To: Brumar89 who wrote (184028 ) 3/23/2006 10:31:59 PM From: neolib Read Replies (1) | Respond to of 281500 Are you saying here that science will negate religion as Dawkins, Provine, and the rest say? I'm saying that is how the ID groups like the Discovery Institute see the issues. I don't see it that way because I see many religious people that accept evolution. It is the more fundamentalist, literal readers of the Bible that can't accept it. For myself, as an engineer, a system that can evolve strikes me as a much more astonishing system than a static one. Just my two cents.What if a supernatural explanation is the correct explanation for some things? Like for example the origin of the universe or the origin of life. Or the fine tuning of the universe. Then science can't comment on it, unless somehow a way is found. So far none have been.This is the first time I've seen anyone refer to the operation of the immune system within an organism as an example of evolution in action. This is a brief description: The model deduced from these findings provides an unambiguous biological example of the power of random mutations and selection. (The current model as understood by molecular immunologists is slightly more complex than described below, but does not differ in any features relevant to the logic of this essay.) When antigen enters the body, it triggers a small number of B lymphocytes -- namely those whose surface antibody can bind the antigen -- to multiply and secrete antibody. These early responding antibody sequences are made of assembled germline gene elements in unmutated form, and frequently have low affinity. Furthermore, these antibodies were not "designed" to bind the antigen; they were proteins that happened to pre-exist in the body before any exposure to the novel challenge with antigen. As the immune response continues, the antigen-activated B cells move to germinal centers. Hypermutation begins, and starts generating antibodies with altered structures. The hypermutation mechanism acts randomly and independently in the different clonal progeny cells, introducing essentially random alterations in the antibody sequence in each cell. Most cells undergoing hypermutation end up producing antibody with unaltered or reduced affinity for the antigen; the latter cells would no longer be activated by antigen. However, rare mutations lead to antibodies of higher affinity for antigen. As the existing antibodies help to remove progressively more antigen from the circulation and the antigen concentration falls, selection for high affinity becomes the crucial factor in determining which cells will be stimulated by antigen. With lower amounts of antigen present, the cells expressing low affinity antibody on their surface become progressively less able to bind and be stimulated by antigen; in the environment of the germinal center, these poorly stimulated B cells are programmed to die by a specific process known as "apoptosis." (Choe et al, J Immunol 157:1006,1996) In contrast, the cells with high affinity antibody continue to bind antigen, and thus continue be stimulated to proliferate and secrete antibody. As the antigen concentration progressively falls while mutation and selection continue, the intensity of the selective pressure for high affinity increases. Repeated cycles of mutation and selection can lead to affinity levels 100-fold higher than that of the original unmutated antibody. The "competition" for efficient antigen binding has been shown to be the selective force driving the rise in antibody affinity, since if antigen is repeatedly administered to prevent the drop in antigen level and thereby eliminate the selective pressure for efficient antigen binding, antibody affinity does not rise (Eisen and Siskind, Biochemistry 3:996, 1964). Furthermore, when selection pressure has been experimentally removed by engineering mice with impaired capacity for programmed death by apoptosis, many B cells are found that make mutated antibodies with low affinity (Takahashi et al. J Exp Med. 190:39, 1999). Late in the course of an immune response, as antigen becomes completely cleared from the bloodstream the amount of antibody secreted gradually falls and the immune response ends; but a subset of the last group of highly efficient cells persists as a quiescent population known as "memory cells," ready to respond with rapid secretion of high affinity antibody should they ever be triggered by another encounter with the same antigen in the future. Next you wroteScience was developed by Christians but they continued to attribute the universe to God, so they weren't philosophical materialists. I'm guilty of using philosophical materialists when I should say methodological naturalists. I don't care about their philosopical views, only how they practice science. Thus theistic evolutionists are IMO, methodological naturalists, they practice science that way. They might not be philosophical materialists. I don't care about that. ID wants to attack the practice of science. That I care about.Yep. I do accept common descent (have you reconsidered your opposition to this in an earlier post, btw?) and I accept an evolution that does not preclude divine activity in the natural world. Then you are a theistic evolutionist, which I have no problem at all with. But why do you make comments saying the evidence for evolution is not compelling in that case? You still have not pointed out what ID brings to the table if you accept theistic evolution. I can't see any point to it in that case. Its only if you want to say that certain elements of the theistic part are actually detectable that it makes any sense, but even then, once you accept common descent, who cares?