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Posts by staterightsfirst

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  • What Birds See [evolution of the eye]

    07/10/2006 9:26:35 AM PDT · 352 of 364
    staterightsfirst to GourmetDan

    And that would be you, Sunny Jim.

  • What Birds See [evolution of the eye]

    07/07/2006 10:31:02 AM PDT · 348 of 364
    staterightsfirst to GourmetDan

    Does this mean you can't defend the specific claim you made regarding gene duplication in "leg development genes?"

  • What Birds See [evolution of the eye]

    07/06/2006 6:41:32 PM PDT · 340 of 364
    staterightsfirst to GourmetDan

    Nice try.

    I joined this conversation because you made the specific claim that a duplication or change in regulation of "leg development" genes will result in a "freak," and that this has been observed.

    Do you have a specific example of this or do you not?

    Do you have a logical biochemical argument for this or do you not?

    Can you clearly define which genes are included in the family of "leg development genes?"

    Can you clearly define as it pertains to ecology the term "freak?"

    Are you avoiding specific answers to my questions because it is far easier to weasel out of ignorant generalizations and subjective nonsense, as opposed to actually discussing science?

  • What Birds See [evolution of the eye]

    07/06/2006 12:21:04 PM PDT · 330 of 364
    staterightsfirst to GourmetDan

    Ahh, good, now we're getting into specifics.

    In your model organism of choice, name a specific gene associated with leg development that, when duplicated or up/down regulated, results in a "freak." I'm assuming you must know one, or have read about one, to have such a strong opinion on the subject.

    This way, we'll hopefully get a clearer picture of what a "freak" is.

    Secondly, my original question still applies. Independent of gene product (though specifically in the family of genes associated with leg development, but you will need to clearly specify which genes are in this family), why is an arbitrary gene duplication event deleterious to the individual?

  • What Birds See [evolution of the eye]

    07/05/2006 10:11:27 AM PDT · 308 of 364
    staterightsfirst to GourmetDan
    You made the claim that gene duplication always results in a "freak," or, a reduction in fitness for successive generations.

    Can you support that claim with a reasoned biochemical and ecological argument or can't you?

  • What Birds See [evolution of the eye]

    07/04/2006 3:05:28 PM PDT · 255 of 364
    staterightsfirst to GourmetDan; b_sharp
    And 'gene duplication' and 'regulatory gene modification' produces only freaks that would be eliminated from the population, not new more fit creatures.

    This statement is trivially false.

    But please, if you disagree, explain clearly to me how a gene duplication event, independent of gene product or expression level, will always lead to a reduction in fitness.

  • What Birds See [evolution of the eye]

    07/03/2006 7:56:11 PM PDT · 206 of 364
    staterightsfirst to Mogollon

    Yeesh. I try and try to stay out of these debates, but...

    Pharmacodynamic tolerance is an acquired trait, not a hereditary one.

    So you're really, really, wrong. Streptomycin resistance is caused predominantly by a hereditary mutation in the ribosomal S12 subunit gene. When the sensitive population was exposed to this drug, this mutation was strongly selected for as predicted by natural selection. Evolution in action.

    But please, if you still disagree, by all means explain precisely how all that we've observed with regards to streptomycin resistance is consistent with pharmacodynamic tolerance.

    Feel free to use references from the primary literature.

  • Deadly Quackery

    06/04/2006 10:17:47 AM PDT · 43 of 46
    staterightsfirst to Steve Van Doorn

    Yeah, the CD4+ T cells are the "helper" T cells.

  • Deadly Quackery

    06/04/2006 10:12:35 AM PDT · 42 of 46
    staterightsfirst to John Valentine

    I notice you don't bother to address my points, only my single use of hyperbole.

    See post #30 - that's fine.

  • Deadly Quackery

    06/04/2006 12:25:51 AM PDT · 30 of 46
    staterightsfirst to staterightsfirst

    OK, considering that the guy who wrote it is purportedly a PhD in Molecular & Cell Biology, I guess "no knowledge of virology" is a little bit harsh.

    :P

  • Deadly Quackery

    06/04/2006 12:11:05 AM PDT · 29 of 46
    staterightsfirst to John Valentine
    Actually, I had read each of these papers long ago and found each of them misleading and esentially dishonest as to their titling.

    I still have the papers. Do you recall any specific problems did you have with their reasoning?

    As for the paper you posted, it's awfully questionable itself. For example, it's clear the authors have absolutely no knowledge of virology (kind of important if you're going to be discussing HIV). For example, at one point they say:

    Despite its spectacular birthday, the HIV-AIDS hypothesis has remained entirely unproductive to this date: there is as yet no anti-HIV-AIDS vaccine, no effective prevention, and not a single AIDS patient has ever been cured.

    Well, that's because:
    1) The HIV vaccine is difficult to develop; animal models are poor, the virus is highly mutagenic, and the receptor-binding portion actually conceals itself in the envelope.
    2) Antivirals have been shown to be effective at preventing AIDS from developing in HIV-positive individuals provided they do not continue to engage in high-risk behavior
    3) Because AIDS only develops after the supply of CD4+ T cells has been depleted it makes absolutely no sense to claim that an inability to cure AIDS somehow means that HIV isn't causing it - (and their 1 in 500 infected/depleted T cell argument is specious at best)

    And when it comes down to it, the best predictor for the development of AIDS is STILL HIV infection, a point noticeably absent from this paper - even though they go into a great deal of detail analyzing and attempting to draw their conclusions from looking pretty much exclusively at sub-groups (such as HIV-positive non-drug users versus drug users, which is another fallacious point: how much more likely is it for a drug user to engage in risky behavior and have a compromised immune system that itself increases the odds of developing AIDS?)

    ...and if you're so sure, why not volunteer for one of the HIV vaccine trials? I mean, you won't get AIDS anyway, right?

  • Deadly Quackery

    06/03/2006 10:50:06 PM PDT · 10 of 46
    staterightsfirst to John Valentine
    You mean besides all of this right?

    If that doesn't turn your wheel, then you can go directly to the primary literature, and take your case up with them. For example:

    HIV Causes AIDS
    W. Blattner, R. C. Gallo, H. M. Temin
    Science, New Series, Vol. 241, No. 4865 (Jul. 29, 1988), pp. 515-516

    How HIV causes AIDS.
    Spartalis MA
    Journal Of The National Medical Association 1995 Mar; Vol. 87 (3), pp. 171, 173.

    HIV causes AIDS: Koch's postulates fulfilled.
    O'Brien SJ; Goedert JJ
    Current Opinion In Immunology 1996 Oct; Vol. 8 (5), pp. 613-8.

    For everybody but the fringe who have offered no alternatives, the debate is over.

  • A revolution for evolution - Intelligent design must not replace hard science in classrooms.

    11/14/2005 4:05:51 PM PST · 146 of 153
    staterightsfirst to johnnyb_61820
    It would be random if it were evenly distributed.

    ... If the organism restricts itself to a single gene, then it is NO LONGER RANDOM.

    So your definition of random is exclusive to a uniform distribution over the entire genome? I can't have random numbers with a normal distribution? Or a Poisson distribution?

    Congratulations on redefining 'random' in order to better your own argument. This is getting to be a common trend with you. Yeesh. Have you even read a single biology/math textbook?

    For the lurkers, here's a simple example. If I have the numbers [1][2][3][4][5] and I flip a coin randomly to change number 4 to either 6 or 8, guess what? The new sequence is random. It may have a narrow distribution, but because the new sequence isn't deterministic (i.e. you can't predict what it will be), it's random.

    Where do you base the idea that this pattern _originates_ from natural selection? ... It is not consistent with natural selection being able to _build_ such a restricting mechanism.

    Natural selection does not originate or build anything. It acts on existing diversity. You're clearly showing your unfamiliarity with evolutionary theory.

    it is the cell actively reconfiguring itself ... Let's say I need a new gene

    This implies intelligence (as does the entirety of the rest of your ridiculous post). This has not been demonstrated and should not be a part of your assertions.

    Cells do not have an 'idea' about how they want to change. They do not 'plan' new phenotypes.

    Genomic change is random through recombination or mutation. Natural selection acts on those changes. It is observed that nature is reactive, not proactive. This is consistent with evolutionary theory.

    Really, why am I bothering to discuss this at all with you? If you're willing to redefine "random" to suit your purposes, there doesn't seem much hope in expecting a rational criticism of evolution from you.

    Also, Dembski? No.

  • A revolution for evolution - Intelligent design must not replace hard science in classrooms.

    11/14/2005 1:15:58 PM PST · 143 of 153
    staterightsfirst to johnnyb_61820
    If you are in the hundreds, I would count that as complex.

    So in other words, your argument against evolution is based on some arbitrary criteria and has nothing to do with evolutionary theory. Thanks, that's what I thought.

    Pseudomonas / DNA Poly IV,V

    Restricting mutagenesis (by whatever mechanism) to a specific part of the genome would give the organism a selective advantage and is consistent with natural selection. Hint: This is why sexual recombination is favorable. Even flu viruses show this pattern of having some parts of the genome more mutagenic than others, because natural selection favours it.

    Also, note that it's very intellectually dishonest to use phrases like, "the cell even knows that" since you're implying higher order intellegence where none has been shown to exist, i.e. at the cellular level.

    Our observations of beneficial change in organisms is almost entirely driven by mechanisms of purpose, not happenstance.

    And yet every example of genetic change we've covered is effectively random. Even if an organism restricts mutation to a single gene, the mutated sequence will be randomly determined because of the fundamental biochemical mechanisms. Natural selection acts on those random mutations.

  • A revolution for evolution - Intelligent design must not replace hard science in classrooms.

    11/14/2005 11:28:05 AM PST · 141 of 153
    staterightsfirst to johnnyb_61820
    But the points at which the recombination take place are not.

    Sure they are. Recombination varies linearly with distance. The further apart two genes are, the more likely a recombination will occur between them, because crossing over is random.

    I noticed you also ignored the point that chromosome segregation is random. Convenient.

    What you seem to be saying here is that neo-Darwinism is untestable. However, there are ways to speed up frequency of mutations in the lab, without affecting their distribution.

    No, I'm saying that what we've observed is consistent with evolutionary theory.

    We understand _some_ of it very well. But, for instance, it seems that E. Coli can actually regulate how well DNA polymerase operates, based on stress conditions:

    First of all, it's DNA Poly III, not IV or V, that performs large-scale replications in E.Coli.

    Second of all, this doesn't change the fact that random errors are introduced by all polymerases; regulating the activity of an error-prone polymerase does not change the random nature of the mutagenesis. It's just another way that prokaryotes can encourage diversity, which is necessary for survival by natural selection - which is consistent with evolutionary theory.

    Finally, I notice you didn't answer my question about complexity, which is at the heart of the issue here. You want to see a complex adaptation, but you refuse to precisely define it.

    How many base pairs are required to make an adapatation complex?

    Can a prokaryote even show a complex adapatation that would satisfy your criteria?

  • A revolution for evolution - Intelligent design must not replace hard science in classrooms.

    11/13/2005 9:28:42 PM PST · 135 of 153
    staterightsfirst to johnnyb_61820
    Most adaptations are complex. There are a few that aren't, mostly that only require changes within one gene of only a few amino acids.

    So you're defining a complex mutation by the number of base pairs that change?

    How many DNA base pairs would need to change to constitute a complex adaptation as compared to a non-complex one? Does it matter where on the genome the DNA changes, considering that tweaking developmental genes leads to exponentially different characteristics whereas changing base pairs in other parts of the genome may do nothing at all?

    On top of that, if you're going to define a complex mutation by the number of base pairs involved (since you effectively disregard recombination as nonrandom) and you want to see this scale of viable mutation in the last hundred years in order to demonstrate evolution in action - then you're actually asking for evidence against evolutionary theory, which indicates that random mutation causes large changes over millions of years, not hundreds.

    Interestingly, I'm pretty sure much of what is considered "errors in replication" are processes we simply don't understand.

    No. Errors in replication are a fundamental part of the chemistry involved in DNA polymerase activity. We understand it very well.

    "Normal sexual recombination is random to a certain extent." ; Are you sure about that? I would ssay that the only thing "random" about it is that we don't understand the process.

    Then you would be wrong. We understand the process very well. Segregation of chromosomes at meiosis during gamete production is a random process. It's a coin flip whether the sperm gets the maternal chromosome or the paternal one. Even genes on the same chromosome are randomly recombined due to crossing over.

  • A revolution for evolution - Intelligent design must not replace hard science in classrooms.

    11/13/2005 4:45:51 PM PST · 133 of 153
    staterightsfirst to RunningWolf
    Science provides sound explanations for the origin and diversity of life, and the origin of the Universe.

    What's the problem with assuming we have the ability to someday elucidate the mechanics of the universe?

    Assuming we can't do something seems like an easy way to never accomplish anything.

  • A revolution for evolution - Intelligent design must not replace hard science in classrooms.

    11/13/2005 4:33:15 PM PST · 132 of 153
    staterightsfirst to johnnyb_61820

    Define "complex adaptation." How do we distinguish a sufficently complex adaptation from a non-complex one for the purposes of your criteria?

    Secondly, what qualifies as a random mutation? Does retrovirus infection count? UV damage? Changes in ploidy? Or only errors in replication? Normal sexual recombination is random to a certain extent. Does that not qualify? Why not?

  • Kansas Fight on Evolution Escalates (Teachers groups punish Kansas school)

    11/07/2005 8:30:21 PM PST · 407 of 410
    staterightsfirst to csense

    "The apples fall this way"

  • Kansas Fight on Evolution Escalates (Teachers groups punish Kansas school)

    11/07/2005 5:30:58 PM PST · 400 of 410
    staterightsfirst to csense

    I didn't say you couldn't _use_ the tools of philosophy. Read my earlier posts. Science uses the tools of logic and mathematics to explain the mechanics of the observable universe, and so is narrower in scope than philosophy, which can presume to explain the unobservable as well.