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There are limitations of the use of a genetic algorithm compared to alternative optimization algorithms:
But obviously the pharmaceutical company has selected one of the studies from the “very good” end of the bell curve.
Mutation accumulation experiments are a very poor way to understand deleterious mutation accumulation. Such experiments do not study actual mutations, they only study performance of strains (the supposed ‘mutations’ are only inferred). In the papers of this type I have examined, zero mutations are actually documented. All that is observed is differential performance of strains. Non-genetic causes, including epigenetic effects or gain/loss of viruses in some bacterial culture, etc., cannot be precluded. More to the point, since the overwhelming majority of mutations are very subtle and do not express a clear phenotype, almost all mutations will be invisible in these experiments, which only monitor gross differences in performance . Only high-impact mutations can be observed in such experiments, and these represent a biased sampling of the actual mutational spectrum. Furthermore, high-impact deleterious mutations will still always be selected away in such experiments, no matter how hard the experimenter tries to preclude natural selection. Therefore there will be a strong tendency to preferentially observe only high-impact beneficials. Since the crux of the genetic entropy argument involves the low-impact deleterious mutations (which will always be invisible in such experiments), these types of experiments have no relevance to this discussion. A final point: in these experiments, fitness is always narrowly defined (., ability to grow on a given medium). For simple, one-dimensional traits like this, any genetic change affecting that trait has a reasonable chance of being beneficial (in a one-dimensional system, any change can only be either up or down, as opposed to improving a real-world complex network of traits where fitness is enormously multi-dimensional).
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