Counteracting viral, microbial, oncology or insulin dysregulation statuses

A, Enlyte or EnlyteRx(essential)

A, Enlyte or EnlyteRx(essential)

B, Lecithin with Vitamin K2(Essential)

C, grapeseed extract and probiotic such as align or leaky gut therapy(essential)

D, L arginine, L citrulline, L ornithine

E, Diverse Mineral Supplement with molybdenum, cobalt, iodide, calcium, vanadium (before, after, but not during cytotoxic therapy)

F, Diverse Multi Vitamin with B12 Methylcobalamin, Vitamin K2 , Vitamin D, and Folate (before, after, but not during cytotoxic therapy)

G, low intensity, short duration, exercise using resistance(essential)

H, EMF Protection Bedding, Clothing and Dwelling Protection (Power outlets, appliances and devices)(essential)

J, DHA docosahexaenoic Acid

K, ARA Arachidonic Acid at levels higher than DHA obtainment

L, Diverse Omega-3, Omega-6 and Omega-9 fatty acid or cholesterol supplement

​J, Berberine 

K, Curcumin

L, active hexose correlated compound AHCC

M, Nattokinase

N, Serrapeptase

O, Retinol

P, All Trans Retinol

Q, Inhibiting Estrogen Receptor Alpha activation which harbors the PEMT inhibitor AP1

R, Causing dn DBC1 to stay as dn DBC1, or preventing DBC1 from integrating with SIRT1 but allowing DBC1 to complex with P53 to repress anerobic glycolysis the canonical disease status at cellular level. DBC1 displaces NAD+ from SIrt1 to exhibit a requisite freeing of (H2e1p)- that enables cellular division.

S, inhibiting availability of DBC1 for complexing with P53 if P53 is genetically impaired or if P53 is impaired only in the diseased cellular microenvironment. Inhibiting DBC1 because free DBC1 escapes Suv39H1 cellular senescence, histone methylation and genetic control programs.

T, Using Iodoacetate and another disease specific therapeutic to disrupt aerobic glycolysis or disrupted increase of glycolysis that counteracts P53 inhibition of glycolysis that occurs when PEMT is inhibited or which occurs in cellular level impairment

U, CART immunological therapy specific to disease phenotype

V, PD1 inhibitor, PDL1 inhibitor

W, Etopaside therapy and an inhibitor of SenP1 to cause cellular deterioration without requirement of P53, escaping potential P53 impairment and causing cellular deterioration in intricate essential mitotic phase mechanisms

X, topical geranyl choline

Y, phage therapy

Z, Se Methylselenocysteine, Methyl Selenic Acid, Methyl Selenol,  Sodium Selenite as Na2SeO3, Selenomethionine as C5H11NO2Se

AHSA, arginine, Citrulline, Ornithine, agmatine, putrescine, spermidine, spermine

AHSB, arginine, histidine, aspartate, glutame, cysteine, phosphoserine, Vitamin K2

AHSC, Iron as Fe++ to promote ferroptosis, including with Se methylselenocysteine

AHSD, Mitophagy Modulation Promotion or Inhibition

AHSE, Autophagy Modulation Promotion or Inhibition

AHSF, Choline kinase alpha inhibitor

AHSG, Proteasome inhibitor (26s, 20s or 19s)

IAHSH, inhibition of Bag1 with nutrient restriction

IAHSI, Inhibition of Bag1 and inhibition of Bag3. 

IAHSJ, Inhibition of SP1(counteracts latent viral disease) to reconstitute CD4+, reconstitued CD8+, inhibit PD1, inhibit PDL1 and disrupt SP1 escaping of diseased cellular entities from AP1 inhibition of telomerase in impaired cellular entities which would rapidly causes senescence if not counteracted by SP1 increasing of telomerase.

AHSK, Telomastatin inhibition of Telomerase

AHSL, Tissue specific ion channel inhibitors, oils, essences, derivatives and therapies

AHSM, S1P Lyase inhibitor

AHSN, S1P receptor Inhibitor

AHSO, GSK3B Inhibitor

AHSP, Deoxyribonucleotide, Ribonucleotide, Ethanolamine, Methylene, Uridine, therapy light or therapeutic light

AHSQ, Crispr genetic repair with biopsy phenotype or crispr genetic repair with known factor genetic repair

AHSR, iNOS/NOS 2 inhibitor, emf protection

AHSS, only obtain meat, chicken, eggs or fish if they are micronized or processed into fine granularity

AHST, relocate to a region that does not use abated being as a sanction, counteracts a correlation

AHSU, remove personal information and contact information from any database and information systems including internet systems and noninternet systems 

AHSV, utilize only unscented, hypoallergenic beauty, cosmetic, hygiene, cleaning and environment cleaning products to conserve methyl groups

AHSW, Interventional Somatostatin

AHSX, Trikafta for conditions involving O2/CO2 exchange

AHSY, Green Tea, Moringa O or Moringa O Tea, Haddock Tea, Burdock Tea

AHSZ, Olive Oil, Green Tea, Dark Chocolate, Moringa O Tea

AHSHSA, Humic Acid, Fulvic Acid, the product Blk Water

AHSHSB, for radiation exposure Humic Acid, Fulvic Acid (Blk Water), Iodide, Phosphatidylcholine, choline

AHSHSC, Prevent myeloperoxidase to prevent impairment to tissues and prevent pathology, enable myeloperoxidase to oxidize lipids and prevent lipid enabling of escape for oncology

AHSHSD, inhibit MDR2 to counteract diverse multiple therapeutic resistance in oncology and other disease

AHSHSE, inhibit S1P Lyase to counteract resistance to therapeutics

AHSHSF, inhibit autophagy to counteract resistance to oncology therapeutics

AHSHSG, inhibit proteolysis to counteract resistance to oncology therapeutics

AHSHSH, Iodoacetate and Iodoacetamide to inhibit increased glycolysis that is the canonical disease syndrome

AHSHSI, Pyst protein or other inhibitor of Dbc1 to counteract aerobic glycolysis, the canonical disease syndrome 

AHSHSJ, Aminophenol therapy for oncology

AHSHSK, Fenretidine for oncology

AHSHSL, MoHL1 and MoHL2 for oncology therapy and glucose metabolisms syndromes

AHSHSM, inhibit gluconeogenesis by inhibiting or disrupting Pepck, Pck1 and Pck2 

AHSHSN, Inhibiting lengthened noncoding RNA FLVCR1 AS1 and FBXL19 AS1 for diverse versions of oncology

AHSHSO, Inhibiting GSK3B

AHSHSP, Exclusion of Yap from beta domain of dystroglycan represses its proliferative potential and diminishes its ability to impair plasticity of extracellular matrix

AHSHSQ, Exclusion of Yap from beta domain of dystroglycan represses its proliferative potential and diminishes its ability to impair plasticity of extracellular matrix

AHSHSR, Crispr genetic gene repair for mitochondrial DNA and Crispr for nucleus DNA to counteract oncology, aging and disease

AHSHSS, Inhibition of Cct beta 3 has the possibility of disrupting autophagy that supports oncology

AHSHST, phosphatidylcholine to enable autophagosomes to close or complete development

AHSHSU, NAD+, Choline, Phosphatidylcholine, methylene dense phosphatidylethanolamine, DNA nucleotides, RNA nucleotides, Ribose, Niagen, NMN, NAM, NR, Niacin, Niacinimide, NAD+, NADH, other NAD+ Sources, Melatonin, and EMF/RF protection to repair genome

AHSHSV, Disrupting Pepck, Pck1 and Pck2 may specifically disrupt oncology relying upon gluconeogenesis for stabilitytunicamycin enablement of endoplasmic reticulum distress can promote apoptosis when proteasome is inhibited by MG132, while  Chop/Gadd153, Kdel chaperones, and potential for increased NADPH oxidase and potential for NOX4 increases, and potential enhancement of protein disulfide isomerase mRNA increase, all are decreased or prevented by proteasome inhibition

AHSHSW, DHA, Arachidonic Acid, both and when integrated into phospohatidylethanolamine particularly activates PEMT

AHSHSX, Inhibiting Tigar can prevent impaired cellular entities from escaping P53 imposition of deteriorationtherapeutic prevention, remediation and imposition of mPOS is emerging as potential to strongly increase the ability to disrupt diminish health status and diminished behavioral health statuses

AHSHSY, inhibiting or enhancing YTHDF2 can impose deterioration of oncology

AHSHSZ, Activators of Nmd3 to enable exit of proteasome from the nucleus pore to enable exit of the 60s Large Proteasome Particle from the nucleus pore include Rapamycin, Cycloheximide, Trichostatin A, MG132 Z leucine Leucine Leucine CHO, Sodium Meta Arsenite, chloroquine Puromycin, and Emetine

AHSHRA, Inhibitors of Nmd3 prevent export of the 60s Large Proteasome Particle from the nucleus pore include Leptomycin B, Actinomycin D, CX5461, Triptolide, BHM21, Homoharringtonine, Rocaglamide, Silvestrol, Mycophenolic Acid, and TunicamycinInhibiting Ras in the Ras associated nucleus protein cycle can prevent export of cargo from the nucleus pore

AHSHRB, Sulfur therapy including MSM, s methylmethionine sulfonium or other along with methyl groups Choline, Phosphatidylcholine, Folate, all trans retinol, Betaine, etc, provide sulfur and methyl groups as major detoxification pathways including detoxification of hormones and steroids

AHSHRC, Estriol and estetrol unevenly and overactivate estrogen receptor alpha more than beta, potentiating pathological overexpression of AP1 which is an inhibitor of PEMT

AHSHRD, The therapeutic delivery, activation and deactivation of mitochondria specifically design to cause apoptosis, sustain apoptosis, support endoplasmic reticulum or otherwise impose specific statuses seems to be a strategy to counteract oncology, detrimental aspects of aging and disease 

AHSHRE, Apetite repression can be enabled by Pyy36 and Extendin4, Pyy36 and cannabinoid receptor 1, or Pyy3/36, Pyy3/36 and leptin, or Pyy3/36 and amylin implementation can repress the motivation for increased nutritional factor obtainment linked to obesity

AHSHRF, JT003, a hyperstimulator of the adiponectin activated AdipoR1 and AdipoR2 receptors which increase fatty acid oxidation and increase glucose absorption, is able to diminish insulin resistance, suppress hepatic stellate cellular entity activation, improve endoplasmic reticulum mitochondria coordination and function, stimulate exhibition of the Pi3k/Akt pathway, thereby suppressing hepatic pathology

AHSHRG, Inhibiting USP10/G3BP1 40s ribosome recycling complex by inhibiting either protein can deteriorate fission/fusion protein loci within mitochondria and prevent its assisting in regulation of functional assembly of mitochondrial associated membrane protein interaction loci ERMCSs

AHSHRH, Cardiolipin supplementation and synthesis should be assure

AHSHRI, Prevention of Mic19 availability introduces distress that can destabilize oncology and lead to mitochondrial deterioration while leading to distress and disease and is toxic.  Assuring or overexpressing Mic19 disrupts the ability of numerous disease and conditions to emerge and persist4

AHSHRJ, Doxycycline increase in mitochondrial associate membrane connectors emerges along with signaling from the mitochondria to the nucleus to initiate the mitochondrial unfolded protein response thereby providing resources from the endoplasmic reticulum to support the mitochondrial unfolded protein response. Doxycycline was found to cause mitochondrial stress, inhibit mitochondrial mDNA expression, increase Chop, C/Ebp beta, mtHsp60, and ClpP, increase interaction between mitochondria and endoplasmic reticulum, increase Ca2+ import into the mitochondria, and increase oxygen usage, all while not causing endoplasmic reticulum stress

AHSHRK, Rapamycin produces cytosolic stress similar to that caused by nutrient deprivation and which includes an increase of endoplasmic reticulum integration loci with the mitochondria along with increased Ca2+ exchange, while focusing newly synthesized integration loci in patterns that are not specific to any particular aspects of subcellular compartments.  This includes increasing the attachment of mitochondria to the nucleus, peroxisomes, endoplasmic reticulum, cytoskeleton and even the plasma membrane

AHSHRL, Tunicamycin introduces endoplasmic distress which can also increase the number of endoplasmic reticulum integration loci with the mitochondria, although exhibiting increased new contact loci near the nucleus complex of the cellular entity correlated with the area of protein folding in the nucleus complex focusing exchange and energy enhancement relevantly

AHSHRM, Calcium availability has emerged as being essential to mitochondrial function and ion channel function which could be beneficial in some instances and be therapeutic in some others, while also in some studies increasing potential for exhibition of oncology. Vitamin K2, and Vitamin D may assist calcium supplementation by changing the ability of calcium to be integrated into and deteriorate epithelial plasticity. If supplementing with calcium, Vitamin K2, Vitamin D, molybdenum and phosphatidylcholine may be useful in promoting homeostasis

AHSHRN, Lithium, Sodium and tetrahydrobiopterin along with folate may be ways of promoting (H2e1p)- sequestration and onboarding

AHSHSRVO, Sodium supplementation is important, as nontoxic versions that do not cause striation of epithelial tissue such as ancient pink Himalayan Sea Salt, because 90 percent and possibly up to 100 percent of oncology in some studies involve low sodium or hyponatremia before diagnosis, since Na+ is used in import of choline, selenium, iodide and other factors determinant of cellular outcomes

AHSHRP, Amobarbital represses complex I of the electron transport pathway including increasing the depletion of glucose and including diminishing hepatic glucose production. Ablation of the NDUFA13 domain of complex I of the electron transport pathway also results in increased glucose depletion along with diminished production of glucose by hepatic tissues. nonAMPK glucose depletion duration NDUFA13 domain inhibition and during repression of complex I of the electron transport pathway has emerged as a diabetic therapeutic pathway

AHSHSRQ, Mitochondria supply ATP to the endoplasmic reticulum in manner that relies upon a Sarco/Endoplasmic Reticulum Ca2+ ATPase reliant or SERCA reliant Ca2+ gradient across the endoplasmic reticulum membrane using the The transporter SLC35B1/AXER which can be inhibited to cause endoplasmic reticulum destabilization, while increasing cytosolic Ca2+ can inhibit endoplasmic reticulum ability to import ATP form mitochondria

AHSHRVR, Gpr120 can cause interleukin 10 expression in a manner that represses colitis, using increased glycolysis and which uses b lymphocyte induced maturation protein 1  

AHSHRVT, Gpr120 can inhibit H4K kinase, inhibiting glycolysis while in CD4+ cellular entities, such as dendritic cellular entities, gpr120 can inhibit CD4+ receptor responses including diminish immunological activity of CD4+ T cellular entities

AHSHRVBU, Cisplatin or other platinum salts are used in oncology therapy, synthesis of 16, 4, N3 or hexadeca 4, 7, 10, 13 tetraenoic acid is resultantly derivatized, resulting in systemic resistance to a diverse group of oncology therapeutics that affect DNA.  The derivatized 16, 4, n3 interacts with and activates g protein coupled receptor Gpr120, also known as FFAR4, of splenic macrophages which causes synthesis of lysophosphatidylcholines that protect DNA from chemotoxicity. Other polyunsaturated fatty acids also activate gpr120. Gpr120 causes sensitivity to insulin, suggesting that it affects glycolysis, therapeutic deactivation of gpr120 can be beneficial to prevent resistance to therapy such as oncology therapy

AHSHRV, Inhibition of Rab5 inhibits early endosomes development into late endosomes while inhibition of Rab7 increases the ability to prevent endosome development into late endosomes

AHSHRW, Inhibition of SLC25A48 deteriorates purine synthesis, prevents G1 to S phase completion and causes deterioration of cellular entities

AHSHRX, Using dichloroacetate to inhibit pyruvate dehydrogenase kinase PDK and using the derivative of the anthraquinones of Rheum known as Rhein to inhibit autophagy, TGFbeta1, and NF kB, the inhibition of glycolysis and inhibition of oxidative phosphorylation can be therapeutically imposed to remove the power sources for oncology cellular entities and cause insurmountable reactive oxygen species increases

AHSHRY, CAR T therapy is useful in oncology therapy

AHSHRZ, valproic acid therapy deteriorates mitochondria and prevents oncology growth that uses nonfermentable sources of nutrients such as glycerol, while it also changes 30 percent of genetic expression in experimental contexts and while it has less diminishing effect on oncology using fermentable sources of nutrients such as glucose. 

AHSHRZA, Selenolase or selenium deficiency

AHSHRZB, Apolipoprotein A IML and 1   palmitoyl  2   oleoyl phosphatidylcholine complex to protect from ischemia and during reperfusion, particularly of cardiac tissue

AHSHRZC, Irinotecan
AHSHRZD, Irinotecan Liposome injections with oxaliplatin, fluorouracil and leucovorin after gemcitabine therapy

AHSHRZE, Fruquitinib for oncology and CRC oncology

AHSHRZF, Irinotecan and Doxorubicin with cardio protection for doxorubicin

AHSHRZG, Mannose 50 mg

AHSHRZH, Serine 100 mg

AHSHRZI, Glycine 100 mg

AHSHRZJ, Cysteine, 75 mg

ASHHRZK, Cystathionine 50 mg

ASHHRZL, Regγ can be inhibited by glucosamine, NIP30 and phosphor NIP30 mimetics. Particular probiotics stimulate Regγ.  Regy causes increased exhibition of cellular cycle particularly in digestive pathways and pancreas although exosomes potentiate export into other aspects of epithelium, lumen, and distal tissues. Regy also directly interacts with gram positive microbes and causes expression of mucus in digestive pathways to separate microbes from digestive pathway membranes.

ASHHRZM, cdk4/6 inhibitor abemaciclib or palbociclib with fulvestrant in HER2+ 
ASHHRZN, cdk4/6 inhibitor ribociclib and fulvestrant in conditions without adequate treatment improvement. 
ASHHRZO, Fulvestrant and tamoxifen relevant modulators of estrogen activity with improved potential including potential or prospective pharmacological capabilities include 4 hydroxytamoxifen, acrylic acids (GW5638, GQ7604, AZD9496, LSZ102, GDC0810), Pyrollidines(SAR14n, SERM OP1156, SERD OP1074, SERM OP1154), fluoromethyl azetidine GDC0927, SERM/SERDs RAD1901 and Bazedoxifene, noncoanonical deteriorators OHBSN13 and PROTAC with the observation that estrogen disruptors potentiate resurgence of different phenotype, such that repression of AP1, AFB1 estrogen receptor moiety which exhibits AP1, and Estrogen Receptor Alpha specifically may be another option, a simultaneous option, or a subsequent option.
ASHHRZP, Smac mimetics small molecules used in oncology therapy such as Birinapant and LCLC161 are used in therapy for myel, gliobl, and sarc oncology versions. 
ASHHRZQ, Inhibiting clAP1, inhibiting clAP2, introduce Smac proteins or causing mitochondrial release of Smac proteins, protecting Rip1 from ubiquitylation or deubiquitylating Rip1 in vivo or in vitro for reintroduction into therapeutic areas, along with assuring resilience of mitochondria, can therapeutic in diverse oncology
ASHHRZR, Ptch1 inhibition can inhibit squam carc.
ASHHRZS, Allocryptopine and Mesalazine are used to counteract IBD.
ASHHRZT, Regγ, Reggamma, promotes oncology, although it inhibits particular MCL oncology. Regγ, Reggamma, can be inhibited with Glucosamine and  NIP30 and phosphor NIP30 mimetics which sensitizes oncology to chemotherapeutics. Fisetin supports or enables Regγ, Reggamma. Particular probiotics stimulate exhibition of Regγ, Reggamma.  Regγ, Reggamma, is major enabler of escape from senescence or surmounted of mitotic inhibition and confluence, being associated with regenerative and pioneering anatomical development. Regγ, Reggamma, is produced in digestive pathways and pancreas while its possible for exosome export to other aspects of lumen, other aspects of epithelium and exhibition at distal tissues. 
ASHHRZU, Quaternary benzophenanthridine alkaloids Sanguinarine, chelerythrine, sanguirubine, Chelirubine, chelilutine, marcapine and sanguilutine are all substantial factors in inhibition of oncology of diverse phenotype. These factors have diverse toxicity characteristics and pharmacological characteristics.
ASHHRZV, Iodoacetate is unstable because of the its C1 linkage and it readily abdicates Iodine and Iodide. Iodide is therapy for oncology particular oncology of glands and biological structure. DMSO and iodoacetate are used together to improve therapeutic effect. Iodoacetate is massively effective in triple negative oncology while being somewhat effective in her2 oncology. Iodoacetate inhibits methylglyoxy metabolism into lactate. Iodoacetate rapidly finds factors exhibiting thyoglycolate and Iodoacetamide has less potency in this regard. Iodacetate is an alkylation factor and promotes alkylation of molecules and microenvironment. Inhibiting availability of pyruvate, acetate and lactate can assist in therapy using iodoacetate. Leucine supplementation can enhance the effectiveness of therapy that uses iodoacetate. Substrate availability for GAPDH, such as glyceraldehyde, can escape the ability of iodoacetate to repress function of GAPDH, thus, suggesting that activated P53 or withholding of glucose nutritional availability can improve the effectiveness of iodoacetate.  Generally substrate availability for affected enzymes, phosphorylation of substrate for affected enzymes, NAD availability and Mg2++ availability, increasingly, as the number of availability of these factors increases result in diminished ability of iodoacetate to effectively promote its pattern of enzyme inhibition.  Thus diminishing phosphate availability, diminishing kinase activity, diminishing NAD availability and decreasing Mg2++ availability can assist in effectiveness of therapy using iodoacetate. Assuring that fluoride is not bioavailable or is not increased in bioavailability can assist in therapy using iodoacetate and iodoacetamide.  Increased availability of Fe++ promote ferroptosis and can enhance therapy using iodoacetate. Cysteine availability enables removal of iodoacetate inhibition of fructose 1,6 diphosphatase.  D glutamate oxidase inhibition is removed by cysteine. Dialysis removes inhibition of arylsulfatase by iodoacetate.  Fe++ removes the inhibition of 3 hydroxyanthranilate. Fee++ decrease may be used if activation of 3 hydroxyanthranilate prevents therapeutic effect. The same study observes that iodoacetate may be among the most specific inhibitors of glycolysis enable specific intervention of aerobic glycolysis, such that it may be applicable to diverse array of diseases, pathology and conditions. Iodoacetate has a diverse pattern of biological enzyme repression.Succinate dehydrogenase is inhibited by iodoacetate. Alcohol dehydrogenase is not clearly able to be inhibited by iodoacetate, although at lower pH or acidity, it is more clearly inhibited. However, Lactate Dehydrogenase is inhibited by iodoacetate, pyruvate decarboxylase is inhibited by iodoacetate and catalase is inhibited by iodoacetate.  It is not clear of the inhibition of pyruvate decarboxylase and lactate dehydrogenase emerges from inhibition of GAPDH. Ribonuclease is inhibited by iodoacetate and iodoacetamide. Creatine kinase or ATP Creatine phosphotransferase is inhibited by iodoacetate. Gapdh inhibitor Iodoacetate causes 70 percent deterioration of triple negative oncology of mammary tissue at 20 uM and causes 30 percent deterioration of ER positive tissue oncology at 40 uM, both at about 4 hours of therapy. 24 hours afterward, triple negative oncology tissues had strongly reemerged while estrogen receptor positive ER positive oncology continued to deteriorate to the point of eradication even at levels less than 10 uM.  Oncology exhibits reprogramming of glycolysis such that the first phase of cellular risk which emerges from PEMT inhibition which causes increases in P53 which result in inhibition of glycolysis to anaerobic glycolysis. Oncology and disease generally is correlated with escape of the P53 repression and decision programs to resume increased levels of glycolysis while P53 continues to be increased and while PEMT continues to be inhibited, a condition known as aerobic glycolysis.  Iodoacetamide has higher potency and lower duration and lower ability to complete eradication of oncology while Iodoacetamide has lower potency, increase duration to therapeutic effect and potentiates more adequate eradication of oncology.
ASHHRZW, Inhibiting Phosphatidylethanolamine can destabilize diverse oncology because phosphatidylethanolamine increases are nearly canonical in at least tissue oncology but also diverse oncology otherwise since inhibition of Pemt, which prevents metabolism of phosphatidylethanolamine into enriched phosphatidylcholine, is considered to be essential to pervasive disease. 
ASHHRZX, Carotenoid and Flavonoids may be therapeutic in oncology because promote optimal pH at the outer and inner aspect of the plasma membrane. 
ASHHRZY, Ceramide increases destabilize the foundation stability of membranes comprising the plasma membrane encapsulated foundational biological compartment.
ASHHRZZ, trastuzimab is used in Her2 and IHC oncology. 
ASRZLA, SP1 and AP1 are typically increased in disease while SP1 counteracts senescence programs exhibited by AP1 to enable escape of impaired cellular entities from P53 selection for apoptosis through Puma and Bax.  Dbc1 also can promote cellular deterioration but this may require inhibition of SenP1 which can replace the activity of Senp2 to prevent SenP1 from rescuing mitotic structural separation destabilization.    SP1 causes overexpression of telomerase, PD1 and PDL1 to enable escape from senescence and enable hiding from the immunological system while SP1 also inhibits cellular surface exhibition of immunological CD4+ and CD8+. Inhibiting AP1, SP1, SENP1 and SENP2 can enable Ddb1 enabled eradication of diseased or eradication of oncology afflicted or oncology impaired plasma membrane encapsulated foundational biological compartment. It may be essential to inhibit Senp2, then inhibit Senp1 or inhibit both Senp1 and Senp2 to modulate Dbc1 ability to stimulate exhibition of apoptosis therapeutically.
ASRZLB, Inhibiting mTorc can prevent 80s large proteasome particle from exiting the nucleus pore.
ASRZLC, Inhibiting sirt1 depotentiates mitosis
ASRZLD, DBC1 represses alternative NFkB signaling and causes exhibition of apoptosis in B Lymphocytes
ASRZLE, Inhibiting MDM2 protects P53 to enable it's making of decisions
ASRZLF, Inhibition of Chk2 and or inhibition of Regy causes 
ASRZLG, Phosphatidylethanolamine is increased resultant of PEMT inhibition and increases in membrane phosphatidylethanolamine represses apoptosis signal transduction while also represses cellular membrane chaperone function. Depleting phosphatidylethanolamine or inhibiting phosphatidylethanolamine synthesis can disrupt structural mechanisms of escape and sustainment of oncology, particularly including escape from immunological intervention.  PEMT2 and PEMT3, both PEMTL versions exhibited in the mitochondrial associated strong deteriorated function in oncology and disease, while PEMT1, PEMTS version occurring at least in areas other than the mitochondrial associated membrane between the endoplasmic reticulum and mitochondria, is increasingly inhibited also in oncology and disease, while in some instances of advanced diseases these can all be strongly deteriorated in function. Mitochondria are preferred to glycolysis because the electron transport pathway is mitochondrial and is regulated by exchange of Ca2+ as substrate from the endoplasmic reticulum to the mitochondria along with products from pr substrate for PEMT1, PEMT2, PEMT3 and acyl transferase such as Ca2+, phosphatidylserine, phosphatidylethanolamine, phosphatidylcholine, and phosphatidylinositol. mPOS or impaired import of proteins by the mitochondria can occur along with either cytoplasm or nucleus accumulation of proteins while dissociation of the mitochondria from the endoplasmic reticulum can occur separately, correlative to, or not occur in synchronization with mPOS. PEMT1 integrally directs anatomical development and layered development activities by Fox pioneering development factors along with inherent ability for foundational biological compartments to respond to metabolic conditions while PEMT2 emerges near conclusion of gestation to regulated PEMT1 activity. This relationship is similar to estrogen receptor beta regulation of estrogen receptor alpha which has a PEMT inhibiting AP1 sequence. 

ASRZLH, Inhibiting factors or conditions that inhibit PEMT can be a strategy in most disease such as inhibiting  choline deficiency, methyl group deficiency, AP1, SP1, methylene cysteine hcy, methylgyoxal, phospholipase D, iNOS/NOS2, oxalate, and numerous other factors including toxins, xenobiotics, and other factors which are methylated by methyltransferase to produce methylene cysteine hcy as a byproduct, thereby competing with PEMT for substrate s adenosyl methionine and also inhibiting PEMT.  PEMT prefers DHA at SN1 positions and Arachidonic Acid at SN1 or SN2 position on its substrate phosphatidylethanolamine(newly synthesized, unglycosylated or lightly glycosylated), resulting in production of PMME, PDME and then phosphatidylcholine that preferably exhibits ether linked fatty acids DHA, extended length arachidonic acid, Oleoylate, Palmitate first fatty acid in fatty acid beta oxidation, and Omega-3.

ASRZLM, typical therapies in these contexts, emerging therapies, Review complete daily regimen, Disease or Diminished Status Regimen, Simplified Factors Insight Version, Therapeutic API A, Therapeutic API B, Therapeutic API C, Foundational Document 1, Foundational Document 2, Foundational Document 3, Destabilizing Oncology Document, and the other documents in this compendium of research. ​​

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These factors implore, suggest, advise and presume the continued or more prevalent exhibition of interactions and consultation with providers of care, facilities that provide care, the foundations and institutions that support research and development which improves care and care outcomes, prioritization by civilizations of the modalities through which human physiological and behavioral outcomes are improved and assured.

​

These factors implore, suggest, advise and presume the continued or more prevalent exhibition of interactions and consultation with providers of care, facilities that provide care, the foundations and institutions that support research and development which improves care and care outcomes, prioritization by civilizations of the modalities through which human physiological and behavioral outcomes are improved and assured.

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