• New longevity genes: (1/2)

    From Treon Verdery@21:1/5 to All on Mon Oct 10 04:58:09 2022
    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.



    it is possible that a new, existing, or optimized cyclomolecule active transport gene could be used to treat or prevent malaria, On finding a cycle-having molecule transport gene, a technologist would think of RNA and DNA drugs, as well as peptides and
    function-causing nestles-together at sockets protein drugs and few AMU molecule drugs to cause the “make more cyclomolecule transport channels” gene to be more active, or also to cause the already there amount of cyclocontaining molecule drug
    transporter channels to heighten their activity, or possibly also modify their specificity to transport more kinds of molecules; There might be something like a drug, mRNA, siRNA, other RNA or DNA drug, peptide, or even harmless, existing, nonengineered
    bacteria or virus, that causes the active transport at the external cell membrane of of cyclic area (like benzenes or various partially saturated on nonsaturated cyclothings) containing molecules to heighten, if there is then it could be coadministered
    with malaria medication, or perhaps any medication containing a cycloarea at its molecule, to create much stronger response per microgram of dosage; that could make malaria medication a few orders of magnitude more affordable from a raw chemical
    ingredient perspective,



    It is possible that a kind of chemical, drug, or gene therapy, or bacteria specific RNA/DNA drug could cuase bacteria to actively transport cyclic structure area containing molecules 2, 4, 8, 16, 32, even 1000 times more actively, that could cause the
    bacteria of focus to be more likely to transport a greater amount of antibacterials (antibiotics) curing bacterial infections; I do not know if this would make it so that 1) amplified active transport of cyclocontaining molecules at bacteria of focus
    simultaneous with 2) antibacterial, antibiotic doses that are 16, 32, or even 1000 times fewer migrograms/picograms/ml would make it so the bacteria of focus transported much more antibiotic, was terminated and the person cured while, beneficially,
    exposing body organisms like other bacteria, to only 1/16 or 1/32nd or even 1/1000 of the actual quantity of migrograms or nanograms of antibacterial or antibiotic; keeping that vast number of different nonfocus bacteria from developing antibiotic
    resistance; it might be effective, and at things like milk cows and egg chickens, could make it so that illnesses that affect these could be mass treated, as they are during 2019, with the 1/16, 1/32, or even 1/1000th 2019 dose of antibiotics,
    simultaneously reducing antibiotic resistance development at all of the other bacteria at the organism, and making the actual medication affordability 1-3 orders of magnitude more affordable



    Modifying active transport with drugs, chemicals, genetics, or possibly RNA/DNA/peptide drugs could cause immunizations to be more effective, perhaps a version that did 2,4,8,16,32 or 1000 times more active transport, possibly with transcytosis, to
    anything, even a many-AMU molecule like an actual antibody would cause heightened effectiveness as well as new therepeutic technologies, like: antibodies doing things at the cytoplasm; what happens to an antibody at the actual cell cytoplasm? Does it
    just sit there in jello? Can it glom entirely new things floating around, causing entirely new, beneficial medical effects? (cytoplasm reaching antibodies could glom deleterious versions of nonfuncting mitochondria, and some petides or proteins
    festooning the at-cytoplasm antibody could communicate to lysosomes, “engulf this nonfunctional organelle (unuseful mitochondria)”; antibodies that glom onto a lysome, noting I read antibodies, at a different thing, cytoexterior, can cause a receptor
    to activate or passivate as the technology makign person prefers, suggests that at-cytoplasm antibodies could make lysosomes much more likely to recycle cytocomponents causing autophagy to increase, that creates a new longevity drug based on a one-dose
    administration of an antigen to produce the antibodies); As a brain and CNS funcion heightening and longevity and young phenotype supporting and increasing technology it is possible that glia, which move around, and benefit the brain, and are descended
    from innunocytes, could, using a drug, chemical, RNA or DNA drug, gene therapy or germline gene modification have their active transport heightened for drugs, chemicals, molecules, peptides, RNA or DNA drugs with particular moeities, perhaps easy to make,
    but rarerly endogenously produced at the body moeities, that cause the glia to do things that are particularly longevizing of CNS brain function, brain CNS capability increasing, and shielding of the CNS brain from anything deleterious at the neurons
    that glia support and travel around through;



    Screening a library of 10 to 100 million or even a billion molecular variants and peptides with a 10 million cells/second flow cytometer could be a 10 second to 100 second (or, with parallel simultaneous dosing of 10 cells per chemical, 20 minute) way to
    find out which molecules and chemicals and drugs cause changes at various kinds of active transport and cytotransport at cells; Once found these chemicals could be enhanced, diversified, and the new library screened; That creates the drugs and chemicals
    that cause the physiologically beneficial, medically beneficial, capability enhancing, as well as longevity, wellness, and healthspan heightening new drugs at cytoplasm effects



    Also, I do not know, but it looks like at cell cytoplasm sized structures, even though pershaps the cells are terminated, antibodies can glom to cytoplasm sized things, even though I think of antibodies as being many-AMU protein things



    This thing says that when you change the nucleus of just one cell, the cells ner it change as well, it calls this “they bystander effect”; are there physiologically beneficial, longevizing, wellness and healthspan heightening bystander effect
    technologies, if, as it says, the bystander effect exists?

    “the nucleus is the target for genotoxic and cytotoxic effects. Reports on the “Bystander Effect” indicate that DNA damage can be caused in cells not directly traversed. Objective: use microbeam to selectively irradiate cytoplasm to determine if
    there are effects on survival or mutation frequency. The Columbia microbeam produces alpha particles of 5.5 MeV, range ~40 μm, LET = 90 keV/μm. Irradiation of each cell takes about 6 seconds. All cells on the dish irradiated, then trypsinized, removed
    and plated for either survival or mutation analysis. Mutation assay is the AL hamster line with one human chromosome. Human chromosome expresses cell surface antigens that make cells susceptible to complement inactivation. Wild-type cells are killed in
    the presence of antibody and complement Cells with mutations in this gene can survive.”



    are there plenums (separation structures) of some kind that divide bystander effect areas from each other, I do not actually have any idea, but I perceive that if I get a beautification chemical peel, it is absent effect on my vagus nerve, what are the
    plenum forms, sizes, lengths, genetics and physiochemistry of the bystander effect; is more bystander effect beneficial, is less of it beneficial, are there human genes, SNPs as well as copy number variants that cause, noting the 100% difference among
    normal humans at some attributes (IQ 200, age at first ovulation, height) it is possible some humans have double or half the bystander effect, among these which have greater longevity, wellness, healthspan, subjectivbe well being (happiness) and
    benevolence?



    Body and other Fluid technology: antibodies can glom to things the size of, I perceive I read, three nucleotides (like 10 or more non hydrogen atoms per adenine, so 30 non hydrogen atoms at a shape), and I do not know how many metal atoms to make a
    glommable thing, but antibodies can react to metals like cobalt, so an antibody might actually be able to change shape around 1 metal atom, although, noting three nucleotides, it is also possible it is 30-300 atoms at a multiatom cobalt particle, that
    suggests it is possible to make an antibody that, without full glomming, although it could also fully glom, a particle at a fluid environment could get the entire antibody protein to change shape and charge; on glomming, the glider’s hydrodynamic wing
    position could change, I suppose I might have heard of one atom changing the conformation and entire quaternary and tertiary structure of a protein, but it seems like it might be possible to make like an antibody glider (like an actual shape) that has
    wings that change their positioning based on sensing one atom, or a few hundred; that could cause an ingredient (antibody gliders in solution) that when placed at a fluid would make the fluid’s containerful effect flowability, even things like physical
    directionality, a kind of chirality, and 3d spatially specifiable adjustable things, possibly as macroscopic as light polarization-size molecules, and even tetris-piece (or fittable modules) accumulations at various areas of fluid velocity, specifiable
    and even algorithmically directable (from some perspectives programmable, also automata-directable); antibodies are $435/gram online; This reminds me of nanoassembly, and one thing to think about is where does the energy to change glider wing postition
    based on 1 atom (or a few hundred come from); ATP is the 20th century reply, but there are a number of triphosphate molecules that might be able to bring conformation-modifying energy to proteins, notablyproteins that have previous biogenic energy
    circuits, UTP, GTP are a couple, but it seems possible that with modelling a new nucleotide, and a bunch more phosphates at a polyphosphate, could make something like a UTP, GTP polymer with like 30 to 300 phosphates on it, which is a couple orders of
    magnitude more energy to bring to the molecule, like a thing-glomming and moving antibody molecule so it can do more thing recognizing, and thing moving around, at higher velocities from an ambient energy source that has like 100 times more molecular
    energy at a form that can power things that have a biogenic (from organisms) protein energy chemistry; some bacteria make polyphosphate crystals, and polyphosphate is a water treatment chemical



    also, as a multiatom molecular technology that reminds me of a nanoassembler, can you just take two or three antibodies, attach them to each other at the base of the Y so they are a certain distance apart and angle, and then glom and position items that
    meet up with them and are the right shape; three of these reminds me of a drill chuck, and the thing about getting them to do things onpurpose could be



    drug amplification technology, wikipedia says, “but lipids and nucleic acids become antigens only when combined with proteins and polysaccharides” suggests that making a nucleic acid drug, or a lipid drug, makes it so that: nucleic acid liposomes, if
    they are possible, or perhaps not, could concentrate at the lymphatic compartment, omitting first pass metabolism, while being immunoinvisible; I read liposomes get glommed with antibodies, nucleic acid thing (drug) containers could last much longer than
    regular liposomes, even though nucleic acid forms are different than autoassmebling phopholipid bags, also RNA and DNA drugs, perhaps made with new nucleic acids, or also really strong new variants on the rails of ladders, could be really really durable
    active drugs, but omit being glommed up; halogenation might keep the liver from metabolising them as well



    Tolerogens cause antibodies to be calmer, It is possible that antibodies that cause some kinds of inflammation, if reduced as to their intensity with tolerogenic therapy, could cause a reduction of physiological accumulated problemness, and preserve
    younger phenotype longer; preserving younger phenotype longer could cause greater longevity, wellness, and healthspan; it is not that linked, but kind of reminds me of, rapamycin being a transplant-rejection blocking (immunomodulating) drug



    things that cause tolerogenic activity: “Semi-mature dendritic cells are tolerogenic. Conditions including the absence of an inflammatory environment result in the incomplete maturation of dendritic cells.”; so if an SNP or gene copy number, gene
    therapy or germline genetic engineering on humans optimizes dendritic cell forms that are tolerogenic, that could be a longevity wellness and healthspan heightening technology, there are numerous technology branches and possibilities to making
    tolerogenic benefits, wikipedia says, “completely protected from symptoms”, “produced IL-10, (an antiinflmmatory cytokine, that is also at intracyte spaces) a cytokine which is able to inhibit the Th1 response”





    Deleting histone deacetylase 2 HDAC2 at mice cause greater cognitive ability, this could be a human intelligence heightening genetic modification, they could find people with an absence of HDAC2 at the population or various SNPs and find out the
    quantifiable effect on g (like IQ), as well as personality (like big5 measurement) of an absence of HDAC2 or also SNP variants and copy number variants on human being as an intelligence increasing gene





    Noting depot drug injections, It could be possible to beneficially immunize children and give them their booster immunization simultaneously, benefitting children’s wellness and well being; online it mentions, “The percentages of primed children with
    hSBA titers ≥8 was low for serogroup A (6–25%) and moderate for serogroups C (27–43%), Y (69–74%) and W (56–69%). For all serogroups, hSBA antibody geometric mean titers (GMTs) tended to be higher in the ACWY-2 than the ACWY-4 group. Post-
    booster/single dose, ≥96% of primed and ≥73% of naïve children had hSBA titers ≥8 against each serogroup, and hSBA GMTs were higher in primed children.” which to my peception might communicate something kind of like “about half of children
    become immune with one dose when they were just a few months old, then with another dose at 60 months then about 4 out 5 or also 19 out of 20 became immune”; At a particular group among a few groups, they gave the children 2 doses of immunizations at
    about a year, then again at 60 months, and got 96% effectiveness; That suggests that if the children had one office visit, rather than three, and that if the one dose at the office visit had microparticles that released immunization chemicals to their
    body at 60 months later, that they could get 96% immunity from one dose and one office visit; just one office visit rather than three could make it so more children and their parents succeeded at the procedure;



    a microbead slurry or 1 ml or less that could be injected at the bellybutton, with the bellybutton location omitting bumpiness as well as being absent sensation or a wiggletropic conceptually noticeable form: It might be possible to do something like
    9600 DPI inkjet printer print 14 or hundreds of sandwich layers of materials with minute squiggles on them, and have the base it is printed on dissolve at a harmless solvent, leaving a bunch of separate inkjet printer ink polymer and protein customized
    geometry sandwitches, or 3D printer print a shape, like things with branches that have branches, that does a math function of how much things soak in to the branches, and how much the branches dissolve per month; sort of like the first 14 months, the
    first branches plump up and dissolve, then the next 14 months the branches sequential to that that plump up and dissolve, and then after that the next group of branches plump up and dissolve, where each dissolving of branches creates a fluid channel with
    like 100 times more spontaneous fluid motion even at the diffusion only next to body-tissue moist environment of a bellybutton injected slurry of microspheres, then at 60 months the branches that, at their sequence, plump up and dissolve, while having
    lots of immunization protein rich branchlets, and possibly even also enzymes that dissolve the polymer that the immunization depot is made of, turning the microspheres to soft wet jello mini blobs, and at 60 months the supplemental dose that raises
    immunity from 6-74% to 96% is administered





    That reminds me of the longevity drug depot injection, thinking about hundreds of years of continuous contribution of longevity drug ethynylfluorarapamycin to thecirculatory system from a gram or less of ethynylfluororapamycin at a way to make the depot
    injection function many centuries is:

    I think that something like eentsy linear strings of protein releasing polymer, sort of like string cheese version of norplant, as microbeads, (kind of a millifiore polymer protein form) could always have high output lines of chemical concentration, as
    compared with like diffusion from a sphere that has layers of different drug concentrations (kind of like candy panning) from the surface;







    I read flow cytometry of yeast can characterize 10 million yeast cells per second; is it possible that an integrated circuit technology could use a 1 cm 10 billion well geometry (although it might be 1 billion, or even 100 million wells because the yeast
    are actually perhaps 2 micrometers large each, and statistically having a plurality at each well has value), with a semiconductor light emitter (laser diode) as well as photodetector at the base, or oblique side, of each well, to do imaging of at a 10
    billion yeast colony well as a parallel chemical, like physiochemical, scientific and manufacturing research and technology, as well as drug reasearch, and other utilizations, screening technology; The flow cytometry version with 9600 DPI inkjet
    printheadf also could be beneficial utilizable technology: although the published flow cytometer only utilizes 10,000 seconds to process 10 billion yeast cytes, if they are at wells at a semiconductor technology produced structure, like about a cm^2 of
    semiconductor wafer, then their row, as well as column location can be related to the chemicals or processes that they have experienced, as well as provides a location with lots of order, minimized unplanned variability; compare the 9600 DPI inkjet
    printer attached to a 10 million yeast cell per second flow cytometer: theoretically a 10 million yeast cells per second could print out say, 5000 yeast cells each containing microdots of fluid, possibly even containing a: preserves living organisms
    chemical, or even a cryoprotectant, and basically 9600 DPI print an array of 46 billion separate, findable, the 5000 different yeast cells could be resorted, yeast cells per square inch, certainly with the option of printing them with a couple diameters
    of space between them to make 46 billion findable yeast on a cryopreservable, or ambient stable chemistry array about 3 inches on a side;



    the 9600 DPI living, viable, or possibly even spore-induced yeast cells on a paper like surface (likely a polymer surface) also could be immunofluorescence dipped



    Interestingly, if the 10 million yeast/second flow cytometer finds or matches, or groups the things it sorts, then it can actually repoduce identical or near identical visual identity form row and column sorted, printed 3 times 3 inch prints, then,
    immunofluorescent dipping of one of the papers/polymer inkjet like arrays, could find yeast of interest, and then because the flow cytometer grouped yeast together, another piece of paper/polymer would have that identical flow cytometry visual (imaging)
    form of yeast geometric arrangement on the paper/polymer, at those same row as well as column coordinates, and a third piece of inkjet printed paper could have the same array, again, printed with cryoprotectant for sharing with other persons or further
    development uses; from the perspective of a person with a liter of yeast fluid, they could print out as many copies of their yeast chemical response and its characterization, or yeast chemical production genetic library, or yeast drug response library
    as they liked; With this system, one person could distribute a 46 billion seperate, and reseparable yeast library to as many people or organizations as they liked;



    Also, using 9600 DPI inkjet technology it could be possible to print a layer of immunofluorescent material onto the printed dot layer of yeast, possibly have ambient moisture, or 9600 DPI printed fluid diffuse or blend sufficiently to visibly
    fluoroimmunolabel the yeast, gaining more data of value; The 9600 DPI inkjetcould also apply chemical reagents to the yeast as well,



    As a longevity technology, printing yeast, then printing a matrix of 300 different longevity chemicals at a row, and 300 different longevity chemicals at a column, possibly even layering yeast, nutritive growth medium, longevity chemical, more yeast, and
    more growthmedium as a 9600 DPI sandwich could produce a 90,000 combined longevity chemical matrix



    Notably, noting the sizes of screenable libraries, autogenerated variations of longevity molecules could have millions or billions of screenable variants; every hydroxyl and hydrogen at rapamycin could be considered as a binary power of 2 with about 2^30
    possible different versions; every location of the oxygen and hydroxyl and unsaturated C=C at a decanoic acid ester (like 10HDA or 10H2DA) is a possible combinatoric library; notably though, as 9600 DPI inkjet printing can make hundreds or thousands of
    identical printed versions of a screened library to distribute to other persons at a company or other scientists, sharing actual organism form, distributing reproductive ready samples, recorded as well as completely new data, archiving, artificial
    intelligence and software queryability and stimulation of the dataset, as well as backup copies are among benefits of 9600 DPI yeast sandwich and sortation printing;



    There are numerous linked technologies: A collaborator at the same company could reload another person’s yeast print into another 9600 DPI inkjet printer, then print a completely different immunofluorescent labeller onto the identical dataset of 300
    times 300 longevity chemicals effect on yeast chemical matrix, Another person might actually physically grab a separated with a gap printed yeast colony dot with 5000 yeast at it, put it in culture medium, grow a few billion of them, and then do a new
    screening, on perhaps an computer modelled group of related longevity chemicals, or completely new chemicals, likely with flow cytometry and 9600 DPI inkjet printing with new chemicals, processes and areas of interest, Another person at another company
    the first company is collaborating with might do flow cytometry with 9600 DPI inkjet printing to compare a human tissue culture chemical sandwich response or also flow cytometry grouping at the 200 times 200 longevity chemical matrix and compare the
    areas of most similar and most different expression and amount of longevity, finding chemicals that had much more effect on humans than yeast, as well as chemicals that effected both similarly: that would suggest that the chemicals that effected only
    human tissue culture cytes have a different genetic and physiochemical longevity producing basis; they could then do tissue culture response at a 300 times 300 longevity 9600 DPI printed chemical sandwich matrix with tissue culture of species far from
    both humans and yeast, like marsupials, platypus, million year lifespan endoliths, 400 year lifespan quahog clams, termite queens, macaws, and naked mole rats; longevity chemical responses at a matrix shared between these would be highly conserved, and
    longevity chemicals with particular concentrations and activity at different but related species could show the different separate occurence of high-longevity capability phenotype, genotype, and what might be called chemotype capabilities; finding those
    origins, their actual genetic nd physiochemical origins, of new longevity chemotypes describes linked physiochemical systems, and gives the possibility of transferring those longevity systems, as genes, to other organisms, to bring that organism an
    entire beneficial useable longevity phenotype, genotype, chemotype to the other species, humans would benefit from clams, and possibly endoliths. The responses of a plurality of species’ tissue cultures to a matrix of chemicals from things like the
    king’s holly (40,000 year lifespan) and creosote bush could also be compared;



    I read that atopic dermatitis, “guidelines for AD include hydrating topical treatment, topical glucocorticosteroids” which made me think, what about other sugars and carbohydrates at he “gluco” part of clucocorticoid? How about a
    ribocorticosteroid (ribose), or e fewer AMU erthritol C3 sugar (glucose is C6) so erythricorticosteroids as a treatment; then I thought about how images of the dermis I have seen have many cell types and layers, and it is possible that different
    medications might localize to these various cytotypes and sort of distances from both skin surface and distance from capillaries could localize differently; if there is a most exterior cytomembrane transported to cytoplasm chemical, like maybe ATP, or an
    ion where if it is at a persons skin it is itchless like Mg, or even Ca. then atopic dermatitis medication with that most highly exterior cytomembrane transported chemical as part of the atopic dermatitis treatment like an ATPhalogenatedcorticosteroid or
    a magnesiumhalogenatedcorticosteroid could be beneficial as it gets much more transport, possible active transport or also transcytosis transport;



    GSK:


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