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Joined 1 year ago
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Cake day: June 15th, 2023

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  • Bad take. Is the first version of your code the one that you deliver or push upstream?

    LLMs can give great starting points, I use multiple LLMs each for various reasons. Usually to clean up something I wrote (too lazy or too busy/stressed to do manually), find a problem with the logic, or maybe even brainstorm ideas.

    I rarely ever use it to generate blocks of code like asking it to generate “a method that takes X inputs and does Y operations, and returns Z value”. I find that those kinds of results are often vastly wrong or just done in a way that doesn’t fit with other things I’m doing.













  • I understand what you’re saying about drift, but I’m not sure that feels sufficient to explain the prevalence of anti-biotic resistance.

    One interesting discovery was the remains of a person in Peru from something like 900 years ago. One really interesting aspect of the discovery was the gut bacteria in the remains. When they sequenced the genome of some of the bacteria they found that they were the same species as we have today. But more importantly was that the genes that encode for antibiotic resistance existed in those bacteria.

    https://www.ancient-origins.net/news-history-archaeology/ancient-peruvian-mummy-surprises-researchers-antibiotic-resistant-genes-020581

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4589460/

    The discussion here isn’t about how antibiotic resistance first came about, the discussion is about how bacteria have been reacting to modern medicine. Why are bacteria becoming harder to treat with antibiotics as time goes on?

    The point I was making is that bacteria already have antibiotic resistance in the genome, but the phenotypic expression is inversely related to bacteriophage resistance.

    Antibiotic resistance needs

    • weaker/more flexible cell walls

    • more efflux pumps

    Bacteriophage resistance needs

    • stronger/stiffer cell walls (to protect against punctures)
    • less efflux pumps (to increase material strength of cell wall)

    In any population group there’s going to be variation in the expression of genes (the phenotype). In that population there are going to be individuals with greater antibiotic resistance and others with greater bacteriophage resistance. When antibiotics are introduced it kills most of the bacteria, but there can be a few individuals with higher antibiotic resistance that can potentially repopulate a new generation with an allele frequency shifted towards higher antibiotic resistance.

    I know what I just described is “natural selection”, but that’s not evolution. Natural selection is one of the processes that is part of evolution, but it is not evolution in of itself.

    Edit: formatting


  • Yes, genetic drift is evolution

    Not “genetic drift”. Although I did forget a critical word. I meant to say “allele frequency drift” which is distinctly different than genetic drift.

    Allele frequency drift simply describes a shift in how common a genetic trait exists, or is expressed, within a population group. The overall genetics of the group are the same. Even if there were no changes to the collective genetics of a population over millions of years (no evolution) you can still have allele frequency drift.

    This is what I mean by “allele frequency drift isn’t evolution”. It’s a mathematical expression of the ratio a gene is expressed within a population group. It doesn’t describe any genomic changes or mutations.

    The first generation can have frequency 1.0 of a trait, gen 2 can have 1.5, gen 3 can have 2.0, and then back down again over the next few generations. But generation 10 can have an (nearly) identical genome to generation 1.