine.dtl
http://www.pnas.org/content/by/year

You first!


"The wretched world lies now under the tyranny of foolishness; things are believed by Christians of such absurdity as no one ever could aforetime induce the heathen to believe." - Agobard of Lyons, ca. 830 AD
This message is a reply to:
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Percy
Member
Posts: 18307
From: New Hampshire
Joined: 12-23-2000
Member Rating: 3.2


Message 32 of 34 (501594)
03-06-2009 9:58 PM
Reply to: Message 29 by Kelly
03-06-2009 7:00 PM


Re: Oops, so sorry it took me so long
Mutations do not explain drug-resistant bacteria. Scientists discovered that bacteria were resistant to certain antibiotics even before the antibiotics were invented.

Well now you're just making stuff up. Bacterial mutations causing drug resistance has been demonstrated time and time again. The possibility of such mutations is why doctors carefully instruct patients to take *all* their medication, the full course of it, not just part of it, because otherwise the body ends up providing an antagonistic but not sufficiently fatal bacterial environment that permits the growth of mutated bacterial colonies. This is very clearly described here in this excerpt from Evolution of drug-resistant tuberculosis: A tale of two species:

How has this resistance evolved? In most instances it occurs because patients either cryptically discontinue one or more of their multiple drugs or take less than the prescribed dosage (12). Alternatively, physicians -- who have become generally less familiar with tuberculosis as the incidence has diminished -- prescribe inappropriately (13). In either scenario, insufficient numbers or dosages of drugs are administered, creating an environment that selects for survival of the drug-resistant mutants. Note that the drugs do not induce the mutations, only tip the balance in favor of the naturally derived variants.

Here's a link to a table of the specific tuberculosis mutations and the drugs they cause resistance to: Summary of the molecular mechanisms of antituberculosis drug resistance

--Percy

Edited by Percy, : Spelling.


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Taq
Member
Posts: 7672
Joined: 03-06-2009
Member Rating: 3.0


Message 33 of 34 (501602)
03-06-2009 10:42 PM
Reply to: Message 29 by Kelly
03-06-2009 7:00 PM


Re: Oops, so sorry it took me so long
quote:
Kelly:

Mutations do not explain drug-resistant bacteria.


Actually, yes they do.

*************************************************************
Yonsei Med J. 2009 Feb 28;50(1):147-51. Epub 2009 Feb 24.

A case of multidrug-resistant Salmonella enterica serovar Typhi treated with a bench to bedside approach.

Yoon HJ, Cho SH, Kim SH.

Department of Internal Medicine, Eulji University College of Medicine, Daejeon, Korea. yhj822@medimail.co.kr

We report a relapsed case of a 25 year-old man with multi-drug resistant Salmonella serovar Typhi (MDRST) bacteremia who had recently returned from travel in India. Due to unresponsiveness to ciprofloxacin and ceftriaxone, we examined the strain's resistance to quinolones and extended-spectrum beta-lactamases (ESBLs). The strain had a single gyrA mutation at codon 83 (Ser83Phe), which explains its decreased susceptibility to fluoroquinolone and resistance to nalidixic acid. In the screening tests of ESBLs, TEM-1 was positive, which is beta-lactamase but not ESBL. The patient was finally successfully treated with meropenem and aztreonam. In the presence of clinical unresponsiveness despite favorable sensitivity tests, further laboratory evaluations are needed, which should include studies of genes related to antibiotic resistance and ESBLs. In addition, further prospective trials should be done about the possible inclusion of antibiotics not yet mentioned in the current guidelines. With MDRST on the rise worldwide, the most optimal and effective line of antibiotic defense needs to be devised.
link
*********************************************************************


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Taq
Member
Posts: 7672
Joined: 03-06-2009
Member Rating: 3.0


Message 34 of 34 (501603)
03-06-2009 10:51 PM
Reply to: Message 23 by Kelly
03-03-2009 3:14 PM


Re: No offense
quote:
But I find that very hard to believe given the fact that no one here demonstrates to me that they know the first thing about what Creation Science is.

Creation science is christian apologetics.

In comparison, evolution is an applied science.

Take, for example, phylogenomics.

With all of the genomic information pouring in from DNA sequencers across the globe there is a real need to make sense of these long runs of A, T, C, and G's. Guess what they use to make sense of this information? You guessed it, evolution.

How? Evolution produces a signal in genomes. That signal is conservation. When a DNA sequence starts to serve a function and a purpose it is built upon by future generations. This causes DNA sequences, and specific bases, to be conserved through generations. By comparing the genomes of species through the lens of evolutionary distance one can identify these conserved sequences. This allows you to assign a probable function to an unknown DNA sequence. This is exactly what scientists have done using a computer algorithm called SIFTER. With just a little information this algorithm, using the theory of evolution, is able to predict protein function with 96% accuracy.

*******************************************************************
PLoS Comput Biol. 2005 Oct;1(5):e45. Epub 2005 Oct 7.

Protein molecular function prediction by Bayesian phylogenomics.

Engelhardt BE, Jordan MI, Muratore KE, Brenner SE.

Department of Electrical Engineering and Computer Sciences, University of California, Berkeley, California, United States of America. bee@cs.berkeley.edu

We present a statistical graphical model to infer specific molecular function for unannotated protein sequences using homology. Based on phylogenomic principles, SIFTER (Statistical Inference of Function Through Evolutionary Relationships) accurately predicts molecular function for members of a protein family given a reconciled phylogeny and available function annotations, even when the data are sparse or noisy. Our method produced specific and consistent molecular function predictions across 100 Pfam families in comparison to the Gene Ontology annotation database, BLAST, GOtcha, and Orthostrapper. We performed a more detailed exploration of functional predictions on the adenosine-5'-monophosphate/adenosine deaminase family and the lactate/malate dehydrogenase family, in the former case comparing the predictions against a gold standard set of published functional characterizations. Given function annotations for 3% of the proteins in the deaminase family, SIFTER achieves 96% accuracy in predicting molecular function for experimentally characterized proteins as reported in the literature. The accuracy of SIFTER on this dataset is a significant improvement over other currently available methods such as BLAST (75%), GeneQuiz (64%), GOtcha (89%), and Orthostrapper (11%). We also experimentally characterized the adenosine deaminase from Plasmodium falciparum, confirming SIFTER's prediction. The results illustrate the predictive power of exploiting a statistical model of function evolution in phylogenomic problems. A software implementation of SIFTER is available from the authors.

link
*****************************************************************

(Also notice that I site peer reviewed sources when I claim that evolution is science. I expect the same when you claim that "creation science" is science.)


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