From: treon3verdery@gmail.com   
      
   They could mutate a bunch of yeast, knoocking out genes, notably 6K genes at   
   microorganisms and 20K at a mammal, find which out of a million (parallel   
   measurement of duplicate knock outs)  omit living longer with a longevity   
   drug, then sequence their    
   genomes to find the missing gene, then look for SNPs or copy number variations   
   of that gene at living organisms with the gene that then cause greater   
   susceptibility and effectiveness of the longevity chemical, then transfer the   
   gene to mice and human    
   tissue culture, see if it is possible to make mice that live 80-200% longer   
   from rapamycin treatment (up from 60%) this way, or 79 to 140% longer from   
   royal jelly ingredients (25/27% longer), possibly decanoic acid esters like   
   10HDA and 10H2DA, or 14 to    
   105% longer from metformin (up from 3-35% longer lifespan); notably if these   
   genes are completely new to being investigated it is possible that rather than   
   using already researched mechanisms they might utilize new mechanisms that   
   favor the effectiveness    
   of numerous longevity molecules and drugs that do not, or do not yet, have   
   published mechanisms of action; so, finding these genes, optimizing SNPs or   
   making new gene nucleotide sequences, as well as changing copy number, could   
   make an organism much more    
   susceptible to a wide range “any” new longevity drugs and chemicals being   
   characterized;   
      
      
      
   It is imaginable that a gene that causes double or halved diameter or quantity   
   of nuclear membrane pores could have effects on anything that gets   
   transcribed, also it is possible to imagine that, noting autophagy happens at   
   numerous, different receptor-   
   differing longevity drug effects, that something that makes autophagy 2,4, 8,   
   16, 32 times more likely to occur at the presence of some cytochemical (a new,   
   or, SNP optimized, copy number optimized, variant of the “autophagy turn-on   
   protein that is    
   much more active at what previously would be traces of chemical that were less   
   than autophagy causing, that now cause autophagy even from 1/16 or 1/32nd   
   amounts) could be the result of enriching the amount or activity of a gene,   
   which if deleted at a    
   yeast, happened to make a sluggish version of an autophagy turn on gene (that   
   required much more endogenous cytochemical to turn autophagy on); so, 180   
   degrees different than the nonresponsive version, the new gene, optimized SNP,   
   or most beneficial copy    
   number would cause greater susceptibility to longevity drugs of numerous   
   kinds, receptors, and mechanisms, including new mechanisms without any   
   previous research as well as new drugs;     
      
      
      
   Finding the genetics of unusually high, hyperresponsiveness to longevity   
   producing drugs and chemicals also brings up the possibility of making   
   laboratory model organisms that are 2, 4, 8, 16, 32 times more responsive to   
   new longevity chemicals and drugs    
   that are possibly being screened as libraries; There is a difference between   
   this and just a genetic variation that causes dose susceptibility;  say an   
   unengineered typical mouse registers a mild 7% longevity increase from   
   smelling the odors of young    
   mice of a sex they can have progeny with, if the gene-response heightened   
   mouse registers a 23% longevity increase then this might suggest that, once   
   the mouse’s nasal receptors got turned on, regardless of the dose above a   
   threshold, the neurons    
   connected to something, or did something that caused 2,4,8,16 times bigger   
   diameter nuclear membrane pores to get utilized, or some neural acivity, which   
   might just barely modify autophagy, is now of sufficient size to cause   
   longevity producing amounts    
   of autophagy, this effect even when the actual dose of the scent is either   
   midrange, or perhaps engineered to be at highest amplitude respponse at nasal   
   neurons already.   
      
      
      
   Laboratory organisms with heightened amplitude of response to longevity   
   chemicals and drugs could create higher prominence (statistically resolvable   
   effectiveness) of new and effective and developable longevity drugs and   
   chemicals at mass screening,    
      
       
      
   Another example could be a “cyclomolecule transport channel active transport   
   gene”; basically this might be a gene that specifies active transport of   
   anything with a cyclic part (benzene, cycloanything) at its molecule, that is   
   kind of a gene for:    
   really likes to transport most few amu drugs directly to the cytoplasm, a   
   yeast without that gene might be unresponsive to many many pharmaceuticals,   
   but a yeast with optimized SNPs, new nucleotides at a new “cylomolecule   
   active transport gene”, or a    
   higher copy number of that gene, might be 2-10 times more responsive to any   
   drug added to its medium, the cyclomolecule transport gene is sort of near a   
   dose responsiveness gene though;   
      
      
      
   One possibility to make more illness more rapidly curable, at a wider variety   
   of treatable tissues, possibly including treating, preventing or curing   
   cancers, is to do gene therapy that puts: 2,4,8,16,32, or even 1000 times more   
   active transport of    
   anything with a cyclic area at its molecule to the cytoplasm gene,    
      
   It is also possible that some kind of loclization could be utilized to   
   localize the gene therapy at a particular tissue or oncocyte area; that way a   
   person could take a longevizing dose of rapamycin, while at any oncocytes,   
   that the cyclomolecule active    
   transport gene therapy had localization at, the rapamycin dose would be   
   32-1000 times higher and block or terminate any oncocytes.   
      
      
      
      
   [continued in next message]   
      
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