Counteracting viral, microbial, oncology or insulin dysregulation statuses II or IIII

A, Enlyte or EnlyteRx(essential)​​

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B, Lecithin with Vitamin K2(Essential)

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

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D, L arginine, L citrulline, L ornithine

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

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

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

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

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J, DHA docosahexaenoic Acid

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K, ARA Arachidonic Acid at levels higher than DHA obtainment

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

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​J, Berberine 

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K, Curcumin

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L, active hexose correlated compound AHCC

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M, Nattokinase

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N, Serrapeptase

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O, Retinol

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P, All Trans Retinol

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

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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.

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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.

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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

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U, CART immunological therapy specific to disease phenotype

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V, PD1 inhibitor, PDL1 inhibitor

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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

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X, topical geranyl choline

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Y, phage therapy

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

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

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

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

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AHSD, Mitophagy Modulation Promotion or Inhibition

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AHSE, Autophagy Modulation Promotion or Inhibition

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AHSF, Choline kinase alpha inhibitor

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

 

IAHSH, inhibition of Bag1 with nutrient restriction

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IAHSI, Inhibition of Bag1 and inhibition of Bag3. 

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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.

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AHSK, Telomastatin inhibition of Telomerase

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

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AHSM, S1P Lyase inhibitor

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AHSN, S1P receptor Inhibitor

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AHSO, GSK3B Inhibitor

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

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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 

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

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AHSW, Interventional Somatostatin

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AHSX, Trikafta for conditions involving O2/CO2 exchange

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

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

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

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

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

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

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AHSHSE, inhibit S1P Lyase to counteract resistance to therapeutics

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AHSHSF, inhibit autophagy to counteract resistance to oncology therapeutics

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AHSHSG, inhibit proteolysis to counteract resistance to oncology therapeutics

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

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

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AHSHSJ, Aminophenol therapy for oncology

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AHSHSK, Fenretidine for oncology

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

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

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

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AHSHSO, Inhibiting GSK3B

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

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

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

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

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AHSHST, phosphatidylcholine to enable autophagosomes to close or complete development

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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

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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

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

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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

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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

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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

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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

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

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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 

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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

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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

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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

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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

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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

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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

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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

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

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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

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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

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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

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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  

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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

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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

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

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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

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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. 

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AHSHRZA, Selenolase or selenium deficiency

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

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AHSHRZC, Irinotecan
 

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

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AHSHRZE, Fruquitinib for oncology and CRC oncology

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AHSHRZF, Irinotecan and Doxorubicin with cardio protection for doxorubicin

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AHSHRZG, Mannose 50 mg

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AHSHRZH, Serine 100 mg

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AHSHRZI, Glycine 100 mg

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AHSHRZJ, Cysteine, 75 mg

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ASHHRZK, Cystathionine 50 mg

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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.

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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.

 

ASHHRZVWXB, 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. 

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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, Counteract H2S and H2S persulfidation in oncological tissues specifically

 

ASRZLN, Disrupt the methylene cysteine H2S paradox that is essential in oncological disease including counteracting transulfuration pathway cystathionine beta synthase,  Cysteine aminotransferase, Thiosulfate sulfurtransferase , 3 mercaptopyruvate sulfurtransferase, Cystathionine gamma lyase, there by preventing H2S promoting of anerobic glycolysis by causing mitochondrial ATP production through persulfidation of ATP synthase, resulting also in directing of glucose to lactate anion regardless of oxygen levels and particularly through increasing lactate dehydrogenase throughput through persulfidation of lactate dehydrogenase at Cyst 163.  H2S is beneficial except when causing resilience and proliferation of oncology.  Decreasing size of inhibitors of H2S and methionine pathways that are more effective than antifolate therapies, such as methotrexate which can be detrimental to reproductive contexts, include PHGDDH inhibitors  CBR5884, NCT503, and includes All trans retinol, and includes serine synthesis inhibitors, and includes inhibiting both Mthfd1L and Mthfd1 together.  H2S can be inhibited with DL propargylglycine which inhibits CSE.  Aminooxy acetic acid inhibits cysteine aminotransferase to prevent synthesis of H2S. HMPSNE is an inhibitor of 3MST and prevents 3MST from producing H2S.  Beta cyano alanine, is another nonspecific inhibitor of H2S synthesis. 

 

ASRZLO, Protecting mitochondrial cytochrome oxidase from Fe3+ scavengers to assure function of the mitochondrial electron transport pathway

 

ASRZLP, Assuring availability of methylcobalamin and transport of methylcobalamin by transcobalamin along with asuring function cubulin receptors of the ileum phenotype foundational biological compartments, all assure absorption and circulatory distribution of the major methyl group donor for methylene cysteine recycling into methionine by methionine synthase and Vitamin B12 methylcobalamin.

 

ASRZLQ, Assuring or modulating thymidylate synthase can disrupt disease and genetic impairment while also disrupting oncology when specifically modulate in oncology tissue to disrupt homeostasis or promote genetic repair 
 

ASRZLR, H2S may have expansive utility in emergency, regenerative and other aspects of medicine. H2S dissociates into HS-, S2-, and H+, while HS- strongly neutralizes reactive oxygen species including Superoxide. H2S abdicated by Na2S and NaHS deactivates Peroxynitrite including that from uncouple iNOS/NOS2, NOS3 and NOS1, while also deactivating oxyradicals, hypochlorous acid and methylene cysteine, Hcy. 

 

ASRZLO, 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. ​​

 

ASRZLP, Alzheimer's Disease  and potentially other neurodegenerative conditions and aspects of demention exhibit energetic deterioration which is more specifically a more substantial context of anaerobic glycolysis compare to diseases otherwise which typically exhibit dysregulated glycolysis known as anaerobic glycolysis in context of inhibited Pemt and deterioration of P53 pathways.   Alzheimer's is correlated increased in HK, and decrease in ATPase activity sourced from oxidative phosphorylation which explains anaerobic glycolysis with glucose accumulation, and increase in Vdac1 expression while anaerobic glycolysis repression of lactate obtained from Astrocytes which support metabolism of other neurons and aerobic glycolysis in neurons along with accumulation of glucose amid fibrils derived from tau and derived from beta amyloid and derived methylene cysteine and derived from microplastics and derived from environmental particulate and derived from unfolded proteins all participate in Alzhiemers such that late onset alzheimers is particular the result of decades of uncontrolled unintervened therapeutically omitted levels of methylene cysteine Hcy. All of these have therapeutic capabilities in place, have massive therapeutic susceptibilities and should no longer be occurring. Phosphorylated tau and beta amyloid, impede Vdac1, such that inhibiting Vdac1 interaction with phosphorylated tau, tau and beta amyloid can also alleviate pathology from Alzheimer’s.

 

ASRZLO, Cobalamin, Ascorbic Acid, Thioretinaco, thioretinaco ozonide, retinamide, Sulfur such as methylsulfonyl methane, S methylselenocysteine, melatonin and cycloastragenol,  NAD+(Niacin, Niacinamide, Melatonin, NMN, NAD+, NMR, NADH and the produce Niagen), phosphate as a phosphate group, retinol, retinoic acid, all trans retinoic acid, napabucasin, Diallyl trisulfide, Iron, Lecithin as mixed phospholipids(phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, phosphatidylinositol), Iodide, hyponatremia therapy, ancient pink Himalayan sea salt, ubiquinones, Cholesterol therapy with Omega 3/6/9 fatty acids, Fenretidine, VDAC1 agonsists and antagonists, VDAC2 agonists and antagonists, Hexokinase antagonists and agonists, small molecules that prevent VDAC1 and VDAC2 from interacting with (Hexokinase,Bax,BaK,BCL2,BcLXL) to modulate aoptosis and resiliancy, VDAC2 in the mitochondrial associated membrane inherently promotes resiliency to apoptosis by sequestering Bak, impaired or inhibited VDAC1 disrupts mitochondrial function and exchange of metabolites between mitochondria and the cytosol while inhibiton of VDAC3 did not produce such effects, inhibition of Hexokinase II complexing with VDAC1 is most linked to oncology providing and impetus for inhibition of both or inhibiting exhibition of the VDAC1/hexokinaseII complex.  Antiapoptosis protein complexing with Vdac1 prevents oligomerization Vdac1, suggesting that homodimers or homotrimers of Vdac1 are an amplification signal for apoptosis, micro rna miRNA7 prevents the opening of the mitochondrial permeability transition pore by inhibiting transactivtion of Vdac1 and preventing exhibition of the Vdac1/HKII complex, Vdac1 homodimers and homotrimers can result in apoptosis without Bax and can cause immediate advancement to MOMP or the phase of immitigable exhibition of apoptosis, Clotrimazole disrupts HK/VDAC Complexes, 3 bromopyruvic acid disrupts HK/Vdac complexes and is an alkylation factor which is a common characteristic of therapeuticAvicins as titerpenoid saponins change Vdac1 gating characteristics to cause apoptosis by lowering , conductance to cause outer membrane permeability, Oblimersen as an 18 mer phosphorothioate antisence oligonucleotide to decrease channel conductance and decrease metabolic exchange across the outer mitochondrial membrane to increase membrane permeability and to cause export of cytochrome c, Cisplatin as a diamminedichloroplatinum II factor reduces Vdac channel activity to cause mitochondrial membrane permeabilization.

 

ASRZLPS, P53 protects and directs neurons while exhibited more apoptosis potential in somatic tissues, particularly because P53s diverse group of senescence, pause, apoptosis, selection, metabolic, genetic regulation and hypertrophic phase pauses produce an interactive environment sensing system that integrates environmental influences into mitosis, DNA repair, DNA replication and mitotic outcomes. The somatic tissues are abdicated more readily in neurons while learning and exposure to new stimuli cause double helix segmentation that are repaired in a context of environment sensing nuances of P53 pathways, leading to an increasingly enhanced focus of environmental change stimuli on resilient neurological tissue. P53 may have been and may be a major factor in emerging, developing and sustained development of neurological tissues, cognitive function and consciousness and Pemt ability to cause expression of oxytocin which performs as a strong foundation for the neurological basis of social behavior and foundation for interpersonal, group, community and civilization development.

 

ASRZLPT, Most proteins imported into the mitochondria utilize translocase of the outer membrane proteins that extend through the outer mitochondrial membrane which attach to the intramembrane translocase of the outer membrane complexes, followed by the inner membrane translocase of the outer membrane complexes then attaching to the translocases of the inner membrane to produce the GIP pore which coordinates proteins with c moiety location sequences to be directed to the outer membrane, intramembrane space, inner mitochondrial membrane or loci within the inner mitochondrial space. Protecting, inhibiting or changing GIP element characteristics can modulate the Major components or mitochondrial membrane permeability homeostasis. The observation that apoptosis promoting proteins nestle themselves between basic alkaline amino acids in the outer mitochondrial membrane explains why a specific amino acid nutritional regiment without choline and acidity are used to reliably produce oncology in experimental conditions and contexts while also acidity is linked to oncology and dysbiosis otherwise. Therapeutics exhibiting alkali or promoting alkalinity are often used as or include in therapeutics.
Curcumin and hydroxychavicol cause Reactive oxygens species activation of mTOR/elF4E/Bax to promote apoptosis.  
Obscuring or inhibiting the c moiety of Bax prevents it from promoting apoptosis because it cannot be attached to or directed to the mitochondria. Staurosporine uses Bax to assist in its cytotoxic effect. 

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ASRZLPU, Inhibiting the complexing of Vdac with Bak causes freeing of Bak which promotes apoptosis. BcLXS separates VDAC2 from Bak and causes apoptosis in topical oncology. Vdac3 is presented as the important sustainer of membrane potential in oncology or neoplasm since the high tubulin levels in oncology are able to interact with Vdac1 and Vdac2 but not Vdac3. Inhibiting tublin and preventing Vdac1 integration with tubulin, inhibiting vdac2 integration with tubulin strongly deteriorates and disorganizes neoplasm and neoplastic potential. Clotrimazole disrupts HK/VDAC Complexes. 3 bromopyruvic acid disrupts HK/Vdac complexes and is an alkylation factor which is a common characteristic of therapeutic. Avicins as titerpenoid saponins change Vdac1 gating characteristics to cause apoptosis by lowering conductance to cause outer membrane permeability. Oblimersen as an 18 mer phosphorothioate antisence oligonucleotide to decrease channel conductance and decrease metabolic exchange across the outer mitochondrial membrane to increase membrane permeability and to cause export of cytochrome c. Cisplatin as a diamminedichloroplatinum II factorreduces Vdac channel activity to cause mitochondrial membrane permeabilization. 

 

ASRZLPV, Inhibiting the complexing of Vdac with Bak causes freeing of Bak which promotes apoptosis. BcLXS separates VDAC2 from Bak and causes apoptosis in topical oncology. Vdac3 is presented as the important sustainer of membrane potential in oncology or neoplasm since the high tubulin levels in oncology are able to interact with Vdac1 and Vdac2 but not Vdac3. Inhibiting tublin and promoting tublin independent of Vdac can modulate mitochondrial membrane potential. Preventing Vdac1 integration with tubulin, inhibiting vdac2 integration with tubulin strongly deteriorates and disorganizes neoplasm and neoplastic potential. Clotrimazole disrupts HK/VDAC Complexes. 3 bromopyruvic acid disrupts HK/Vdac complexes and is an alkylation factor which is a common characteristic of therapeutic. Avicins as titerpenoid saponins change Vdac1 gating characteristics to cause apoptosis by lowering conductance to cause outer membrane permeability.  Oblimersen as an 18 mer phosphorothioate antisense oligonucleotide to decrease channel conductance and decrease metabolic exchange across the outer mitochondrial membrane to increase membrane permeability and to cause export of cytochrome c. Cisplatin as a diamminedichloroplatinum II factorreduces Vdac channel activity to cause mitochondrial membrane permeabilization. 

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ASRZLPW, OYE old yellow enzyme protects the actin cytoskeleton from oxidative impairment, counteracting and major component of sickled erythrocyte circulatory monocyte disease, disulfide exhibition of position C285 to C374, that can typically otherwise occur and be persistent until culling when sickled pathology emerges.  OYE delta genetic polymorphism and its pathology are diminished, counteracted or prevented when there is impairment of either of these disulfide interactant C285 or C374 are structurally impaired or positionally ameliorated.  Actin exhibition of C285 to C374 intramolecular disulfide exhibition is pathology feature linked to oxygenic distress and impaired redox that is also a feature of sickled erythrocyte circulatory monocyte disease, while also this pathology can be counteracted by OYE enzyme function and while OYE polymorphism delta potentiates in a manner in which positional or structural amelioration of C285 or C374 prevents OYE polymorphism delta from producing such pathology. OYE was discovered by the same researchers who revealed Anaerobic glycolysis pathology, although OYE is linked to research in 1933 and while Anerobic Glycolysis is linked to the decade in which the first global geopolitical conflict emerged, the 1910s. Both of these discoveries and about 20 others, might have vastly caused ablation of diminished human outcomes beginning in about 1760 to about 1960, with numerous changes of divergence from the geopolitical, civilization and individual level epidemiological occurrences in this expanse, such that this opportunity was ablated by emerging or enhancement of obfuscation utilized to promote and protect industrialism, stereotypes, political and social power and control, and revenue generating outcomes instead. The function of old yellow enzyme OYE including integration into and activation of phenolic ligands and the result is a redox interaction that produces between 800 nm and 500 nm wavelength polarity transfer which might be characterized as (H2e1p)-‘ic’ redox interactions that exchange eV- in this polarity range.   OYE can be reduce or integrated with using NADPH which is a factor reduced by or carrying (H2e1P)- as the H in NADPH.   OYE and is (H2e1p)- cargo can reduce or transfer, typically, to acceptor domains exhibiting quinones, oxygen, alpha,beta unsaturated aldehydes, and alpha,beta unsaturated ketones.   Observation of acceptor complexes in phenolic ligands asparagine 194 and histidine 191, and their adhesion to hydrogen, as stabilizers of at least transfer of (H2e1p)- using FMN as a source. Asparagine 194 and histidine 191 are described as putative stabilizers that interact with the nicotinamide ring of NADPH.  Genetic polymorphism of structure, position and interaction of asparagine 194, histidine 191, positions 191 and 194, even when an OYE transcriptive product was directly integrated, each deteriorating phenolic ligand integration affinity and polarity transfer, polarity transfer completion and receiving or absorption of polarity transfer. NADH was decreased in effective electron transfer, correlated with (H2e1p)- synapse function, 15 times more substantially than NADPH decrease in efficiency by changing phenolic ligand factor position and structure. This observation signals why ATP, ADP, AMP, Adenosine and phosphate may be integral factors into which (H2e1p)- is integrated, stored, distributed, etc. CH2 may be caused to integrate electrons by strong electron withdrawing groups while the electrons can be moved and replaced, or the electrons can be released upon dissociation of CH2 or the electrons can be donated or acquired in oxidation or reduction interaction or might donated or abdicating in molecular interactions.   ATP, ADP, AMP, adenosine and phosphate, however, seem to have been produces to specially encapsulate potentials of the (H2e1p)- synapses as mobility factors to move through systems in a manner that might be similar to storage of (h2e1p)- in nutrition sources derived in farming and distributed through mechanisms of industrialization, systems of economics and nutritional sustenance provision, etc.  ATP, ADP, AMP, adenosine, phosphate may encapsulate (H2e1p)- in modality similar to how CH2 methylene is encapsulated and protected to prevent aberrant polymerization such as in ethanolamine or phosphatidylethanolamine. The potentials of these factors can then be regulated, released, encapsulated, stored and moved in ways that prioritized directed biological activity, developmental programs and metabolic programs. Old yellow enzymes are a modality of obtaining (H2e1p)- from the external environment, enabling resourcing of (H2e1p)- from the universes level, biome level, and environment levels of (H2e1p)- fields. Physiology, aquatic entities, the biome and aspects of the universes comprise dense (H2e1p)- lakes. These factors describe why phenolic compounds such as polyphenols can be therapeutic in oncology or other disease.  Polyphenol use may prevent oncology, and some instances can be therapeutic, while antioxidant capabilities can diminish the effect of cytotoxic therapy and can diminish the effect of cytotoxic immunological function.

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ASRZLPX, The research links senescence to shortening of telomeres as in by AP1 inhibition of Telomerase although without AP1 and otherwise telomeres are lengthened by ALT and Telomerase, homocysteine, and increased acid beta galactosidase. Among the theories of again, all of which involve factors exhibited in when Pemt is inhibited P53 is upregulated, P53 repression is escaped or methylene cysteine, Hcy, and apoptosis exhibition compared oppositely to resiliency, include displacement of thioretinaco ozonide oxygen/ATP complex from the mitochondrial permeability transition pore, such that both oncology and aging at the cellular level  converge in this displacement, unifying the opposing oncology patterns with the detrimental aspects of aging.  Heretofore, this analysis presents oncology and beneficial aging as having similar patterns except that the exhibition of disease results in oncology. This particular perspective presents oncology as a detrimental context and diminished aspects of aging at the foundational biological compartments as convergent factors at the mitochondrial permeability transition pore/Thioretinaco ozonide oxygen interaction.   This interaction is comprised of oxidative phosphorylation enablement of ATP synthesis the active synthesis locus, along with exhibition of thioretinaco ozonide oxygen NAD+ phosphate which supports coupling of NAD+ to phosphate using polymerization by donation to oxygen in a reduction that uses nutritionally derived electrons. Pathogenic opening of the mitochondrial permeability transition pore linked to displacement of thioretinaco ozonide oxygen from the pore is linked with pathology in aging and pathology as oncology, while opening of the mitochondrial transition pore can be inhibited by melatonin and cycloastragenol. In an somewhat pivotal finding, the same research article reveals the EMF exposure and mycotoxins in plaque of vasculature and plaque of the brain, each promote oncology and detrimental aspects of aging through dissociation of the thioretinaco ozonide oxygen from the mitochondrial permeability pore opening which causes deterioration of the active the correlated active locus of oxidative phosphorylation. Furthermore, dissociation of thioretinaco ozonide oxygen from the mitochondrial permeability pore opening is confirmed by this causal context being linked to decrease in cobalamin enzymes in the aging brain, diminished NAD+ integration into Sirt1, and rescuing effect of retinoids which promote recoupling of the mitochondrial pore opening with thioertetinico ozonide oxygen. The active site of oxidative phosphorylation where ATP is produced is presented as being comprised of thioretinaco and thioretinaco is presented as being a complex of two molecules of thioretinamide along with cobalamin as a complex, which can be oxidized to the disulfide thioretinaco ozonide, and then can be complexed with oxygen, nicotinamide adenine dinucleotide, ATP and inorganic phosphate. The concluding complex at the active loci of oxidative phosphorylation can be reduced by electrons during the catalysis of the mitochondrial electron transport complexes such that the concluding thioretinaco ozonide complex can release such ATP from the active locus integrated complex.  The result is exhibition of nicotinamide riboside, hydroperoxide and which results in membrane potentials as protons are responsively transported to the active locus. It is a deterioration, deficiency or inadequacy of melatonin  or opening of the mitochondrial permeability transition pore which the literature links directly with dissociation of the thioretinaco ozonide complex from the membrane at active site of oxidative phosphorylation, which can occur correlative to increase age or in correlation with dementia, although electrophile carcinogens, microbial factors, oncology promoting viral vector, reactive oxygen species from ionizing radiation, and catecholamines which can decompose the disulfonium active site, and which have the ability deplete sulfur exhibiting s adenosyl methionine through increased polyamine synthesis which competes with Pemt and Inmt for substrate s adenosyl methionine. Ancillary effects of decomposition of the active disulfonium complex at the active site of oxidative phosphorylation include impaired oxidative phosphorylation, impairment of the proton pump, impairment of membrane potential, produces oxidative stress, produces calcium influx, cases aerobic glycolysis, produces apoptosis, and causes mitochondrial dysfunction that is observed in canonical effects oncology derived from chemicals, oncology derived from microbes, multiple impairments occurring with TBI brain injury, dementia and detrimental aspects of aging. INMT is an enzyme which exchanges s adenosyl methionine bidirectionally for a adenosyl methylene cysteine while also adding and removing methyl groups to sulfurs, amine, amides and diverse other molecules and proteins.  

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ASRZLPAWXA, Methylene cysteine, hcy, can be derivative to methylene cysteine Hcy thiolactone and this occurs in typical conditions while in atypical conditions, Hcy thiolactone can become increased when conditions including impaired ability to oxidize the sulfur atom of methylene cysteine, hcy, occurs. A derivative of homocysteine is presented in a particular study as the cause of impaired oxidation of the sulfur from methylene cysteine, hcy. This metabolite of methylene cysteine thiolactone, hcy thiolactone,  which prevents oxidation of the sulfur from methylene cysteine, hcy, however, is diminished in exhibition or not exhibited in oncology resultant of oncology promoting microbes, oncology promoting chemicals, oncology promoting radiation and other factors, potentially including exposure to EMF. Methylene cysteine thiolactone, hcy thiolactone, in oncology tissue exhibits, typically, attachment to free amino groups of proteins, attachment to nucleic acids, attachment to glycosaminoglycans, using methylene cysteine groups or hcy groups.      The result can be nucleoprotein complex exhibition similar heterogenous fibril development, increase in proliferation and oncology development, ameliorated expression genes suppressed by developmental program, membrane deterioration which disrupts ascertainment of the encompassing structure of the foundational biological compartment, and oxidative metabolism amelioration such as exhibition of anaerobic glycolysis. Antineoplastic derivatization studies using methylene cysteine thiolactone, hcy thiolactone, particularly in search of factors that oxidize or lyse the sulfur from methylene cysteine Hcy, revealed N substitution exhibiting derivatives which are lipid soluble, exhibit carbonyl groups adjacent to the Nitrogen of methylene cysteine thiolactone, also known as hcy thiolactone, is systemically considered to be unsaturated, while also presented as exhibiting a transition metal atom.  Putative catalysis is presented as Methylene cysteine thiolactone, hcy thiolactone,  interaction with retinoic acid which results in synthesis of thioretinamide, TR, as N methylene cysteine thiolactonyl retinamide, which occurs in organic processes. 2 molecules of thioretinamide catalytically interact with cobalamin, resulting in thioretinaco TR2Co as N methylene cysteine thiolactonyl retinamido cobalamin, N hcy thiolactonyl retinamido cobalamin. Thioretinamide and thioretinaco  exhibit potent antineoplasm, antineoplastic, inhibiting activity observed in oncology produced experimentally from oncology promoting factors while also exhibiting such potency also in neoplasm moved into nonhuman small mammalian organisms.  Essentially, the active locus of oxidative phosphorylation emerges when oxygen and ATP complex with thioretinaco ozonide of the C1 complex in the Mitochondrial membranes. Sulfonium cations of thioretinaco oxonide are integrated into by the alpha and gamma phosphate anions of ATP. The information seems to suggest that comparative competing influences of methylene cysteine promoting of dysbiosis and apoptosis, compared to H2S promotion of resilience are factors in disease and oncology.  Disulfonium exhibition in the thioretinaco ATP complex at the locus of oxidative phosphorylation would be affected by methylene cysteine, Hcy, direction toward transsulfuration proteolysis to result in H2S along with the thioretinico complex derivative methylene cysteine thiolactone protection of the ability of sulfur to be removed from methylene cysteine.  Inability to remove sulfur from methylene cysteine, hcy, would impair the ability of the transsulfuration pathway to to produce H2S from methylene cysteine Hcy and would impair the availability sulfonium to comprise the disulfonium in the thioretinaco complex of the active site of oxidative phosphorylation. 

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ASRZLPY, Regarding crispr perfect genetic repair, Crispr might even be utilize to place functional enzymes into specific foundational biological compartments. Activating or sensing molecules can be used to determine what conditions exist in the foundational biological compartment, phenotype, proteasome or genetic structure, followed by release of specific activation factors which then interact with intramolecular or intermolecular domains to release precise payloads that respond to dynamic and changing conditions at the foundational biological compartment level, within the biological compartment level or organelle level, microenvironment, tissue level, systemic level or dynamic level.  These enable therapeutic development of sensors, payload, interactions, absorption or transduction level, or other levels to occur with specificity to genetics, phenotype, disease or other conditions. Crispr can even affect microbes and result in eradication of microbes directly with microbial toxic affect, inhibition using antisense inhibitors, genetic interaction with microbes, genetic removal when integrated into Human genome, metabolically or in other ways.  

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ASRZLPZ, Sabatolimab represses Tim3 from interacting with phosphatidylserine and diminishes Tim3 interaction with Galectin9.  Spartalizumab prevents apoptosis ligand 1 / 2 by integrating with PD1.  Together, these factors promote strong therapeutic influences in oncology.

Cobalamin requires adequate sodium to be efficiently utilized, and typical table salt can have striates that scratch vasculature causing increased cholesterol to repair vasculature. Salt is sometimes recommended to be avoided because of this.  However, hyponatremia can be exhibited proximate to vast aspects of newly diagnosed oncology.  This is because selenium, choline, iodide, Vitamin B12(cobalamin), and other factors that determine oncology status compete for sodium to use as transport into the foundational biological compartment. Factors preferred by oncology thus utilized available sodium and deselects factors harmful to oncology. Also, cholesterol not made in a laboratory is harmful when exorbitantly high and oxidized, such that foundational biological compartments are comprised of about 87 percent cholesterol and such that the conditions causing the oxidative stress are the most accurate cause of oxidized cholesterol.  Correlatively, B12 adenosyl cobalamin and B12 methylcobalamin are natural B12 vitamins while other versions are synthetic including B12 cyanocobalamin which exhibits the toxic cyano molecule used for centuries to abate vital being. Cyano molecules used in producing B12 cyanocobalamin are used because of industrial priority and the metabolism of synthetic B12 versions requires used methylation resources and competes and inhibit Pemt while also causing increase methylene cysteine.  Hyponatremia therapy and ancient pink Himalayan Sea salt are recommended during oncology therapy and generally, particularly in place of table salt. Some conditions such as hepatic conditions can make B12 cyanocobalamin toxic at low levels. 

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ASRZLPZAGA, therapeutic thioretinaco ozonide therapeutic molecule is putatively presented as (NHTR)2CblO302ATP.

Information, “Enhanced Liposomal Thioretinaco Ozonide Compositions and Liposomal Carrier.”  Patent Number US66960082B2.

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optimal pH characteristics including a systemic background pH near, about or at pH 7.4 

 

Methylene cysteine is optimal near, about or at 3.7 um/L (statistically 6 or 7 um/L or lower) and when adenosyl methylene cysteine is lower than 0.012 um/L 

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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.

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