Pupillometry predicts creativity; so do activities that cause similar pupillometric behavior as creative tasks cause more creativity? COuld children’s toys measure the amount of imagination pruring play to make better toys and play suggestions? (CCA;
cortana child advisor, voluntary amazon alexa echo speaking guidance of play

https://www.tandfonline.com/doi/full/10.1080/10400419.2018.1530533



Creative play is teachable, “This study investigated the effects of a pretend play intervention on 45 first and second grade children 2–8 months post-intervention. It was hypothesized that pretend play would be improved in the intervention groups and
that they would score higher than controls on measures of play, creativity, and emotional processes. Subjects were randomly assigned to an affect, imagination, or control group. The imagination group significantly increased on multiple play scores from
baseline to follow up and compared with controls, scores on frequency of positive affect expression were significantly higher. Differences on other scores were not found. Results indicate that play skills can be improved and cognitive play skills may
have a stronger impact on affective processes than anticipated.”



Female university students (n = 104) were randomly assigned to a coloring intervention or a logic-puzzle control group. Participants completed an inventory of psychological measures (depressive symptoms, stress, anxiety, flourishing, resilience,
mindfulness) and then participated in a 1-week intervention of either daily coloring or logic-puzzles. Following the intervention, participants again completed the inventory of psychological measures. Coloring participants showed significantly lower
levels of depressive symptoms and anxiety after the intervention, but control participants did not.



Increasing the well being of girls may increase their creativity, “The development of analytical abilities was predicted by visual and verbal short-term memory and self-concept, the development of creative abilities by visual short-term memory and well-
being” among 6th graders.

Physical “outward bound” programs, are to my perception, described as increasing self esteem and might increase well being. Could a computer graphic form of “outward bound” be possible?



Nifty thing zaps antibiotic resistant bacteria, “attached a cephalosporin molecule to a secondary antibiotic called ciprofloxacin.”…”When resistant bacteria encounter the combined drug they cleave the cephalosporin, setting the ciprofloxacin free
to kill the bacteria.” https://www.imperial.ac.uk/news/191213/decoy-antibiotics-could-around-bacterias-defences/

An upside version of the same mechanism: could NMN linked to another molecule visit (get more use at) known good mitochondria, then cleave to put another beneficial molecule in place? Possibly a “fission (duplicate) this mitochondria” chemical or
nucleotide? Finding the healthiest 10% of cytes at the body, with the most mitochondria, then causing them to do mitosis could cause higher quality tissue, promoting wellness and healthspan. It is possible that doing mitosis on the ones with the most
mitochondria at the tissue of 80-120 year olds could beneficially increase the mitochondria per cyte numbers.



Some probiotics could reduce risk of stroke, “Regulatory T [(RT)] cells have a beneficial inflammatory effect, protecting an individual from stroke. But gamma delta T cells produce a cytokine that causes harmful inflammation after a stroke.“



Probiotics that increase RT, or not: ”After 10-d treatment with Bifico capsules (combined bifidobacterium, lactobacillus and enterococcus)”, “a combination of Lactobacillus gasseri, Bifidobacterium bifidum, and Bifidobacterium longum”, “
Probiotics (Lactobacillus gasseri KS-13, Bifidobacterium bifidum G9-1, and Bifidobacterium longum MM-2” However, “Regulatory T cells, which are anti-inflammatory cells of the immune system, increased during the study in all participants but there
were no differences between the probiotic and placebo group.”



Longevity technology:



Online https://www.longecity.org/forum/topic/94224-manipulating-mitochondrial-dynamics/ it says that NR, which is kind of like NMN, to be available has to be enzymatically divided into niacinimide and ribose to affect NAD levels. “Perfused or intact
intestine rapidly hydrolyzed NMN to nicotinamide riboside, which accumulated, but was not absorbed. It was slowly cleaved by an enzyme associated with the mucosal cells to nicotinamide, which was the major if not the only labeled compound absorbed.”
Notably Ribose is only $36/Kg at amazon, and I think nicotinamide is about $11 for 90 grams. so verifying that NR gets cleaved prior to ever reaching cytes suggests the mouse 20g human equivalent dose a day benefits from ribose with nicotinamide. One
plausible thing the person at imminst/longecity says is that nicotimide does lots of mitochondrial fission. “see my Exercise Like a Girl post. http://www.longecity.org/forum/topic/93915-exercise-like-a-girl-a-protocol/ In particular my last reference
that indicates NR must be cleaved by enzymes to be absorbed. So taking nicotinamide plus a greater than stoichiometric dose of ribose is essentially taking a predigested NR, except you won't have to wait hours for maximum effect on NAD, and more of the
nicotinamide will be converted into NR in the body with the excess of ribose.” … “For fission, my dose is 2g NAM + 5g ribose (equivalent to >4g NR)”



So with a plasma half life of 3.5 hours for nicotinamide and “70” minutes for ribose (D-ribose was rapidly absorbed (Tmax=36–44 minutes) and rapidly disappeared from plasma (within <140 minutes). Additionally, D-ribose was partially (18–37.5%)
recovered from urine) that suggests 4 times a day dosing for about a month. Ribose tastes yummy though.



I perceive NMN and NR are similar.



A probiotic that produces ribose and nicotinamide could be a wellness probiotic.



Actually, my perception is that lots of eentsier mitochondria where mitophagy, removing nonfunctional mitochondria is favored, sounds nifty, Caloric restriction increases mitophagy, as, the NR workalike I read about says it does..“work in S. cerevisiae
links optimal mitochondrial quality with longer lifespan (Higuchi et al. 2013).” also, “an increase in mitochondrial fission would create many fragmented mitochondria, which has been shown to be useful for eliminating damaged mitochondria and for
creating smaller mitochondria for efficient transporting to energy-demanding areas” Distal parts of cytes like dendrites could benefit. It could support endogenous pre-existing stem cyctes as well, “stem-like cells division is asymmetric; some cells
inherit mainly “old” mitochondria and loose their stemness properties (self-renewal and pluripotency), whereas others get young mitochondria and stay stem-like. This indicates that a mechanism exists to sort old and young mitochondria and highlights
the importance of mitochondrial turnover and quality in maintaining “stemness””, also, supporting some mitochondrial fission, “a huge increase in fusion are detrimental. These include studies that show mitochondria hyperfilamentation that is
apparent in brain from patients or mouse model of AD and leads to cellular senescence” So at a human, a month of mitochondrial fissioning NR workalike could cause mitochondrial improvement. The thing is that at yeast, fewer, and larger mitochondria go
with greater highest longevity, “ Also, at yeast and rodents, caloric restriction causes less fissioned mitochondria, “On the other hand, caloric restriction has been shown to decrease the expression of mitochondrial fission factors Drp1 and Fis1 and
to upregulate the fusion factor Mgm1, resulting in a more filamentous network (Goldberg et al. 2009). In Rat, caloric restriction leads to the same effect and an increase in cristae number has been observed” That suggests a temporary fission fest could
be beneficial but a mitochondrial fusion fest could also have value. “MtDNA mutations tend to accumulate when the fusion/fission cycles are less frequent and there is less mtDNA mixing. Fusion appears to be important for mixing content of different
mitochondrions (Tam et al. 2013; Chan 2012) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4935730/ LCA and lactic acid might cause mitochondrial fusion:

At a concentration of 50μM, exogenously added LCA (“Lithocholic acid, also known as 3α-hydroxy-5β-cholan-24-oic acid or LCA, is a bile acid that acts as a detergent to solubilize fats for absorption. Bacterial action in the colon produces LCA from
chenodeoxycholic acid by reduction of the hydroxyl functional group […] It has been implicated in human and experimental animal carcinogenesis.[2] Preliminary in vitro research suggests that LCA selectively kills neuroblastoma cells, while sparing
normal neuronal cells and is cytotoxic to numerous other malignant cell types at physiologically relevant concentrations)

was found to extend the mean and maximum chronological lifespan of yeast.[6] The bile acid accumulates in the inner and outer mitochondrial membranes, altering the mitochondria's lipid composition by promoting or inhibiting various enzymes.[7] The
remodelling of the membranes changed the shape and number of mitochondria in the cell by (1) increasing their size, (2) decreasing their numbers, (3) decreasing the number crista extending from the IMM and (4) increasing the number disconnected crista in
the mitochondrial matrix.[7]Then, after the month or two of eenstsier high mitophagy mitochondria, an actual person might prefer a different more ATP generative sizeier size of mitochondria. LCA or Lactic acid might work: “Lactic acid exposure
increases the size of muscle mitochondria thus improving the lactate threshold.” I suppose that suggests like, lactic acid with sucralose, or yogurt.



The imminst/longecity person’s emphasis is that their NR workalike will I perceive, that like NMN it could cause youthful phenotype at a variety of tissue types. From fMRI, It is possible thinking exercises the brain, although I think I read that
people get really neurally efficient at things they are mentally good at.



Trehalose as a mitophagy inducer, “in the mouse where old mice have been fed with trehalose, a mitophagy inducer. These mice displayed an improvement of the levels of the mitochondrial quality controls mediators, especially PARKIN, BNIP3, SIRT3 and
PGC1α, when compared to controls mice (LaRocca et al. 2014). Their artery walls do not stiffen and these results were reproduced ex vivo on arterial rings. As reported earlier, caloric restriction diet leads to increased mitophagy and decrease in both
mitochondrial damage and markers of senescence in rats” The mice received “Controls received regular drinking water, and treated animals received 2% trehalose (Sigma-Aldrich) supplemented water for 4 weeks” So at a human that would be 20g a day in
a liter of water, or 33g because it tastes good and a Kg doses a human for 4 weeks. Trehalose is at ebay and tastes good.



The mitochondria in oocytes might be super well preserved or in a state where they are prompted to be absent degrading while keeping the oocyte alive, as every 2019AD human mitochondria is the product of a species-lengthy chronological maternal lineage
of 100% mint mitochondria. The biochemistry of keeping those mitochondria fresh could possibly have longevity chemical and research applications. Are those oocyte mitochondria just the right volume and shape, running at just the right amount of ATP
produced per nanogram of tissue, possibly even optimally located compared to other oocyte organelles on actin traces. If so, then making mitochondria throughout the body produce that much ATP per nanogram of mitochondria, that mitochondria size and
morphology, and that area of actin line support; of course cytes at tissues differ very much, but that could be an aim-for guide to mitochondria that were at active living yet pristine preserved shape at all ages; that could be a healthspan, wellness,
possibly also longevity technology.



Mitochondria have a construction molecular transport molecule-mover that works on a bunch of stuff, “Precursor proteins will be transported to one of four areas of the mitochondria, which include the outer membrane, inner membrane, intermembrane space,
and matrix.[10][11] All proteins will enter the mitochondria by a translocase on the outer mitochondrial membrane” So mitochondrially active drugs could among other transport channels use that translocase, possibly to move really large proteins into
the mitochondria.



Longevity technology: Oral or probiotic broad brush enzymes: The broad brush approaches like “more histones” to organismal wellness and longevity could have other members. It is possible that enzymes that take a broad brush to materials in the
cytosol/cytoplasm could have wellness and longevity effects; a monoxygenase, an acetylase, a methylase, an ethylase, a benzene-opener enzyme, a deaminase, an alpha-helix remover, as well as others could all be linked to a cytomembrane molecular transport
protein or peptide, then these enzymes reach the cytosol at all the tissues, where they have a 1-10% broad brush effect. A bunch of these enzymes can be made into a library and then screened as to longevity hieghtening effects.



If it has not been previously mentioned I read that gene therapy on the liver was more than 99% effective during about 2005 AD, so if any of the broad brush enzymes have a longevity effect a dose of gene therapy to the liver to produce them would cause
them to be endogenously produced and placed in circulation for a one dose longevity treatment. On verification of hieghtened longevity and human well being making the broad brush enzymes a part of the human germline is beneficial.



(no clue: would a ribozyme be more or less durable than a protein enzyme?)





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4935730/ Research on a disease could result in cognitively enhanced, longer lived humans. Mice knocked out for Surf1 (Surfeit locus protein 1) “not only these animals failed to show spontaneous
neurodegeneration at any age, but they also displayed markedly prolonged lifespan, and complete protection from Ca(2+)-dependent neurotoxicity”, and also, “enhanced memory in Surf1 KO mice”; however at 2019 AD humans some Surf1 genetic variants
were unwell, but it is possible a new engineered gene variant of Surf1 could be lifespan increasing intelligence enhancing, and neurobeneficial at human beings.



This paper describes links between preeclampsia and things that could be treated with longevity drugs. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6556237/ telomere length, mtDNA quality, mitochondrial function;

Noting trehalose causes softer blood vessels and mitophagy it might have some benefit to pregnant women and fetuses, “They established that high lipid peroxidation levels are a result of escalated mitochondrial mass in poor vascular flow to meet energy
requirements in preeclampsia” If it an actual thing that trehalose, or possibly ribose, is a thing that benefits pregnant women and fetuses then these sugars could be genetically engineered into fruit so there can be a weller baby, easier pregnancy
fruit



“Apart from mitochondrial dysfunction, inflammation and inflammatory mediators are evident in premature ageing of the placenta. Certain ageing-associated inflammatory markers such as Senescence-Associated Secretory Phenotypes (SASPs) are elevated in
preeclampsia” suggests boswellia active chemical could be tested in mice, then humans to see if it improves pregnancy and baby wellness, “The active ingredient is boswellic acid, which has been shown to exhibit anti-inflammatory, anti-cancer,
analgesic and immunostimulant properties.

Studies have linked both asthma attacks and inflammation to excessive amounts of leukotriene in the body. Leukotriene is a substance that is produced by 5-lipoxygenase.

Boswellia contains four different acids that can neutralize leukotriene. Of the four, Acetyl-11-keto-beta-boswellic acid (AKBA), is considered to be the most potent when it comes to reducing inflammation.”



Another drug they could test on pregnant mice and then if it causes benefit, humans, are longevity fungi; Reishi causes mice to live 9-20% longer https://www.lifeextension.com/Magazine/2013/2/how-reishi-combats-aging/Page-01 so could address some of the
preeclampsia mechanisms. 1/5 less maternal and baby risk from a herb-at-a-glance prior to further drug development is a beneficial possibility of reishi. Also, Reishi has many component chemicals so it is likely that a partial set of those is more
optimal for pregnant women and their fetuses.

Noting the researcher’s paper that likely causes many people to think that longevity technologies could benefit mothers and babies:

It is nifty to think of a matrix experiment where they have pregnant mice getting reishii, boswellic chemicals, trehalose, metformin (a mitophagy chemical), LCA(mitochondrial fusion), and NR (mitochondrial fission) or NMN at various concentrations and
combinations and finding the optimization of maternal and baby wellness.

they could find out if prenatal metformin causes greater longevity in the progeny; earlier use in rodents is associated with greater longevity; what does prenatal do? Also, what effects on personality? Clonal mice behavior quantitative measurement.

Human longevity immunizations and one dose drugs are described at things I have written about, it is possible, although I do not immediately know of any, that some of these one dose longevity drugs could benefit women who are planning a pregnancy, or
with research, women who are pregnant as they could reduce the preeclampsia risks. The paper notes, “before exposure to 3% plasma from preeclampsia pregnancies, it resulted in significant reduction in cellular superoxide production, normalization of
mitochondrial functioning, and reduction in inflammatory influx”, so, noting that preeclampsia pregnancies have circulating chemical nonoptimalities it is possible that immunizing against these nonoptimal chemicals could benefit mother, fetus, and baby.


What might be a longevity peptide at Reishi is called Ganoderma lucidum peptide. Also, “ergothioneine is a water soluble amino acid that has been shown to be cytoprotective”



“An evaluation of all available clinical trials on the use of Reishi in cancer treatment was published in June 2012.

While there was insufficient data to demonstrate efficacy Reishi by itself, when Reishi was given alongside radiation and/or chemotherapy, patients were 50% more likely to respond positively compared to those given chemo/radiation alone. the results in
cancer patients receiving Reishi showed the expected increases in immune cells known to enhance tumor response and stimulate host immunity.” reminds me of how RT immunocytes reduce risks from stroke. A month of pre-dosed Reishi could be measured as to
wellness and cognition preserving effects after ischemia as a result of its immunosystem effects.



Polysaccharides like glucans that have drug activity could be genetically engineered into plants to benefit human beings.



Genetically engineering, or growing it on a flavored medium, to make the reishi fungus to taste delicious could cause a larger number of humans to benefit from the 9-20% longevity increase. Also, they could test it on mice, and mutate fungal versions
that have the optimal dose at a fewer gram quantity of fungus, that would also make the pills more affordable. Has anybody tried putting one day’s dose in a chunk of chocolate for easier enjoyment? The cheapest mushroom powder on amazon is near 53
cents an ounce.

“The NIA Interventions Testing Program (ITP) has to date reported on four drugs with consistent major effects on mouse lifespan in one or both sexes and found evidence for significant but less dramatic effect of four other drugs. Rapamycin, started at
9 months of age, was found to increase median lifespan by as much as 26% in females and 23% in males. Acarbose can lead to an increase of 22% in median lifespan in male mice, and to a significant, but smaller, 5% increase in female mice. A third drug, 17-
α-estradiol (17aE2), a nonfeminizing congener of the well-known estrogen 17-β-estradiol, increases lifespan of male mice by 19%. Lastly, NDGA (nordihydroguaiaretic acid) has been shown to increase lifespan of male mice only, with an increase of 12% in
median lifespan.

Drug delivery; paracellular transport is transporting things across an epithelium by passing through intercellular spaces, “Some claudins form tight junction-associated pores that allow paracellular ion transport.[12]

The tight junctions have a net negative charge, and are believed to preferentially transport positively charged molecules. Tight junctions in the intestinal epithelium are also known to be size-selective, such that large molecules (with molecular radii
greater than about 4.5 Å) are excluded.[13][14] Larger molecules may also pass the intestinal epithelium via the paracellular pathway, although at a much slower rate and the mechanism of this transport via a "leak" pathway is unknown but may include
transient breaks in the epithelial barrier.

Paracellular transport can be enhanced through the displacement of zona occludens proteins from the junctional complex by the use of permeation enhancers. Such enhancers include medium chain fatty acids (e.g. oleic acid), chitosans, zona occludens toxin,
etc.”

If a female mouse is pregnant with a clone of herself, and the plaenta is bypassed with surgery to connect the two bloodstreams does the pregnant mouse live longer or show tissue regeneration? In an extreme sense, if so, then a uterine blob, perhaps
even a nonfetal version could have a longevising effect.

Heart transplants cause 15 years greater lifespan in ill persons. Interestingly, “During heart transplant, the vagus nerve is severed, thus removing parasympathetic influence” That suggests the possibility that modulating parasympathetic nervous
system could have a longevity effect. Drug localization could reduce side effects on areas of the parasympathetic nervous system that are harmless or beneficial.

“The parasympathetic system is responsible for stimulation of "rest-and-digest" or "feed and breed"[3] activities that occur when the body is at rest, especially after eating, including sexual arousal, salivation, lacrimation (tears), urination,
digestion and defecation.

some things that I have read have something to do with lifespan are dopaminergic activation, “feed and breed” (CR, enunch), digestion (morphology of GI tract and LKM512)

“As in the sympathetic nervous system, efferent parasympathetic nerve signals are carried from the central nervous system to their targets by a system of two neurons. The first neuron in this pathway is referred to as the preganglionic or presynaptic
neuron.”

Suggests that like deprenyl preserves the suubstantia nigra something could localize at the parasympathetic long neurons and preserve it or grow it like (NGF, BDNF, VEGF, stem cells). Youthful (teenage) function parasympathetic nercous system could be a
healthspan or possibly longevity technology.

“Its cell body sits in the central nervous system and its axon usually extends to synapse with the dendrites of a postganglionic neuron somewhere else in the body. The axons of presynaptic parasympathetic neurons are usually long, extending from the
CNS into a ganglion that is either very close to or embedded in their target organ. “ Really long neurons reaching organs on an each-organ basis.

Another area of localized neuronal preservation could be the CNS connector to the vagus, “vagus in Latin literally means "wandering"), has parasympathetic that originate in the dorsal nucleus of the vagus nerve and the nucleus ambiguus in the CNS”. �
�Upon leaving the medulla oblongata between the pyramid and the inferior cerebellar peduncle, the vagus nerve“, “two distinct branches of the vagus, both of which originate in the medulla”

I perceive deprenyl might sort of look like dopamine, and thus concentrate at dopminergic neurons, so perhaps something that looks like Vagus nerve neurotransmitter chemicals at either the vagus or the CNS connectors to the vagus could carry
preservatives or things like BDNF, NG, others; sort of like acetylcholine (or any of 30 different nuerotransmitters) connected to half a deprenyl molecule could be a vagus preservative. Deprenyl has a PEA then a nitrogen attached to an ethynyl group, so
acetylcholine with a N-C≡(triple equals) on it, and perhaps a polyglycine to keep it out of the CNS, could be a bodyside vagus drug. Perhaps the ethynyl could be at the N of acetylcholine, “The parasympathetic nervous system uses chiefly
acetylcholine (ACh) as its neurotransmitter, although peptides (such as cholecystokinin) can be used.[15][16] The ACh acts on two types of receptors, the muscarinic [M2] and nicotinic cholinergic receptors.”

A youthful form cardiac neuroagent or neuropreservative could cause greater longevity and wellness, “vagus nerve acts on sinoatrial node slowing its conduction thus actively modulating vagal tone accordingly. This modulation is mediated by the
neurotransmitter acetylcholine and downstream changes to ionic currents and calcium of heart cells.”, “increased vagal tone (and thus vagal action) is associated with a diminished and more variable heart rate.” So along with the idea of a cardiac
neuroactive or neuropreservation chemical, the possibility that regular heart rate might be beneficial could go with a cardiac Acetylcholine reducer that a drug would be better kept out of most of the body, notably the CNS. Some organisms make
acetylcholine regulators, so those could be a molecule source.



I perceive I read baseline lung capacity is correlated with wellness. Could drugs that effect breathing tidal volume affect wellness and longevity? 20-33% deeper (or shallower, or more rapid, or less rapid) might be non-noticed and possible with a
localized stimulant. Pulmonary (vagus?) localized deprenyl or even caffeine, or a diaphragm stimulant could have a beneficial effect.



As a result, the postsynaptic parasympathetic nerve fibers are very short.“The vagus nerve does not participate in these cranial ganglia as most of its parasympathetic fibers are destined for a broad array of ganglia on or near thoracic viscera (
esophagus, trachea, heart, lungs) and abdominal viscera (stomach, pancreas, liver, kidneys, small intestine, and about half of the large intestine).”



Drugs that affect the Vagus, rather than the CNS, could have quantifiable effects on mental wellness, “Baseline vagal tone can be used either as a potential predictor of behavior or as a signal of mental health (particularly emotion regulation, anxiety,
and internalizing and externalizing disorders).” Vagus mental wellness effects are also supported, “Children with more secure attachments with their mothers exhibited greater empathetic responsiveness, less social inhibition, and higher vagal tone�
� Breathing to calm down, and a pause before reacting to stabilize cardiac rate might be automatic with vagus drugs, “unflappable, but able to joyfully rise and run around and dance” could be a beneficial vagus drug.

It is likely there is a genetics of vagus morphology. Do those genes correlate with wellness, longevity, and personality, notably happy personality.



New drug delivery technology, “Blood capillaries are a well-known site for transcytosis,[5] though it occurs in other cells, including neurons,[6] osteoclasts[7] and M cells of the intestine.” “Transcytosis (also known as cytopempsis)[1] is a type
of transcellular transport in which various macromolecules are transported across the interior of a cell. Macromolecules are captured in vesicles on one side of the cell, drawn across the cell, and ejected on the other side.”

It seems like anything that gets things through capillary epithelium is a drug transport molecule or moeity. “Pharmaceutical companies, such as Lundbeck, are currently exploring the use of transcytosis as a mechanism for transporting therapeutic drugs
across the human blood–brain barrier”

Transcytosis can work on things as large as bacteria, suggesting things like nanomachines being delivered to and across cytes. “Transcytosis has been shown to be critical to the entry of Cronobacter sakazakii across the intestinal epithelium as well as
the blood–brain barrier.[15] Listeria monocytogenes has been shown to enter the intestinal lumen via transcytosis across goblet cells.[16] Shiga toxin secreted by enterohemorrhagic E. coli has been shown to be transcytosed into the intestinal lumen.”,
“[transcytosis] activation mediated by prolactin in the rabbit mammary gland during pregnancy.[13]”, “transcytosis is regulated positively by TSH” perhaps hormonally nonactive version of prolactin or some nonthyroid active version of TSH could
be linked to some other active drug molecule.

Is there anything which exported from a cyte will increase longevity? Glutamate (of glutamate toxicity), nonoptimally glycosylated proteins, tau or other alzheimers proteins, transcytosis also exports things as well as transports through. Possibly
sulfur containing amino acids like methionine, metalloproteins containing iron, or worn out organelles (noting it can possibly work on things as large as bacteria); lactic acid or lactate export could make it so people were absent feeling tired after
lots of motion; effortless hiking.



GSK: Better stethoscope, Heart rate microvaries with areas of breathing cycle, it is possibly diagnostic of disease; a stethoscope that computationally combines breathing change with heart rate at microintervals could be linked to a deep learning AI that
connects RSA and heart sounds with various diagnosable things, including normality or even better than well status. Micropressure sensor could record breathing microchest movements separate from cardiac sounds. Could also be GSK for amateur unsupervised
patient use and upload to the cloud for longitudinal data on patient wellness; “Respiratory sinus arrhythmia (RSA) is typically a benign, normal variation in heart rate that occurs during each breathing cycle”, “RSA is frequently used as a
noninvasive method for investigating vagal tone, in physiological, behavioral, and several clinical studies.[16][17][18] This can be done using electrocardiography (ECG) recording,[19] although other methods are also being developed that take advantage
of the interactions between ECG and respiration.[20][15] Interpretation of RSA measurements must be done with care, however, as several factors including differences between individuals can change the relationship between RSA and vagal tone.”, “RSA
is less prominent in individuals with diabetes and cardiovascular disease.[27]”


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