From: treon3verdery@gmail.com   
      
   Longevity technology: Scientists have already found the differences between   
   the longest and shortest lived bats. They found 2089 gene variants between the   
   two. Noting about 1000 of those genes are likely shared with humans (Homo   
   sapiens and branch    
   species), those thousand genes can be installed with gene therapy into mice,   
   at 21 groups of 49 genes each, and 11 mice per group to get a p value on   
   longevization effects. That is just 232 mice. It may be possible to do this   
   with even fewer mice using a    
   fractional matrix design procedure. After that, two to four rounds of   
   different simultaneous potential longevity gene concentrating admixtures can   
   be accomplished. Biomarkers of aging could be used to determine reduced aging   
   prior to actual determination    
   of 98th percentile longevity. Using biomarkers allows faster rounds of   
   selection and remixing. Another completely different approach is to use the   
   high N outdoor mouse dorm, combined with crispr/cas9 to generate mice with   
   just 11 long lived bat genes per    
   mouse among those genes that are shared with humans. The outdoor mouse dorm   
   mice then have sex and babies. As these generations of mice reach 6-18 months   
   they may have readable aging biomarkers, and the least aging mice grouped   
   together to have babies    
   again. Those progeny mice are then screened for most minimal aging at   
   biomarkers of aging, making a round. This can also be done with bowhead whale   
   genes, and 400 year lifespan tortoises and 400 year lifespan quahog clam   
   genes. The abstract of comparing    
   bat longevity genetics says, "Bats are the longest-lived mammals given their   
   body size with majority of species exhibiting exceptional longevity. However,   
   there are some short-lived species that do not exhibit extended lifespans.   
   Here we conducted a    
   comparative genomic and transcriptomic study on long-lived Myotis myotis   
   (maximum lifespan = 37.1 years) and short-lived Molossus molossus (maximum   
   lifespan = 5.6 years) to ascertain the genetic difference underlying their   
   divergent longevities. Genome-   
   wide selection tests on 12,467 single-copy genes between M. myotis and M.   
   molossus revealed only three genes (CCDC175, FATE1 and MLKL) that exhibited   
   significant positive selection. Although 97.96% of 12,467 genes underwent   
   purifying selection, we    
   observed a significant heterogeneity in their expression patterns. Using a   
   linear mixed model, we obtained expression of 2,086 genes that may truly   
   represent the genetic difference between M. myotis and M. molossus. Expression   
   analysis indicated that    
   long-lived M. myotis exhibited a transcriptomic profile of enhanced DNA repair   
   and autophagy pathways, compared to M. molossus. Further investigation of the   
   longevity-associated genes suggested that long-lived M. myotis have naturally   
   evolved a    
   diminished anti-longevity transcriptomic profile. Together with observations   
   from other long-lived species, our results suggest that heightened DNA repair   
   and autophagy activity may represent a universal mechanism to achieve   
   longevity in long-lived    
   mammals." Another way to gain greater mouse and human (Homo sapiens and branch   
   species) longevity is to consider the M, Myotis bat as normal, and the shorter   
   lived bat as having deleterious genes, a third bat midway between the two   
   could also be    
   characterized. This way it is possible to search for and likely find things   
   the M. Molossus produces that actually decrease lifespan (interleukins,   
   beneficial network or cascade "slowdown" physiochemicals, proteins like Brd2).   
   The researchers method    
   could be applied to long and short lived tortoises as well as quahog clams and   
   the clams' shortest lived clam relatives.   
      
   Well baby genetics, rounds of mouse and marmoset genetics, epigenetic drug   
   benefits humans   
      
   Persons at the 90th percentile of intelligence and above who have zero family   
   history of birth defects may have a traceable genetics of being absent birth   
   defects that can be made into RNA drugs and gene therapies that after testing   
   at mice can be tested    
   by volunteers who are planning a pregnancy.   
      
   Diacetyl melatonin night be measured as being especially longevizing at the   
   brain, while melatonin palmitate could especially benefit lipid rich regions,   
   and the free base of melatonin can reach the other regions, it could be   
   especially longevizing to    
   take all three together,   
      
   Longevity technology, the least change to an amino acid sequence that creates   
   quaternary protein structure could be used at longevity producing proteins to   
   make new varieties of those proteins likely with unique effects, possibly   
   encouraging longevity,    
   similarly at longevity proteins the least amino acid sequence change that   
   removes quaternary structure could also make improved protein longevity drugs,   
   a variety of protein structures for any particular near identical amino acid   
   sequences could be    
   screened at mice to see which is the most active at longevization form to turn   
   into a human protein drug or gene therapy tested by volunteers.   
      
      
   Precluding pattern recruitment at people under 18 or older with amygdala size   
   reduction that is absent effect on cognitive g, is genetics that preclude   
   acting in anger and is beneficial.   
      
      
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