Annoying creationists

[joobz]

I like how evolutionists like to speculate that changing the number and intensities of selection pressures is how blizzards transform lizards into buzzards with gizzards.

Did you think of the rhyme while dressed as a wizard, eating lunch with Eddie Izzard, after your date fun with Miss. Herd while thinking of a fizz word?

 

[kleinman]

Annoying Creationists

Combination selection pressures profoundly slow the mutation and selection sorting/optimization process. That is what Dr Schneider’s peer reviewed and published mathematical model shows and that is what the empirical evidence shows.
http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html

The combined antiviral effects of indinavir and RT inhibitors dramatically suppressed the emergence of resistance to these agents, in a bi-directional fashion, relative to the rates observed during inhibition of the protease or RT alone. This suggests that the durability of viral inhibition can be increased by combining indinavir with one or more inhibitors of the reverse transcriptase, suppressing the viral replication that drives the evolution of resistance.

http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html

Multidrug combinations are increasingly important in combating the spread of antibiotic-resistance in bacterial pathogens1, 2, 3. On a broader scale, such combinations are also important in understanding microbial ecology and evolution4, 5. Although the effects of multidrug combinations on bacterial growth have been studied extensively, relatively little is known about their impact on the differential selection between sensitive and resistant bacterial populations1, 6, 7. Normally, the presence of a drug confers an advantage on its resistant mutants in competition with the sensitive wild-type population1. Here we show, by using a direct competition assay between doxycycline-resistant and doxycycline-sensitive Escherichia coli, that this differential selection can be inverted in a hyper-antagonistic class of drug combinations. Used in such a combination, a drug can render the combined treatment selective against the drug's own resistance allele. Further, this inversion of selection seems largely insensitive to the underlying resistance mechanism and occurs, at sublethal concentrations, while maintaining inhibition of the wild type. These seemingly paradoxical results can be rationalized in terms of a simple geometric argument. Our findings demonstrate a previously unappreciated feature of the fitness landscape for the evolution of resistance and point to a trade-off between the effect of drug interactions on absolute potency and the relative competitive selection that they impose on emerging resistant populations.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8595505&dopt=Abstract

Monotherapy does not give long-term suppression of viral replication and evolution, and combination therapy is viewed as a potentially more effective long-term approach based on increased and more durable suppression of HIV replication.

http://www.apsnet.org/education/advancedplantpath/topics/Resistan/Resistan_Lesson_5.html

Many manufacturers of systemic, single-site fungicides are now marketing them formulated as combinations with multi-site fungicides, with the intent of "preventing" the evolution of resistance to the systemic fungicides. Similarly, alternate applications of fungicides with different modes of action or "cocktails" of two or more fungicides applied in the same spray or have been used as a means of combating fungicide resistance. The often-stated rationale for these fungicide combinations is that they prevent the buildup of resistance because the multi-site fungicide in the spray program kills any mutants resistant to the single-site fungicide.

This explanation of the effectiveness of fungicide combinations is not entirely correct, since a multi-site fungicide such as captan is no more effective against a benomyl-resistant Venturia population than it is against the wild-type population. However, even partial suppression of the resistant population will reduce the rate of selection of fungicide resistance and give the grower time to react before there is a catastrophic crop failure. Fungicide combinations, therefore, are a good tactic, not because they prevent resistance, but because they slow down the selection of resistance and thus can prevent crop loss.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219

Although no resistance to B. thuringiensis subsp. israelensis has been reported under field conditions, studies in the laboratory have shown that high levels of resistance can be developed when larval populations are selected against recombinant bacilli that produce only one, two, or three of this bacterium's mosquitocidal Cry proteins. For example, when populations of C. quinquefasciatus were selected against a strain producing only Cry11Aa at a concentration that killed 95% (LC95) of the larvae, the level of resistance was 1,000-fold after 28 generations (9). When the same species was selected at the same level with a strain of B. thuringiensis subsp. israelensis that produced Cry11Aa, Cry4Aa, and Cry4Ba, resistance was 217-fold after the same number of generations (9). Interestingly, the level of resistance was only 3.3-fold when C. quinquefasciatus was selected with wild-type B. thuringiensis subsp. israelensis which, in addition to the Cry endotoxins, produces Cyt1Aa (9). The implication of these results is that combinations of Cry endotoxins, and especially combinations of Cry endotoxins and Cyt1Aa, are responsible for delaying resistance.

Now you evolutionists have asserted that variations in the weather are what drive evolution. In other words, blizzards transform lizards into buzzards with gizzards!

That’s almost as funny as chemicals cooperating to spontaneously form life.

I looked out the window the other day and it was snowing, I thought I saw a lizard turning into a buzzard but it actually was chemicals cooperating to spontaneously make life. You evolutionists really know how to explain mutation and selection.

 

[Mr. Scott]

Now you evolutionists have asserted that variations in the weather are what drive evolution. In other words, blizzards transform lizards into buzzards with gizzards!

No evolutionist said anything like that. Preference to attack straw men instead of real evolution theory illustrates you are aware of the fatal weakness of your thesis.

Even your supporters would appreciate it if you stopped evading and specifically refuted the importance of variability in selective pressures.

 

[kleinman]

Annoying Creationists

You evolutionists continue to have a problem understanding how variation in intensity and number of selection pressures affects the mutation and selection sorting/optimization process. This citation which I just posted explains exactly how variation in selection pressures works.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219

Although no resistance to B. thuringiensis subsp. israelensis has been reported under field conditions, studies in the laboratory have shown that high levels of resistance can be developed when larval populations are selected against recombinant bacilli that produce only one, two, or three of this bacterium's mosquitocidal Cry proteins. For example, when populations of C. quinquefasciatus were selected against a strain producing only Cry11Aa at a concentration that killed 95% (LC95) of the larvae, the level of resistance was 1,000-fold after 28 generations (9). When the same species was selected at the same level with a strain of B. thuringiensis subsp. israelensis that produced Cry11Aa, Cry4Aa, and Cry4Ba, resistance was 217-fold after the same number of generations (9). Interestingly, the level of resistance was only 3.3-fold when C. quinquefasciatus was selected with wild-type B. thuringiensis subsp. israelensis which, in addition to the Cry endotoxins, produces Cyt1Aa (9). The implication of these results is that combinations of Cry endotoxins, and especially combinations of Cry endotoxins and Cyt1Aa, are responsible for delaying resistance.

This empirical example shows exactly how variation in the number of selection pressures accelerates the evolutionary process. This citation shows that if you reduce the number of selection pressures it accelerates the ability of the population to evolve against the remaining selection pressures. Dr Schneider’s computer simulation shows this same effect mathematically.

This following citation which was so kindly posted by an evolutionist shows what happens if you subject a population to single selection pressures sequentially.

http://www.pnas.org/cgi/content/full/104/34/13711

Fig. 5. A schematic view of fitness landscapes and evolution under fixed goal and MVG. (a) A typical trajectory under fixed goal evolution. The population tends to spend long periods on local maxima or plateaus. (b) A typical trajectory under MVG. Dashed arrows represent goal switches. An effectively continuous positive gradient on the alternating fitness landscapes leads to an area where global maxima exist in close proximity for both goals.

The top image shows the trajectory that the population takes on the fitness landscape to get to the global optimum for goal 1. The second and third images show the trajectory the population takes when the goals are switched back and forth from goals 1 and 2. The bottom image shows the trajectory the population takes to achieve both goals sequentially. Now if goals 1 and 2 are applied simultaneously, you have two different selection conditions pushing the population on two different trajectories. Selection condition 1 is trying to push the population to the global optimum 1 and selection condition 2 is trying to push the population to global optimum 2. A step that would be advantageous for one condition is disadvantageous for the other condition which confounds both selection conditions in their search for their new optimums. This is why combined selection pressures confound the evolutionary process. This is the same reason ev becomes very slow converging for longer genomes.

What this citation shows is the recipe for producing multi-drug resistant microbes. Treat microbes with monotherapy and then when the population evolves resistance to this monotherapy change to a new monotherapy and when the population evolves resistance to that drug change to a new monotherapy… That is the recipe for producing superbugs. This citation shows what you need in order to accelerate evolution. You evolutionists have been so good at describing how the mutation and selection sorting/optimization process works; we all thank you for giving us MRSA.

 

[kjkent1]

I think it worthwhile to explain in more detail why huge populations have only a small effect on the rate of evolution when compared to the number of selection pressures. The following example concerns the evolution of resistance to Beta-lactam drugs (Penicillin class antibiotics).

“Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins”, Daniel M Weinreich, Nigel F Delaney, Mark A DePristo, Daniel L Hartl. Science. Washington: Apr 7, 2006. Vol. 312, Iss. 5770; pg. 111
"Five point mutations in a particular Beta-lactamase allele jointly increase bacterial resistance to a clinically important antibiotic by a factor of ~100,000. In principle, evolution to this high-resistance Beta-lactamase might follow any of the 120 mutational trajectories linking these alleles. However, we demonstrate that 102 trajectories are inaccessible to Darwinian selection and that many of the remaining trajectories have negligible probabilities of realization, because four of these five mutations fail to increase drug resistance in some combinations. Pervasive biophysical pleiotropy within the Beta-lactamase seems to be responsible, and because such pleiotropy appears to be a general property of missense mutations, we conclude that much protein evolution will be similarly constrained. This implies that the protein tape of life may be largely reproducible and even predictable. "

I think that this cite by kleinman is worth responding to, lest someone be mislead to believe that the scientific community is drawing a consensus that evolution is impossible.

The above-quoted cite is an experiment intended to reveal the possible outcomes of "point mutation." The article specifically states: "Seen as an analysis of clinical cefotaxime resistance evolution, our treatment makes several simplifying assumptions about the mutational and selective processes. For example, we have disregarded horizontal gene transfer and have limited attention to only five mutations. Furthermore we have assumed that selection acts only to increase resistance to cefotaxime, whereas microbes are exposed to a spatial and temporal diversity of antibiotic compounds in nature as well as in clinical settings."

The point is that kleinman has seemingly intentionally limited the scope and use of this article so as to bolster his position that evolution is impossible, while the article itself states that the experiment is only intended to analyze clinical cefotaxime resistance by examining a specific five mutations. That is, the experiment is deliberately limited and in no way is an attempt to deal with the unlimited real-world potential of non-point mutation mechanisms, such as "horizontal gene transfer."

Another day, another self immolation -- courtesy of Dr. Alan Kleinman.

 

[Paul C. Anagnostopoulos]

nsp = number of selection pressures
gfc = generations for convergence.

That's confusing. In math, juxtaposition of letters indicates multiplication. This is not economics.

~~ Paul

 

[m_huber]

Well, Alan, you've made nice, long posts about how evolution can't possibly work.

Let's imagine a world in which evolution doesn't occur.

For this to be the case, all forms of life currently on the planet must have been on the Earth from either the beginning of time or the "seeding" of the planet by some being(s). Since fossils are abundant at ages of greater than 600 million years, it is reasonable to think that this "seeding" occurred around that time. Of course, stromatolites and other simple plants are dated much older than that, but we will assume that these were "early experiments." Life continues until the Permian, roughly 350 million years later, at which time 90% of all fossil species go extinct. Life then continues for roughly 300 million years, at which time 65% of all fossil species go extinct (including the dinosaurs). Then, over the next 65 million years, almost all large mammals go extinct. That brings us to today, when humans are a major factor in driving animals to extinction.

The question, then, is how does life survive in steady state? Large objects hit the earth. These wipe out large numbers of life forms. The climate of the planet changes significantly. This effects what niches are available. Swings in earth's temperature may be in the order of 40ºC, which is not a small number! how do you propose that life, in steady state, has dealt with all of these extinctions and changes in the planet?

Evolution alleviates this problem. The mechanisms may be simple or complex. What you are looking at does not answer the question of mechanism.

 

[kleinman]

Annoying Creationists

There are some evolutionists who think that if you really scramble a genome it accelerates evolution and that it somehow overcomes the mathematical and empirical fact that combination selection pressures profoundly slow the evolutionary process. HBV does frame shifts but combination therapy still profoundly slows the evolution of this virus.
http://www.emedicine.com/med/topic3180.htm

Increasingly, combination therapy with more than one nucleoside or nucleotide analog is contemplated for patients with chronic hepatitis B. Combination therapy may be more effective than monotherapy in patients who have exhibited drug resistance. It remains to be determined whether combination therapy is appropriate for patients with chronic hepatitis B who are drug naive.

And
http://www.cirquemeded.com/AGA/FCU2006/Kwo.pdf

221649: Evolution of Multi-Drug Resistant HBV: Implications on Rescue Therapy. Hyung Joon Yim, Munira Hussain, Stephen Wong, Ying Liu, Scott K Fung, Anna S Lok

Background: Multi-drug resistant HBV have been reported in patients who received sequential treatment with nucleoside monotherapy. In vitro studies showed that HBV constructs with mutations resistant to lamivudine (LAM) and adefovir (ADV) have marked reduction in sensitivity to combination of LAM+ADV, while constructs with mutations resistant to either drug remain sensitive to the other drug. Aims: To determine if mutations conferring resistance to multiple antiviral agents are present on the same HBV genome in vivo and to describe the evolution of these mutations. Methods: Sera from 6 patients found to have dual-resistant HBV mutations on direct sequencing were cloned after nested PCR, 18-20 clones from each sample were sequenced. Results: Mutations to both therapies were present on the same genome in 163/195 (84%) clones from 10 samples with dual-resistant mutations to LAM+ADV, LAM+HBIG, or LAM+entecavir (ETV) on direct sequencing, 32 (16%) clones had mutations to one drug. Evolution of mutations was examined in 3 patients. Patient 1 received LAM+ETV after LAM breakthrough, all 18 clones had L180M and M204V/I at month 0 (start of ETV), clonal analysis first detected ETV-resistant mutation (T184L) at month 20, 6 months earlier than direct sequencing. Both treatments were stopped at month 34 (T184L: 20/20 clones); 6 months later, T184L was detected in 12/20 clones while L180M and M204V/I remained detectable in 19/20 clones. Patient 2 was switched to ETV monotherapy after LAM breakthrough, all 20 clones had L180M+M204V at month 0. At month 36, ETV-resistant mutation I169T was detected in 15 and S202G in 4 clones. At month 41, S202G was present in 17 clones and I169T in 4 clones, LAM-resistant mutations remained detectable in all 20 clones. Patient 3 developed HBV recurrence after transplant despite receiving LAM+HBIG. All 18 clones had M204I and sG145R when HBV recurrence was diagnosed. ADV was added and LAM stopped 7 months later. ADV breakthrough occurred after 41 months of ADV when all 18 clones had ADV-resistant N236T. Four months after reintroduction of LAM, all 20 clones had L180M+M204V, 12 clones had additional V173L change. However, N236T was replaced by a different ADV-resistant mutation P237H. Conclusions: Our study showed that mutations conferring resistance to multiple antiviral agents are present on the same viral genome, suggesting that combination therapy directed against mutants resistant to each treatment may not be adequate in suppressing dual-resistant HBV. Sequential antiviral therapy leads to selection of multi-resistant HBV; mutations evolve during continued treatment resulting in mutants with increased replication fitness.

And here is an example of a deletion with HIV and we all know that combination therapy works for HIV.
http://jvi.asm.org/cgi/content/full/81/9/4713

Deletions, insertions, and amino acid substitutions in the ß3-ß4 hairpin loop-coding region of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) have been associated with resistance to nucleoside RT inhibitors when appearing in combination with other mutations in the RT-coding region. In this work, we have measured the in vivo fitness of HIV-1 variants containing a deletion of 3 nucleotides affecting codon 69 (

69) of the viral RT as well as the replication capacity (RC) ex vivo of a series of recombinant HIV-1 variants carrying an RT bearing the 69 deletion or the T69A mutation in a multidrug-resistant (MDR) sequence background, including the Q151M complex and substitutions M184V, K103N, Y181C, and G190A. Patient-derived viral clones having RTs with 69 together with S163I showed increased RCs under drug pressure. These data were consistent with the viral population dynamics observed in a long-term-treated HIV-1-infected patient. In the absence of drugs, viral clones containing T69A replicated more efficiently than those having 69, but only when patient-derived sequences corresponding to RT residues 248 to 527 were present. These effects could be attributed to a functional interaction between the C-terminal domain of the p66 subunit (RNase H domain) and the DNA polymerase domain of the RT. Finally, recombinant HIV-1 clones bearing RTs with MDR-associated mutations, including deletions at codon 69, showed increased susceptibilities to protease inhibitors in phenotypic assays. These effects correlated with impaired Gag cleavage and could be attributed to delayed maturation and decreased production of active protease in those variants.

And we also know that HIV does recombination, as does Malaria and numerous other microbes yet combination selection pressures slow the evolution of all these life forms. It is not the type of mutation which dominates the mutation and selection sorting/optimization process; it is the number of selection pressures applied to the population which determines the rate of evolution. If you evolutionists taught this to naïve school children instead of blizzards transform lizards into buzzards with gizzards, it may not have taken David Ho years to figure out that combination therapy was what was needed to treat HIV. Thank you evolutionists for teaching children to be completely ignorant of the mutation and selection sorting/optimization process, of course you did this by teaching these children everything you know about mutation and selection.

 

[kjkent1]

There are some evolutionists who think that if you really scramble a genome it accelerates evolution and that it somehow overcomes the mathematical and empirical fact that combination selection pressures profoundly slow the evolutionary process. HBV does frame shifts but combination therapy still profoundly slows the evolution of this virus.
http://www.emedicine.com/med/topic3180.htm

And
http://www.cirquemeded.com/AGA/FCU2006/Kwo.pdf


And here is an example of a deletion with HIV and we all know that combination therapy works for HIV.
http://jvi.asm.org/cgi/content/full/81/9/4713

And we also know that HIV does recombination, as does Malaria and numerous other microbes yet combination selection pressures slow the evolution of all these life forms. It is not the type of mutation which dominates the mutation and selection sorting/optimization process; it is the number of selection pressures applied to the population which determines the rate of evolution. If you evolutionists taught this to naïve school children instead of blizzards transform lizards into buzzards with gizzards, it may not have taken David Ho years to figure out that combination therapy was what was needed to treat HIV. Thank you evolutionists for teaching children to be completely ignorant of the mutation and selection sorting/optimization process, of course you did this by teaching these children everything you know about mutation and selection.

Another complete self immolation by Alan Kleinman, above.

In his first two cites, kleinman argues that frame shifts are irrelevant against HVB and combination therapies. Unfortunately, neither of the citations say word one about frame shifts -- thus the articles are totally irrelevant and don't support kleinman's position at all. Whereas the citation I posted a few weeks back showing that HVB with a frame shift actually escaped despite combination therapy, directly falsifies kleinman's position on this point.

In kleinman's third citation, the article states: "In summary, the 3-nucleotide deletion (69) along with S163I in the context of an MDR RT genotype favored the ex vivo Replication Capacity under drug pressure, in agreement with its in vivo emergence and evolution in a long-term-treated HIV-1-infected patient."

This statement shows that the experiment actually demonstrated the exact opposite of what kleinman hoped to show. The deletion provided more resistance to combination therapy.

I love the smell of naplam in the morning. In this case, there's no strawman to burn -- just a total error on kleinman's part. He really ought to read his articles before he posts them.

 

[kleinman]

Annoying Creationists

Over the past year, evolutionists have argued that recombination, frame shifts, huge populations, the weather, you name it makes the theory of evolution mathematically possible. Unfortunately for you evolutionists, you have neither the mathematics nor the empirical evidence to counter the mathematically and empirically proven fact that combination selection pressures profoundly slow the evolutionary process. Dr Schneider’s peer reviewed and published model of random point mutations and natural selection shows how mutation rates, genome length, population all affect the generations for convergence. Even though Dr Schneider’s model does not include the above named mechanisms of gene transformation, the empirical evidence fills that gap. There are no measurable, repeatable examples of mutation and selection which show that combination selection pressures don’t profoundly slow the mutation and selection sorting/optimization process. It doesn’t matter whether there are frame shifts, recombination or blizzards, combination selection pressures profoundly slow the mutation and selection sorting/optimization process. It should be obvious to everyone that making the sorting conditions more complex profoundly slows the ability of a population to sort beneficial and detrimental mutations. If this were understood and taught by evolutionists, we may have been able to avoid MRSA, multi-drug resistant gonorrhea, years in delay in understanding that HIV required combination therapy and the numerous other examples of poly-resistant microbes, weeds, cancers and other diseases subject to the principles of mutation and selection phenomenon. Mutation and selection doesn’t give common descent but it does cause many problems in fighting disease. You evolutionists interfere in this fight and contribute to the premature death of millions of people suffering from diseases subject to the mutation and selection phenomenon. You evolutionists don’t understand the mathematics but here are some more empirical examples which may penetrate your evolutionist programmed minds.

http://www.bioone.org/perlserv/?request=get-document&doi=10.1603%2F0022-2585(2003)040%5B0985%3AEFSOIR%5D2.0.CO%3B2

Pyrethroid-treated nets are an efficient tool for reducing malaria transmission and morbidity. The recent evolution of pyrethroid resistance in several Anopheles species represents a major threat for the future success of roll back malaria in Africa. The possible use of nonpyrethroid insecticides, such as carbamates, on nets is a promising alternative solution because these insecticides are effective against susceptible and pyrethroid-resistant populations of Anopheles and Culex mosquitoes. Unfortunately, carbamate resistance as a result of insensitive acetylcholinesterase has recently been detected in Anopheles gambiae s.s. populations from Côte d’Ivoire. Using biochemical assays on surviving Anopheles mosquitoes from an experimental hut trial, we showed evidence for selection for an insensitive acetylcholinesterase mechanism by carbamate impregnated bednets. However, no such selection has been found with nets treated with pyrethroid alone or pyrethroid/carbamate “two-in-one”-treated nets. Because pyrethroid-impregnated nets were suspected to select for the Kdr mutation in An. gambiae, we propose that use of two-in-one nets could be a promising alternative strategy for the management of insecticide resistance in malaria vectors.

http://www.journals.uchicago.edu/JID/journal/issues/v192n7/34874/34874.html

There is consensus that combination therapy in general and ACT in particular is the way forward in antimalarial chemotherapy. Maybe the optimal future combination will be a 3-drug ACT including 2 intersynergistic quinoline drugs with similar, relatively long half-lives, protecting each others' efficacies after the fast elimination of the artemisinine derivative. Additionally, the expected complex multigenic mechanism needed for quinolone-based antimalarial resistance would be expected to slow down the emergence of this resistance to these drugs.

http://www.bact.wisc.edu/themicrobialworld/bactresanti.html

• Patients should be give combinations of antibiotics, when necessary, to minimize the development of resistance to a single antibiotic
• Patients need to be given another antibiotic or combination of antibiotics if the first is not working

http://content.healthaffairs.org/cgi/content/abstract/25/2/325

Artemisinin-based combination treatments (ACTs) are seen as an important tool in the global effort to roll back malaria. With parasite resistance to chloroquine increasing rapidly in many parts of the world, there is greater recognition of the need for a globally coordinated strategy to ensure that artemisinins are not used as monotherapy, which has the potential to cut short their useful therapeutic life. We find that even a partial subsidy could delay the emergence of resistance and that a delay in implementing a subsidy for ACTs could facilitate the emergence of resistance and lower the economic value of ACTs.

Where are all your evolutionist citations? Where is all your evolutionist mathematics? You have a peer reviewed and published evolutionist mathematical model which when it shows what you don’t want to hear, you discredit the model. Well, Dr Schneider’s mathematical model is correct, it does capture the essentials of the mutation and selection sorting/optimization process. Dr Schneider said it well when he posted this on the internet:

A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.

Well done model Dr Schneider, and Paul, you did a very nice job producing the online java version of the program.

 

[m_huber]

Selection pressures are not what we need evidence of. To demonstrate that evolution is false, you need some form of test that would show that, for example, reptiles and birds are not related. Instead, when we test them genetically, they come up as similar. When we observe the fossil lineage, we find that dinosaurs provide a common ancestor. We find that some reptiles can reproduce asexually; in some cases, (1 in 100, I am told), a chicken can reproduce asexually. So, morphological similarities aside (Ever look at a chicken's foot?), there are numerous logical pathways that can be used to arrive at the conclusion that reptiles and birds are related. This has been guessed since the early 1800's, and evidence backs it up. When we look at steady-state ideas, which were largely disposed of in the 1800's, we find that there is no evidence to suggest that things remain constant over history. While there are periods of stasis, eventually, the only thing that stays the same is that everything changes. In other words, evolution happens.

Alan, I would love to see you expand your worldview. Even if you don't accept evolution, it would be nice to see you talk about something other than a computer program.

 

[kleinman]

Annoying Creationists

Some evolutionist draw the erroneous conclusion that just because things look alike they evolved from each other. With that type of thinking, a cloud, a watermelon and a jellyfish must have evolved from each other because they are all mostly water. It is this type of nonsensical speculation that forms the basis for the theory of evolution. The fundamental principle that forms the basis of the theory of evolution is the mutation and selection sorting/optimization process and it simply does not work the way evolutionists allege. In fact evolutionists have failed to properly elucidate how this phenomenon actually works and it has hurt millions of people with diseases subject to mutation and selection in the process. Diseases like HIV have force people to come to grips with how the mutation and selection sorting/optimization process actually works and this process doesn’t use blizzards to turn lizards into buzzards with gizzards. Here are more empirical examples of how the mutation and selection sorting/optimization process actually works.
http://jac.oxfordjournals.org/cgi/content/full/52/1/11

Since many bacterial species have two intracellular targets for the fluoroquinolones (DNA gyrase and DNA topoisomerase IV), these agents have been investigated for dual targeting.58 Several new compounds (moxifloxacin, gatifloxacin, gemifloxacin and clinafloxacin) approach the dual target situation with S. pneumoniae, as judged (i) by very low mutation frequencies,59 (ii) by decreased susceptibility of both gyrA and parC resistance mutants (clinafloxacin),59 and (iii) by a diminished plateau (inflection point) in plots of mutant recovery versus fluoroquinolone concentration (moxifloxacin).24 Thus dual targeting appears to be a good approach for refining compounds to restrict resistance.

And

According to these ideas, restricting the development of resistance requires that antimicrobial concentrations at the site of infection be kept above MPC. If that cannot be done for a given agent–pathogen combination, the agent should be used as part of a combination therapy involving agents with different targets. Such an approach is likely to be required for plasmid-borne resistance.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1863594

Single agent therapy is unlikely to be successful for very long because the emergence of resistant strains of tumor cells is almost the rule in such circumstances. Only combination therapy using different types of drugs that attack a target at different sites on a molecule or attack other key molecules can prevent resistance in most cases.

http://jcm.asm.org/cgi/content/full/43/1/208

Infection with cytomegalovirus (CMV) remains a significant cause of morbidity and mortality among hematopoietic cell transplant (HCT) recipients. We describe two pediatric HCT recipients who developed persistent and severe drug-resistant CMV infections. CMV resistance to foscarnet and ganciclovir was detected after only 6 and 11 weeks of therapy, respectively. Viral pol mutations associated with drug resistance in these patients included T838A (a novel mutation) and D588N, which were shown by marker transfer to confer foscarnet and multidrug resistance, respectively. Each of these mutations significantly reduced in vitro replication of CMV, suggesting that they may decrease viral fitness. This finding was further supported by the disappearance of mutations upon withdrawal of antiviral pressure in one patient. Novel antivirals or combination therapy may be required for the treatment of drug-resistant CMV in HCT recipients and perhaps in other severely immunocompromised patients.

http://www.malariajournal.com/content/3/1/2

The effect is extremely dependent on the size of infection. As an example, if a human is inoculated with a drug-sensitive clone and there are 10^11 parasites in the host and the mutation rate to the drug resistant form is 10^-8, then there will be a sub-population of 10^3 resistant parasites. Following drug treatment, the sensitive forms will be eliminated and the sub-population of 10^3 resistant forms will expand to dominate the infection. Needless to say, if the mutation rate to resistance is 10^-8, then infection sizes of less than ten thousand would rarely contain the appropriate mutation. Current antimalarial drug deployment strategies utilise this effect by using drugs in combination. If mutation rates to resistance are 10^-8 for each drug in a two-drug mixture, then even an infection of 10^12 individual malaria parasites is highly unlikely (a probability of 0.0001) to simultaneous contain a spontaneous drug-resistant mutation in each gene.

 

[tsig]

This is a serious issue, dammit!

Straw men have constantly been subject to torture and abuse in this thread, and it just needs to stop. Enough is enough. This cruelty will not stand!

Not yet I still need more straw to mulch my garden.

 

[kleinman]

Annoying Creationists

Oh no, an evolutionist has used the all powerful strawman argument. I guess that’s what you evolutionists do when you don’t have any mathematical or empirical data. Since I have both, why don’t I give you some more empirical examples of how the mutation and selection sorting/optimization process works, which is combination selection pressures profoundly slow the process.
http://www.touchbriefings.com/pdf/886/lth041_negredo.pdf

The main objective of antiretroviral drug resistance testing in clinical practice is to improve the outcome of therapy by helping to choose the most effective combination regimens.

and

Other factors related to the evolution of drug resistance concerned or associated with antiretroviral therapy, such as inadequate drug prescription, drug–drug interactions, previous sequential monotherapy or pre-existing resistance.

http://www.malariajournal.com/content/5/1/48

This improved understanding of the evolution of drug resistance has come from a relatively simple situation. Until recently, the number of antimalaria drugs in common use was small: chloroquine and sulfadoxine-pyrimethamine in Africa and the Americas, with mefloquine and more recently, mefloquine-artesunate in Southeast Asia[13]. As chloroquine and sulfadoxine-pyrimethamine have lost their efficacy, combination drugs have been strongly endorsed as the most effective next step [14].

http://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.html

Despite the emergence of multidrug-resistant strains of hepatitis B virus (HBV) and previous success with combination therapy for other chronic viral infections, we are still using sequential monotherapy for chronic HBV infection.

http://www.dissectmedicine.com/resistance

"Long-term endocrine therapy with either aromatase inhibitors (AIs) or tamoxifen may lead to endocrine resistance and disease progression. Recent years have seen advances in our understanding of the complex biological mechanisms associated with resistance. Growth factor signaling pathways appear to be upregulated in hormone-resistant tumours and interact with oestrogen-receptor (ER) signaling, which remains functional even after long-term endocrine deprivation. Signaling through the human epidermal and insulin-like growth-factor receptor (HER and IGFR, respectively) pathways may promote ligand-independent ER gene transcription and stimulate growth factor signaling. Therapeutic agents that inhibit these signal transduction pathways, when combined with AIs, may offer breast cancer patients new hope for more robust, longer-term remissions. Preliminary data from phase II studies of combination therapies are encouraging. There is a large programme of ongoing randomised, controlled trials, the results of which should pave the way for integrating combination therapies into clinical practice. To identify which patients will respond best to particular combinations of treatments, biomarkers and gene expression profiles are being investigated as predictors of sensitivity or resistance. In time, breast cancer treatment will become truly individualised because physicians will be able to match patients with a variety of disease phenotypes to optimal combination therapies." British Journal of Cancer (2006) 95, 661-666.

 

[kjkent1]

Oh no, an evolutionist has used the all powerful strawman argument. I guess that’s what you evolutionists do when you don’t have any mathematical or empirical data. Since I have both, why don’t I give you some more empirical examples of how the mutation and selection sorting/optimization process works, which is combination selection pressures profoundly slow the process.

You have both? Hmmm...I wonder why you've never provided any for us, then?

Curiouser and curiouser.

 

[kleinman]

Annoying Creationists

Some evolutionists are having a hard time seeing the mathematical and empirical evidence that evolutionbymutationandselectiondidn’tdoit. So let’s post some more empirical citations for those myopic evolutionists who forgot their glasses.
http://www.mitpressjournals.org/doi/abs/10.1162/106454698568431

An understanding of antiviral drug resistance is important in the design of effective drugs. Comprehensive features of the interaction between drug designs and resistance mutations are difficult to study experimentally because of the very large numbers of drugs and mutants involved. We describe a computational framework for studying antiviral drug resistance. Data on HIV-1 protease are used to derive an approximate model that predicts interaction of a wide range of mutant forms of the protease with a broad class of protease inhibitors. An algorithm based on competitive coevolution is used to find highly resistant mutant forms of the protease, and effective inhibitors against such mutants, in the context of the model. We use this method to characterize general features of inhibitors that are effective in overcoming resistance, and to study related issues of selection pathways, cross-resistance, and combination therapies.

http://www.imbim.uu.se/forskning/swedbergresearch.html

Several antimalarial drugs act on the folate metabolism affecting synthesis of DNA precursors, especially dTTP. Examples are Fansidar, which is a combination of pyrimethamine and sulfadoxine, and LapDap, which is a combination of chlorproguanil and dapsone. We still do not know exactly how these compounds interfere with the folate pathways, which include both de novo synthesis and salvage of folates from the host. To be an efficient antimalarial, a drug or drug combination should act on both pathways.

http://www.cropscience.org.au/icsc2004/symposia/2/5/1401_powles.htm

It is clear that herbicides remain the most efficient technology for large-scale weed control, worldwide. However, the continued increase in evolved herbicide resistance in prominent weed species must lead to change in the way herbicides are used. As there is a paucity of new herbicide modes of action being commercialised there is an imperative to maximize the longevity of the available herbicide resource. To do this requires more pro-active herbicide usage than has been the case until now. Herbicide resistance management strategies need to be implemented that aim to maximise herbicide longevity in farming systems. Maximising the diversity of crops and weed control tools employed is essential for sustainable crop weed management. In the future, bio-economic and population genetics simulation models will assist more sustainable herbicide usage. Careful crop and herbicide rotation together with herbicide sequences and mixtures will be required. Equally, non-herbicide agronomic and biological techniques will be employed to reduce herbicide reliance thereby helping to ensure greater longevity of the precious herbicide resource.

http://www.conservationmedicine.org/papers/Kilpatrick/Kilpatrick_2006_BiolCons.pdf

In some cases it is the combination of multiple stressors that lead to the decline of species or groups of species; e.g., amphibians by nematodes (Johnson et al., 1999), increased UV radiation and pollutants (Hatch and Blaustein, 2003; Beebee and Griffiths, 2005), and disease (Collins and Storfer, 2003; Daszak et al., 2003). Conserving endangered species and facilitating their recovery is one the main environmental challenges of the 21st century. Unfortunately, history has shown that in most cases permanent removal of stressors has not been possible and species often need to be

managed indefinitely to ensure their persistence; of the 1263 species listed under the Endangered Species Act of the United States less than 2% have been de-listed (US Fish and Wildlfe Service, 2004).

Now if I only had some fossil Rorschach tests.

 

[Shalamar]

You have both? Hmmm...I wonder why you've never provided any for us, then?

Curiouser and curiouser.

I think he knows he has no evidence or proof for his claims, but if he says it often enough, people will stat to believe him.

'Creationism, apply directly to the buttocks...'

 

[delphi_ote]

I'm just wanted to stop by and continue my protest of kleinman's unethical treatment of straw men/women. I don't care if they're made of straw or wood or even bricks, forcing these fragile people to take insane positions and then torturing them with terrible arguments is wrong!

Strawpeople are people, too!

 

[joobz]

I'm just wanted to stop by and continue my protest of kleinman's unethical treatment of straw men/women. I don't care if they're made of straw or wood or even bricks, forcing these fragile people to take insane positions and then torturing them with terrible arguments is wrong!

Strawpeople are people, too!

He also believes in torturing these poor poor strawindividuals with terrible rhymes.

 

[Ottis]

Just one question. Do these strawpeople wear watches that were designed spontaneously? or did the watch design EVOLVE over thousands of years from hour-glasses and sun-dials???
Just wondering....