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A massive oxygenation event in the earlier development of the Earth caused Oxygen to become among the strong biosynthetic electron withdrawing groups and to be participated in electron withdrawing groups other than cyano molecules which can be toxic. The oxygenic even assists in increase the size of organisms and promoted exhibition of organisms with more than 1 foundational biological compartment.  Oxygen is distributed by mechanisms including circulatory factors to reach the ;mitochondria where Thioretinaco Ozonide complexes in the cristae of the inner mitochondrial membrane initiate the electron transport pathway which involves using 4 complexes to modulate proton and electron movement across membranes to result Thioretinaco Ozonide becoming the ATP synthase complex which produces ATP while also enabling the function of Oxidative phosphorylation which produced 30, 32 or more molecules of ATP from glucose as aerobic glycolysis when P53 is not exhibited while this is reduced to 6, 9 or more molecules of ATP from glucose when P53 is exhibited as Anaerobic glycolysis.   Aerobic glycolysis typically is used to indicate that Pemt is repressed, P53 should be exhibited but is in some way subverted and glycolysis is dysregulated to produce maximal or more energy molecules used in a different way compared to typical levels.  

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Hydrogen anion (H2e1p as hydrogen with another high energy electron) is an important factor in enabling and sustaining celestial entities and the extra high energy electron om Hydrogen (H2e1p instead of hydrogen as H1e1p) can be released as eV or fluorescence. Glycolysis captures this energy, forwards it to the Krebs cycle, then the Krebs cycle forwards it to the electron transport pathway, as between 6 and 9, more or less, high energy electron carrier substrate for the electron transport pathway (anaerobic glycolysis or P53 repression of Glut glucose absorption, P53 repression of Insulin receptor, and P53 inhibition Glucose 6 phosphate dehydrogenase enabled entry of glucose into glycolysis/pentosephosphate/hexosemonophosphate pathways) or about between 32 and 38 more or less high energy electrons in carriers available as electron transport pathway substrate (canonical function or anaerobic glycolysis with protection of Pemt function, both of which compare to the pathology syndrome of the same or more level of electron transport pathway substrate when aerobic glycolysis is not protected by Pemt function and when this energy pathway becomes dysregulated in disease known as the pathology syndrome aerobic glycolysis ) of carriers of high energy electrons(NADH/NAD+, FAD/FADH2, other).   

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Aerobic glycolysis exhibits conditions that commandeer available glycolysis resources and redirect these away from possible pathways as NADH and Pyruvate redirection to NAD+ and lactate ion because repression of glucose 6 phosphate dehydrogenase by p53 decrease the ability of pathways to produce nucleotides and nadph and Acetyl - CoA.   Parp signaling in Homologous and nonHomologous DNA repair uses NAD+ and is prolonged because of inadequate nucleotides for DNA repair, resulting in a pathway of increasing DNA impairment, increasing strength of gradient NAD+ gradient to strengthen direction of pyruvate and NADH to lactate anion ad NAD+, increasing DNA impairment, causing apoptosis of among already differentiated tissue, causing stemness reserves to enter development while be prevented from completing differentiation while also being prevented from complete escape from stemness, training of an overly resilient phenotype, increasing methylene cysteine from nicotinamide remnants left over from Parp removal of ribose from NAD+ because Parp uses ribose redistribution to produce gradients to recruit ribose exhibiting RNA and recruit ribose exhibiting DNA,  depleting NAD+ which causes Parp to complex with Dbc1 which is a causal indicator of functional and genetic advanced aging, causing P53 to promote its own genetic and protein/protein pathway deterioration, finally producing phenotype of oncology, disease and detrimental aspect of aging phenotype. 

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Pi3k is linked with oncology and resistance to oncology because Pi3k inhibits the major oncology suppressor p53, causing Glut receptors to move to the plasma membrane to vastly increase glucose absorption and causing glucose 6 phosphate dehydrogenase to increase entry of glucose into glycolysis, pentose phosphate and hexose monophosphate pathways. P53 repression, also, unrepresses the insulin receptor, and the unrepressed insulin receptor can functionally amplify the activity of the phosphofructokinase activity and interact with lysosomal ragulator complexes to recruit and activate mTorc1 catalytic activity.  This review has found hundreds of molecules, pathways, therapeutics and strategies able to be used now and in the future to abrogate what is known of as disease and aging, while some have been achieved in nonhuman contexts and Homo Sapiens tissue.  Most, if not all,  are directly or indirectly linked to Pemt, Hydrogen Anion, Carriers of Hydrogen Ion, conditions directly linked to these or other. Most, if not all, in some way were galvanized by organizations, groups, systems and institution of civilizations along with patterns exhibited in Human events, philosophical and other contexts, including human outcomes within and outside of civilization's contexts. The key factor is a requirement for integrative program management which is able to focuse these into solutions to be reduced to practice and reduced to solutions for implementation. 

 

The electron transport pathway frees high energy electrons from carriers to supply thioretinaco ozonide complex with resources  in the cristae of the inner mitochondrial membrane to cause it to become complex 5 of the electron transport pathway, then supplies resources also the complex 5 which is ATP synthase which performs oxidative phosphorylation to produce ATP as an easily regulated and control source of energy against natural gradients as a characteristics of life.  This pathway has to be commandeered, redirected, or removed in detrimental aspects of age, disease and for vital being to no longer be exhibited.  High energy electrons also are sequestered by CH2 when CH2 is activated by strong electron withdrawing groups to polymerize the ribose and deoxyribose in production of RNA, DNA, NAD+/NADH, NADP+/NADPH and diverse other molecules.

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Hydrogen anion, (H2e1p), in carriers, structure, membranes, and alkaline strong ions promote biology enabling background foundational alkaline disequilibrium. Other alkaline factors in tissues and structure, or monocytes, can also potentially promote a background alkaline influence.  Fatty Acid alkanes are examples of factors also promoting alkalinity in the background.  H+, H+ derivatives and other cations produce acidic or positive polarity compared to the negative polarity of alkaline factors.  The strong ions are a group of alkaline or acidic and positively polarized cationic molecules that are reviewed in medicine, essential care contexts, to determine their cumulative comparative polarity, pH, proton balances, acidity or alkalinity. Specifically, NAD+ and NADPH, along with FAD and FADH2, NADP+ and NADPH and other redox molecule pairings are a synapse in which the ionized molecules such as NAD+ has abdicated, released or had oxidized from its structure the hydrogen anion, compared to NADH which has been reduced by acquisition of either a high energy electron or hydrogen with a high energy electron.  The high energy electrons, when not acquired, are unbounded by quantization exist not in version that has been collapsed into particle version, but as eV, fluorescence, energy, superposition, or quantum characteristics. 

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Essentially the eV- potential of the unbound hydrogen anion exists in the NAD+ and NADH synapse as multiplicity or potential multiplicity between being acquisitioned by NAD+ to produce NADH compared to being abdicated by NADH to produce NAD+. 80,000 molecules have NHD domains, nudix homology domains, that are essentially inflated by or functional differently upon acquisition of NAD+ to participate in such Hydrogen anion dynamics or synapse. High energy electrons or high energy electrons encapsulated within molecules to make them safe compared to electrons from artificial light or electrical components which can be detrimental.  Photons, as light quanta, and phonons, as sound or thermal quanta, can be translated into electrons in the photoelectric effect, using melanin, neuromelanin, metals, and crystalline lattisces which vibrate to allow the bosonic character of phonons to produce electron interactions which can translated into energy.  

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High energy electrons or Hydrogen anion which exhibits a high energy electron, can be acquired through nutrition, supplements, light or phonons, CH2 acquisition of electrons (to polymerize RNA, DNA, Fatty Acids, Fatty Acid Alkanes, NAD+, NADH+, NADP+, NADPH and numerous other factors), paramagnetic interactions, quantum spin liquid(quantum entangled relationships that potentially interact at up to 30,000 times the velocity of light and reach into already exhibited eras and which reach into future eras, elemental conjugates of Hydrogen anion, high vapor pressure elements such as Sodium and Lithium which sequester Hydrogen anion from the numerous low vapor pressure elements, biosynthetic processes and in other modalities.   

Hydrogen anion is included as at least one of the hydrogens in methyl groups, CH3.  CH3 or a methyl group is included in methionine. Methionine can be produced in number of modalities, including Methionine Synthase complexes CH3 with methylene cysteine to produce methionine, when BHMT uses Betaine (n,n,n glycine Betaine or trimethylglycine) and methylene cysteine to produce methionine, when the enzyme BHMT uses S-methylmethionine sulfonium and methylene cysteine to produce methionine,  when PEMT uses S-adenosyl methylene cysteine and S-adenosyl methionine to produce methionine, other more obscure pathways, and when one of the most abundant enzymes in physiology known as THMT (thetin - methylene cysteine methylpherase) uses a number of substrates (2 methylthetin, trimethylsulfonium, and others) to produce methylthioglycolic acid and methionine.         

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THMT is interesting because it is among the most abundant enzymes in physiology and because of inadequate sulfur availability. THMT has intramolecular sulfide linkages which complex with sulfide from outside of the molecular structure.  Sulfur inadequacy causes these intramolecular sulfide linkages to complete themselves instead of using extramolecular sulfide, resulting in the THMT entering a gelatinous inactivated phase in tissue where it is exhibited. THMT is a major vector of depleting methylene cysteine depletion, although THMT produces both L-methionine and S-methylthioglycolic acid.   s-methylthionglycolic acid exhibits glycolic acid which, in the early 1900s, became regarded as either the center or a center of medicinal chemistry because it naturally derivatizes conditions and molecules to more environment specific metabolites and substrates.  This process potentiates derivation of specific therapeutic interventional and supportive molecules in vivo and in vitro.   Thioglycolic acid was used beginning in the 1880s when a 1878, 1870 and 1882 series of research studies found that it was produced THMT using a synthetic metabolite (2 methylthetin) to deplete Methylene cysteine.  Physiologically, Methylthioglycolic acid is important because it exhibits a methyl group, sulfur which is natural sequestering factor for hydrogen anion in physiology and in the biome, and work to support glycolic acid capacity of derivatizing interventional molecules while also supporting the role of glycolic acid as a desquamation vector like other alpha hydroxy acid. Methyl groups and sulfur also resolve a number of dysbiosis in biosynthetic, metabolic, structural, hormonal and other pathways. 

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S-adenosyl methionine synthase, then, is able to complex ATP with methionine to produce S-adenosylmethionine.  The ATP complex exhibits Hydrogen anions multiplicity packed into the oxonium exhibited between the Phosphate Groups of ATP.  The literatures observes that 2 eV- is freed from each molecule of NADH that has H oxidized from it, although both FADH2 and NADH are used by the Electron transport pathway's 4 complexes.  The electron transport pathway also uses FADH2 and other factors as substrate to obtain and transfer Hydrogen anion's multiplicity. Thioretinaco Ozonide is also supplied with high energy electrons causing it to become metabolized into becoming complex 5 of the electron transport pathway, also known as the ATP Synthase complex.  The ATP Synthase complex then use Oxygen, Ozone, and high energy electrons to perform what is known of as Oxidative Phosphorylation, essentially translating the about 42, 43, or 44 percent of the original 2 eV- derived from Hydrogen anion oxidation (release) from NADH by packing these fractal amounts of hydrogen anion multiplicity into the oxonium that is exhibited between the phosphate groups of ATP, ADP and in AMP.  

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S-adenosyl methionine synthase complexes ATP with methionine to produce S-adenosylmethionine, such that the complexing of these factors activates a carbocation rearrangement, known as Hydrogen anion shift, (H2e1p)'ic' shift or methyl shift.   The hydrogen anion multiplicity of ATP is redistributed about the complete S-Adenosylmethionine structure, resulting in ionization of the Sulfur of the methionine structure and turning S-adenosyl methionine into a "enzyme."  Pemt removes the CH3 and potentially removes a hydrogen anion multiplicity fractal, then attaches this CH3, its hydrogen anion multiplicity fractal and its lone pair of electrons to one of the three open locations of the lead ethanolamine group of newly produced, lightly glycosylated or unglycosylated phosphatidylethanolamine.  The first of three sequential CH3 transfers by PEMT enzyme produces PMME, then the second produces PDME and the third produces brand new, de novo, choline as the lead group of newly synthesized phosphatidylcholine. This newly produced phosphatidylcholine selectively exhibits fatty acids DHA, Arachidonic Acid, Palmitoyl fatty acid, oleoyl fatty acid and Omega-3, which resolution phase and resolution eicosanoid potentiators.  

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Derived from nutrition, the CDP-ethanolamine pathway, phosphatidylserine decarboxylase 1 in the mitochondrial inner membrane, phosphatidylserine decarboxylase 2 in the Golgi/Vacuolar complex, and possibly in other pathways, phosphatidylserine participates with PMME, PDME, enhanced fatty acid phosphatidylcholine with newly synthesized choline and methylthioglycolic acid to causes abiotic/biotic phase separation, sequestration of biological useful factors for import into the biological phase, desquamation of squamous tissue factors, removal of aberrant polymerizations including methylene cysteine polymerizations which can be a foundational factor in disease, structural deterioration of oncology causing molecules, promotes production of tissue plasminogen activator's super clot busting activity, production of serine protease to proteolyze proteins to foundational levels for plasticity levels mimicking gestational plasticity, and enables expression of oxytocin which is a foundational molecule in human social, emotional, group, individual, population level, civilization level and species level connections and prioritization.   

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CH2 or methylene is in a biologically activated status, although not necessarily activated by strong electron withdrawing groups, such that CH2 exhibited in methylene cysteine (clinically known as Hcy) is in structurally deactivated status in which Sulfur in methylene cysteine acquires the ability of CH2 to sequester electrons.  The sulfur in methylene cysteine, thus, is able to sequester electrons and participate in redox transactions to acquire electrons and acquire hydrogen anion multiplicity which causes protonating of tissue, monocytes, enzymes, structure and other factors to become protonated, essentially exhibiting hydrogen anion with the high energy electron removed to remove the specific use of hydrogen anion in the biological context and essentially potentially exhibiting hydrogen without an electron which is canonically a "proton" comprised of Nucleus, 1 proton and no electron. Methylene Cysteine is different from typical cysteine in this regard, changing the function of cysteine in structure.  Cystathionine beta synthase metabolism of methylene cysteine to cystathionine and H2S followed by cystathionine gamma lyase production cysteine and H2S from cystathionine care only some of these enzyme's catalytic activities. Cystathionine Beta Synthase is inhibited by methylene cysteine, while cystathionine gamma lyase is not inhibited by methylene cysteine, is inhibited by decreased cystathionine, inhibits itself by its own production of H2S, and helps cystathionine beta synthase escape repression by methylene cysteine by increasing cystathionine beta synthase access to H2S.  Cystathionine beta synthase requires use of s-adenosyl methionine to become activated.  

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Cystathionine beta synthase is increased in expression by either noncanonical HRE response element HIF signaling and or canonical HRE HIF response signaling in specific conditions including gestation to prevent detrimental apoptosis before the gestational nutritional supply complex emerges and separately in oncology.  Pemt2 L which emerges along with Pemt3 L at conclusion of gestation to regulate Pemt1 S which emerges relevantly to conception, presents a correlation because Pemt2 L, Pemt3 L both are "obliterated in function" in correlation to advancement of oncology and other disease, although the dissociation of the only known habitat for Pemt2 L and Pemt3 L known as the mitochondrial associated membrane participates in repressing the function of PEMT2 L and Pemt3 L.  Pemt1 S can also be inhibited in oncology and disease.  However, when Pemt2 S, Pemt3 S and Pemt1 S are all activate, the gradient for competition for the supply of S-adenosyl methionine to Pemt can be improved to compete with other methyltransferase including DNA methyltransferase and methyltransferase otherwise which are primary toxic factor intervention pathways for hormones, xenobiotics, metals, other toxins, and particularly being used by nicotinamide methyltransferase detoxification by methylation for nicotinamide produces produced Parp signaling which removes ribose from NAD+ because the ribose is redistributed to local substrate to produce a gradient upon which Ribose exhibiting DNA and ribose exhibiting RNA can be recruited to the loci of DNA repair.  S-adenosylmethionine synthase competes for ATP with such as pathways phosphorylation cascade and choline kinase which is increased in almost every disease and almost every version of oncology, if not every disease and every version of oncology.  Pemt enzymes then compete with other methyltransferases and other enzymes such as cystathionine beta synthase for available s-adenosyl methionine.  

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However, cysteine is a foundation for methylene cysteine which has a methyl group and cysteine with the CH2 of cysteine being structurally deactivated to delegate participation in redox transactions.  Methylene cysteine is known clinically as Hcy, while this review found that methylene cysteine is so toxic, that using the word to often can cause detriment, thus presenting the opportunity to use a more accurate description of methylene cysteine which represents the CH2 exhibited within Cysteine, along with a methyl group.  Also, methylene cysteine is methylated to produce methionine.  Methionine is used as priming sequence in the production of 99 percent or more of proteins.  methionyl-tRNA Synthetase can mistakenly use methylene cysteine instead of methionine in its translation of methionine for methionine encoded tRNA.   Also, the variant MARS1 is known to be linked to oncology.  However, methylene or CH2 is often used therapeutically such as methylene blue and specific types of light.  Concludingly, CH2 methylene is integrated into Cysteine with an active delegation of its redox potential to the Sulfur along with exhibition of a methyl group to comprise methylene cysteine. Methylene cysteine is methylated to produced methionine. ATP is attached to methionine to produce S-adenosyl methionine. and S-adenosylmethionine becomes an enzyme, while S-adenosylmethionine is used by a number of interventional methyltransferase to remove the methyl group and produce methylene cysteine. 

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Pemt removes a methyl group from s-adenosylmethionine and uses a molecule of methylene cysteine to produce methionine and another molecule of nontoxic methylene cysteine which is considered to be clinically nontoxic, explaining how different methylene cysteine levels in different physiological instances can have sometimes very disparate health statuses.  Choline requirements per day for Adults can be more than 1000 mg, although between 4 and 7 mg per kg of anatomical mass per day was derived in this review using early developmental status data and more advanced phases of being data.  Maternal choline supplementation became advised resultant of studies which caused choline to be placed among required nutrients in the later 1990s. Breast feeding with choline adequate and folate adequate Human breast milk can cause substantial improvement in development, cognition, health status, cognitive performance, expanse of being and other indicators. Supplemental repression of methylene cysteine has been correlated in the search with reconstitution of vital being in the clinical setting. NADH supplementation and methylene cysteine repression have been experimentally able to complete abolish small nonhuman mammal differences in early developmental and advanced aging including visual, cognitive, mobility, and other differences.  Other factors in extreme homeostatic aging have been linked to repression of mTorc1 signaling and sustainment of mTorc2, including FoxO sustainment of stemness tissue reserves and FoxO sustainment of mTorc2.  mTorc2 sustains the mitochondrial associated membrane which is the habitat for Pemt2 L and Pemt3 L. 

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Other studies have already produced at least a 200 percent increase in expanse of being and elimination of diseases exhibited in Human physiology by removing processed and thermodynamically prepared nutritional factors from the nutritional regimen of a small mammalian species. The studies suggests that clinical formulation of required daily nutrients is required regardless of nutritional obtainment if using thermodynamically prepared nutritional factors and because absorption levels of nutrients can be as low as 5 percent.  

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However, sustained regulation of the mitochondrial permeability pore through which ATP is exported and other factors are imported has emerged as an important factor in diverse aspects of homeostasis.  The electron transport pathway and complex 5 ATP synthesis, are initiated by the Thioretinaco ozonide complex in the cristae of the inner mitochondrial membrane. Dysbiosis of the mitochondria is integral in sustained disease or sustained impairment. Essentially, the mitochondria is where ATP synthesis occurs and supply of phosphatidylethanolamine for PEMT function, regulated supply of Ca2+ from Endoplasmic Reticulum or other organelles is essential to production of ATP, mitochondrial signaling is important in interactive control of the cytoplasm and foundational biological compartment, proteins from signals outside of the plasma membrane and outside of the mitochondria and from the nucleus all can require entry into the mitochondria to maintain mitochondrial DNA, manage metabolisms, participate in metabolism and determine if and when a foundational biological compartment should continue to exist or should systematically deteriorate. Mitochondria number can change dynamically and can increase requirements for oxygen and other material, while separation of the mitochondria from the endoplasmic reticulum, deterioration of the ability of the mitochondria to import proteins known as MPOS which occurs along with among accumulation of unimported proteins, impaired ability for mitochondrial apoptosis signals to be exported, availability of autophagy and proteolysis to clear such accumulated proteins, and nonresolution phase signaling which occurs to potentiate export of a disease phenotype using ESVs or exocytic vesicles to other tissues and foundational biological compartments, and decreased mitochondrial membrane potentials which cause mitophagy recycling of mitochondria into discrete smaller mitochondria which experience autophagy if membrane potentials are too deteriorated each present or experience complexing with other mitochondria if membrane potentials are adequate, each present information about how important the supply of energy, materials and signaling from mitochondria are to complex organisms.  

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A number of specific apoptosis signals from the mitochondria are linked to oncology when being prevented from becoming exported or are not produced because MPOS repression of mitochondrial protein import. A diverse array of antibiotics have emerged to exhibit intricate mechanisms that change biological function, RNA function, DNA function, and change other factors, which is a different perspective from that which is typically communicated to clinicians and communicated in clinical care contexts. Doxycycline, for instance, is known to cause the mitochondrion to attach to the endoplasmic reticulum.  However, doxycycline also promotes impaired exchange of signals between DNA in the mitochondria and DNA i the nucleus, resulting in accumulation of unfolded proteins in the mitochondria which produces the Unfolded Protein Protective Response. The increase in contact points between the mitochondrion and the endoplasmic reticulum produced by doxycycline did not surmount the impairment of protein exchange produced by doxycycline, resulting in protection of some versions of oncology, although the possibility of use in combination therapy for cytotoxic effect may emerge. 

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Tfam is a protein imported into the mitochondria from its transcriptional activation in the nucleus, while Tfam exclusion from the mitochondria prevents its ability to participate in maintaining, repairing and transcriptionally activating mitochondrial proteins.  Repression of Tfam activity, like Dbc1/Parp complexes, decreased NAD+, methylene cysteine, s-adenosyl methylene cysteine, AP1, SP1, iNOS/NOS2, methylglyoxal, oxalate, increased insulin signaling, reactive oxygen species, increase in choline kinase, decreased Pemt function, removal the mitochondrial associated membrane, and repression or removal of Pemt2 L and Pemt3 L, all are linked to disease and detrimental aspects of advancing age. 

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S-adenosyl methylene cysteine is a product of at least INMT methyltransferase activity which bidirectionally converts S-adenosyl methylene cysteine with s - adenosyl methionine. This can be a rescue pathway for S-adenosyl methionine synthesis to support Pemt and other methyltransferases. S-adenosyl methylene cysteine is metabolized to methylene cysteine by SAH hydrolase (S adenosyl methylene cysteine hydrolase, S adenosyl Hcy Hydrolase, SAH). SAH hydrolase is bidirectional and it can produce adenosine and methylene cysteine from S adenosyl methylene cysteine according to gradients of availability of these factors and according to NAD+ availability in its typical ratio of NAD+/NADH.  SAH hydrolase can also produce S adenosyl methylene cysteine from adenosine and methylene cysteine, correlative gradients of these factors and comparative NADH increase which diminishes the NAD+/NADH ratio. The literature presents that aggregate typical ratio in mammalian tissue can be near, about or at a NAD+/NADH ration of 3/10.  However, within the plasma membrane, the cytoplasm can typically exhibit NAD+/NADH ratio near, about or at 700/1 which favors a gradient toward derivation of NADH which is reasonable because sequestration of the boundless multiplicity of hydrogen anion enables synthesis of NADH and FADH2 used in supply of substrate(pyruvate and NADH) to pathways such as from glycolysis to Krebs cycle toward electron transport pathway and from glycolysis to Lactate Anion and NAD+ toward Parp signaling, supply of substrate from Krebs to the Electron Transport Pathway.  

INMT methyltransferase can produce trimethylation products for amines, amides, sulfur, selenide and other factors, resulting also in trimethylsulfonium which can either use trimethylsulphonium and dimethylsulfide to produce dimethylsulfide and 5-methyltetrahydrofolate, followed 5-methyltetrahydrofolate being directed toward MTHFR and then to methionine synthase production of methionine. Also, trimethylsulphonium can be directed to THMT to use methylene cysteine and trimethylsulphonium to produce methionine and methylthioglycolic acid.

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Among the pathways of metabolizing methylene cysteine, cystathionine beta synthase and cystathionine gamma lyase are transsulfuration pathway components which do not recycle methyl cysteine, These components and the transulfuration deteriorate methylene cysteine to Cysteine and H2S, although these components have other catalytic activity.  Cystathionine beta synthase produces H2S and cystathionine in particular, while cystathionine gamma lyase produces cysteine and H2S in particular.

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Methionyl-tRNA synthetase is known to mistakenly use methylene cysteine in place of methionine because these molecules differ by a methyl group, which causes Methionyl-tRNA to intervene this condition by producing methylene thiolactone which is toxic, similarly to methylene cysteine'eic'acid as Hcy'eic' acid and methylene cysteine. Each should be prevented and intervened therapeutically.  Cystathionine beta synthase and its structurally attached heme oxygenase can use methylene cysteine thiolactone to produce retinoic acid from retinol, retinamide from retinoic acid, and thioretinamide from retinamide.  Influx of Ca2+ increases cystathionine beta synthase activity above baseline and increases cystathionine gamma lyase activity above baseline. 

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The diversity in pathways that decrease methylene cysteine, Hcy, and S-adenosyl methylene cysteine, S-adenosyl Hcy, are important because genetic status, tissue, metabolic conditions and environment can result in expression of different enzymes in different tissue and expression of enzymes at different levels in different tissue.  

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Folate, methyltetrahydrofolate and Vitamin B12 methylcobalamin are substrate for methionine synthase.    

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Enlyte, EnlyteRx and advanced formulations of EnlyteRx are each foundational therapies of methylene cysteine, Hcy, repression.  Statistically, methylene cysteine, Hcy, should be suppressed to lower than 6 or 7 um/L toward a therapeutic objective of about 3.7 um/L, while S-adenosyl methylene cysteine should be suppressed to be lower than 0.012 um/L.  

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Between about to about 9 or molecules of high energy electron carriers, NADH and FADH2, are culminatingly supplied to the electron transport pathway per cycle from Glycolysis, to Krebs cycle, to the electrons transport pathway, during P53 repression of glucose 6 phosphate dehydrogenase linked to anaerobic glycolysis, while some of the literature observes between about 32 and 38 molecules of NADH and FADH2 are culminatingly supply to the electron transport pathway  when P53 is not expressed.  P53 expression produces syndrome or context where P53 pathways and genetic sequencing become increasingly susceptible to impairment or surmounting, resulting in dysregulation of glycolysis, while anytime glycolysis occurs without the protection of Pemt enzyme activity, there is also a likelihood of either dysregulation of potential for dysregulation of glycolysis. The dysregulation of glycolysis involves unhindered glycolysis that can include producing more glycolytic products that is typical per cycle and including potential directing of the glycolytic products toward the multiple pathways of glycolysis potentially including an increasingly focused directing of pyruvate and NADH toward lactate anion, NAD+, Parp signaling and the dysbiosis syndrome parthanatos, although the potential for overproduction of substrate toward the electron transport pathway does not seem to be presented strongly in the research and literature. 

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NAD+ is essential to Glucose 6 Phosphate Dehydrogenase enablement of glucose to enter glycolysis which becomes available for glycolysis, pentose phosphate and hexose monophosphate pathways.  There are a number of pathways which obtain substrate from glycolysis including pyruvate dehydrogenase directing of NADH and Pyruvate toward lactate anion and NAD+ which can be used by Parp signaling at loci of DNA repair.  Parp removes ribose from NAD+ and produces Nicotinamide remnants which can be salvaged into NAD+/NADH cycling, can repress or obscure the Sirt1 NHD Nudix homology domain to cause Sirt1 to abdicate its deacetylase activity for a number of other catalytic activities, or can become detoxified using nicotinamide methyltransferase which causes increased levels of methylene cysteine.  

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Thus within the cytoplasm, a near, about or at 700/1 ration of NAD+/NADH is presented in the research literature, while near, about or at 3/10 ratio of NAD+/NADH is presented as occurring in mammalian tissues, occurring as a synapse in which these factors can attach to the Nudix Homology Domains, NHD, of 80,000 or more carriers of NAD+/NADH synaptic components in biology. NAD+ and NADH or paralleled by NADP+/NADPH which are linked to different activity, sometimes considered to be NAD linkage to catabolic activity to derive biologically factors while NADP is liked to anabolic activity.  Other carriers of hydrogen anion can exhibit correlation with particular pathways and kinds of activity also. The ratio of NADP+/NADPH is presented as being 0.005.   

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About 40 percent or as much as 70 percent of NAD+ is found in the mitochondria, according to the literature. NAD+ is produced, recycled and regenerated by metabolic and circadian pathways, which can involve use of the Earths fields and possibly light from celestial entities as pathways including in producing, recycling and sequestration of hydrogen anion multiplicity into NAD+ or other carriers of hydrogen anion. NaAM, NR, NMN, Niacin, Niacinamide, and nicotinic acid potentiate NAD and NAD potentiates NADP. 

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This review found information that confirms that hydrogen anion in the boundless condition can donate, and even receive to reconstitute, its multiplicity in fractal levels.  This confirms that it exists in the boundless condition as a field and exists in the reduced to particle version (electron) as a disjoint field with other hydrogen anion in the universes and in possibly in the universe of universes. These suggest an aether exists that is captured and sequestered by physiology and interacted with to the universes level which occurs at up to 30,000 times the velocity of light, resulting in an interactive systems of systems that allows humans to interact with material of the universe and expanse of the universe before factors exhibit characteristics that Humans can observe. 

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Clearly, this potentiates that human activity, cognition, perception, creativity, expression, admiration, exploration, sense of wonder, constructive activity, captured representation of and understanding of the universes, extend to the most incipient instances of creative forces and creative nuance, while also changes or bends the universes into multiplicities. Some such multiplicities such as particle functions and release from superposition seem completely unnecessary except to support Human observation, cognition and the support of the conditions essential for life, particularly intelligent life.  Certainly, life, intelligent life, interactively extends to the creatively incipient aspects of the universe, while understanding, appreciation, acknowledgement of that creative influence and fulfillment of the potential that the favor of such incipient creative nuance has potentiated, continues to bend the universes to the benefit of humanity and to the benefit of the Human experience. Every scientific and philosophical context exhibit nuance of the uncertainty principle where some aspects of everything cannot be completely explained or represented in canonical models. This uncertainty is more than likely to be the result of modalities in which the Universes are changed interactively by Life, particularly intelligent life.  This review looked for confirmation of these context in material aspects of activity and found that in instances before massive levels of EMF emerged to compete with physiological Human interactivity with the Universes and found that in instances of events with massive detrimental effect to vital being there was also a correlated increase massive displacement of stability among the universes celestial entities.  

 

Humans were intended to be here, were intended to live their lives and were intended to exhibit vital being indefinitely, thus bringing the otherwise inanimate aspects of the universe, too, to life. The universes, too, for every Human has some aspect the uniquely interacts with them.  Abated being would not cause such a universes level tumult if it were not displacing outcomes and factors in the future which were intended and if it were not displacing factors that have emerged in other eras, if it were not affective to Human consideration, and if the most incipient of human inclination and activity were not preventative of its detrimental potential. 

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The synapse between redox paired molecules that carry or potentially carry Hydrogen anion exhibits a polarity that can be used by molecules, acquired by molecules, become translate into biologically enabling and sustaining factors or characteristics, and can contribute to fields and potentials used to maintain a pH near, about or at pH 7.4 used in essential medicine care contexts as an indicator of awareness, cognitive function, vital function and physiological stability. 

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Environmental, aquatic, atmospheric and other toxins, hydrocarbons, dioxins, polycyclic aromatic and other particular or impaired physiology potentiate decreased percentage composition of oxygen in the atmosphere or physiology which cause activation HRE response element which can be mistakenly activated by toxins even if oxygen levels are not diminished which cause the HRE and other response elements to be activated including SRE Serum Response elements, while also apoptosis of foundational biological compartments are also repressed to prevent physiological impairment in low oxygen conditions.     This can disrupt Thioretinaco Ozonide Function and potentiate pathology linked to proliferation of tissue.  

Thioretinaco Ozonide becomes the ATP complex, although Thioretinaco can also be displaced by EMF, Ionizing Radiation, methylene cysteine, oncology causing toxins, dental plaque, vascular plaque, brain plaque, potentially plaque of Islets which repress Insulin synthesis, microbial proteins, viral proteins, and disease.    

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Oxidative disease is that which maintains Thioretinaco Ozonide function and ATP synthesis at ATP Synthase while glycolytic disease involves either repression of Thioretinaco Ozonide and glycolytic production of energy or a massive increase glycolytic energy production along with activate Thioretinaco Ozonide.   

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High energy levels improve resilience and cause apoptosis to be avoided.  HRE response can be involved in repressing apoptosis,  Inhibition of the enzyme Pemt production of resolution phase fatty acid dense de novo choline as phosphatidylcholine causes increased levels of the CDP-Choline pathway which does produce such new resolution phase fatty acid dense de novo choline as phosphatidylcholine.  The CDP-Choline pathway produces phosphocholine, S1P, S1P receptor activation, GPCR receptor activation, and diverse other factors that provide high energy high resistance and highly resilient repression of apoptosis.    Phosphorylation cascades also supply cytokines with energy and resources to activate diverse pathways potentiating numerous outcomes including high energy repression of apoptosis and nonresolution phase signaling linked to pathology.   Immunological signaling can involve such phosphorylation cascade.    

 

The CDP-Choline pathway attaches ATP to choline, while ATP is used by massive phosphorylation cascade activity.  Displacement of Thioretinaco Ozonide and disruption of ATP synthase can be replaced by deregulated glycolysis which produces massive amounts of energy for phosphorylation cascades.  

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Another modality of response to toxins, xenobiotics, allergy potentiating factors are methyltransferases which attach CH3 methyl groups to the factors to deactivate and metabolize such factors.     Methyltransferases compete with the enzyme Pemt for methyl groups and for substrate S-Adenosylmethionine. 

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Pi3k/Akt/mTorc1 signaling causes growth in response to mTorc1 reading of Ragulation complexes at the lysosome which arrange themselves or reading according sensing of growth factors, carbohydrate, nutrients, amino acids or Oleoyl phosphatidic Acid 18/3 species, resulting in use of energy resources including ATP.    Pi3k/Akt signaling is linked with resistant disease and represses P53 to promote disease, dysregulated growth and other factors. 

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Glycolysis and its production of energy from glucose including NADH and pyruvate, which can be repressed by P53 as anaerobic glycolysis or becomes dysregulated as disease promoting aerobic glycolysis when Pemt is represses and when P53 is surmounted, impaired or circumvented.   Glycolysis can be commandeered particularly when P53 is exhibited because P53 decrease glucose entry into pentose phosphate, hexose monophosphate and glycolysis pathways, resulting in massive decrease in Acetyl-CoA, massive decrease in NADPH, massive decrease in pyruvate and massive decrease in nucleotide synthesis. Resultantly, Parp signaling at loci of DNA impairment, DNA repair and DNA replication increases awaiting deficient nucleotides to arrive as Parp removes the ribose from NAD+ and attaches the ribose to local substrate to enable ribose gradients that recruit Deoxyribonucleic DNA, recruit Ribonucleic Acid RNA and await other material to repair DNA.  Parp signaling prevents optimal DNA repair, causes ribosylation of hemoglobin and increases Hb1ac levels, causes nicotinamide increases which prevent Sirt1 deacetylase activity, causes increased methylene cysteine resultant of methyltransferase detoxificaiton of nicotinamide, causes competition with Pemt for S-Adenosylmethionine, represses Pemt with methylene cysteine, and produces a strong gradient of NAD+ because DNA repair can occur in 1 million or more instances in each foundational biological compartment each day, and causes much of the available pyruvate and NADH in glycolysis to be directed toward lactate and NAD+ to satisfy Parp signaling.  These are aspects of parthanatos.    

 

This presents how Glycolysis can be commandeered and dysregulated to produce resources that are directed toward pathology conditions and presents how phosphorylation and ATP redirection along with commandeering of glycolytic potential can independently causes deterioration of the electron transport pathway, deterioration of the supply of ATP to S-adenosylmethionine synthesis and deterioration of S-adenosylmethionine availability for Pemt, along with causing repression of Pemt. 

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The redirection of energy and ATP away from S-adenosylmethionine synthase production of S-Adenosyl methionine, and redirection of S-Adenosylmethionine away from usage by Pemt2 L and Pemt3 L, but possibly expanding to Pemt1 L, are the causing of detrimental aspects of aging and are foundational factors in pervasive if not all disease.   

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Pemt2 L and Pemt3 L emerge near conclusion of gestation to regulate the growth potential of Pemt1 S which occurs in the endoplasmic reticulum and which is active at conception.  Pemt2 L and Pemt3 L have their only known habitat as the shared membrane between the mitochondria and the endoplasmic reticulum known as the mitochondrial associated membrane.   mTorc2 signaling promotes association of the Mitochondria and Endoplasmic Reticulum and performs along with some other factors in linking the Mitochondria and Endoplasmic reticulum to enable transport of phosphatidylethanolamine, phosphatidylserine, Ca2+ used in ATP synthesis and other factors.   

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Rapamycin is known extend expanse of being because it represses mTorc1 while allowing mTorc2 to function.  Also, the gompertz makeham sigmoidal graph presents risk for abated being by age and has nearly perfectively correlated shape and correlation to typical methylene cysteine by age.  Methylene cysteine, clinically Hcy, is a primary inhibitor of Pemt enzyme function. While redirection of ATP, increase in choline kinase alpha, increase nonresolution phase using ATP, and deterioration of thioretinaco ozonide function, ATP synthase Complex 5 function, Oxygen availability, and commandeer of  Glycolysis supply to Krebs cycle and commandeering of Krebs cycle supply of high energy electrons encapsulated in NADH and FADH2, present perspective of detrimental aging and disease at the foundational biological compartment level.  The factors causing repression of Pemt, mitochondrial production and ATP synthesis are largely known, at least in particular linear metabolic pathways, such that preventing and alleviating these diminished conditions are strongly possible.

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Pemt transfer of CH3 from S-adenosyl methionine to in three sequential catalytic actions for complexing with three open locations in the energy levels and orbitals of the ethanolamine lead group of phosphatidylethanolamine in the foundational biological compartment membranes to regulate such growth factors which activate mTorc1 such as Vegf, TGF, and others.  Essentially, CH3, in the homeostatic  condition, can be exhibited on at least a 1 to 1 basis with growth factors in foundational biological compartment membranes while attaching themselves also to the leading edges of expanding structural lattices to prevent unregulated growth.  Functional Pemt can increase the duration between mitotic cycles by between 200 and 300 percent, which, if one considers the Hayflick Limit is about between 200 or 300 percent increase in expanse of being, although the Hayflick limit has found to be inaccurate and to be too low an estimate of potential for expanse of being.

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CH3 also promotes a foundational biological alkaline disequilibrium near, and this participates in a redox factor synapses (NAD+/NADH, NADP+/NADPH, FAD/FADH2, others) which releases the boundless status of the high energy electron within the hydrogen anion or releases the hydrogen anion into its boundless condition.  Hydrogen anion is among the three hydrogens of CH3.  The resultant synapse is comprised of released 2eV-, fluorescence, energy, nonquantized, wave function potential, particle function potential, superposition multiplicity. The synapse promotes a background pH near, about or at pH 7.4, supported by similar alkaline factors carriers of hydrogen anion in tissue, structure, enzymes fatty acids, fatty acid alkanes, and circulatory monocytes, and which compares to H+ derivatives in the foreground which produce a gradient upon which biology enable potentials are foundationally derived while also produce a gradient from which energy is derived to enable biological activity to occur against gradients as fundamental self-determination characteristics of life.  Pemt2 L and Pemt3 L are linked to mTorc2 function, association of mitochondria with the endoplasmic reticulum and supply of phospholipids, nutrients and Ca2+ to mitochondria to support electron transport pathway and Thioretinaco Ozonide performance in the ATP synthase  complex. 

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There are potentials, opportunities and capabilities derived or able to be derived which prevent, alleviates and intervenes each of the detrimental potentialities in these regard.  individuals, groups, populations, organizations, systems and civilizations must only galvanize themselves in focused achievement thereof, regardless of the social, political and other inertia that has for so long repssed advancements that now seem to have lagged since the 1700s and 1800s, or earlier.  The incipient impetus for Humanity to exhibit their being among one another is the systematic observation, consideration, resolution, alleviation and prevention of disparate outcomes and achievement of comprehensive assuring of Human Welfare, Social Welfare and other nuances of Human Welfare including access to care, quality of being and sustained nuances of vital being. 

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(H2e1p)- the energy that supplies Celestial entities or Stars with high energy molecules to use in catalytic function, release of energy and light production, is integrated into membranes using modalities that include Pemt, along with Pemt de novo synthesis of choline as phosphatidylcholine, and focused exhibition of resolution phase fatty acids in such phosphatidylcholine including Docosahexaenoic Acid, extended length Arachidonic Acid, Oleoyl fatty acid, Palmitoyl first fatty acid in fatty acid beta oxidation pathway, and Omega-3 fatty acids.

Methylene cysteine is methionine with a removed methyl group and methylene cysteine is is toxic, sequesters electrons from tissues, sequesters electrons from carriers of (H2e1p) which is a version of hydrogen with an extra electron used at Universes level for energy, sequesters electrons from enzymes, structure and material otherwise, which can deteriorate the ability of CH3 packed into membranes as methyl groups from promoting a background pH near, about or at pH 7.4.   There are numerous factors that transport, carry and exhibit (H2e1p) version of hydrogen, including CH3 which has at least 1 (H2e1p), including Choline which has 3 molecules of CH3, including phosphatidylcholine which exhibits resolution phase fatty acids an 3 CH3 methyl groups, and other factors, while CH3 is typically exhibited on at least a 1 to 1 basis with growth factors in membranes and attach themselves to the leading edge of expanding or growing lattices in membranes to discontinue growth.   

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Cystathionine beta synthesis catabolizes methylene cysteine and produces cysteine and H2S while H2S produces resilience to apoptosis, such that cystathionine beta synthase is increased in early gestation before development of a structure to supply nutrients from the maternal host to the emerging gestational complex emerges, and is also increased in oncology.  HRE hypoxia response element and its activation of numerous response elements that can occur in the same genetic locus such as the SRE serum response element, also represses apoptosis promotes enhance resilience in stem/pluripotent tissues which can be in areas deep in epithelium which are not primary recipients of circulatory system nutrients.  P53, expressed when Pemt is repressed, represses absorption of Glucose and represses entry of glucose into glycolysis, pentose phosphate pathway and hexose monophosphate pathway which causes a syndrome known as parthanatos involving rapid DNA polymorphism, apoptosis among already differentiated tissue, rapid emergence of pluripotent tissue into development, repression of complete removal of stemness and repression of completion of differentiation which programs physiology toward disease.  mTorc1 promotes a senescence phenotype that is toxic and exports disease while P53 promotes senescence, and Ap-1 promotes replicative senescence by repressing telomerase expression which causes chromosome fusion when telomeres become depleted. 

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Telomeres are depleted or removed every time a foundational biological compartment experience mitosis during DNA replication, such that when telomeres are depleted chromosomes fuse and mitosis cannot occur. This depletion of telomeres known as the Hayflick limit was once regarded as a limit to age, until it was found that telomerase and Alt replenish telomeres and a major cause of telomere depletion was a choline deficiency and inhibition of the enzyme Pemt. 

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Ap1 is interesting because, like parthanatos, it is a training context for highly resilient, highly adaptive, resistance potentiating diseased and oncology exhibiting tissues.   Sp-1, which has extra copies exhibited in G quadruplexes typically within telomere regions, increases Telomerase activity to protect its extra copy habitat while Sp-1 represses CD4+, represses CD8+, increase Pd1 and increase PdL1, all of which deteriorate the adaptive immunological protein presentation, training, monitoring, and response, resulting in obscuring of diseased foundational biological compartments to allow these develop, differentiation, and proliferate into latent disease vectors, oncology and other pathology.   Essentially, Sp-1 becomes an escape mechanisms for highly trained, highly adaptive, high pathology and pathology exporting foundational biological compartments. 

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A study by a physician found that two separate populations of about 10,000 exhibited risk for abated being of 500 over a decade of observation when methylene cysteine was above 6 or 7 µmol/L, while the cohort with an instantaneous diagnostic result of methylene cysteine lower than 6 or 7 µmol/L exhibit only 1 instance of abated being over a decade of observation. 

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Another study found that a graph of the Gompertz and Makeham statistical representation of risk for incurring abated being by age  produces a sigmoid that is nearly perfectly correlated to the average typical level of methylene cysteine by age, including high correlation with peculiarities in the graph exhibited beginning with octogenarian status. 

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Growth, Energy, high Insulin signaling, Phosphorylation cascade, increase in the CDP-Choline pathway, displacement of Thioretinaco Ozonide, displacement of the ATP synthase Complex, glycolytic dysregulation, repression of Pemt2 L, repression of Pemt3 L, disruption of the mitochondrial association membrane, and then dysregulation of Pemt1 S and deterioration of Pemt1 S,  conclusively have emerge as central factors in pervasive disease and the cause of diminished aspects of aging.   

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Glucose enters glycolysis when not prevented by P53 and not prevented by inadequate NAD+.  Glucose products energy factors that can be transported to mitochondria, uses by the foundational biological compartment and become transported to the Krebs Cycle.  The Krebs cycle then synthesizes energy molecules that can be used by the foundational biological compartment and transported to the Electron Transport Pathway.  The electron transport pathway takes energy most as NADH and FADH2 and produces ATP by releasing the electron within the Hydrogen as (H2e1p) or hydrogen with an extra electron.  The electrons, 2 eV-, fluorescent light, and energy are used to produce ATP by packing the energy into the Oxygen as Oxonium between the phosphate groups of ATP, while the electrons are used to reduce 02 which interacts with 2H+ to produce water.   

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Repression of Thioretinaco Ozonide, repression of the ATP synthase complex, or both, can occur in a way that causes either Glycolysis or Glycolysis and the Krebs cycle to perform without the ability to produce ATP in the electron transport pathway.  This results in production energy  in a dysregulated modality that is ATP and mostly NADH which compromises the NAD+/NADH ratio, while also being susceptible to dysregulation and commandeering by pathology and pathology vectors. The Electron Transport Pathway typically occurs most stably in mitochondria receiving Ca2+ from endoplasmic reticulum through the mitochondrial associated membrane although mitochondria can receive Ca2+ from other organelles and directly from the cytoplasm. 

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The use of Protac to specifically remove and detrimental toxin or enzyme, use CRISPR perfect Genetic Repair to counteract Genetic causalities of Disease, Enzyme replacement to counteract genetic impairment, therapies that decrease methylene cysteine,  Usag-1 repression to cause regeneration of renal tissue, Usag-1 repression to cause regeneration of dental structure, Agrin insertion into cardiac matrix to cause regeneration of the complete cardiac complex, IGF-1 enabled regenerate of Islet production of Insulin, and other emerging capabilities are changing the Human condition, while in order to assure advancement of Humanity, comprehensive assurance of Human, Social, Care, Care Coverage, Housing, Nutrition, Opportunity, Financial, Information and Data aspects of welfare are essential. 

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There are therapeutics, pharmacological factors, nutraceuticals, natural factors, foods, surgical and diverse other capabilities able to counter the full stack of disease enabling factors.  It only requires clinician and other resources to determine phenotype of disease and link these to multiple therapies to counteract potential for less than therapeutic effect.