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author | Bryan Bishop <kanzure@gmail.com> | 2025-08-13 13:53:07 -0500 |
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committer | Bryan Bishop <kanzure@gmail.com> | 2025-08-13 13:53:07 -0500 |
commit | d4f403e3c3a6f78e637e7a1f2bc4a8339ce449b9 (patch) | |
tree | fb91f6eac49fc4f50863f1c1b921f9bc6da634ce | |
parent | 35f3715e348e886fe441ecb4ebe9961d0d1dd4d1 (diff) | |
download | diyhpluswiki-master.tar.gz diyhpluswiki-master.zip |
-rw-r--r-- | genetic-modifications.mdwn | 24 |
1 files changed, 14 insertions, 10 deletions
diff --git a/genetic-modifications.mdwn b/genetic-modifications.mdwn index 5fcc073..f38f1c3 100644 --- a/genetic-modifications.mdwn +++ b/genetic-modifications.mdwn @@ -1004,8 +1004,6 @@ What about radiation resistance? Here's a case in the literature where radiation * kidney/liver size increase, or <a href="http://gnusha.org/logs/2017-04-30.log">supernumerary kidneys (extra kidneys)</a> -* <strike>hippocampus size</strike> (done) - * sleep: anti-tiredness (might be a form of insomnia?) * sleep: can we combine night owl + morning person? @@ -1014,7 +1012,7 @@ What about radiation resistance? Here's a case in the literature where radiation * copy-paste some of the gene therapies from earonesty's list: <https://web.archive.org/web/20150907230432/http://www.documentroot.com/2014/08/gene-therapies-i-want-to-see-developed.html> -* olfactory receptor genes, see <http://gnusha.org/logs/2017-09-01.log> and <a href="https://www.biorxiv.org/content/biorxiv/early/2018/06/28/358739.full.pdf">A scalable, multiplexed assay for decoding receptor-ligand interactions</a> +* olfactory receptor genes, see <http://gnusha.org/logs/2017-09-01.log> and <a href="https://www.biorxiv.org/content/biorxiv/early/2018/06/28/358739.full.pdf">A scalable, multiplexed assay for decoding receptor-ligand interactions</a>. Copy olfactory receptor genes from canines. * gallstone disease - variants in ABCG8 and TRAF3 <a href="https://www.biorxiv.org/content/early/2018/02/20/265728">ref</a> @@ -1030,7 +1028,7 @@ What about radiation resistance? Here's a case in the literature where radiation * optional or delayed puberty (trigger puberty later or whenever the child wants- wait 5 years? 20 years?) -* fertility upregulation, such as early ovarian hypertrophy during gestation, enhanced ovarian reserves such as through <a href="https://www.nature.com/articles/ncomms2861">Foxo3 overexpression</a> +* fertility upregulation, such as early ovarian hypertrophy during gestation, enhanced ovarian reserves such as through <a href="https://www.nature.com/articles/ncomms2861">Foxo3 overexpression</a>; enable or upregulate post-natal oogenesis. * blood types @@ -1042,14 +1040,12 @@ What about radiation resistance? Here's a case in the literature where radiation * tay-sachs allele and IQ ? -* Cas9 immunity, Cas9 tolerance (be permissive or restrictive about future CRISPR dosages) - -* disable germline transmission of certain modifications (germline editing is primarily required for zero mosaicism by modifying pre-conception or post-conception a single cell embryo, but this is only a delivery detail not something specifically related to desiring inheritance; long-term inheritance is a secondary goal that could be toggled on and off) - * personality - see <a href="https://www.biorxiv.org/content/biorxiv/early/2018/11/26/476010.full.pdf">ref</a> (?) This system is conserved across various mammalian species. SNORD copy number variations. "Particularly significant are SNORD115 and SNORD116\_2. The latter is the variant that is predicted to bind to Ankrd11 exon X, while the possible target genes for the other two SNORD116 variants are not yet clear. These latter ones show generally only little copy number variation (Table 1). However, we note that the direction of the correlation is different between rodents and humans. In humans, the relatively higher anxiety group has the smaller number of copies, while it is the other way around in the three tested rodent species (see above)." -- regulation of behavioral variance using snoRNAs. * TODO: review <a href="https://en.wikipedia.org/wiki/Human_accelerated_regions">human accelerated regions</a> (segments of the human genome that are conserved throughout vertebrate evolution but are strikingly different in humans, especially compared to chimpanzees); and long non-coding RNAs (lncRNAs). See also "<a href="https://www.nature.com/articles/nature10530">A high-resolution map of human evolutionary constraint using 29 mammals</a>. Note also that thee are human-specific deletions compared to chimpanzees in otherwise conserved sequences. "A study examining intragenic clustering of human accelerated elements found that the transcription factor neuronal PAS domain-containing protein 3 (NPAS3) has the largest population of noncoding-accelerated regions. NPAS3 is active during mammalian brain development and the human accelerated elements within this locus predominantly appear to act as transcriptional enhancers." +* find areas of "accelerated evolution" in recent human genome; look at common mutations in the population; most mutations are probably detrimental or neutral. It's possible to figure out which genes (and alleles in particular) have been spreading rapidly throughout the population, so we should look at that information. Compare against neanderthal genome and other ancient human genomes that have been sequenced. Compare also to great ape genomes, chimpanzee, orangutan, macquee, etc. + * improved anti-cancer apoptosis stuff * [telomerase stuff](http://gnusha.org/logs/telomerase.log) @@ -1070,14 +1066,22 @@ What about radiation resistance? Here's a case in the literature where radiation * anti-sunburn, sunburn protection- see SOD pathway upregulation -* find areas of "accelerated evolution" in recent human genome; look at common mutations in the population; most mutations are probably detrimental or neutral. It's possible to figure out which genes (and alleles in particular) have been spreading rapidly throughout the population, so we should look at that information. - * <a href="https://www.gwern.net/Embryo-editing">gwern.net/Embryo-editing</a> * figure out what makes <a href="https://diyhpl.us/~bryan/papers2/neuro/Human-specific%20ARHGAP11B%20increases%20size%20and%20folding%20of%20primate%20neocortex%20in%20the%20fetal%20marmoset%20-%202020.pdf">human ARHGAP11B</a> cause mammalian brains to grow so much larger +* Cas9 immunity, Cas9 tolerance (be permissive or restrictive about future CRISPR dosages) + * encode CRISPR-Cas9 or even dCas9 fusion proteins into the germline genome such that future payloads can rely on Cas9 or dCas9 availability for future genetic upgrade delivery into adults. +* disable germline transmission of certain modifications (germline editing is primarily required for zero mosaicism by modifying pre-conception or post-conception a single cell embryo, but this is only a delivery detail not something specifically related to desiring inheritance; long-term inheritance is a secondary goal that could be toggled on and off) + +* if you can cause ancephalic human fetal development via embryo engineering (such as for human cloning), then i wonder if you could introduce an engineered non-ancephalic neural cell line into the embryo (hybrid, mosaic or chimeric embryo) and have it develop the cortical neural tissues instead of the ancephalic cell line. this reduces concerns of non-brain pleitropy. The metabolic and other biological requirements in neurons is likely to be vastly different from the demands of the other cell types in the body; an increase in separation of concerns can reduce undesirable or unintended side effects including non-genomic other-tissue/other-organ "off-target effects". + +* reduce human skin attractiveness to mosquitos, possibly related to carboxylic acid secretions + +* optimize metabolism and nutrition for modern dietary demands + ## Microbiome ### dental caries vaccine |