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Re: [psychiatry-research] News: Connection between faulty neural activation and schizophrenia revealed

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  • anonymous_9001
    Among others. http://www.ncbi.nlm.nih.gov/books/NBK26836/
    Message 1 of 8 , May 4 9:25 PM
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      Among others.

      http://www.ncbi.nlm.nih.gov/books/NBK26836/

      --- In evolutionary-psychology@yahoogroups.com, james kohl <jvkohl@...> wrote:

      >I think what you're trying to say is that only random mutations alter the
      > genome sequence. Am I right?
      >
      >
      > James V. Kohl
      > Medical laboratory scientist (ASCP)
      > Independent researcher
      > Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the
      > socioaffective nature of evolved behaviors. Socioaffective Neuroscience &
      > Psychology, 2: 17338.
    • james kohl
      ... From: anonymous_9001 Among others. http://www.ncbi.nlm.nih.gov/books/NBK26836/ Excerpt with my emphasis: The number of genes is
      Message 2 of 8 , May 5 4:14 AM
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        --- In evolutionary-psychology@yahoogroups.com, james kohl <jvkohl@...> wrote:

        >I think what you're trying to say is that only random mutations alter the
        > genome sequence. Am I right?


        From: anonymous_9001 <anonymous_9001@...>
        Among others.


        http://www.ncbi.nlm.nih.gov/books/NBK26836/

        Excerpt with my emphasis: The number of genes is only very roughly correlated with the phenotypic complexity of an organism. Thus, for example, current estimates of gene number are 6,000 for the yeast Saccharomyces cerevisiae...

        Thanks for helping me to make my point.

        See: Extensive transcriptional heterogeneity revealed by isoform profiling

        Abstract excerpt: Our findings have implications for genome compaction, evolution and phenotypic diversity between single cells.

        My comments (with my emphasis):

        Genetically homogenous populations of yeast cells were grown in two conditions.
        1) with glucose as the carbon source;
        2) with galactose as the carbon source.

        In a genome containing 6,000 open reading frames, the authors report detection of approximately 1.88 million unique transcript isoforms (e.g., 776,874 supported by at least two sequencing reads defined by a unique combination of end sites at single-nucleotide resolution).

        If nutrient-dependent adaptive evolution were not pheromone-controlled, accumulated mutations might result in species differences in adaptively evolved neurogenic niche construction and differences in neural activation. However, there is no evidence for that! There is also no model for that. Instead, in species from microbes to man, adaptive evolution and species diversity is nutrient-dependent and pheromone-controlled.

        Attempts to explain adaptive evolution via mutations theory can be compared to a model that accurately represents how the difference in two nutrients results in approximately 2 million changes. The changes obviously contribute to epistasis (as is required for species diversification), which  must be pheromone-controlled.  Participants in intelligent discussion should be struck by the degree of systems complexity (e.g., in neuronal architecture in species from nematodes to man)  that cannot be explained via current mutations theory, but can be explained via what's currently known about biological facts.

        I am struck by your ignorance and implied assertion -- by offering the reference above -- that you know anything at all about this topic.

        Thanks again,

        James V. Kohl
        Medical laboratory scientist (ASCP)
        Independent researcher
        Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.




      • anonymous_9001
        None of that refutes anything I ve said. I will remind you again what this was originally about: Chromatin remodeling? Epigenetic. Does not alter base sequence
        Message 3 of 8 , May 5 9:09 AM
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          None of that refutes anything I've said. I will remind you again what this was originally about:

          Chromatin remodeling? Epigenetic. Does not alter base sequence at all. All it
          does is change how the genome is packaged to regulate access of transcription
          factors and RNA polymerases. Does not alter genome sequence.

          Silencing? Epigenetic. Silencing can be a result of chromatin remodeling,
          production of repressors/breakdown of activators, RNA interference, etc. Does
          not alter genome sequence.

          Alternate splicing? Epigenetic. Splicing is post-translational. Does not alter
          genome sequence.

          --- In evolutionary-psychology@yahoogroups.com, james kohl <jvkohl@...> wrote:
          >
          > --- In evolutionary-psychology@yahoogroups.com, james kohl <jvkohl@> wrote:
          >
          > >I think what you're trying to say is that only random mutations alter the
          > > genome sequence. Am I right?
          >
          >
          > From: anonymous_9001 <anonymous_9001@...>
          >
          > Among others.
          >
          >
          > http://www.ncbi.nlm.nih.gov/books/NBK26836/
          > Excerpt with my emphasis: The number of genes is only very roughly correlated
          > with the phenotypic complexity of an organism. Thus, for example, current
          > estimates of gene number are 6,000 for the yeast Saccharomyces cerevisiae...
          > Thanks for helping me to make my point.
          > See:Extensive transcriptional heterogeneity revealed by isoform profiling
          > Abstract excerpt: Our findings have implications for genome compaction,
          > evolution and phenotypic diversity between single cells.
          > My comments (with my emphasis):
          > Genetically homogenous populations of yeast cells were grown in two conditions.
          > 1) with glucose as the carbon source;
          > 2) with galactose as the carbon source.
          > In a genome containing 6,000 open reading frames, the authors report detection
          > of approximately 1.88 million unique transcript isoforms (e.g., 776,874
          > supported by at least two sequencing reads defined by a unique combination of
          > end sites at single-nucleotide resolution).
          > If nutrient-dependent adaptive evolution were not pheromone-controlled,
          > accumulated mutations might result in species differences in adaptively evolved
          > neurogenic niche construction and differences in neural activation. However,
          > there is no evidence for that! There is also no model for that. Instead, in
          > species from microbes to man, adaptive evolution and species diversity is
          > nutrient-dependent and pheromone-controlled.
          > Attempts to explain adaptive evolution via mutations theory can be compared to a
          > model that accurately represents how the difference in two nutrients results in
          > approximately 2 million changes. The changes obviously contribute to epistasis
          > (as is required for species diversification), which must be
          > pheromone-controlled. Participants in intelligent discussion should be struck
          > by the degree of systems complexity (e.g., in neuronal architecture in species
          > from nematodes to man) that cannot be explained via current mutations theory,
          > but can be explained via what's currently known about biological facts.
          >
          >
          > I am struck by your ignorance and implied assertion -- by offering the reference
          > above -- that you know anything at all about this topic.
          > Thanks again,
          >
          > James V. Kohl
          > Medical laboratory scientist (ASCP)
          > Independent researcher
          > Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the
          > socioaffective nature of evolved behaviors. Socioaffective Neuroscience &
          > Psychology, 2: 17338.
          >
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