Longevity technology: (2/2)
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Treon Verdery@21:1/5 to
All on Tue Oct 4 05:34:31 2022
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So like 100 milligram of antibodies gets used up on the highly 8:1 decorated transport channel-blocking molecules, while well cytes have a graphical distribution displaying the number of glommable plugs as centering on just one or even zero; It would
take 24 hours to make another entire 100 milligrams of antibodies, so noting the decorated plug molecules wear off before that 24 hours while the body is producing the next 100 mg, the 24 hours that pass make cause just 1/4 of 1/8th the decorative plugs
to be at well cytes. The well cytes only get 1/32nd the immunoreaction cleaning dose of immune system response. Meanwhile the deleterious cytes still have a plurality of decorative plugs at each cyte, labelling them for glomming and removal.
Longevity technology:
So is there a sequencable series of natural allergens, or even easy to find and get harmless colds that can be screened, like a screenable library, to do this glom at the places beneficial senolytics are active, gently wash well cytes to experience
immunoharmlessness, and also up immunocytes purposefully to terminate the labelled deleterious cytes? That would be a sequence made from preexisting viruses and allergens at the 2019 AD typical population, where a human body proceeding through that
sequence actually gets greater longevity, wellness, healthspan, and youthful phenotype.
So, uh, BCG, and possibly, MAO-B receptors on blood cyte surfaces, and perhaps there is something natural that occurs at capillary epithelial cytes; could blenderized pollen, perhaps with oil to make GI tract passaging liposomes, cause immunoreaction at
the circulatory system? Also what about things like mushrooms, fugu, and other species immunoreaction physiological products? Are there things like blenderized e. coli variations of particular kinds that cause varied immune response, which can be bred
or engineered to be longevity, healthspan, wellnes,, and youthfulness of phenotype beneficial senolytics, because they have different lipopolysaccharides on their membranes?
Find the receptors or molecule transport channels that are at the exterior cytomembrane of senescent cytes, the kind longevity, wellness, healthspan and youthful phenotype producing senolytics effect. Optimally find external cytomembrane molecular
biology characteristic structures, senescent cyte-only receptors and molecule transport channels unique to senescent cytes. Then gather a bunch of those unique molecular biology object-features, like proteins, molecule transport channel membrane protein
structures, or possibly lipid raft like cytomembrane fragments with a stable, typical to living structures of a molecular biological form of the kind of deleterious cyte terminating senolytics terminate, Then screen libraries of wild-type bacteria, fungi,
plants, and even virus products to find out if they effect, modify, block, cause hypertransport at, or disintegrate these molecular biology structures.
Also, a novel thing, place a bunch of the actual molecules and proteins that are the unique biomolecular structures of the kinds of cytes senolytics terminate, at a culture medium, perhaps a (1000 times 1000) million multiwell plate, that contains a wide
survey of bacteria, wild yeast, and variations on what humans think of as beneficial bacteria (probiotics); possibly use micropositioning to place a zone of molecular biology unique structures, a diffusion gap. and then a bacterial growth area: this
causes material that diffuses across the zone to be measurable as to its quantitative effect on the unique molecular biological structures of the kind of cytes senolytics direct their effects at; When some of the million sample multiwell plates find
bacteria, fungi, even viruses hosted by human tissue culture cytes products’ or other materials that cause plugging, blocking, hypertransport amplification, or disintegration of the unique molecular biological structures of the kind of cytes senolytics
terminate, then organisms that produce new senolytics have been identified and can be quantified as longevity, wellness, healthspan, and youthful phenotype producing drugs. These wild type organisms can also be bred to have much higher amounts of
senolytic chemicals. That is a new source of senolytic drugs.
As a technology, an immune response generating functions-like-a-senolytic yeast beverage or yogurt, plant, or plant pollen, bscteria, or even physiologically and attentionally nonperceptible dermal bacteria, similar to a probiotic, that is a senolytic
from immunofunctioning, that is the immunosensitizing bacteria, plant, fungi or even virus causes greater longevity, wellness, healthspan, and youthfulness of phenotype like senolytics do. The humans, that is person’s or people’s immune response to
optimally, the organisms or ok, but less nifty as it goes with actual human sustained production of concentrates, organism material concentrates, where both and either of these causes the immune system to be sensitized to glom and terminate the kind of
cytes senolytics terminate.
So, perhaps: blenderized e coli membranes, combined with cytomembrane molecule transport channel plugs that preferentially populate deleterious chemokine and deletarious cytokine export channel (efflux) transport channels, also combined with some oil to
make liposomes that make it through the GI tract;
So where do the at-wild, at 2019AD society, efflux blocker molecules come from? Organisms at a culture medium with chemical travel zone and an area of chemically changeable molecular biology structures to measure the modification efficacy of each of
the organisms forms is described. As another source of efflux channel blocking molecules that are combinable with immunosensitizing decorations on the efflux blocking molecule, for immunoglomming and removal, which has a senolytic function effect.
It seems like it would be possible to screen a library of naturally occuring materials and molecules,proteins, peptides,andother things, as well as genetically engineered materials like new or enhanced proteins and peptides, to find out if there are any
that plug the efflux channels that are effluxing deleterious biochemicals.
It might be that to a molecular biologist this is sort of easy, like “the transport channel is n angstroms wide and w angstroms tall. Anything hydrophobic/hydrophilic you make with an angle bend, a beta sheet or an alpha helix on it will block the
efflux channel of that size and form. If you make a 20 amino acid peptide tail and put iton the plugging protein, you can use an amino acid that is absent any environemental or body-wide previous immune sytem antigen stimulation, or immune system
activity. Immunocytes that react to the unique 20 mer peptide, after the “immune system alerting dose” are unlikely to react to any other physiological biochemical, minimizing immunological reactions drift, thus keepin nearer optimal human,
immunofunction, human longevity, human wellness, and youthful phenotype form at the human.
The technology is that if just those cytes are immunoterminated which have a bunch of efflux channels where deleterious cytokines, chemokines, and matrix protein messer-uppers are effluxed, then that immunotermination functions like a senolytic:
Gene therapy, that transfects and terminates deleterious cytes with something like apoptosis, gene therapy that produces immunoequivalents to senolytic drugs, or gene therapy that actually produces proteins or peptides that are senolytic in their own
right. Technology of senolytic longevity, wellness, healthspan, and phenotypic youthfulness of form are developing. At 2019 AD, at any deleterious cyte where a senolytic accumulates at but previously did not terminate as it would more optimally do, gene
therapy could be a way to get the 30% that fisetin does not reach, the 50% that curcurmin does not reach, or the numerous kinds of cytotypes and tissues that any known senolytic might not reach the cytoplasm of (cartilidge, eye lenses, osteocytes, other
nonvascularized tissues).
Curcurmin and fisetin are published senolytics; could curcurmin as well as fisetin molecules with an antibody alerting moeity or tail, attached with: an enzyme endogenous to the cytoplasm that divides the curcurmin or fisetin from the immune system
alerting moeity, which then travels to the outer surface of the exterior cytomembrane, which alerts the immune system to terminate the cyte that the senolytic has already localized and concentrated at. That only works if fisetin, curcurmin, andother
senolytics actually localize to deleterious cytes. If they just go to allcytes, but only terminate deleterious ones, then a different technology would be the thing to make. If senolytics do localize and concentrate at deleterious cytes then putting
immunoactivators on them would cause them to be even more senolytic as the immunocytes seek them out.
wellness technology: somehow leukocytes, macrophages and WBCs notice they are more effective at being an active and beneficial immune system when they travel past the capillary epithelia to actual cytotypes that provide a utility definition to a tissue (
chondrocytes, pneumocytes, cardiocytes, dermatocytes, beneficial only immune responses to neurons, glia, mesentary, hepatocytes) to have a curative beneficial effect; that is they make their way past the epithelia to reach pneumocytes to engulf
pneumocytes that have viruses and cure pneumonia when they do that. So, is there a chemical peptide or protein that causes luekocyctes and other immunocytes to move past, or between, epithelial cytes twice as often, twice as fast, or even travel
preferntially along tissue cytes and omit a travel path that is along epithelial lined passgaeways like capillaries? Those would be drugs that multiply the effectiveness of the immune system at interacting with and vanquishing infections. Kindof like
the utility of antibiotics, it could be possible to terminate twice as many infected cytes orinvasive organismsevery 24 hours, rapidifying recovery from illness and improving wellbeing.
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