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Somewhat Comprehensive New and Original
Somewhat Comprehensive New
A massive oxygenation even 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.
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.
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.
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.
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.
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.
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.
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.
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 share 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.
in the foundational biological compartment membranes to regulate such growth factors while CH3 can attach itself to and deactivate the leading edges of growing lattices in membranes. 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.
CH3 also promotes a foundational biological alkaline disequilibrium near, about or at pH 7.4. 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.
(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.
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 response element and its activation of numerous response elements that can occur in the same genetic locus such as the SRE, 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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Somewhat Comprehensive Overview Original
PEMT2 emerges at conclusion of gestation to regulated the growth and development which PEMT1 enables at conception. Mitochondria of maternal origin proliferates even before gestation while male contributed mitochondria are either inhibited or deproliferate. Mitochondria attach to numerous intracellular organelles and exchange such as endoplasmic reticulum, nucleus, golgi, cytoskeleton peroxisomes, etc, to obtain Ca2+, phosphatidylethanolamine, phosphatidylserine, phosphatidylinositol and other factors, while Ca2+ is used in electron transport pathway to produce ATP, resulting in a closed loop feedback system of atp production and supply of atp from mitochondria to their interaction partners.
Pemt1 is Pemt S, short. Pemt L, for lengthened, is Pemt2 and Pemt3. The membrane shared between the endoplasmic reticulum and mitochondria is knows as the mitochondrial associated membrane. Pemt L as Pemt2 and Pemt3 are better able to traverse the increased depth or complexity, from a membrane perspective, of the mitochondrial associated membrane.
The reason that PemtL and Pemt2 in particular are pervasively diminished in disease, oncology and particularly diminished in advanced phases of conditions, is that these often involve either Impaired ability of mitochondria to import proteins, known as mPOS, or dissociation of the mitochondrial associated membrane which the literature now presents as the central loci of Pemt2 function, or both.
Improved aging involves cellular entities that behave like oncology with unusual resilience to advanced mitotic lineage including genetic, telomeric, apoptosis and mitochondrial resiliency. Oncology and disease involves similar resilience that results in paradoxes in order to achieve such resiliency.
Exhibition of senescence or differentiation to the point that cellular entities do not experience mitosis because of AP1 enabled inability of telomerase to replace telomeres, exhibition of P21, exhibition of P27 or senescent status imposed by tissue level communication such as basolateral/apical polarity.
Extracellular exosomes are used to export and import phenotype, nutrients, enzymes, metabolites, autophagic cargo, and proteins, between cellular entities in lumen or epithelium to promote uniformity. rear / front polarity is used to determine chemotaxis patterns for monocytes used for immunology or stem cellular replenish of tissue specific aggregates of stem cellular entities.
Cellular resilience and deterioration are controlled by diverse programs involving immunological, tissue level, or intracellular signaling, typically cause Bax or Bak factors promotion of apoptosis compared to Bcl2 factors counteracting apoptosis potential signaling. However, mitochondria are used in almost every pathway of programmed apoptosis or cellular level deterioration both in initiation and sustainment of signaling which results in apoptosis.
The ability of Fox proteins which enable and sustain pioneering anatomical development are now known to be result of cellular entities and stem cells to respond to the metabolic characteristics of the environment to exhibit functions of anatomical tissue inherently and aggregate and develop into such anatomical factors in layered phased development process that is less comprised of only very complicated linear development of cellular entities. This new perspective of Fox development increase the potential for pervasive regenerative outcomes including already exhibited ability to regenerate the thymus with only 1 fox protein and the ability to regenerate Islet beta cellular entities with Igf1.
PEMT inhibition results in P53 which inhibits endocytosis of glucose, inhibits entry of glucose into glycolysis, pentose phosphate and hexose monophosphate shunt pathways, causes anaerobic glycolysis, directs available pyruvate to lactate because it produces NAD+ from NADH to sustain parp signaling that can occur about 1 million times in each cellular entity each day, depletes NADH, allows parp to deplete nad+, increase Hb1ac because parp removes the ribose from NAD+ to attach it to material in promotion of a gradient upon which repair material is recruited to loci of DNA repair, and increase methylene cysteine (clinically hcy) because the nicotinamide remnants from nad+ relieved of ribose have to be detoxified by methyltransferase. Dbc1 removes its heterodimer dn from dn Dbc1 to produce Dbc1 which integrates with Sirt1 and displaces nad+ from the Sirt1 NHD nudix homology domain, resulting in Dbc1 interaction with P53 that is essential to P53 being able to convince impaired cellular entities to experience apoptosis through increases in Puma and increase in Bax. Tigar can rescue cellular entities from outcomes impose by P53, although P53 can also promote resilience. Mdm2 causes acetylation of P53 to cause it to rapidly deteriorate, although PTEN protect P53 from Mdm2.
P53 inhibits glycolysis because it is anabolic, risks genetic instability by allowing cellular entities to escape programmed apoptosis, promotes adaptation, promotes resilience, is extremely inefficient in its production of ATP compared to mitochondrial electron transport pathway and compared oxidative phosphorylation. All of these are beneficial during incipient phases of injury or impairment, while, however, promoting disease when exhibited for extended duration and without incipient phase of injury and impairment.
Aerobic glycolysis emerges when PEMT function including PEMT2 is not in place to protect a cellular entity exhibiting impaired, inadequate or nonexisting P53 function.
mPOS or isolation of mitochondria from import of proteins and dissociation of the mitochondrial associated membrane between the mitochondria and the endoplasmic reticulum, each or both results in impaired ability for decisions at the immunological, tissue and cellular level regarding resilience or apoptosis from being affected or imposed. Mitochondria can also experience resilience, and there can be hundreds of mitochondria in a cellular entity while mitochondria can move between cellular entities and exist outside of cellular entity membranes. Mitochondria dissociated from the endoplasmic reticulum or otherwise not involved in organelle exchange of Ca2+ and ATP, can import glycerol, import Ca2+ and import other metabolites directly from the cytosol and cytolplasm while causing impairment of capabilities such as exit of ribosome 80s, 60s and 40s large particles form the nucleus pore. These can cause resilient aging or resilient cellular function in impairment or injury to promote diseases.
Strategies that dissociated, reassociate, enable protein import, disable protein import, reconstitute apoptosis signaling and reconstitute resilience signaling, along with repair of mitochondrial DNA by crispr and along with repair of nucleus DNA by crispr, at some instance, possibly in the near future, are going to abrogate what is known as disease, while even now these factors may be in clinical study and development to abrogate nuances of most disease. Agrin grafts to cardiac extracellular matrix is already known to cause complete regeneration of the cardiac complex. Inhibition of Usag1 and enabling BMP7 expression are already known to cause complete regeneration of dental structures and are known to cause complete regeneration of renal structure and tissue. Inhibition of CD20 is known to stabilize even advanced renal disease. Oncology vaccines are, in some instance, having 100 percent success in producing stable and lasting remission. Populations should be acutely aware of these initiatives, fund these, move these rapidly into practice because these foundationally advance the Human experience.
The paradoxes between extreme stable homeostatic aging have emerged are possible to implement, although practice in these areas are continuing to be developed. Almost in every instance, systems’, information and information systems’ interaction with outcomes and events have caused almost every outcome or event to precise homologues to biology and have caused outcomes and events to elute precise information about the causal factors and potential resolution of pervasive aspects of diminished outcomes. Why and how outcomes occur pervasively present themselves as opportunity review, understand, counteract, prevent, learn and develop ways to improve the Human experience.
The reason that glycolysis is not preferred over oxidative phosphorylation and electron transport pathway include that glycolysis is inefficient at producing ATP from glucose, mitochondrial interaction with organelles and structure is regulated by level of Ca2+ obtained from the interaction partner causing a linking of ATP production directly to the status of the organelle partnered with mitochondria, mitochondria interaction directly with cytosol/cytoplasm derives an expansive resource partner for sterol, glucose, Ca2+, and other factors, potentiating overproduction or dysregulated production of ATP which can cause over activation of ‘ases’ such as ATPase, which can cause subsequent overactivation of phosphate (ADP, ATP, AMP, and linked metabolites, etc) availability for kinase overactivation, these can cause GSK3B activation, g protein coupled receptor activation, S1P receptor activation, and cause enhanced resilience to apoptosis signaling.
Choline kinase is hyperactivated when PEMT is inhibited, this causes the cdp choline pathway to become hyperactivated in production of unenriched diminished DHA/Arachidonate/omega-3 fatty acid phosphatidylcholine along with overproduction of ATP attachment to choline as phosphocholine, and overproduction of S1P. Depletion of S1P by S1P lyase is a major therapeutic and immunological resistance pathway. Hyperproduction of phosphocholine provides substrate for proteolysis that release the ATP for proteolysis and systemic cellular level availability while also producing available of choline for hyperactivation of choline kinase, and while hyperactivation of cdp choline pathway is an allergen, xenobiotic and toxicity response that diminishes plasticity and causes utilization of methyltransferase which compete with Pemt for resources.
Phosphocholine is an allpurpose substrate for pathology and vectors that cause pathology including hyperactivation of resiliency signaling, while also being a subclinical activator of the complements immunological system and while also being able to directly activate platelets.
Inhibition of glycolysis by P53 when Pemt is diminished in availability and function also results decreased acetyl CoA which prevents choline from being stored as acetyl choline by choline acetyltransferase, enhancing the cycle of choline direction toward the cdp choline pathway.
Basolateral apical polarity and rear/front polarity are polarities determined by enzyme expression and location in cellular entities which promote epithelial and lumen tissue stability in the instance of basolateral polarity and which determine chemotaxis patterns with regard to rear/front polarity. Confluence is the ability of cellular entities to inherently sense when they have encountered tissue or structure over a percentage of the cellular surface using ligands that attach the cytoskeleton to external tissue or structure and using cellular/cellular junctions and proteins such as gap junction proteins. Confluence involves P21, P27, and P53 to impose tissue competent growth inhibition and chemotaxis inhibition while Hippo, Yap, Tax, Lat1 and Lat2 are mitotic signals involved confluence most centrally. The factors present in this information typically result in escape from confluence or escape from tissue stability imposed growth and chemotaxis inhibition.
An inducible version of a particular enzyme which uses Ca2+, for instance, causes strong gradients of Ca2+ from solid structure of physiology that can change systemic chemotaxis patterns for monocytes and result in patterns of condition advancement observed in pathology. Sirt1 overactivation is common modality linked to escape from senescence, although this can be differentially directed toward different outcomes if Dbc1 displaces Nad+ from the nudix homology domains that are exhibited in about 80,000 proteins in biology as a environmental modality of regulating biology.
Nad+ is interesting to understand because sparse, dense and very dense (H2e1p)- lakes span the universes and exhibit networks that include nearest neighbor (H2e1p)- carrying enzymes, proteins, tissue, molecules and biologically activity factors, while interacting at 30,000 times the velocity of light. Comprise, possibly, are interact networks that continuously emit influence, receive feedback and guide outcomes toward those which sustain, stabilize and support the status quo, while such adjudicative interactions potentiate also the emergence of competing outcomes in other eras which then impose deterministic influence on the status quo. This is why methylene cysteine below 6 or 7 um/L, access to stable nutrition, accesses to stable housing, access clean and stable water supplies, economic stability, social stability, education, social development, and other factors are so important in their ability to prevent competing outcomes in other eras from causing massive destabilizing of vital being, health, cognition and other aspects of the Human experience.
Carriers of (H2e1p)-, thus, operate in a synapse that includes + or oxidized phase, as in Nad+, exist as NadH in the reduced phase, while also are exhibited as the molecule NAD although in biology, unless involved in another molecular configuration, the oxidized and reduced versions are most mentioned in the information and while NAD is at least mentioned in the research information. There are numerous other carriers of (H2e1p)-. The synapse between NADH oxidized (H2e1p)- and NAD+, including fluorescence and eV- released when (H2e1p)- is oxidized from NADH in particular, exists as interactive statuses that provide influence, power, translatable influence into energy molecules, and even is able to be translated into mechanical force, each of which assist in powering biology.
(H2e1p)- can be derived from paramagnetic and quantum spin liquid networks that move e-, nutritional pathways that provide carriers and sources of energy molecules and (H2e1p)-, lithium and Sodium which have high vapor pressure and allows them to siphon (H2e1p)- from networks of other element molecules harboring (H2e1p)-, along with other more controversial vectors which are confirmed in some instances and in other instances continued to be debated such as Human rubisco, Human pigment synthesis of energy and even phonons which involve sound's ability to produce energy along with substantia nigra in which neurons generate energy from interactions in fields of influence in the universe, some of which have not been conclusively ascertained. Darkening of the substantia nigra are linked to development of coordinated movement in early development,
The interaction of Human physiology, constructive activity and creative activity, interactivity, expression and other productive potentialities, extend into fields that reach to all aspects of the Universes and can be amplified in their effect to the Universes by the trillions of interactive systems within each human, among humans and in human contexts such as civilizations.
The human cognitive function, interactive function, and physiological interaction, thus, interacts into distant antecedent and emerging eras and produces a stabilization oscillating context which can be presented as an interaction with any observed artifact that extends at 30,000 ;times the velocity of the light that reaches human observation of such artifact in a manner that affects the observed artifact come to exhibit those characteristics that observed by the observer. This may inherently promote stability. Quantum levels of observation may not be inherently possible without assistance or assistive capabilities because it may provide flexibility in deriving the observed status quo. Physiology presents relevant nuances of nanoplasm, through space electron jumps, just in time electron transfer, and ability for atoms to exhibit characteristics of other atoms when required to sustain stability.
The most intricate perspective in this regard is that inhibition of PEMT increases methylene cysteine (clinically hcy) which performs as inherent apoptosis signal that cause release of multiple apoptosis factor such as cytochrome C and others, requiring resilience signaling to be increase to counteract massive levels of apoptosis that emerge when Pemt is inhibited, although Pemt1 is naturally regulated in this regard by Pemt2 which emerges at conclusion of gestation. Methylene cysteine above 6 or 7 um/L and s adenosyl methylene cysteine above 0.012 um/L begin to cause clinical levels of apoptosis signaling, sequesters electrons from tissues, sequesters electrons of carriers of (h2e1p)-, sequesters electrons from biological active proteins/enzymes, and begins to cause a reliance upon major anatomical structures, enzymes, ion channels, molecules, adventitia and buffering system to maintain background pH at its optimal levels near, about or at pH 7.4.
Pemt moves CH3, exhibiting Carbon, 2 Hydrogens as H1e1p and 1 hydrogen as (H2e1p)- into cellular membranes, packing cellular membranes and tissues with (H2e1p)- the molecule integrally enabling stars to shine. This packing of membrane hydride enables tissues, structure and other factors to promote a background pH near, about or at pH 7.4 while also providing a source of (H2e1p)- that can be mined to provide (H2e1p)- integrated into carriers such as FAD, FADH2, NAD(H), NADP(H), and other factors which are used by the electron transport pathway in mitochondria efficiently, and with substantial regulation, to produce ATP. Removal of the electron in (H2e1p)- or carriers of (H2e1p)- is characterized as “protonation” because Hydrogen directly or indirectly since (h2e1p)- becomes distributed canonically across the expanse of a protein or molecule, resulting in Hydrogen becoming either (H1e1p) from (H2e1p)- or resulting in (H1e1p) becoming H1p without an electron.
Diminishing pH levels are linked with cellular entities increasing the protein content of extracellular exosomes while increasing the absorption of exosomes by cellular entities, explaining an important link between acidity in development of pathology in the microenvironment, particularly oncology. Pathology affected cellular entities may export pathology phenotype to epithelium, lumen and cellular entities in these contexts, including even distal tissues. Cellular entities may also internalize and endocytose phenotype, protein cargo, and enzymes exhibited in exosomes. their are diverse opportunities at replacing, preventing and counteracting the export and import of pathology phenotype while there are even more substantial opportunity to distribute optimal micelles, lipid droplets, exosomes and other modalities of importing, controlling and optimizing phenotype, genotype, and proteasomes of cellular entities.
These conditions deteriorate the neurological basis of social behavior, frontal cortex control function, behavioral conditioning, recall of conditioned stimuli/response pairs in different contexts, resiliency to externally imposed stimuli/response pairings, and include diminished Pemt ability to produce tissue plasminogen factor super clot buster, serine proteases which promote early developmental plasticity, and oxytocin which performs centrally in producing human emotional, social, group, community, civilization and species level connections and prioritization.
methylene cysteine lower than 6 um/L produces an study observed decrease from 500 instances of abated being for those with more than 6 or 7 um/L of methylene cysteine (hcy) to 1 instance of abated being among those with methylene cysteine (hcy) below 6 or 7 um/L, using two comparative populations of about 10000 participants in each group over a decade of observation.
The paradigm of programmed apoptosis and resilience are central to diminished status at physiological and behavioral levels, while also presented an important paradox between extremely resilient aging.