Annoying Creationists
Hey, I saw that movie. I wonder what will replace us when they make the next “meteor hits” movie.
Sure I know where you can buy a ticket where one ticket can win a million lotteries. Evolutionists are selling that ticket all the time which also explains why you are not incredibly wealthy. Yes sol, your formula is correct. The probability that the theory of evolution is true is not 1 in 10^400, it is 1 in 10^360. Do you want to buy a ticket to that lottery? They are on sale, a quarter each or increase your chances with 3 for a dollar.
Here’s a couple more examples how mutation and selection actually works, no charge for these tickets.
http://mic.sgmjournals.org/cgi/content/full/153/10/3211
http://www.springerlink.com/content/7441316203717r82/
Why should I even waste my time trying to refute your computer program? If you can provide one real example of your model then I’ll spend some time trying to understand your algorithm. On the other hand, it is very easy to find real examples of combination selection pressures slowing the evolutionary process and that is what Dr Schneider’s peer reviewed and published model shows. Do you want me to help you find examples of your algorithm? Try googling “nonexistent” “examples” “evolution”.Kleinman said:When you produce a single real example that shows n+1 selection conditions evolve more rapidly than n selection conditions, I’ll take a look at your program.rocketdodger said:Or, in other words, you are a fraud who knows none of the mathematics you claim to know and are completely unable to refute any of my mathematics.
Kleinman said:Belz, I’m not ignoring your posts, I’m waiting for one of you evolutionists to post a citation showing that n+1 selection pressures evolves more rapidly than n selection pressures.Belz… said:Easy.
Kleinman said:Belz… said:
Dinosaurs live and die for millions of years, with n selection pressures affecting them.
Meteor hits. Selection pressures: n+1. Lots of death. Suddenly mammals are all over the place.
Hey, I saw that movie. I wonder what will replace us when they make the next “meteor hits” movie.
Yes, I think so, that’s what makes dinosaurs turn into mammals after meteor hits. I really like the Bugs Bunny and Road Runner cartoons they show with the movie.Kleinman said:If you want to talk about beggaminases, that alright with me.Belz… said:Yes, let's talk about that. Remember what it means ?
Sadly, that experiment is being done.Kleinman said:Kjkent1, I have never said that there can not be variants of genes. There are hundreds of forms of human hemoglobin. Just because there may be two variants of a particular gene that may confer resistance to a particular drug does not mean there is no goal for evolution as you allege. All you have shown is that there are only a small number of possible genetic sequences that improve fitness for the virus from the huge number of possible combinations available. The transformation of reptiles into birds requires a trajectory on a fitness landscape that transforms thousands of genes which always gives fitness to reproduce. When you give an example which shows only two possible variants that give improved fitness to reproduce, how do you explain the transformation of thousands of genes when you have so few variants that give improved fitness to reproduce?kjkent1 said:In the current example there are demonstrably at least two pathways to resistance (maybe more, no way to know without repeating the experiment at least a few million times).
Kleinman said:Sol, forget the 100 generations, show us how to use probability theory to win a million lotteries only 14 times longer than winning one lottery. You must be incredibly wealthy after winning all those lotteries.sol invictus said:I already did - if you can find me a million lotteries where each ticket has a chance to win all of them. That's not so common in real lotteries... but the math is identical to the case we were discussing, which is why I mentioned it.
Kleinman said:sol invictus said:
In any case you've already agreed my formula was correct, and yours was wrong. Are you flipflopping again?
Sure I know where you can buy a ticket where one ticket can win a million lotteries. Evolutionists are selling that ticket all the time which also explains why you are not incredibly wealthy. Yes sol, your formula is correct. The probability that the theory of evolution is true is not 1 in 10^400, it is 1 in 10^360. Do you want to buy a ticket to that lottery? They are on sale, a quarter each or increase your chances with 3 for a dollar.
Here’s a couple more examples how mutation and selection actually works, no charge for these tickets.
http://mic.sgmjournals.org/cgi/content/full/153/10/3211
Candida albicans drug resistance – another way to cope with stress said:Exposure of C. albicans to antifungal drugs induces immediate phenotypic stress responses that may permit drug tolerance. This tolerance allows the selection, or evolution, of stable stress responses that confer higher levels of resistance. All micro-organisms contain a plethora of genes that can potentially confer resistance to new environmental stresses (Wright, 2007). C. albicans is a diploid fungus with several gene families that have probably arisen by gene duplication. We have discovered that alleles of CDR1 and CDR2 within the same strain differ functionally and that CDR2 alleles are continuing to evolve (Holmes et al., 2006). Thus there are a large number of pumps with different substrate specificities that, if overexpressed or mutated, could confer resistance to ‘novel’ antifungals with intracellular targets.
Candida albicans drug resistance – another way to cope with stress said:
This perspective on antifungal drug resistance suggests several possible ways of overcoming, or preventing, drug resistance. Combination therapy can be used to attack two different targets simultaneously with a low probability that resistance to both drugs will arise, or to attack a drug target and its resistance mechanism (cf. augmentin). While combination therapy sounds attractive, and it has been reported that antimicrobial combinations can actually select against the development of resistance (Chait et al., 2007), clinical results are variable and there are increased efficacy testing requirements.
http://www.springerlink.com/content/7441316203717r82/
The clinical challenge of imatinib resistance in chronic myeloid leukemia: emerging strategies with new targeted agents said:Abstract Chronic myelogenous leukemia (CML) is a progressive and often fatal hematopoietic neoplasm. The disease is characterized by the presence of the Philadelphia chromosome, which arises following a balanced translocation between chromosomes 9 and 22, creating the BCR-ABL fusion gene. It is often stated that the only proven curative option is allogeneic stem cell transplantation (allo-SCT), which is indicated for only a limited subset of patients. The Bcr-Abl tyrosine kinase inhibitor (TKI) imatinib mesylate (IM) represented a major advance over conventional CML therapy. Following IM treatment, more than 90% of patients obtain complete hematologic response, and 70–80% of patients achieve a complete cytogenetic response. Resistance to IM represents an increasing clinical challenge and is often a result of point mutations causing a conformation change in Bcr-Abl, which impair IM binding. Novel targeted agents designed to overcome IM resistance, including multitargeted TKIs and farnesyl transferase inhibitors, are in various phases of development. Dasatinib, which has recently become available in the clinic, is a Bcr-Abl TKI that also inhibits Src, c-Kit, platelet-derived growth factor receptor, and ephrin A receptor kinases. In a phase II randomized trial in patients resistant or intolerant to IM, patients receiving dasatinib had better hematologic and cytogenetic responses than those on high-dose IM, irrespective of the presence or absence of mutations. Nilotinib has also shown promising activity. Combining IM with conventional chemotherapy, interferon, and targeted agents including TKIs is being actively pursued. Diagnostic testing may enable individualized targeted treatment so that patients receive the most effective agent first-line.