Christie Laura Grace Profile picture
Nov 5, 2023 40 tweets 10 min read Read on X
1/ 🚨🧵DNA plasmid contamination in modRNA "vaccines"
DO NOT HAVE TO ENTER THE NUCLEUS
to impact
GENE EXPRESSION, and be implicated in CANCER RISK!
(I said this on April Moss TV MONTHS ago talking about proteomics and gene expression!)
STUDY BELOW in somewhat LAYMAN'S TERMS
Image
2/ Study citation: Gao JJ, Diesl V, Wittmann T, Morrison DC, Ryan JL, Vogel SN, Follettie MT. Bacterial LPS and CpG DNA differentially induce gene expression profiles in mouse macrophages. J Endotoxin Res. 2003;9(4):237-43. doi: 10.1179/096805103225001431. PMID: 12935354. Image
3/ In the study, the researchers investigated the impact of CpG DNA and LPS on gene expression. They exposed macrophages to CpG DNA and LPS (lipopolysaccharide), which are known immune stimulants. CpG DNA is recognized by Toll-like receptor 9 (TLR9) and can Image
4/ trigger immune responses. LPS, on the other hand, is a component of the cell wall of certain bacteria and is recognized by Toll-like receptor 4 (TLR4).
In more layman's terms, the researchers wanted to understand how genes in the immune system cells (macrophages) react when Image
5/they're exposed to CpG DNA and LPS.
They used a "microarray" to see what was happening. A microarray is like super microscope for genes. This allowed them to look at thousands of genes at the same time. It's like looking at a huge puzzle with thousands of pieces all at once. Image
6/Imagine each gene is a light bulb, and when it's turned on, the gene is doing something. The researchers wanted to see which genes got turned on or off when they added CpG DNA and LPS to the cells.
So, they put the macrophage cells in a dish and added Image
7/CpG DNA and LPS to the dishes. Then, they used the microarray to see which genes in the cells started to "light up" or "turn off" in response to the CpG and LPS. The researchers got to see how the genes in the cells reacted to CpG DNA and LPS. Image
8/ It's like the researchers watched how different genes in cells respond to to the CpG DNA motifs (same motif in the DNA PLASMID CONTAMINATION), like watching a light show of genes turning on and off. This helped them understand how CpG DNA and LPS impact cellular genetics. Image
9/ it is very important to note, the CpG DNA pieces were NOT in the NUCLEUS when gene expression was witnessed! The screenshots are posted above of all the genes they saw impacted by the CpG motif of the DNA and the LPS.
The CpG DNA molecule does not need to enter the cell
10/ nucleus to act on gene expression. CpG DNA engages by interacting with cell surface receptors and in cellular compartments other than the nucleus.
Heavy science: CpG DNA is recognized by Toll-Like Receptor 9 (TLR9), which is located on the cell surface and in endosomes
11/(a cellular compartment). TLR9 specifically recognizes CpG motifs within DNA.
Then CpG DNA binds to TLR9, it triggers a signaling cascade within the cell, leading to the activation of transcription factors like NF-κB and AP-1.
These activated transcription factors then
12/ influence gene expression. They can induce the expression of various genes, including those involved in the immune response, inflammation, and other cellular processes, such as cancer.
The following are genes in the screenshots that are implicated in cancer, and the types:
13/ (not a complete list)
SCYA4 MIP-1b: breast cancer and colorectal cancer.

Vasodilator-stimulated phosphoprotein (VASP): lung, prostate, colorecta, and breast cancer.

Fas antigen (FAS): liver, breast, ovarian, and cervical cancer.

Plasminogen activator inhibitor, type II
14/ (SERPINB2): Implicated in various cancers, including breast, prostate, and colorectal cancer.

Tissue inhibitor of metalloproteinase-1 (TIMP-1): breast, lung, and colorectal cancer.

Plasminogen activator inhibitor, type I (SERPINE1): breast, lung, and ovarian cancer.
15/ CD44 antigen (CD44): breast, pancreatic, head and neck cancers, and other cancers.

Selenoprotein W, muscle 1 (SEPW1): Although not directly associated with cancer, it is involved in antioxidant defense, which may have implications in cancers related to oxidative stress.
16/ Glia maturation factor-b homolog (GMFB): plays a role in neuroinflammatory diseases, which may indirectly relate to some cancers through inflammation-related pathways.

These genes may play roles in various cancer types, either directly contributing to cancer progression or
17/ through mechanisms related to inflammation, oxidative stress, and metastasis.
Also, in some cases, abnormal DNA methylation patterns, including changes in CpG methylation, have been linked to cancer.
These genes are implicated in cancer. Cancer is a VERY COMPLEX PROCESS.
18/ These single genes are most likely not enough alone to directly drive cancer, but they are involved in it. These genes are being impacted OUTSIDE of the nucleus, and do not take into account if the DNA plasmid pieces in the lipid nanoparticle enter the nucleus.
19/ These are some of the genes implicated in the immune system and various DISEASE:
Interleukin 1b (IL-1b): various inflammatory diseases.
SCYA5 Rantes: inflammation
SCYA7 Intercrine: inflammation.
SCYA2 MCP-1: inflammatory diseases.
TNF-a: Tumor necrosis factor-alpha
20/ is associated with inflammation and autoimmune diseases.
CSF3 (G-CSF): Granulocyte-colony stimulating factor, plays a role in regulating white blood cell production.
PBEF: various diseases, including metabolic and inflammatory conditions.
21/ Vasodilator-stimulated phosphoprotein: cardiovascular and vascular diseases.
IL-1 receptor antagonist: inflammatory diseases.
TNFRsf1B: autoimmune diseases
TNFRsf5: autoimmune disease
Adenosine A2b receptor: Linked to cardiovascular and inflammatory disease
22/ 🚨PLAUR: Urokinase plasminogen activator receptor: cancer and tissue remodeling.
Fas antigen: Associated with apoptosis and autoimmune diseases.
Fc-g-R1: autoimmune diseases
Ubiquitin specific protease 18: ubiquitin system, associated with cancer and neurological diseases.
23/ Plasminogen activator inhibitor, type II: blood clotting and fibrinolysis.
Tissue inhibitor of metalloproteinase-1: Regulates tissue remodeling, various diseases, including cancer.
Plasminogen activator inhibitor, type I: Regulates fibrinolysis and blood clotting disorders.
24/ Cathepsin C: immune responses and genetic disorders.
CD44 antigen: cancer and inflammation.
Glia maturation factor-b homolog: neuroinflammatory diseases.
Integrin-associated protein: various diseases.
these genes in disease can be complex and may vary depending on context
25/ and the specific disease in question. These genes are often involved in multiple pathways and processes, making their roles in disease multifaceted.
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26/ The genes impacted by the CpG motif:
Interleukin 1b: Associated with immune response.
SCYA5 Rantes: Involved in immune response.
SCYA7 Intercrine: Associated with immune response.
SCYB2 MIP2: Related to immune response.
Interleukin 1 alpha: Part of the immune response.
SCYA2 MCP-1: Associated with immune response.
TNF-a: Involved in the immune response.
SCYA3 MIP-1a: Part of the immune response.
SCYB10 IP-10: Has a role in the immune response.
SCYA4 MIP-1b: Associated with immune response.
CSF3; G-CSF: Cytokine involved in immune response.
SCYA12 MCP5: Associated with cytoskeletal/extracellular matrix function.
Interleukin 10: Immune-related.
SCYA9 C10-like: Involved in immune response.
Interleukin 18: Part of the immune response.
PBEF: Associated with proliferation/differentiation.
Adenosine A2b receptor: Related to oxidative stress.
PLAUR: Involved in oxidative stress.
Glycoprotein 49 B: Part of the oxidative stress response.
Fas antigen: Related to apoptosis.
Ornithine decarboxylase: Part of the enzyme category.
2¢-5¢ oligoadenylate synthetase 1A: Involved in protein synthesis.
Purine-nucleoside phosphorylase: Enzyme related.
Hyaluronan synthase 1: Related to signal transduction.
TBX1 protein: Part of signal transduction.
DNA segment, Chr 17: Unknown function.
27/ More genes impacted by the CpG motif:
m15131 (Interleukin 1b) - Immune response
u02298 (SCYA5 Rantes) - Immune response
z12297 (SCYA7 Intercrine) - Immune response
X53798 (SCYB2 MIP2) - Immune response
x01450 (Interleukin 1 alpha) - Immune response
m19681 (SCYA2 MCP-1) - Immune response
x02611 (TNF-a) - Immune response
x12531 (SCYA3 MIP-1a) - Immune response
m33266 (SCYB10 IP-10) - Immune response
m35590 (SCYA4 MIP-1b) - Immune response
m13926 (CSF3; G-CSF) - Immune response
u50712 (SCYA12 MCP5) - Cytoskeletal/extracellular matrix
m84340 (Interleukin 10) - Immune response
u19482 (SCYA9 C10-like) - Immune response
D49949 (Interleukin 18) - Immune response
aa691772 (PBEF) - Proliferation/differentiation
X98475 (Vasodilator-stimulated phosphoprotein) - Unknown function
w71236 (WD40 repeat protein 1) - Signal transduction
m74294 (IL-1 receptor antagonist) - Receptor/cell surface
m59378 (TNFRsf1B) - Receptor/cell surface
m83312 (TNFRsf5) - Receptor/cell surface
U05673 (Adenosine A2b receptor) - Receptor/cell surface
ET61664 (Fc-g-RIIB) - Receptor/cell surface
C76481 (PLAUR) - Enzyme
u05265 (Glycoprotein 49 B) - Enzyme
m55637 (HAM-1) - Enzyme
M83649 (Fas antigen) - Apoptosis
M31314 (Fc-g-R1) - Enzyme
u55060 (Lectin, galactose binding, soluble 9) - Enzyme
AA178227 (CD83 antigen) - Protease/inhibitor
x67809 (PPICAP) - Unknown function
m11284 (MHC class I Qa-Tla) - Transport
AA034646 (CC chemokine) - Transport
u59463 (Proprotein convertase subtilisin/kexin type 3 receptor 1-like 2) - Enzyme
M65027 (Glycoprotein 49 A) - Enzyme
aa690738 (ABCA1) - Enzyme
x66081 (CD44 antigen) - Enzyme
AA072961 (Integrin-associated protein) - Enzyme
u16985 (Lymphotoxin B) - Enzyme
aa177433 (Fc epsilon beta) - Transport
u77460 (Complement C3a) - Transport
M73696 (SLC2A1 glucose receptor 1) - Transport
I13732 (SLC20A1 phosphate transporter 1) - Transport
aa691772 (Complement C3a receptor 1) - Transport
I04275 (Scavenger receptor) - Transport
D14883 (CD82 antigen) - Transport
U21795 (Interleukin 2 receptor, gamma chain) - Receptor/cell surface
X54149 (Myeloid differentiation primary response 118) - Proliferation/differentiation
C76739 (Macrophage C-type lectin) - Receptor/cell surface
L10244 (Immediate early response 3) - Signal transduction
m64291 (COX-2) - Enzyme
x03479 (Serum amyloid A 3) - Enzyme
L32973 (Thymidylate kinase TDKI) - Enzyme
m92649 (Mouse nitric oxide synthase) - Enzyme
aa445671 (Glycerol kinase) - Enzyme
U44088 (T-cell death associated gene) - Apoptosis
s64539 (Ornithine decarboxylase) - Enzyme
m33863 (2¢-5¢ oligoadenylate synthetase 1A) - Protein synthesis
x56548 (Purine-nucleoside phosphorylase) - Enzyme
u19118 (Activating transcription factor 3) - Transcription factor
D82964 (Hyaluronan synthase 1) - Signal transduction
m22326-2 (Early growth response 1) - Transcription factor
D17571 (Zinc finger protein 147) - Transcription factor
L10244 (Spermidine/spermine N1-acetyl transferase) - Enzyme
AA163244 (Fructose-6-phosphate 2-kinase) - Transcription factor
Y11666 (Jumonji) - Transcription factor
aa051486 (HMG protein 14) - Transcription factor
aa245216 (Flavo-binding protein) - Unknown function
W44201 (SEC23B homolog) - Signal transduction
U88328 (Cytokine inducible SH2-containing protein 3) - Signal transduction
U19119 (Interferon inducible protein 1 receptor alpha) - Signal transduction
X61940 (Tyrosine phosphatase, non-receptor type 16) - Signal transduction
x81627 (LCN2, 24p3) - Signal transduction
m83218 (S100 calcium binding protein A8) - Signal transduction
U53219 (IFN-g induced GTPase) - Signal transduction
M63630 (IFN-g inducible protein, 47 kDa) - Signal transduction
X17459 (Recombining BP suppressor of hairless) - Signal transduction
U20159 (Lymphocyte cytosolic protein 2) - Signal transduction
aa462486 (Map kinase phosphatase A2) - Signal transduction
aa185007 (Proteasome alpha type 6) - Enzyme
j03023 (Hemopoietic cell kinase) - Signal transduction
U36277 (NF-kB inhibitor) - Signal transduction
m33203 (Heme oxygenase 1) - Enzyme
m65029 (Translation initiation factor 2 alpha kinase 2) - Enzyme
k01496 (Complement factor B) - Enzyme
x16440 (Feline sarcoma viral oncogene homolog) - Enzyme
X80638 (Aplysia ras-related homolog 9) - Enzyme
D87691 (ETF1) - Enzyme
u51907 (NF-kB activator) - Signal transduction
x00246 (Histocompatibility 2, D region locus 1) - Unknown function
AF006040 (Fas death domain-associated protein) - Unknown function
AF019249 (N-mcy (and STAT) interactor) - Unknown function
m57696 (Yamaguchi sarcoma viral oncogene homolog) - Unknown function
AA097231 (RAS-related C3 botulinum substrate 2) - Unknown function
L16462 (B-cell leukemia/lymphoma 2) - Unknown function
X76850 (MAP kinase-activated protein kinase 2 related protein A1a) - Unknown function
u78031 (Bcl2-like) - Unknown function
AA170444 (Ube11 similar to ubiquitin) - Unknown function
x84797 (Hematopoietic cell specific Lyn substrate 1) - Unknown function
AF001863 (FYN binding protein) - Unknown function
aa407010 (KIAA0970) - Unknown function
J03368 (Myxovirus resistance 2) - Unknown function
AF013114 (Epstein-Barr virus induced gene 3) - Unknown function
AF026124 (Phospholipase D3) - Unknown function
W40735 (EH-domain containing 1) - Unknown function
aa184871 (DUS6 dual specificity phosphatase) - Unknown function
aa273574 (E2 ubiquitin conjugating enzyme) - Unknown function
U14103 (Guanine nucleotide dissociation stimulator, -like 1) - Unknown function
U70139 (Carbon catabolite repression 4) - Unknown function
AA060409 (Glia maturation factor-b homolog) - Unknown function
aa673503 (Riken 1300002F13) - Unknown function
m59821 (Immediate early response 2) - Transcription factor
X61800 (C/EBP-d) - Transcription factor
J03776 (Interferon regulatory factor 7) - Transcription factor
m58691 (Zinc finger protein 36) - Transcription factor
U06924 (STAT 1) - Transcription factor
M31885 (Inhibitor of DNA binding 1) - Transcription factor
L20315 (Macrophage expressed gene 1) - Transcription factor
Y08460 (Degenerative spermatocyte homolog) - Transcription factor
L20315 (NF-kB p105) - Transcription factor
@brucep13
(Check out the other threads--especially the ones on zeta potential. Highly negative zeta potential on LNPS cause an impact on biodistribution. Positively charged LNPSs have a tropism for the lungs. neutrial go to liver. Slightly negative go to spleen. Very negative leak into vasculature, and impact vascular (and heart). The DNA plasmid contamination will increase the LNPs to form a DNA/RNA polylipoplex--which will shoot the zeta potential on these things from -3 mV to when they were measured in bulk solvent, which are actually almost -9 in the bloodstream, to farther closer to at least -20 or higher, causing it to bing with the endothelial, causing the RNa to express spike right into the bed of the vesselsas it remodels the endothelium and impacts the permeability, and can lead to hypercoaggulation.
@DJSpeicher Got plasmids?
@TheChiefNerd This is really bad. No genome integration has to occur.
28/ IN MOST CASES, NO GENOMIC INTEGRATION IS REQUIRED. LITIGATION TIME
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More from @_HeartofGrace_

Mar 26
🚨💉🦠PREPRINT! Journal has it now. NEW theoretical MULTI AXIS MECHANSM by spike protein, SHARED DISEASE and worse between LONG C@VID and C@VID V@CCINATION via ion channel dysfunction, and AUTO ANTIBODIES TO THE PROTEINS OF THE SODIUM CHANNEL!
Short summary below👇

THIS IS THE SHARED THEORETICAL MECHANISM:

I am about to release two more papers to preprint and journals in next 24 hours on worse symptoms, clots, and cancer.

I cannot write the summary I wanted, I have to go back to writing. This is al I got.
I must get back to writing, and sleep sometime.

✅Ion channels are tiny gateways in our cells that control how ions (like sodium, potassium, and calcium) move in and out. This

is crucial for sending signals in our nerves, regulating our immune system, and keeping our cells functioning properly.

This spans ALL of our physiological processes--ALL CELLS.

When ion channels don’t work correctly— ion channel dysfunction can cause a wide range of health issues, including neurological disorders, chronic pain, and immune system problems. Mast cell. So many things--head to toe. Not just nerve symptoms. All symptoms. Clots, All of it. Vascular permeability. All of it.

I am completing deeper dive on this because there just was not enough room in the paper to do it--exact further mechanisms on organ injury and cancer. This includes but not limited to myocarditis and organ injury. Antibodies against the areas and more with dysfunction of the ion channels in tandem with cGAS STING, MACROPHAGE, ZETA PPOTENTIAL, HORMONES, GENETIC MUTAIONS, PAMPS and DAMPS, and more.

Both C@VID-19 infection and v@ccination MIGHT, theoretically, contribute to ion channel dysfunction through immune system overactivation, chronic inflammation, and the production of autoantibodies that mistakenly attack ion channels.

The cGAS-STING pathway, which detects viral threats, can become overactivated, leading to persistent inflammation and autoimmune reactions. Additionally, the spike protein from SARS-CoV-2 shares structural similarities with certain ion channel proteins, which may lead the immune system to mistakenly target these channels, causing transient or chronic dysfunction. In some cases, this immune response may be self-limiting, resolving over time, while in others, it may lead to long-term autoantibody production, resulting in sustained neurological, cardiovascular, and muscular symptoms.

cGAS AMPLIFIES the feedback loops, while macrophages get dysregulated in the consumption of the charged lipids, the vessels in capillaries and arteries become permeable, clots--next paper in 24 hours will show full on mechanisms--tissue damage. The eyes, the whole body. Brain. IN SOME PEOPLE.

Can cause people to have all kinds of things getting misdiagnosed or as secondary effects. Bed bound. Death

This could if, THEORETICALLY, with severe gain of function mutations present in ion channel encoding for proteins in ion channel, cause cascade of immune system, autoantibody attack against proteins of ion channel, appear sepsis like, and cause death.

Heart attack.. SIDS. Sudden adult death.

FOR WOMEN--this paper shows that estrogen has an impact on ION CHANNELS and how that if a woman is menstruating and still has estrogen present, each month, a flare may occur, and cause worsening autoimmunity, which is not to say men have not suffered, but why WOMEN are suffering from these symptoms MORE. Could be worse all the time. Immune reaction worse. Initial injury worse.

Also, WHITE EURPOEANS and middle eastern background compared to African, Asia, and indigenous, while still suffering harms, have higher levels of STING activation due to variation in STING pathway making more susceptible to dysregulation, meaning more autoimmunity and harms than others in white and middle eastern background.

ALSO--women have dysregulation in gut brain axis due to estrogen.

Due to their role in nerve signaling, muscle function, immune regulation, and cardiovascular stability, dysfunctional ion channels can lead to widespread symptoms, including
SFN LIKE symptoms, AIDP LIKE symptoms. GBS like symptoms, transverse myelitis,
tachycardia, bradycardia, palpitations, arrhythmias, hypotension, hypertension, dizziness, fainting, syncope, chest pain, blood pooling in the legs, poor circulation, orthostatic intolerance, POTS-like symptoms, brain fog, migraines, chronic headaches, vertigo, tingling, numbness, neuropathy, tremors, muscle weakness, myoclonus, ataxia, seizures, hypersensitivity to light and sound, temperature dysregulation, fatigue, autonomic dysfunction, memory problems, difficulty concentrating, muscle cramps, muscle spasms, muscle stiffness, twitching, myopathy, exercise intolerance, paralysis episodes, myalgia, difficulty swallowing, loss of fine motor control, nausea, vomiting, bloating, diarrhea, constipation, gastroparesis, IBS, abdominal pain, acid reflux, swallowing difficulties, shortness of breath, hunger, hyperventilation, irregular breathing, chest tightness, chronic cough, respiratory muscle weakness, hormonal imbalances, ovarian dysfunction, irregular periods, amenorrhea, infertility, PCOS, thyroid dysfunction, insulin resistance, unexplained weight loss or gain, frequent urination, bladder dysfunction, incontinence, difficulty urinating, interstitial cystitis, kidney dysfunction, chronic inflammation, autoimmune disease, increased susceptibility to infections, mast cell activation syndrome, histamine intolerance, allergies, skin rashes, hives, anxiety, panic attacks, depression, mood swings, irritability, insomnia, hypersomnia, depersonalization, derealization, heat intolerance, cold intolerance, excessive sweating, lack of sweating, lightheadedness, vision disturbances, difficulty adjusting to light changes, tinnitus, and sensitivity to sound, smell, or touch.

This is NOT the complete list!

Organ injury, hypo or hyper thyroid like symptoms--that whole list on the Pfizer data dump: run through them. Specific ion channels are 4--also acetylcholine channel.

The cGAS-STING pathway detects foreign or self damaged DNA inside cells, triggering an immune response.

When SARS-CoV-2 infects cells or lingers as viral remnants, it can overactivate, leading to prolonged immune responses that may mistakenly target self-proteins, including ion channels. This process can contribute to autoantibody formation against ion channels, which may explain persistent symptoms following COVID-19 infection or, in rare cases, vaccination. THIS is combined with macrophage polarization and spike protein on ion channels-theoretical.

Because the spike protein shares structural similarities with certain ion channels, the immune system may temporarily mistake ion channels for the virus, leading to transient dysfunction. In some cases, once the immune system resets, symptoms resolve. However, in other individuals, this misdirected immune response is chronic, leading to persistent autoimmune-mediated ion channel dysfunction.

This could explain why some individuals experience long-term neurological, cardiovascular, or muscular issues after infection or vaccination.

This does not say that sv40 and biotech plasmids with other properties of spike are not present. This paper could not address that and does not discount.

Add in dna plasmids amplifying cgas sting and macrophage and charged lipids impacting further, and recipe for disaster.

The possibility of transient versus chronic ion channel dysfunction due to cGAS-STING activation and autoantibodies is URGENT need for testing for ion channel autoantibodies in individuals experiencing post-COVID or post-vaccine symptoms.

Identifying these autoantibodies could lead to better-targeted treatments, distinguishing between cases that may resolve over time versus those requiring immunotherapy. Research into the mechanisms behind autoimmune ion channel dysfunction will be crucial for improving diagnosis and treatment options for those affected by these complex conditions.

There is current drugs present that cost under ten dollars for ion channel dysfunction like tegretol. I am not a medical doc and this is not treating or DXing anything. Always check with your doc.

People are suffering spread the word. This is theoretical.

For those with labs, get testing!!!!

I have to go now and write.
I am ONLY answering emails and calls right now form doctors I am arranging meetings with. If you have questions, ask the experts in your circles.

I cannot chat about this or answer questions. If you want summaries, load into grok or whatever you choose. I must go.

I have work to do and messaging slows me down.Image
2/ The cGAS-STING Pathway, Ion Channel Dysregulation, and Immune Responses: Implications for Autoimmunity, Inflammation, Long COVID, and Post-Vaccination Responses

osf.io/preprints/osf/…Image
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People told me to wait-I cannot. I am writing fast and two more are coming in 48 hours.
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Read 12 tweets
Feb 24
1/ 🚨💉🧬 Hot off the presses, March 2025, almost one year later, "next gen mRNA"

"CpG ODN-adjuvanted, alum-adsorbed, virus-like particle (VLP) vaccine displaying the hexaproline stabilized Spike (S) protein and the Nucleocapsid, Membrane, and Envelope proteins of SARS-CoV-2." Image
2/

(This requires access, so I will screen shot) sciencedirect.com/science/articl…Image
3/ The sentence reads like a nightmare to me: " CpG ODN-adjuvanted, alum-adsorbed, virus-like particle (VLP) vaccine displaying the hexaproline stabilized Spike (S) protein and the Nucleocapsid, Membrane, and Envelope proteins of SARS-CoV-2."
Read 29 tweets
Feb 23
The material that has gone into humans is research grade at best. That means RG. Fit for animals but not humans.
I dare say it was even fit for animals.

I know because it was my job.

I know the difference between research grade, cGMP (which still has its issues, One just need to research any 483 form with the FDA, or having worked designing the stuff).

I designed recombinant proteins custom, fusion proteins with specialty RNA, lipids, custom work for those who have suffered from genetic disease and cancer.

Those are small batches for clinical trials that are highly filtered by expert teams with all eyes on every vial, clean as can be, with small cohorts of maybe a few dozen people, and a liter of material. And with all that, there is still side effects because that platform is flawed on multiple levels. I can cite study after study right now on the reasons why it that is, and to pull them all from my profile, and so could others.

Sludge was allowed to be injected into over 5 billion people.

Non-coding RNA can cause cancer. Fact.

Multiple studies including done by experts who out rank anyone here in the US or the UK over in Korea have done the tests stating that the modified RNA is breaking inside the LNP. This renders it non coding, which means it can't make anything and it's only function is going to be to interfere with other cellular mechanisms with the concern of causing cancer. It can cause transient concerns which can activate pathways regardless if it is degraded in the cells.

The lipids themselves have been used in multiple studies injected into animals and have been found to cause disease and cancer because of the disruption of the continual injection and what damage has occurred as a result of exhaustion of the mononuclear phagocyte system. That's something you are not familiar with and what I'm stating here is not known to most people reading this.

Positively charged lipids have an impact on cellular function and if they aggregate an areas they can do damage.

The modified RNA has been shown to have oncogenic properties.

This modified RNA also has been known to frame shift inside the ribosome causing junk proteins to be made which is irrelevant because....

Moderna did their own study with their own researchers only a couple of years ago which they paid for using special equipment and they found (packer et Al 2021) that the impurities in the positively charged lipids are covalently bonding to any nucleic acid they come in contact with including the modified RNA inside the lipid nanoparticle creating what is called an adduct and it is occurring in about 10 spots per piece of RNA in each of the particles which, will cause the same issue and cause the slippage in the ribosome causing non-coding issues which means we're back to the cancer possibility with the junk protein being made with aggregation and misfold of a spike protein that is already known to have amyloid properties related to neurodegenerative disease.

The lipid nanoparticle itself contains high levels of the original starter biotech plasmid which was housed in e coli and grown up to make the modified RNA. On this piece of plasmid which is circular which you can look up anywhere, It contains multiple parts and the one moderna used is slightly different than the one Pfizer used. There is a spot for the protein gene of interest. I can show you a video of you would like and you are a smart guy and it was done by a biotechnology student. There's also an antibiotic resistant gene, And a few other sections and on the Pfizer plasmid there is what is called the SV40 promoter which is minus the large T antigen However is still a very strong promoter. The CMv promoter also a strong promoter.

These are circular and they were not digested properly or removed from any of the batches and it all went into humans.

The scale of harm that could theoretically be on deck is unlike anything our civilization has ever seen when it comes to the potential harms.

I've heard people say they don't want to scare people.

The amount of cancer and autoimmune around myself and others is staggering. People in their 30s at my clinic have cancer. People in their twenties. 17-year-olds with brain tumors. A 9-year-old boy just got taken to the children's hospital here a couple months ago with myocarditis right after... Guess what?

That promoter can have transient expression in ways I'm not typing here because I'm writing a paper on it and when it's shown exactly what it is doing in cells aside from its other activity and how it can interfere with the proteome, in ways that people are not currently checking which will take time and sales turn over and the proteome is going to start replacing and making adjustments and fusion proteins are going to start to occur in some people (if they aren't already.... Fusion protein is often present in lymphoma, piers).

Then we have the issue with biodistribution and they lied about the whole thing including studies that prove more than once with full data to back peer-reviewed that the particle itself has a different biodistribution in pregnant animals compared to non-pregnant animals that it goes to the lymph nodes 8 times more and that means everything is going to the lymph nodes eight times more including eight times the spike protein eight times the RNA 8 times the positively charged lipids eight times the DNA plasmid contamination and any other god-awful contamination that exists that we know about which is occurring often like bacteria and other plasmids and cross-contamination from other projects because it is a well-known fact that this occurs and any 483 will show you this in every other plant on the planet.

This thing was never going to save anyone.

This needs to be taken very seriously.
@piersmorgan PS

I ranted that all from my phone using voice to text. I apologize for any grammatical errors
1/ plasmid dna can be taken up by a lymphocytes when injected into the muscle.

That's the biotech plasmid.

In pregnant females this happens at eight times the volume regarding lipid nanoparticles going into their lymph nodes while they are experiencing changes in their immune system but it also goes to the placenta.

Typing from my phone here

x.com/_HeartofGrace_…
Read 35 tweets
Jan 25
1/ Digital Twins and Cancer.
This has already begun.
There's talk about how this translates into the human, physical world. This has already begun with the use of what are called organoids, which Harvard was and others were investigating, before it gained traction. Image
2/ you can read here about the use of a digital twin and cancer.

. sciencedirect.com/science/articl…Image
3/ the use of organoids for customized, personalized cancer treatment is already happening, privately. You're just not hearing about it. In 2017, HARVARD researchers started using organoids. Image
Read 19 tweets
Dec 31, 2024
1/ 🚨"35-year-old woman contracted Lou Gehrig's disease after her first Pfizer dose."
ACTIVATION of DORMANT GENES in BOTH ADENOVIRUS AND RNA BASED.
These "products" like adenovirus and RNA/DNA can be DORMANT (see linked thread) and then become ACTIVE. Not just cancer :(
READ👇 Image
2/ Charcot's disease is amyotrophic lateral sclerosis

'Charcot's Disease' is a progressive and fatal

progressive death of motor neurons

.ama-assn.org/delivering-car…
3/ "New-Onset Amyotrophic Lateral Sclerosis in a Patient who Received the J&J/Janssen COVID-19 Vaccine"

pmc.ncbi.nlm.nih.gov/articles/PMC10…
Read 26 tweets
Dec 31, 2024
1/ 🚨 THEY KNEW.
"REACTIVATION" potential of ADENOVIRUS VECTORS used for "gene therapy", including the use of DNA PLASMID with LATENT and REACTIVATED STATES for BOTH and why this is important for SHEDDING and DISEASE.

🚨DATE of ISSUE: JANUARY 2020. COINCIDENCE? Image
2/ Pierre Kory and others have talked a lot about shedding--they are correct. The studies are on viral vectors--these are viral vectors. There are studies I have and so do others on this, but to drive it home--right here:

gillettechildrens.org/your-visit/pat…Image
3/ back to the first document: this was released 01/2020, right before the world was about to go into forced measures against the people, demanding they get injected with something that needs FIFTEEN YEARS of testing. The US had the gene sequence form CHINA in this moment. Image
Read 33 tweets

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