🚨🚨💉Nice chronological list below. Lawyers you might be interested.
I would like to submit the date of August 17th, 2018.
(b. Elimination of roles of the RAC in HGT and biosafety.)
And it was taken over by the FDA, OSP, and IBC. This is very important!

"In a Federal Register notice issued on August 17, 2018 (83 FR 41082), the NIH proposed a series of actions to the NIH Guidelines for Research Involving Recombinant or Synthetic Nucleic Acid Molecules (NIH Guidelines) to streamline oversight of human gene transfer research (HGT), and to focus the NIH Guidelines more specifically on biosafety issues associated with research involving recombinant or synthetic nucleic acid molecules."

This is what was decided:

"Elimination of HGT protocol submission and reporting requirements to the NIH, and individual HGT protocol review by the Recombinant DNA Advisory Committee (RAC)."

The recombinant advisory committee was the group that was in charge of biosafety and ethics for the use of things like RNA with lipids. They were the one thing we had standing in the way (if they were doing what they were supposed to do).

"Modification of roles and responsibilities of investigators, institutions, Institutional Biosafety Committees (IBCs), the RAC, and the NIH to be consistent with these goals including:

a. Modification of roles of IBCs in reviewing HGT to be consistent with review of other covered research.

b. Elimination of roles of the RAC in HGT and biosafety."

Do you know what they did here, and who was in charge?

"After careful consideration of public comments, the NIH is amending the NIH Guidelines in the following areas:

1. Elimination of HGT protocol submission and reporting requirements to the NIH, and individual HGT protocol review by the Recombinant DNA Advisory Committee (RAC).

2. Modification of roles and responsibilities of investigators, institutions, Institutional Biosafety Committees (IBCs), the RAC, and the NIH to be consistent with these goals including:

a. Modification of roles of IBCs in reviewing HGT to be consistent with review of other covered research.

b. Elimination of roles of the RAC in HGT and biosafety."

what this means is that the RAC will no longer review individual HGT protocols. This function will be fully transitioned to Institutional Biosafety Committees (IBCs) and the Food and Drug Administration (FDA).
But also the NIH Office of Science Policy (OSP), and in 2018, that was David T. L. Lee, PhD.

Also, the IBC does not have the experience to work with pediatric populations.

Experiments categorized as Major Actions under Section III-A-1-a must be submitted to the Office of Science Policy (OSP), NIH
These proposals must be published in the Federal Register for a minimum of 15 days to allow for public comment and must receive specific approval from NIH before initiation.

"The deliberate transfer of drug resistance traits to microorganisms that are not naturally known to acquire these traits will require NIH Director approval. This is to ensure that such transfers do not undermine the ability to control disease agents in human, veterinary medicine, or agriculture contexts."

The DNA plasmids that have contaminated the Pfizer and Moderna RNA injections contain an antibiotic resistance part to them--that is standard issues when you use plasmids to make RNA. That is plasmid biotech 101.

Before initiating experiments involving the deliberate transfer of recombinant or synthetic nucleic acid molecules into human research participants, researchers must obtain approval from their IBC and all other applicable institutional and regulatory authorities.

The criteria for synthetic nucleic acids that require IBC approval now include:

Length:
Nucleic acids containing more than 100 nucleotides.
Biological Properties:

Nucleic acids with properties enabling integration into the genome, such as cis elements.

Replication Potential:
Nucleic acids that have the potential to replicate within a cell.

Transcription/Translation Potential:
Nucleic acids that can be transcribed or translated.
Now, according to the NIH Guidelines for Research Involving Recombinant or Synthetic Nucleic Acid Molecules, the COVID-19 injections, which contain synthetic nucleic acid molecules (mRNA), would require Institutional Biosafety Committee (IBC) approval prior to initiation.
Specifically, these injections fall under the category of experiments involving the deliberate transfer of synthetic nucleic acid molecules into humans, as outlined in Section III-C-1.

The mRNA in the COVID-19 injections qualifies as synthetic nucleic acid molecules.

As per Section III-C-1, any experiment involving the deliberate transfer of recombinant or synthetic nucleic acid molecules into human research participants requires approval from the IBC before initiation.

Now the thing to look up, is who were the people involved with the IBC for PFizer and Moderna? federalregister.gov/documents/2019…

🚨 Infections and Cancer: CDC states a current increase n bacterial infections. Some share on social media they've had covid many times, more bacterial infections, and some people (common denominator?) keep getting prolonged infection. Drug resistance is one thing. However, Multiple injections of lipids?

Our immune system needs to SEE things that are there to clear or deal with what is called a pathogen. A pathogen can be bacteria, a virus, but another thing it sees as a pathogen is a pharmaceutical lipid.

We have things in our body called Pattern Recognition Receptors (PRRs).

PRRs can detect PAMPs (pathogen-associated molecular patterns)

PRRs detect the PAMPs. PRRs also detect DAMPs

PAMPs are common structures found on pathogens, such as bacterial cell wall components, like that of listeria. DAMPs are parts of us that are released when our cells are damaged.

Our cells that are part of our immune system can recognize things that are not us, like pharmaceutical liposomes that are part of the lipid nanoparticle that is being used to not only deliver the RNA for the covid injections, but now, it appears the word is spreading, that traditional attenuated vaccines are now going to switch over to the lipid component.

Not only is this bad from the cGAS STING aspect (the change over) but lets look at what is called the MPS--mononuclear phagocyte system (read about the MPS below).

The body need to first MARK the pathogen for clearance. It recognizes a pathogen, but it has to MARK it, like placing a flag on something, or if your car was stranded at night, and maybe you have a flare to put out--a signal to say "This is where I am!"

Our immune systems MAKES proteins that are there to help MARK bad things that enter us, like viruses, bacteria, and pharmaceutical lipids (there are 4 kinds of lipids in the lipid nanoparticle: cholesterol, DSPC, ionizable lipids that can be charged (and some that already have a charge), and the PEG on the outside of the lipid nanoparticle.

The PEG was placed on the outside of the lipid nanoparticle to essentially cloak it from our immune system so our PRRs could not see it right away. It is like a cloaking shield a Romulan ship would use, and studies have shown this can last for a day or up to over 50 hours of cloaking time. It does not guarantee the shielding from our immune system detecting it, but it gets in the way.

Once the immune system sees the lipids that are there, it wants to attach proteins to the surface of it.

We have different proteins in our body that attach to things to mark them for removal (destruction). These are called Opsonins.

We also have things called macrophages. Some of you might have seen cool videos of macrophages chasing a bacteria, engulfing it, and digesting it. These are not an opsonin. These surround the bad guy, envelop it, and digest it.

Here are the types of flags, and the list of what is usually going to mark which thing.

There is overlap on which opsonins can bind to what things. The immune system usually wants to launch a hefty response and get a few things in the area to deal with what is going on (comprehensive).

The lipids in the RNA injections are detected by our immune system, once the cloaking time is up.

Then our body goes in to mark all of those things (there are a LOT of them in the injections!!!!)

1st opsonin protein: C3B
This is something that "sticks" to the outside of that pathogen, and the lipid. C3B also binds to some bacteria and viruses!

Then we have the opsonin C4B. This also binds to bacteria, virus, and pharmaceutical lipids! Same with iC3b but it does not bind with all the viruses. C3B is one of the main markers of those pharma lipids.

Then we have our immunoglobulins.
IgG!
IgG can bind to viruses, bacteria, and pharma lipids

IgM can also bind to all three.

Then we get into things like C-Reactive Protein, lactoferrin and MBL, but those are not the main players here.

Studies have shown (the time frame varies by person, current infection state, health, etc) that if you inject pharma lipids like DSPC and PEG in vivo, that if you repeat injections of those lipids, depending on time frame, they can take longer for the immune system to clear because the POOL of our PROTEINS to MARK the INVADERS gets DEPLETED!
This means that in these studies, it now took the immune system LONGER to clear the lipids out, because there were imply not enough opsonins to mark them all. So they just hung out. And we know these in themselves can cause inflammation.

So in the beginning of 2021, if you all remember, people, starting with the frontline workers, and THEN the doctors hit the immune compromised who have/had current autoimmune conditions and other immuno comprised states like CANCER. And this was really bad, considering spike protein came in, DNA plasmids came in (no level is safe!! I do not care what FDA says on this! They've been compromised anyways by pharma and their own malfeasance), but also a HUGE NUMBER of PHARMA GRADE LIPIDS were injected to people ONCE and then what did they tell people? When were people getting the next dose again? (Insert profanities here)
Those doctors ta the FDA, those scientists, docs at hospitals--they injected people again 3 weeks later, during COVID! They injected people with something that depletes the opsonin system, twice in three weeks. (insert profanities)

Consider this, if you deplete your protein pool, your opsonin pool, what if you get strep? What if you get the flu? What if you get a urinary tract infection? What if you get covid?

This system can replenish itself, but, some things CAN occur here, including impacts on cancer.

We do not have this unlimited supply of opsonins.

So not only if you keep getting injected with these lipids can harm occur from inflammation, they can also reduce the number of opsonins you have because remember, they were injected all over the body, head to toe.

Not only can the pool of these proteins be depleted, they can be ALTERED.

If repeated exposure to liposomes alters opsonin levels or immune function, the immune system might adapt by changing the types of antibodies it produces.

Antibody
class
switch

Does a paper need to be written for this stuff too for it to be taken seriously? Is it only true if it is peer reviewed?
I linked it below for you.

So, if we have a depleted pool of opsonins meant to flag the bad guys in our body that do not belong, the immune system might have a tougher time, and in this process, the body can class switch, it can change what is coming in, because certain opsonins (proteins) have been depleted fighting one thing, and might change.

CANCER:
Cancer cells can be marked by complement proteins. Opsonins!
For instance, complement components like C3b can bind to cancer cells, leading to their recognition and uptake. This is called complement-mediated cytotoxicity.

C3b marks cancer cells for phagocytosis (engulf--eat them).
Depletion of the complement system reduces the opsonization of tumor cells, leading to decreased recognition and clearance by phagocytes like macrophages and neutrophils.
If you have depleted opsonins, and you do not have enough or less to mark cancer cells, that can cause tumor progression. This can lead to not only tumor growth, but mestasis.

Did you hear of anyone who had their cancer advance after ....?

They knowingly gave a blast of lipid pharmaceuticals to people who had/have cancer.

This depletion can also impact the effectiveness of monoclonal antibodies (cannot mark the cells, antibodies cannot SEE them!)

This might also impact immune checkpoint inhibitors and CAR T therapy.

And now, scientists (do not just blame the FDA) want to use RNA and lipids going forward.

This is bad news bears, and might be a big piece of the puzzle beyond the spike protein and other factors, why people this past year or so, some people, have been getting sick with multiple infections. sciencedirect.com/science/articl…

🚨 How plasmid DNA will track to the nucleus (with extra steps) before it gets degraded in the cell. First it gets recognized by cGAS, but that is not the only thing that will recognize it, and actually PROTECT it from being broken down, and zip it right to the nucleus.

DNA plasmid will be recognized by the cGAS STING pathway immediately upon cell entry. This is the first part of the cell that recognizes it with rapid speed. cGAS is the cell's main "smoke detector" that recognizes things that do not belong, like viruses, bacteria, double stranded RNA and DNA.

But here's the thing--DNA will cause the strongest response, and it is also LENGTH dependent--longer pieces of DNA plasmid will cause cGAS STING to cause the strongest response of all, even at lower amounts.

You can have a mixture of different lengths of DNA. Small pieces will activate the immune system in a mold to moderate way. Medium sized pieces of DNA will trigger a stronger response--the small pieces will actually act as "pass interference" (US football term here) and stop the larger pieces from binding.

The longer pieces of DNA will cause a very strong immune system response--one that can be dangerous, and cause a hyperactivation of our immune systems and cause it to attack us, destroy tissue, and cause us injury, including but not limited to autoimmune concerns.

There is also an order to the organs in our body (eyes, brain, bladder, heart, etc) with how other things will impact the cellular damage (I am explaining on podcasts coming up, and why myocarditis (heart damage) aside from immune issues and clots, are the highest injuries seen (followed by bladder, etc).

Back to what is happening in the cell. There is an order of operations in our cells for how things are taken care of regarding foreign entry of plasmid DNA. Right now we will just speak to entering the nucleus.

There are multiple proteins inside the cell that can bind to plasmid DNA, and some do not care what kind of DNA, they see it as "bad" because DNA does not belong free floating around in our cells.

The proteins:
✅cGAS (cyclic GMP-AMP synthase)
✅IFI16 (Interferon Gamma Inducible Protein 16)
✅Other DNA-Binding Proteins (like HMGB1 (High Mobility Group Box 1) and DDB2 (Damage-Specific DNA Binding Protein 2)
✅Motor Proteins (DYNEIN!!!!!)

And then we have the thing that breaks down the DNA plasmid:
✅TREX1

☑️1. DNA plasmid has now entered the cell vis a lipid nanoparticle

☑️2. Initial Interactions with cGAS

cGAS-STING Pathway (IFI16 as well):

cGAS STING and IF116 rapidly detect cytoplasmic DNA, particularly double stranded DNA (like plasmid DNA).

IFI16 specifically senses foreign DNA and activates immune responses similar to cGAS-STING.

The cGAS-STING pathway is known for its rapid response to foreign DNA, triggering signaling cascades within minutes of detection. cGAS STING, the smoke detector for our cells, is coming in fast and hard, and is the first on the scene.

cGAS (the smoke detector) has the evolutionary advantage in binding to newly arrived cytoplasmic DNA to trigger an immune response quickly.

☑️3. Dynein time!

Dynein is going to come in with rapid speed too--about the same time cGAS does, or just behind it. Dynein is what is called a MOTOR PROTEIN!
It looks like this little ball with feet, and it can attach to plasmid DNA, it will bind to it! It will attach to the DNA plasmid, and carry it on its back like Luke Skywalker carrying Yoda (except on a tight rope to the nucleus, it is now walking it to the nucleus).

(see video below of Kinesin protein walking on a little rope thing we call microtubules, it will look like it is walking on a tight rope. It is simlar to Dynein).

However, when Dynein binds to plasmid DNA it is now protected from being broken down! It is now shielded, like Luke Skywalker shielding Yoda from harm.

☑️4. Size of DNA plasmid matters!
Size Variation and Transport Efficiency:

Small Plasmids (20-120 base pairs):

Smaller plasmid fragments diffuse more readily and are easily transported by dynein-microtubule interactions. T
Their smaller size allow them to move through the nuclear pore complex more easily.

Medium Plasmids (120-2000 base pairs):

Medium-sized plasmids benefit significantly from active transport mechanisms.
Their interaction with dynein and microtubules ensures they reach the nucleus without being degraded or immobilized within the cytoplasm.

Large Plasmids (2000-4000 base pairs):

Larger plasmids might face more difficulty due to their size but are still effectively transported by the cytoskeletal network.

☑️5. Dynein can bind to plasmid DNA either directly or via adaptor proteins that recognize the DNA.
Dynein moves the DNA towards the cell center (minus end of microtubules), directing it towards the nucleus.

☑️ NO SV40 needed to get it into the nucleus, there are CHARGE MEDIATED localization reactions here--meaning the CHARGE is driving it into the nucleus!

The negative charge of DNA, due to its phosphate backbone, can interact with positively charged molecules or proteins within the cell.

☑️6. Another way DNA plasmid can enter the nucleus During Telophase

Our cells are dividing, and when this happens, DNA plasmids can enter the nucleus.

Cell Division Phases
Prophase: Chromosomes condense, and the nuclear envelope begins to break down.
Metaphase: Chromosomes align at the cell's equatorial plane.
Anaphase: Chromatids separate and move to opposite poles of the cell.
Telophase: Nuclear envelopes re-form around each set of chromosomes, and the cell begins to split into two daughter cells.

The nuclear envelope is more permeable during reformation, allowing easier entry of exogenous DNA.
The temporary absence or incomplete formation of the nuclear envelope reduces physical barriers to DNA entry.

☑️ 7. So now, we have cGAS that has bound to DNA plasmid, and we have DYNEIN that has walked the DNA plasmid pieces right to the nucleus, carrying it like a snuggie on its back.

☑️ 8. TREX 1 comes into the picture. TREX 1 is the thing that is going to break down DNA plasmid, but Dynein-bound DNA is likely less accessible to nucleases because it is associated with a large protein complex. TREX has a difficult time interacting with the motor protein carrying the DNA plasmid on its back.

☑️9. Association with other proteins!
In addition to dynein, plasmid DNA can associate with other cellular proteins that shields it from degradation. These proteins can form complexes that obscure the DNA from nucleases like TREX 1.

HMGB1 (High Mobility Group Box 1)
Can bind DNA and influence its stability and interaction with other cellular components.
Acts as a DNA chaperone and can also participate in the immune response.

IFI16 (Interferon Gamma Inducible Protein 16)
A DNA sensor that can detect foreign DNA in the cytoplasm.
Activates immune responses, similar to the cGAS-STING pathway.

DDB2 (Damage-Specific DNA Binding Protein 2)
Involved in DNA repair and can bind damaged DNA.
Participates in recognizing and responding to DNA damage.

☑️10. Limitations of cGAS-STING Pathway
The cGAS-STING pathway can become saturated if there is an overwhelming amount of dsDNA in the cytoplasm. Saturation occurs when the amount of DNA exceeds the pathway's capacity to process and respond effectively.
The response of the cGAS-STING pathway is dose-dependent, meaning that higher concentrations or continuous exposure to dsDNA can lead to prolonged or sustained immune activation. This can potentially lead to chronic inflammation or immune dysregulation, and damage to organs causing injury to people, and autoimmune disease.

The ability of cells to handle dsDNA can vary between different cell types and under different physiological conditions. Some cells may have higher tolerance thresholds for dsDNA, while others may be more sensitive (I will explain this on the podcast coming up!)

☑️11. cGAS can have altered functionality for a few reasons. This has been discussed in other threads, including by RACE (your RACE determines what kind of cGAS you have, er smoke detector in your body! There are also what are called HLA mutations (DR) that can cause a dysregulation in immune response.

Genetic Mutations: Mutations in genes encoding cGAS, STING, or associated proteins can impair the pathway's ability to detect or respond to dsDNA properly.

Certain diseases or conditions may interfere with cGAS-STING signaling, either enhancing or dampening its response to dsDNA. For example, viruses may encode proteins that inhibit or exploit cGAS-STING signaling to evade immune detection.

Drugs or therapies that modulate immune responses, including those targeting cGAS-STING pathway components, can also alter immune responses in desired or undesired ways.

☑️12. So lastly, TREX 1 comes in and this is the thing that cleans up DNA, and it is the last thing to arrive on the scene in your cell, after cGAS has already had its way with it, after the immune system has already been activated, and after the plasmid DNA has already been transported to the nucleus. It is the slowest moving part of your cell's defense mechanism. 2/ Here is what a motor protein looks like walking along a microtubule, this is Kinesin, not Dynein, but it will carry that DNA plasmid like Luke carrying Yoda on its back, and it will walk it right to the nucleus

sciencedirect.com/science/articl…

1/ 🚨💉🦠MYOCARDITIS: I need help confirming what I found. I compared the DNA sequence in the DNA plasmid used in mRNA COVID vaccines that codes for the SPIKE protein, to that of another sequence. I wanted to see if there is a match. There is a 99% consecutive match, no gaps. There is a 99% match of the DNA to code for this one smaller protein, imbedded inside of the larger DNA sequence, that codes for the spike protein.

I had to first convert this smaller sequence, the other sequence. That smaller sequence was a protein sequence (not the spike protein, but it codes for a different kind of protein), and I had to "reverse" the sequence to that of a DNA sequence.

I have to get confirmation this was done correctly, by other scientists. I need confirmation of what I am seeing, and if this is correct.

I need confirmation that this is accurate. If this is accurate, I am very fearful of what I just discovered.

I had to take the full plasmid sequence first that is used in the production of the mRNA COVID vaccines by Pfizer.

Then I took the whole DNA sequence that is part of that full DNA plasmid, and I started with Pfizer. I looked at the whole DNA sequence for the plasmid itself, and then I looked at the part that codes just for the spike protein.

I was curious because I was looking at two other studies, at least, that used a very specific peptide chain.

Peptides are short chains of amino acids.

The research I found in more than one study, that was done with mice took a very small, peptide chain and they mixed it with different things, to immunize the mice.

This was injected into mice with different things, and it was not even used with any kind of lipid. It was not used inside of a lipid nanoparticle, which would be much, much worse of an outcome.

This very small protein sequence that I am talking about, that I converted to a DNA sequence, that was used in more than one study, was injected, with a combination of things, to induce myocarditis in mice.

The specific peptide chain (there is actually more than one, a variation is used in another study) was injected into mice, and was found to cause myocarditis.

The researchers induced myocarditis in BALB/c mice by injecting them with a peptide derived from the cardiac myosin heavy chain, specifically amino acids 614-643 (known as M7Aα). This is the chain I looked at, and I converted to its DNA sequence form. This is the sequence that I compared to the much larger sequence of DNA that is part of the sequence that we know of, in the DNA plasmid, that makes the spike protein, specifically the sequence found in the mRNA COVID VACCINE made by PFIZER.

There is another study at least that I found, where this peptide was used to induce myocarditis in mice, but so was another peptide, similar to that one, a variant of that peptide. It is still a peptide derived from the cardiac myosin heavy chain.

BALB/c mice are important mice used in research, as they are very similar to one another, and they usually respond very much the same in research when used to test for cancer, or autoimmune disease.

I was curious about this peptide as I was reading articles this evening. and I wondered, is this embedded anywhere in the PLASMID DNA that is used in the PFIZER VACCINES to make the RNA that makes the spike protein?

DNA makes RNA makes a protein.

In the first study with mice, the researchers
The researchers found in one study, that CD4+ T cells recognize the M7Aα peptide when presented by MHC class II molecules on antigen-presenting cells (APCs).

Certain amino acids within the M7Aα peptide trigger an autoimmune response against cardiac tissue.
This is what we call molecular mimicry.

M7Aα Peptide is derived from the cardiac myosin heavy chain, and this is implicated in autoimmune myocarditis.
It can induce an autoimmune response in susceptible individuals, mediated by CD4+ T cells that recognize this peptide in association with MHC class II molecules.

Now, if this is combined with the spike protein, the concern is, there could potentially be cross-reactivity between T cells or antibodies generated against the spike protein and those recognizing the M7Aα peptide. This cross-reactivity might occur if there are structural similarities or shared epitopes (molecular mimicry) between the spike protein and the M7Aα peptide.

If cross-reactivity occurs, it could lead to an immune response targeting cardiac tissues due to recognition of both the spike protein and the M7Aα peptide. This mechanism could potentially induce myocarditis similar to what is observed with autoimmune responses to the M7Aα peptide alone or in conjunction with other triggering factors.

But what I am saying here is that the M7Aα peptide alone is known to cause autoimmune myocarditis.

the M7Aα peptide alone has been shown to induce myocarditis in experimental models, particularly in BALB/c mice.

This peptide corresponds to a specific sequence (amino acids 614-643) from the cardiac myosin heavy chain. When administered to these mice, it triggers an autoimmune response mediated by CD4+ T cells. These T cells recognize the M7Aα peptide presented by MHC class II molecules on cardiac tissues, leading to inflammation and damage to the heart muscle, characteristic of myocarditis.

The autoimmune mechanism involves molecular mimicry, where the M7Aα peptide shares structural similarities or epitopes with other antigens, such as peptides from pathogens, exacerbating autoimmune myocarditis in susceptible individuals.

Therefore, the M7Aα peptide alone, under specific conditions, can induce myocarditis by triggering an autoimmune response against cardiac tissues.

But also, we have the spike protein that is there, and we also have presence of DNA plasmid pieces, which also create issues.

However, the concern is, the sequences I just checked tonight, twice in BLAST, are at a very high match percentage.

The DNA sequence that I tracked when I reversed the protein for the heavy chain of myosin, when compared to the full DNA sequence on the DNA PLASMID that codes for the spike protein, that is used in the PFIZER VACCINES, is showing me, when I checked it twice, to be a consecutive match, with NO GAPS, to have a max possible score of 1343, with a total score of 1343, with a query percent of 99% and with a percent identified as 96.88.

I need confirmation if I am correct, or if I am seeing this correctly please.

I am going to post the sequences that I have, and then the data from the BLAST comparison that I found.

The query sequence (lcl|Query_7196259) has a length of 808 base pairs. This is the sequence that makes the M7Aα peptide. This is the peptide used in studies that was injected into mice to cause myocarditis.

The subject sequence (Sequence ID: Query_7196261) has a length of 3822 base pairs. This is the full DNA sequence that is part of the DNA plasmid vector that is used to make the mRNA COVID VACCINES--this is the very specific data sequence that is used by PFIZER.

This is the sequence of the DNA plasmid, the portion that encodes for the SPIKE protein that is used in making the current PFIZER mRNA VACCINES for COVID:
ATGTTCGTGTTCCTGGTGCTGCTGCCTCTGGTGTCCAGCCAGTGTGTGAACCTGACCACCAGAACACAGCTGCCTCCAGCCTACACCAACAGCTTTACCAGAGGCGTGTACTACCCCGACAAGGTGTTCAGATCCAGCGTGCTGCACTCTACCCAGGACCTGTTCCTGCCTTTCTTCAGCAACGTGACCTGGTTCCACGCCATCCACGTGTCCGGCACCAATGGCACCAAGAGATTCGACAACCCCGTGCTGCCCTTCAACGACGGGGTGTACTTTGCCAGCACCGAGAAGTCCAACATCATCAGAGGCTGGATCTTCGGCACCACACTGGACAGCAAGACCCAGAGCCTGCTGATCGTGAACAACGCCACCAACGTGGTCATCAAAGTGTGCGAGTTCCAGTTCTGCAACGACCCCTTCCTGGGCGTCTACTACCACAAGAACAACAAGAGCTGGATGGAAAGCGAGTTCCGGGTGTACAGCAGCGCCAACAACTGCACCTTCGAGTACGTGTCCCAGCCTTTCCTGATGGACCTGGAAGGCAAGCAGGGCAACTTCAAGAACCTGCGCGAGTTCGTGTTTAAGAACATCGACGGCTACTTCAAGATCTACAGCAAGCACACCCCTATCAACCTCGTGCGGGATCTGCCTCAGGGCTTCTCTGCTCTGGAACCCCTGGTGGATCTGCCCATCGGCATCAACATCACCCGGTTTCAGACACTGCTGGCCCTGCACAGAAGCTACCTGACACCTGGCGATAGCAGCAGCGGATGGACAGCTGGTGCCGCCGCTTACTATGTGGGCTACCTGCAGCCTAGAACCTTCCTGCTGAAGTACAACGAGAACGGCACCATCACCGACGCCGTGGATTGTGCTCTGGATCCTCTGAGCGAGACAAAGTGCACCCTGAAGTCCTTCACCGTGGAAAAGGGCATCTACCAGACCAGCAACTTCCGGGGCAGCCCACCGAATCCATCGTGCGGTTCCCCAATATCACCAATCTGTGCCCCTTCGGCGAGGTGTTCAATGCCACCAGATTCGCCTCTGTGTACGCCTGGAACCGGAAGCGGATCAGCAATTGCGTGGCCGACTACTCCGTGCTGTACAACTCCGCCAGCTTCAGCACCTTCAAGTGCTACGGCGTGTCCCCTACCAAGCTGAACGACCTGTGCTTCACAAACGTGTACGCCGACAGCTTCGTGATCCGGGGAGATGAAGTGCGGCAGATTGCCCCTGGACAGACAGGCAAGATCGCCGACTACAACTACAAGCTGCCCGACGACTTCACCGGCTGTGTGATTGCCTGGAACAGCAACAACCTGGACTCCAAAGTCGGCGGCAACTACAATTACCTGTACCGGCTGTTCCGGAAGTCCAATCTGAAGCCCTTCGAGCGGGACATCTCCACCGAGATCTATCAGGCCGGCAGCACCCCTTGTAACGGCGTGGAAGGCTTCAACTGCTACTTCCCACTGCAGTCCTACGGCTTTCAGCCCACAAATGGCGTGGGCTATCAGCCCTACAGAGTGGTGGTGCTGAGCTTCGAACTGCTGCATGCCCCTGCCACAGTGTGCGGCCCTAAGAAAAGCACCAATCTCGTGAAGAACAAATGCGTGAACTTCAACTTCAACGGCCTGACCGGCACCGGCGTGCTGACAGAGAGCAACAAGAAGTTCCTGCCATTCCAGCAGTTTGGCCGGGATATCGCCGATACCACAGACGCCGTTAGAGATCCCCAGACACTGGAAATCCTGGACATCACCCCTTGCAGCTTCGGCGGAGTGTCTGTGATCACCCCTGGCACCAACACCAGCAATCAGGTGGCAGTGCTGTACCAGGACGTGAACTGTACCGAAGTGS4CCCGTGGCCATTCACGCCGATCAGCTGACACCTACATGGCGGGTGTACTCCACCGGCAGCAATGTGTTTCAGACCAGAGCCGGCTGTCTGATCGGAGCCGAGCACGTGAACAATAGCTACGAGTGCGACATCCCCATCGGCGCTGGAATCTGCGCCAGCTACCAGACACAGACAAACAGCCCTCGGAGAGCCAGAAGCGTGGCCAGCCAGAGCATCATTGCCTACACAATGTCTCTGGGCGCCGAGAACAGCGTGGCCTACTCCAACAACTCTATCGCTATCCCCACCAACTTCACCATCAGCGTGACCACAGAGATCCTGCCTGTGTCCATGACCAAGACCAGCGTGGACTGCACCATGTACATCTGCGGCGATTCCACCGAGTGCTCCAACCTGCTGCTGCAGTACGGCAGCTTCTGCACCCAGCTGAATAGAGCCCTGACAGGGATCGCCGTGGAACAGGACAAGAACACCCAAGAGGTGTTCGCCCAAGTGAAGCAGATCTACAAGACCCCTCCTATCAAGGACTTCGGCGGCTTCAATTTCAGCCAGATTCTGCCCGATCCTAGCAAGCCCAGCAAGCGGAGCTTCATCGAGGACCTGCTGTTCAACAAAGTGACACTGGCCGACGCCGGCTTCATCAAGCAGTATGGCGATTGTCTGGGCGACATTGCCGCCAGGGATCTGATTTGCGCCCAGAAGTTTAACGGACTGACAGTGCTGCCTCCTCTGCTGACCGATGAGATGATCGCCCAGTACACATCTGCCCTGCTGGCCGGCACAATCACAAGCGGCTGGACATTTGGAGCAGGCGCCGCTCTGCAGATCCCCTTTGCTATGCAGATGGCCTACCGGTTCAACGGCATCGGAGTGACCCAGAATGTGCTGTACGAGAACCAGAAGCTGATCGCCAACCAGTTCAACAGCGCCATCGGCAAGATCCAGGACAGCCTGAGCAGCACAGCAAGCGCCCTGGGAAAGCTGCAGGACGTGGTCAACCAGAATGCCCAGGCACTGAACACCCTGGTCAAGCAGCTGTCCTCCAACTTCGGCGCCATCAGCTCTGTGCTGAACGATATCCTGAGCAGACTGGACCCTCCTGAGGCCGAGGTGCAGATCGACAGACTGATCACAGGCAGACTGCAGAGCCTCCAGACATACGTGACCCAGCAGCTGATCAGAGCCGCCGAGATTAGAGCCTCTGCCAATCTGGCCGCCACCAAGATGTCTGAGTGTGTGCTGGGCCAGAGCAAGAGAGTGGACTTTTGCGGCAAGGGCTACCACCTGATGAGCTTCCCTCAGTCTGCCCCTCACGGCGTGGTGTTTCTGCACGTGACATATGTGCCCGCTCAAGAGAAGAATTTCACCACCGCTCCAGCCATCTGCCACGACGGCAAAGCCCACTTTCCTAGAGAAGGCGTGTTCGTGTCCAACGGCACCCATTGGTTCGTGACACAGCGGAACTTCTACGAGCCCCAGATCATCACCACCGACAACACCTTCGTGTCTGGCAACTGCGACGTCGTGATCGGCATTGTGAACAATACCGTGTACGACCCTCTGCAGCCCGAGCTGGACAGCTTCAAAGAGGAACTGGACAAGTACTTTAAGAACCACACAAGCCCCGACGTGGACCTGGGCGATATCAGCGGAATCAATGCCAGCGTCGTGAACATCCAGAAAGAGATCGACCGGCTGAACGAGGTGGCCAAGAATCTGAACGAGAGCCTGATCGACCTGCAAGAACTGGGGAAGTACGAGCAGTACATCAAGTGGCCCTGGTACATCTGGCTGGGCTTTATCGCCGGACTGATTGCCATCGTGATGGTCACAATCATGCTGTGTTGCATGACCAGCTGCTGTAGCTGCCTGAAGGGCTGTTGTAGCTGTGGCAGCTGCTGCAAGTTCGACGAGGACGATTCTGAGCCCGTGCTGAAGGGCGTGAAACTGCACTACACATGA

This is the sequence I converted from the myosin heavy chain peptide (The M7Aα peptide sequence is: MDLLLGSKVQDTILALLGNAEELRQKVEPLLEEAGLLSSK)
I converted it to :
ATGGACGGTGTTCAATGCCACCAGATTCGCCTCTGTGTACGCCTGGAACCGGAAGCGGATCAGCAATTGCGTGGCCGACTACTCCGTGCTGTACAACTTCGCCCCCTTCTTCGCATTCAAGTGCTACGGCGTGTCCCCTACCAAGCTGAACGACCTGTGCTTCACAAACGTGTACGCCGACAGCTTCGTGATCCGGGGAAACGAAGTGCGGCAGATTGCCCCTGGACAGACAGGCAACATCGCCGACTACAACTACAAGCTGCCCGACGACTTCACCGGCTGTGTGATTGCCTGGAACAGCAACAAGCTGGACTCCAAAGTCGGCGGCAACTACAATTACAGGTACCGGCTGTTCCGGAAGTCCAATCTGAAGCCCTTCGAGCGGGACATCTCCACCGAGATCTATCAGGCCGGCAACAAGCCTTGTAACGGCGTGGCAGGCGTGAACTGCTACTTCCCACTGCAGTCCTACGGCTTTAGGCCCACATACGGCGTGGGCCACCAGCCCTACAGAGTGGTGGTGCTGAGCTTCGAACTGCTGCATGCCCCTGCCACAGTGTGCGGCCCTAAGAAAAGCACCAATCTCGTGAAGAACAAATGCGTGAACTTCAACTTCAACGGCCTGACCGGCACCGGCGTGCTGACAGAGAGCAACAAGAAGTTCCTGCCATTCCAGCAGTTTGGCCGGGATATCGCCGATACCACAGACGCCGTTAGAGATCCCCAGACACTGGAAATCCTGGACATCACCCCTTGCAGCTTCGGCGGAGTGTCTGTGATCACCCCTGGCACCAACACCAGCAATCAG

This was the result I got twice from using BLAST:

Score: 1343 bits, which indicates a highly significant match.
Expect: 0.0, suggesting that this alignment is unlikely to occur by chance.
Identities: 777 out of 802 bases matched (97% identity).
Gaps: 0 gaps reported, indicating a continuous alignment.
Strand: Plus/Plus, indicating both sequences are aligned in the same orientation.
These alignment statistics confirm that the sequence from position 1019 to 1820 in the subject sequence (Query_7196261) matches consecutively with the entire length of the query sequence (Query_6853905).

If I am looking at this correctly, the DNA sequence to make the Myocarditis producing the peptide derived from the cardiac myosin heavy chain, specifically amino acids 614-643 (known as M7Aα), is hanging out, in almost its entirety, in full form, inside, the part of the DNA plasmid, that encodes, for the spike protein, that is currently being used, in the mRNA vaccines, made by pfizer.


2/ These are the studies I looked at which utilized a peptide called M7Aα that produces myocarditis in mice.
This is the sequence I looked at to see if it was a match to the spike protein.
Please confirm what I am seeing here.


Generation of Humanized Mice Susceptible to Peptide-Induced Inflammatory Heart Disease

science.org/doi/10.1126/sc…
ahajournals.org/doi/10.1161/01…

🚨💉🧬DNA plasmid can integrate into the genome, drive cancer, without a "promoter" (SV40), and drive FOREIGN PROTEIN formation WITHOUT RNA. DNA integration studies on REAL cancer tissues exist. Specific sites of integration explained, by specific cancer, and junk protein creation:

II. We know the current mRNA injections that are housed inside of a lipid nanoparticle fromm Moderna and Pfizer contain plasmid DNA contamination, proven by several scientists in the world. This does not discount the other issues with this platform--but we will focus on the DNA plasmid part, and speak to the existing studies which have already been performed, on human cancer tissue, from human cancer patients, the very specific cancers involved, and specifically, WHERE exactly, in the human genome, the DNA pieces are integrating and the impact this is having on cancer, without any SV40.

Pfizer is getting studied right now--people with cancers and other concerns who are injured--and there is much talk about the SV40 promoter that exists in the plasmid of the Pfizer vaccine, but this does not explain why someone who had the Moderna vaccine, would develop cancer.

That is because, the integration of a piece of DNA plasmid itself at different sites in the human genome, without the existence of any kind of promoter will do it, and again, this has already been sequenced in human cancer tissue.

III. First, a bit about this occurring within human cells with bacteria:

Bacteria can release DNA through direct secretion or in the form of OMVs (Outer Membrane Vesicle). These vesicles can fuse with the membrane of human cells, delivering bacterial DNA into the cytoplasm. The cytoplasm of the cell is the part outside of the nucleus of the cell, which protects our genes.

Other bacteria have what is called "Type IV Secretion System", or a T4SS. T4SS allows bacteria to transfer DNA and proteins directly into the host cells.

example: Bartonella henselae, which uses its T4SS to transfer its plasmid DNA into human endothelial cells.

Bacterial DNA can enter the human cell by endocytosis, where the cell engulfs extracellular material, or via membrane fusion when OMVs merge with the human cell membrane, thus, releasing their contents into the cytoplasm.

The nuclear pore complex (NPC) facilitates the bidirectional transport of molecules between the nucleus and the cytoplasm. While DNA is typically too large to pass through NPCs, smaller bacterial genetic material can interact with nuclear transport proteins to enter the nucleus. This means that smaller pieces of DNA plasmid can make it in, through active diffusion of the nuclear core complex, because the DNA of a bacterial plasmid has a negative charge, and it is attracted to some of the components of interior of the nucleus which has a positive charge, because positive charges and negative charges are attracted to one another. Another way this can happen is integration during the cell cycle, specifically telophase.

bacteria can introduce double stranded breaks (DSBs) into the human genome (see the tweet below this one I am hopping off).
Bacteria can induce DSBs in human DNA through various mechanisms, like secretion of colibactin by E. coli, which alkylates DNA and induces DSBs. These breaks provide opportunities for bacterial DNA to integrate into the host genome during the repair process (see the post linked up below for more details on this process).

Bacteria can also engage in host DNA methylation and histone modification, affecting chromatin structure and gene expression, causing genomic instability, making it easier for foreign plasmid DNA to integrate.

Another way is through this mechanism called horizontal gene transfer. Once inside the nucleus, bacterial DNA can integrate into the human genome at sites of DNA breaks or within regulatory regions, such as promoters or enhancers, which can alter gene expression. Our DNA has its own promoters and enhancers, and it does not need an outside promoter like the SV40 to make an impact.

IV. How the DNA plasmids are going to effect different parts of our genome, and some highlights, regardless if this is coming from bacteria, or DNA plasmid contamination housed inside of a lipid nanoparticle:

Common Integration Sites

Intronic Regions (36%)
Non-coding regions within genes. DNA plasmid integration here might affect gene splicing and regulation.
Exon Regions (22%)
Coding regions of genes. Integration can disrupt gene function or create novel proteins. Novel proteins, as in junk what the heck is this doing in our bodies protein, the immune system is not going to be happy.

3’ UTR Regions (17%)
Regions involved in post-transcriptional regulation. Integration can impact mRNA stability and translation.

Hotspot Genes of Concern if we saw DNA plasmid Integration Occurring:

SNORD141A/B:
Ribosomal RNA processing.
MIR4507:
A microRNA that can regulate gene expression.
MALAT1:
A long non-coding RNA associated with cancer metastasis.
CD74, HLA-B, HLA-C:
Genes involved in immune response.

DNA plasmid pieces can be integrated nearby a tumor suppressor gene (which slows the growth) or a promoter, which allows for uncontrolled growth of cells/tumor. This does not ever ever have to be SV40 coming in, or any other promoter--it just needs a piece of DNA plasmid to land next to this site.

Activation of Proto-Oncogenes (pro cancer)

Integration of bacterial DNA into genes like CEACAM5 and CEACAM6 (upregulated in gastric adenocarcinoma) can convert proto-oncogenes into active oncogenes, leading to uncontrolled cell growth and cancer. No SV40 need. No RNA needed. No spike needed.

Inactivation of Tumor Suppressor Genes

Insertion into the TP53 gene, which encodes a critical tumor suppressor protein involved in DNA repair and apoptosis, can lead to loss of function, allowing cells with damaged DNA to proliferate, grow out of control, and drive cancer fast and hard.

V. Order of operations of DNA plasmid pieces entering a cell, specific sites of integration, how this is occurring, and how this could drive cancer, without the presence of ANY promoter:

1. plasmid DNA contamination which is enclosed in lipid complexes enters human cells via membrane fusion or endocytosis.

2. DNA transport to the nucleus is now occurring.
Once inside the cell, the plasmid DNA can interact with nuclear transport proteins to pass through the nuclear pore complex. It can also enter by diffusion, or by the charge signaling that acta as what is called NLS, a nuclear location signal. The negative charge on that DNA can force it through by attraction to the positive charges in the nucleus.
During cell division, plasmid DNA can enter the nucleus as the nuclear envelope disassembles.

3. DNA double-strand breaks, which can be induced by various cellular factors, provide sites for plasmid DNA integration. This is explained in detail in the other post I am piggybacking off of regarding DNA lesions, and active sites of repair, which are constantly happening, in the cells in our bodies.

4.Epigenetic modifications such as DNA methylation and histone modification may also occur, leading to chromatin remodeling, making integration more likely.

5. Integration can occur in intronic, exonic, or regulatory regions, affecting gene function.

6. Activation or Inactivation of Genes
A. Integration into proto-oncogenes or their regulatory regions can activate oncogenes.
B. Integration into tumor suppressor genes can inactivate them, removing growth inhibition.

7. Induction of Cancer.
Altered gene expression leads to uncontrolled cell proliferation, survival, and metastasis.

plasmid DNA in the genome further contributes to genomic instability and cancer progression.

VI. Cancers of concern, and spots in the genome if integration occurred, which can drive very specifics cancers to form:

Brain Cancer:
Proto-Oncogenes: EGFR, MYC, PDGFRA, MDM2
Tumor Suppressor Genes: TP53, PTEN, RB1, CDKN2A

Breast Cancer:
Proto-Oncogenes: HER2/ERBB2, MYC, CCND1, FGFR1
Tumor Suppressor Genes: TP53, BRCA1, BRCA2, PTEN

Uterine Cancer:
Proto-Oncogenes: PIK3CA, KRAS, CTNNB1
Tumor Suppressor Genes: PTEN, TP53, ARID1A

Pancreatic Cancer:
Proto-Oncogenes: KRAS, MYC, EGFR
Tumor Suppressor Genes: TP53, CDKN2A, SMAD4, BRCA2

Liver Cancer:
Proto-Oncogenes: CTNNB1, MYC, MET
Tumor Suppressor Genes: TP53, ARID1A, AXIN1

Lung Cancer:
Proto-Oncogenes: EGFR, KRAS, ALK, MYC
Tumor Suppressor Genes: TP53, RB1, STK11, CDKN2A

So how this works, is that pieces of the DNA plasmid, if the proper size, under the correct conditions, can integrate, and if those pieces of DNA plasmid, just ONE, can make an impact.

Integration Proximity
The integration of plasmid DNA into the human genome does not have to occur right next to a cancer-related gene (proto-oncogene or tumor suppressor gene) to have a significant impact.

However, the location of integration can influence the extent and nature of the effect.

Proximity to Proto-Oncogenes:

Activation of Oncogenes:
If the plasmid DNA integrates close to a proto-oncogene, it can disrupt regulatory elements or introduce strong promoters/enhancers that upregulate the expression of the oncogene. This can convert a proto-oncogene into an active oncogene, leading to uncontrolled cell growth and cancer.

Proximity to Tumor Suppressor Genes:

Inactivation of Tumor Suppressors:
Integration near or within a tumor suppressor gene can disrupt its coding sequence or regulatory elements, leading to a loss of function. This removes growth inhibition, allowing cells to proliferate uncontrollably.

Integration in Regulatory Regions:

Epigenetic Changes:
Integration in regions that regulate gene expression (such as promoters, enhancers, or insulators) can alter the chromatin structure and gene expression patterns. This can indirectly affect the expression of cancer-related genes even if the integration site is not immediately adjacent to them.

Intronic and Exonic Regions:

Gene Disruption:
Integration within introns or exons of cancer-related genes can disrupt normal gene function by introducing mutations or altering splicing patterns. This can lead to either a loss of function (tumor suppressor genes) or gain of function (proto-oncogenes).

Genes Implicated in Various Cancers and Their Potential Impact by Integration with a bit more information:

Brain Cancer:
Proto-Oncogenes:
EGFR, MYC, PDGFRA, MDM2Integration near these genes can upregulate their expression, leading to uncontrolled cell growth.
Tumor Suppressor Genes:
TP53, PTEN, RB1, CDKN2AIntegration disrupting these genes can inactivate them, removing growth inhibition.

Breast Cancer:
Proto-Oncogenes:
HER2/ERBB2, MYC, CCND1, FGFR1Upregulation due to integration can promote oncogenic activity.

Tumor Suppressor Genes:
TP53, BRCA1, BRCA2, PTEN
Disruption of these genes can lead to loss of tumor suppression.

Uterine Cancer:
Proto-Oncogenes:
PIK3CA, KRAS, CTNNB1Increased expression from integration can activate oncogenic pathways.

Tumor Suppressor Genes:
PTEN, TP53, ARID1A, inactivation from integration can lead to cancer progression.

Pancreatic Cancer:
Proto-Oncogenes:
KRAS, MYC, EGFR
Integration-induced activation can drive cancer development.

Tumor Suppressor Genes:
TP53, CDKN2A, SMAD4, BRCA2
Integration causing loss of function can lead to tumorigenesis.

Liver Cancer:
Proto-Oncogenes: CTNNB1, MYC, MET
Upregulated expression from integration can promote liver cancer.

Tumor Suppressor Genes:
TP53, ARID1A, AXIN1Disruption from integration can remove growth control.

Lung Cancer:
Proto-Oncogenes: EGFR, KRAS, ALK, MYC
Integration near these genes can lead to their activation.

Tumor Suppressor Genes:
TP53, RB1, STK11, CDKN2A
Integration disrupting these genes can contribute to lung cancer development.

So, if one was to look at whole genome sequencing from someone who was exposed to DNA plasmid with potential for integration, these would be some very important sites in the human genome to look especially if one was sitting there with a paraffin block from a liver cancer patient or colon cancer patient who had a recent DX of cancer after getting injected with an experimental drug that had no proper testing on it, especially genotoxicity testing, to see that perhaps, you could prove, the site of integration that correlates to the cancer tissue staring right back at you.

Colon cancer:
Proto-Oncogenes:
KRAS, MYC, BRAF, PIK3CA
Increased expression from integration can activate oncogenic pathways:
Integration of plasmid DNA near these proto-oncogenes can upregulate their expression. This activation can drive uncontrolled cell growth and proliferation, contributing to the development and progression of colon cancer.

Tumor Suppressor Genes:
APC, TP53, SMAD4, CDKN2A
Inactivation from integration can lead to cancer progression: Integration disrupting these tumor suppressor genes can result in their inactivation. Loss of function in these genes removes critical checks on cell growth and division, allowing for unregulated cell proliferation and the progression of colon cancer.

VII. The making of JUNK and HARMFUL PROTEINS, without ANY RNA, just the pieces of DNA plasmid:

Integration of Bacterial Plasmid DNA in Exon Regions

Exon Regions
These are the coding regions of genes that are transcribed into mRNA and translated into proteins. DNA makes RNA makes a protein. If you feck with that DNA, you will feck with your proteins.

Impact of Integration
Disruption of Gene Function
Frameshift Mutations without ANY RNA!
Integration of plasmid DNA within an exon can cause a frameshift mutation.

This occurs if the insertion disrupts the normal triplet reading frame of the gene, leading to the production of a nonfunctional or truncated protein.

For example, if bacterial DNA is inserted within the middle of an exon, the resulting protein might be significantly altered, losing its normal function, which could lead to disease or contribute to cancer development.

Nonsense Mutations
Integration can introduce a premature stop codon, leading to the truncation of the protein. This can produce a shortened, nonfunctional protein that may be rapidly degraded by the cell.

Missense Mutations
The insertion can change one amino acid in the protein sequence, potentially altering the protein's function. This can either reduce the protein's normal activity or, in some cases, confer new, potentially harmful functions.

Creation of Novel Proteins, AKA JUNK AND HARMFUL PROTEINS

Novel Fusion Proteins:
If integration occurs in a way that fuses plasmid DNA with host exon sequences, it can create a novel fusion protein.

This fusion protein may have new, unforeseen functions, some of which could be oncogenic (cancer-promoting).

For instance, fusion proteins can combine the functional domains of two different proteins, potentially activating signaling pathways that lead to uncontrolled cell growth.

Gain-of-Function Mutations (which is not to be used in the phrase gain of function that you typically see talked about, although, you could say this is double whammy gain of function)

Integration might lead to a gain-of-function mutation where the new protein formed has a novel, aberrant activity that promotes cancer progression.

For example, if the bacterial DNA integrates in a way that enhances the protein's stability or activity, it could lead to continuous cell signaling conducive to cancer.

Alteration of Protein Interactions:

Disruption of Protein-Protein Interactions
Proteins often function in complexes with other proteins.

Integration within an exon could alter the protein's interaction domains, disrupting its ability to form necessary complexes.

This could impair crucial cellular functions, such as DNA repair or cell cycle regulation, contributing to genomic instability and cancer.

Aberrant Localization:
Integration might affect the cellular localization signals within a protein.

This can mislocalize the protein within the cell, potentially placing it in a part of the cell where it can cause harm, such as in the nucleus where it might interfere with DNA replication or repair processes.

No SV40 needed. just pieces of DNA plasmid driving junk and harmful proteins to be expressed, that could drive autoimmune processes that have nothing to do with the RNA (that is also bad, we know this) and cancer. frontiersin.org/journals/cellu…

1/ Hydroxychloroquine. Many used this to treat C@vid, and recently Dr Drew on his show asked what drug is even considered safe in pregnancy--Hydroxychloroquine! But, it's not just antiviral.
Look what it is doing to cGAS! Could this treat those with specific vaccine injuries? 2/ "attenuating the underlying activation of the STING pathway mediated by cGAMP."

furthermore, "HCQ/CQ interfere with other pattern recognition receptors (PRRs) essential to the anti-viral response namely the cGAS–STING and RIG-I–MAVS pathways (Figure 1 and Table 1). "

1/ 🚨💉 Happy day (wherever you are). Regardless of current conditions, without jynxing it, "we" will hopefully be having a talk soon, and cGAS STING is going to come up. Layman's terms in these threads.

https://twitter.com/_HeartofGrace_/status/1794772733487624505

2/ "STING regulates intracellular DNA-mediated, type I interferon-dependent innate immunity"

ncbi.nlm.nih.gov/pmc/articles/P…

If you've heard of people with vaccine injuries feeling better after fasting, there's a reason for that and it has nothing to do with autophagy, it has to do with restriction of a certain amino acid and the interaction with cGAS STING (if the injuries are related to cGAS STING).
And with that being said you don't need to restrict your eating you just need to restrict a specific amino acid to achieve the same result (if it makes you feel better). There's literature on this. It's the restriction of a certain amino acid.
Methionine.
Methionine deprivation acts as a switch and it interacts with the release of cGAS from chromatin.
Methionine restriction allows for the engagement of chromatin untethering through demethylation. I'm not an MD and I can't DX or RX--check with your doctor always before starting anything

But methionine restriction diet is prescribed even with those who have cancer and the reason it has an impact on them is because of its interaction with cGAS STING.

🚨💉Here is a list of many types of cells that are tied to cGAS STING. cGAS STING can be activated by pieces of DNA plasmid that exists currently as contamination in the current mRNA covid vaccines that utilizes plasmids. MAST CELL--is but one type that has involvement.

Mast cells are involved in allergic reactions and defense against pathogens. They express cGAS and STING.
"Enrichment analysis showed that cGAS-STING was profoundly implicated in diverse immune-related pathways in KIRC, KIRP, and PCPG. Significant positive correlations were noticed between cGAS-STING score and TIICs, including activated CD8+ T cells, activated CD4+ T cells, monocytes, and mast cells"

NK cells are a type of cytotoxic lymphocyte critical for innate immune responses against virus-infected cells and tumors. They express cGAS and STING, contributing to their activation and effector functions.

Smooth muscle cells are found in blood vessels and various organs. They express cGAS and STING, contributing to vascular inflammation and immune responses in the context of vascular diseases.

Adipocytes, or fat cells, have been reported to express cGAS and STING. Their activation of the pathway may influence metabolic inflammation and immune responses in adipose tissue.

Cardiomyocytes are muscle cells of the heart. They express cGAS and STING, contributing to inflammation and immune responses in cardiovascular diseases--such as myocarditis

Osteoblasts and Osteoclasts are cells involved in bone formation (osteoblasts) and bone resorption (osteoclasts) express cGAS and STING, influencing immune responses and bone homeostasis.

Liver cells, known as hepatocytes, express cGAS and STING, contributing to immune responses during liver inflammation.

Renal Tubular Epithelial Cells are cells lining the renal tubules in the kidney express cGAS and STING, playing a role in kidney diseases.

Retinal pigment epithelial cells are cells in the retina express cGAS and STING, influencing immune responses and inflammation in the eye.

Smooth muscle cells are found in blood vessels and various organs. They express cGAS and STING, contributing to vascular inflammation and immune responses in the context of vascular diseases.

Dendritic Cells also known as DCs are crucial antigen-presenting cells of the immune system which express cGAS and STING.

Macrophages are phagocytic cells that also express cGAS and STING.

Neutrophils are another type of innate immune cell that expresses components of the cGAS-STING pathway.

Neutrophils are among the first responders to infection and inflammation.

B cells, which are responsible for antibody production, have been shown to express cGAS and STING, although their specific roles in B cell function are still being elucidated.

Endothelial cells lining blood vessels have been reported to express cGAS and STING, contributing to their function in immune surveillance and response.

Epithelial cells lining various organs and tissues, such as epithelial cells in the respiratory tract and gut, also express cGAS and STING, participating in local immune responses and barrier function.

Fibroblasts are connective tissue cells that support tissue structure and repair.
They have been found to express components of the cGAS-STING pathway, influencing their role in immune responses and tissue homeostasis. Mast Cell and cancer data:
ncbi.nlm.nih.gov/pmc/articles/P…

👀🚨💉🧬T CELLS (CD 4 and CD 8), have their OWN cGAS STING Pathway! DNA PLASMIDs can interact w/ cGAS STING OF T CELLS, causing FUNCTION of T CELLS to be: IMPAIRED, cause T CELL DEATH, IMPEDE T CELL PROLIFERATION, hindering an effective immune response, and CANCER progression.

(multiple studies will be employed--layman's terms throughout and at the end)

1. What are T Cells and where are they?

T cells are a type of lymphocyte central to the adaptive immune system. They are found throughout the human body, primarily in lymphoid tissues and organs.

T cells mature in the thymus gland, hence the name "T cells." The thymus is located in the upper chest behind the sternum, where immature T cells from the bone marrow mature and differentiate into various types of T cells that are capable of recognizing specific antigens. Differentiate means they go through a process which changes them into the "final product", into something that is more specialized in what it does, or what we would call the final thing. We have many cells in our body that do this.

Lymph nodes are small, bean-shaped structures distributed throughout the body along lymphatic vessels, which act as filters for lymphatic fluid, where T cells along with other immune cells encounter pathogens and antigens. Lymph nodes are abundant in areas such as the neck, armpits, groin, and abdomen.

The spleen is an organ located in the upper left abdomen, which filters blood and serves as a reservoir for immune cells, including T cells.

Although T cells do not originate in the bone marrow, it is a site where hematopoietic stem cells differentiate into precursor cells that eventually migrate to the thymus for maturation into T cells.

Mucosal tissues contain T cells, like the lining of the intestines, respiratory tract, and genitourinary tract. These tissues are entry points for many pathogens, and T cells play a crucial role in defending against infections at these sites.

T cells circulate throughout the bloodstream, allowing them to quickly respond to infections and move to sites of inflammation or infection.

2. What could go wrong?

So would you think it would be a bad thing, if you did not have properly functioning T cells in these areas, or that if a bunch of them died off, the body might have a more difficult time fighting off an infection?

This is a very complicated process--we are just looking at highlights form some studies that found activation of the cGAS STING pathway, the special cGAS STING that is for T Cells, can cause them to not function properly, change them into something else, or kill them.

The first study used many methods and controls to look at what happens to T Cells when their own cGAS STING pathway is activated (we are sticking with the smoke alarm analogy for T cells).

3. Diving a bit deeper into what happens when the cGAS STING of T cells become activated (by DNA plasmid would do it):

Activation of the cGAS-STING pathway in CD4 and CD8 T cells leads to the production of antiviral cytokines such as IFNβ and IP10, which are part of the immune response against viral infections.
However, despite the beneficial antiviral response, the activation of cGAS-STING in T cells has several detrimental effects:

Increased Cell Death
There is an increase in apoptosis (programmed cell death) of T cells.

Impaired Proliferation
T cell proliferation is significantly impaired, which hinders their ability to expand and mount an effective immune response.

Metabolic Impairment
There are disturbances in cellular metabolism, including impaired glycolysis and mitochondrial function, which are critical for T cell energy production and function.

4. Heavy science time for a bit, and then swinging back around to terms that are more understandable at the end:

The impairments observed in T cells upon cGAS-STING activation involve mechanisms that are both IRF3-dependent and IRF3-independent. IRF3 is a transcription factor involved in the expression of interferons and other immune response genes. The specific pathways leading to impaired T cell function include NF-κB-mediated antiproliferative effects, ER stress-induced cell death, and IRF3/IRF7-mediated inhibition of mTORC1, among others.

5. Let's look at the cGAS STING pathway that T cells do possess (and how it has been proven):

STING Activation in Human T Cells (the study)
STING, a key component of the cGAS-STING pathway, is functional in human primary T cells. When these T cells were treated with the physiological STING agonist 2′‐3′‐cGAMP (cGAMP), it induced phosphorylation of STING (pSTING) and IRF3 (pIRF3), which are critical steps in signaling through this pathway.
While cGAMP alone induced some level of STING and IRF3 phosphorylation, the activation was significantly enhanced when T cells were simultaneously activated through their T cell receptor (TCR) using αCD3/CD28 antibody-coated beads. This suggests that TCR engagement is necessary for robust activation of the cGAS-STING pathway in T cells.

The activation of STING in conjunction with TCR stimulation led to the production of antiviral factors such as IFNβ and IP10. These cytokines are critical for mounting an immune response against viral infections, indicating that T cells can indeed utilize the cGAS-STING pathway to produce these protective factors.

The study also emphasizes that the synergistic effect of STING and TCR stimulation occurs at a cell-intrinsic level, implying that T cells themselves are capable of integrating these signals to initiate an immune response.

6. How activation of this pathway in T CELLS can lead to an impaired or dysregulated response (or T cell DEATH)

Activation of STING in T cells leads to increased apoptosis (programmed cell death). This process is mediated by the transcription factor IRF3, which upregulates pro-apoptotic BH3-only proteins such as Noxa (PMAIP1). This mechanism was observed in both human and murine T cells (Gulen et al., 2017).

STING activation in T cells also inhibits their ability to proliferate. This effect is independent of IRF3 and is mediated through a distinct domain within STING's C-terminal tail (miniCTT), which disrupts the mTORC1 pathway involved in cell cycle progression (Cerboni et al., 2017).

Activation of STING alters metabolic pathways in T cells, impairing their ability to perform glycolysis and mitochondrial respiration, which are essential for energy production and cell function during activation and proliferation (Imanishi et al., 2019).

While type I interferons (IFNs) are produced upon STING activation in T cells, they do not rescue the impaired functions. Instead, they contribute to the overall dysregulation of T cell function observed in these contexts (Benoit-Lizon et al., 2022).

WHY DOES THIS MATTER?

A.) T CELLS ARE NO LONGER FUNCTIONING PROPLERY AFTER THEIR OWN cGAS STING PATHWAY HAS BEEN ENGAGED!

B.) Activation of the cGAS-STING pathway in T cells leads to increased cell death, impaired proliferation, and compromised metabolism.
This can diminish the overall effectiveness of T cell responses against viruses because T cells are critical for coordinating and executing adaptive immune responses--rendering them ineffective.
USELESS T CELLS!

C.) While the cGAS-STING pathway can trigger the production of antiviral cytokines like type I interferons, this activation also disrupts essential T cell functions, limiting the ability of T cells to proliferate and differentiate into effector cells needed to combat viral infections effectively.

D.) Long-term bad news bears
Prolonged or excessive activation of the cGAS-STING pathway in T cells could have long-term consequences for immune system health. It may lead to chronic immune dysfunction or contribute to conditions where T cell responses are dysregulated, such as autoimmune diseases or chronic viral infections, and CANCER.

E.) CANCER IMPLICATIONS:

T cells are essential for mounting an effective immune response against cancer cells.
Activation of the cGAS-STING pathway in T cells leads to functional impairment, including decreased proliferation and increased apoptosis, which reduce the ability of T cells to effectively target and eliminate cancer cells, thereby weakening the antitumor immune response.
STING activation in T cells also disrupts metabolic pathways necessary for their activation and function. This metabolic impairment can limit the energy and resources available to T cells, compromising their ability to sustain their needed defense against cancer.

In some contexts, STING activation has been associated with promoting tumor growth and immune evasion mechanisms. While STING activation can induce an initial immune response, chronic activation or dysregulation may lead to mechanisms that support tumor survival and growth, potentially through effects on the tumor microenvironment or regulatory T cells (Tregs).

******************************************************
Layman's Terms for what this means :

Imagine cGAS-STING as a smoke alarm system inside your house (representing T cells).
Its job is to detect danger signals (like DNA or damaged cells) and alert the immune system (like alerting the homeowner to a potential fire).

Impairment of T Cell Function

Normally, T cells are like firefighters that detect and eliminate cancer cells. When cGAS-STING is overly active, it's like the smoke alarm constantly going off, which exhausts the firefighters (T cells). They become less effective at finding and fighting cancer cells.

Energy Drain Time (Metabolic Dysregulation)

cGAS-STING activation in T cells disrupts their energy production, making it harder for them to stay active and fight cancer. It's like the firefighters not having enough energy to respond quickly to fires.

Mixed Signals Time (Promotion of Tumor Growth)

Sometimes, the smoke alarm (cGAS-STING) sends confusing signals. It might initially help by alerting the immune system, but if it keeps going off, it can disrupt the immune response and even help the fire (tumor) grow instead of putting it out.

The Immune System Gets WEAK

Weakened Defense: Overactive cGAS-STING in T cells weakens their ability to defend against infections and cancer. It's like having tired firefighters who can't respond effectively to emergencies.

Chronic Stress Hurts the T Cells

Continuous activation of cGAS-STING stresses out T cells, making them more prone to dysfunction. It's like the smoke alarm constantly buzzing, which wears out its batteries and makes it less reliable.
Impact on Cancer:

Mixed Bag

While cGAS-STING activation can initially boost the immune response against cancer, prolonged or excessive activation might paradoxically support tumor growth.

It's like the smoke alarm causing confusion: sometimes it helps detect the fire (cancer) early, but if it malfunctions, it might inadvertently make things worse.

Has anyone talking about how the mRNA vaccinations are impairing T cell function?

It would be really bad if there was a bunch of DNA in there, or something else in there activating the cGAS STING in T cells--and ni the thread below, you will see, that even in SMALLER AMOUNTS, LONGER pieces of DNA while HAMMER on the switch for cGAS STING.

That would be bad if it hit your cGAS STING of your T cells, would it not?

There ya go. 2/"STING agonism turns human T cells into interferon-producing cells but impedes their functionality"
ncbi.nlm.nih.gov/pmc/articles/P…

🚨💉🧬COVID-19-Induced Sporadic Inclusion Body Myositis" case study..."she has been vaccinated with two-dose series of the COVID-19 vaccines..."
Now we tie cGAS STING to GSK-3, and the implications of disease, especially, amyloid (no spike needed!) Layman's terms at end!

Case Study:
A 54-year-old female with a history of asthma, hyperlipidemia, and type II diabetes mellitus presented with persistent fatigue and myalgias affecting her extremities.

Despite ruling out autoimmune causes and statin-induced myalgias, symptoms worsened.

Muscle biopsy revealed features of acquired inflammatory myopathy with rimmed vacuole-type structures, TDP-43-p62 positive intranuclear inclusions, and amyloid-like inclusions, consistent with sporadic inclusion body myositis (sIBM).

GSK-3 and Inclusion Body Myositis (IBM)

GSK-3β, is implicated in sIBM due to its role in protein aggregation similar to that seen in Alzheimer's disease.

GSK-3β regulates inflammatory responses and may contribute to chronic inflammation observed in IBM through pathways involving NF-κB, IL-1β, and TNF-α.
Its role in tau phosphorylation and inflammatory
signaling suggests a link to the pathological features observed in sIBM, including amyloid-like inclusions.

DNA Plasmid Exposure and cGAS-STING Pathway Activation--GSK-3 downstream effects:

DNA plasmid exposure can activate the cGAS-STING pathway.

cGAS detects cytoplasmic DNA, including plasmid DNA, leading to the production of cGAMP and activation of STING.

STING activation drives an immune response characterized by type I interferon production and inflammatory cytokine release.

Chronic activation of cGAS-STING can exacerbate neuroinflammation and promote protein aggregation, similar to observations in AD and potentially in IBM.

Case study analyzed through cGAS GSK-3 lens:

The patient's symptoms and biopsy findings align with chronic inflammation and protein aggregation seen in IBM.
GSK-3β's role in inflammatory pathways and protein regulation may exacerbate these pathological processes.
Exposure to DNA plasmids could further activate inflammatory pathways via cGAS-STING, contributing to disease progression.

Laboratory findings such as elevated CRP and myoglobin may reflect ongoing inflammation and muscle damage associated with sIBM.

:The integration of GSK-3β in inflammatory pathways, DNA plasmid exposure, and cGAS-STING activation just may account for the chronic inflammation and pathological protein aggregation observed in sIBM.

Further breakdown:

GSK-3 is a key player in how proteins are managed in our cells. It's known to help proteins clump together, similar to what happens in Alzheimer's disease.
In this woman's case, GSK-3 might be playing a role in causing inflammation in her muscles through pathways that involve chemicals like NF-κB, IL-1β, and TNF-α.
It also seems to affect how another protein called tau behaves, which is crucial for healthy nerve function. When tau is altered, it can lead to problems with the nerve cells.

When DNA plasmids get into our cells, they can set off a "smoke detector" system called cGAS-STING. This system is there to alert our immune system that something foreign is inside our cells.

When cGAS senses the DNA plasmids, it starts a chain reaction that leads to the production of certain signals. These signals then activate STING, which tells our immune system to get ready for a fight by releasing substances that cause inflammation.

If this system stays active for too long, it can lead to more inflammation and even cause proteins to clump together inside cells, similar to what happens in diseases like Alzheimer's and possibly in sIBM.

This woman's symptoms and what was found in her muscle biopsy fit with what we know about sIBM—a condition where muscles become inflamed and proteins clump up inside cells.

GSK-3 might be making things worse by causing more inflammation and affecting how proteins behave in her muscles.

If she was exposed to DNA plasmids—it could have triggered her immune system through the cGAS-STING pathway, adding to the inflammation and protein clumping. /2

ncbi.nlm.nih.gov/pmc/articles/P…

🚨💉FOIA Update: Response I am sending to the FDA to Appeal their decision to not release contamination records at all sites Pfizer and Moderna (Catalent). I am flying Han Solo on this one (no legal assist, yet).
CEBR/FDA will see it shortly (you might as well see it too). I am sending this over, with the safety signals quoted, and a few other nuggets (I cited their own provisions and some landmark cases):

💉1. 21 C.F.R. § 20.67: Disclosure of Identities of Confidential Sources
Regulation quoted by the FDA in the denial of the FOIA:

21 C.F.R. § 20.67(a): "The names or other information which would identify a person providing information to the FDA concerning a possible violation of the laws administered by the FDA will not be disclosed."

✅My Argument:

Contamination records typically do not involve confidential sources or informants. Therefore, this regulation should not apply, as the primary concern is public health, not the identity of sources.

The FDA's recall process involves public notifications about contaminated products to protect consumers (21 C.F.R. § 7.40-7.59).

FDA’s mission (21 U.S.C. § 393) focuses on protecting public health.

💉2. 21 C.F.R. § 20.61: Trade Secrets and Confidential Commercial Information
Regulation quoted by the FDA in the denial of FOIA release:

21 C.F.R. § 20.61(b): "Commercial or financial information which is privileged or confidential means valuable data or information which is used in one's business and is of a type customarily held in strict confidence or regarded as privileged and not disclosed to any member of the public by the person to whom it belongs."

21 C.F.R. § 20.61(c): "Data and information submitted or divulged to the Food and Drug Administration which fall within the definitions of a trade secret or confidential commercial or financial information are not available for public disclosure."

✅My Argument:

The information requested does not qualify as trade secrets or its disclosure is necessary for public safety.
Public interest in accessing contamination records outweighs the potential harm of revealing trade secrets.

The case Public Citizen Health Research Group v. FDA, 704 F.2d 1280 (D.C. 1983): Favored the disclosure of adverse reaction reports, emphasizing the significance of public access to safety information.

FDA’s mission (21 U.S.C. § 393): Emphasizes the importance of protecting public health.

💉3. 21 C.F.R. § 20.83: Special Disclosure of Records Related to Health and Safety
Regulation quoted by the FDA in the denial of FOIA release:

21 C.F.R. § 20.83: "The Commissioner of Food and Drugs may, in his discretion, disclose records or information that are exempt from mandatory disclosure whenever he determines that such disclosure is in the public interest and promotes the objectives of the act and the agency."

My Argument:

Contamination records are critical for public health and safety and should be disclosed under this provision.
Public health and safety take precedence over confidentiality concerns when it comes to potential health hazards.
FDA’s discretionary disclosure policy allows for the release of information when it is in the public interest.

Supporting References:

National Archives and Records Administration v. Favish, 541 U.S. 157 (2004): The public interest in disclosure can outweigh the need for confidentiality.

Public Citizen Health Research Group v. FDA, 704 F.2d 1280 (D.C. 1983): Disclosure of adverse reaction reports is important for public safety.

Environmental Defense Fund, Inc. v. U.S. Department of Health, Education, and Welfare, 428 F.2d 1083 (D.C. 1970): Supports disclosure of information affecting public health and safety.

FDA’s mission (21 U.S.C. § 393): Emphasizes the importance of protecting public health.

4. 21 C.F.R. § 20.81: Data and Information Previously Disclosed to the Public

💉Regulation quoted by the FDA in the denial of the FOIA:

21 C.F.R. § 20.81(a): "Any data or information that has already been disclosed to the public in an authorized manner is available for public disclosure."

✅My Argument:

If any portion of the contamination data has been previously disclosed, the remainder should also be disclosed to ensure completeness and public understanding.
The public has a significant interest in complete information.

Supporting References:

Environmental Defense Fund, Inc. v. U.S. Department of Health, Education, and Welfare, 428 F.2d 1083 (D.C. 1970): Supports the disclosure of information affecting public health and safety.

Public Citizen Health Research Group v. FDA, 704 F.2d 1280 (1983): Favored the disclosure of adverse reaction reports, emphasizing the importance of public access to safety information.

Washington Post Co. v. U.S. Department of Health and Human Services, 690 F.2d 252 (D.C. 1982): Discusses the balance between public interest and confidentiality of commercial information, favoring disclosure when public health is concerned.

Department of the Air Force v. Rose, 425 U.S. 352 (1976): Held that Exemption 6 of the FOIA (personal privacy) does not cover information that has already been made public.

FDA’s mission (21 U.S.C. § 393): Emphasizes the importance of protecting public health.

💉5. Rebuttal to Glomar Response ("Neither Confirm Nor Deny")
FOIA Exemption and Glomar Response:

"The FDA can neither confirm nor deny the existence of records that would be responsive to your request, as doing so could reveal confidential commercial information."

✅My Argument:

The public interest in accessing contamination records, especially those related to public health and safety, outweighs the potential harm of revealing confidential commercial information.

Contamination records related to public health concerns do not typically contain confidential commercial information.

Supporting References:

The case National Archives and Records Administration v. Favish, 541 U.S. 157 (2004): Acknowledged that FOIA exemptions must be balanced against the public interest in disclosure.

Public Citizen Health Research Group v. FDA, 704 F.2d 1280 (D.C. 1983): Favored the disclosure of adverse reaction reports, emphasizing the significance of public access to safety information.

Environmental Defense Fund, Inc. v. U.S. Department of Health, Education, and Welfare, 428 F.2d 1083 (D.C. 1970): Supports the disclosure of information affecting public health and safety.

FDA’s policy of transparency (21 C.F.R. § 20.61):
Details the types of information exempt from disclosure, but allows for the release of safety-related information.

FDA’s discretionary disclosure (21 C.F.R. § 20.82): Allows the Commissioner to disclose records when it is in the public interest.

FDA’s mission (21 U.S.C. § 393): Emphasizes the importance of protecting public health.

I will be adding a bit more language, and a few other integral pieces to the rebuttal.

Fingers crossed! @drdrew
@DrJBhattacharya
@drjamesbjoyce
@SenatorRennick
@ABridgen
@FLSurgeonGen
@RepThomasMassie

🚨💉🏥

.researchgate.net/figure/Chloroq…

🚨💉"Severe ulcerative colitis induced by COVID-19 vaccination
Takashi Taida et al. Clin J Gastroenterol. 2024 Jun."

And

"A molecular subtyping associated with the cGAS-STING pathway provides novel perspectives on the treatment of ulcerative colitis"--June 2024

.pubmed.ncbi.nlm.nih.gov/38349435/#:~:t…

🚨💉⚕️This is how I figured out PROGRANULIN is a MAJOR player in MANY VACCINE INJURIES. It was not just looking at current treatments, it was looking at TWO drugs that made things WORSE. I've been posting to help MDs help the vaccine injured.
It started with cGAS STING:

A. First it started with threads I made last year on cGAS STING, and I was making substack posts about it. The more I looked, and with the work of those who tracked DNA plasmid levels in vials versus VAERS reports--Speicher, Weissman, and others found a correlation between the amount of DNA plasmid in a vial was correlated to the number of VAERS records. When I looked at the website, How Bad is My Batch, I looked up the batch numbers they linked up, and myocarditis was at the top. So I knew cGAS STING was implicated.

cGAs STING is the thing that can detect foreign DNA plasmids, DSRNA, viruses, DNA from our own cells, from mitochondria, and bacteria. cGAS STING actually has an on/off switch, called CRL5-SPSB3 ubiquitin ligase, but it is such a recent discovery, no scientist that I know of on the planet has started researching how to turn it OFF.

cGAS STING is implicated in inflammation, stroke, autoimmune, myocarditis, aortic dissection, neuropathies, and sadly, CANCER.

So I broke down cGAS STING, and drew it out on a piece of paper, and then I looked at what is called the cGAS STING AXIS. cGAS STING isn't just a pathway, it is an AXIS.

B. I saw the work of Patterson and Yogendra. I heard they were prescribing Doxycycline, Maraviroc, and something else for some people for mitochondria dysfunction. I looked at their panels they post on IncellDX. I looked at each marker they were testing for, and everything seemed inflammatory. This did not make complete sense to me, because I had heard people had burning pain but not so much inflammation. I heard vaccine injured had small fiber biopsies done, and lumbar puncture, and lip biopsy, and there were people that mainly had this burning pain, but no sign of real inflammation. And they all kept saying it was spike. And it had to be inflammatory. And I knew that in some cases, YES to cytokine because some vaccine injured shared their labs with me--but the labs I knew had to be incomplete.

So I wrote down their tests, and I looked up to make certain the full action of both those drugs, on cGAS STING and the whole AXIS. I made a chart. I wrote down each part of the cGAS STING AXIS that doxycycline and Maraviroc acted on.

C. I knew some people were taking prednisone. I knew others, VERY FEW were on IVIG. I looked at the mechanism of action for both of those, on the cGAS STING pathway.
( I have all of the specifics written down).

D. THEN, I had heard there were two supplements/drugs that people with burning pain who are vaccine injured, existing burning pain, had taken, that made them WORSE. And it was the first one I looked at, that was key. I knew that because this supplement was being given because doctors (you tried, I do not blame you for that, but this is not a pathway you can just throw a wrench at, it is delicate, and I wondered if it actually SWUNG the response BACK in the other direction, because it is a MODULATOR of sorts and like LDN, some got worse, and that is because MODULATORS of the immune system, or other things, do not just fine turn like a radio dial to this perfect number that works for people, that is incorrect. It will either suppress the immune system, or drive it back harder. OR it will do something else.

What was the supplement that doctors told their vaccine injured patients to take for the burning pain?

Alpha Lipoic Acid.

I was lucky enough, to find one very serious research article on the exact mechanism of alpha lipoic acid, and that it not only works on the PAIN RECEPTORS (which can be ACTIVATED WITH OR WITHOUT CYTOKINES--YOU DO NOT NEED INFLAMMATION FOR PAIN RECEPTOR ACTIVATION).

So then, I went after that mechanism, and I traced it back to the pathway and AXIS of cGAS STING and where it was interacting, and with what.

This study, looked at :
Serum PGRN levels (Progranulin)
Serum levels of TNFα
Oxidized low-density lipoprotein (oxLDL)
Intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) measurement

And I looked back at IncellDX, and it was cytokine, spike panels, VEGF etc, but no progranulin, and no ICAM-1 or VCAM-1

The above markers are what was measured in patients who were taking alpha lipic acid for diabetic neuropathy.
The study used 54 patients, including a control group. And they tested other markers too, but these were the four of significance.

E. So then I looked at the pathways again--and I looked at all of the moving parts not just of cGAS STING, but of the entire AXIS itself.

These are some of the markers on my list:
Cytokines and Interferons
Type I Interferons (IFNs)IFN-α
IFN-β
Pro-inflammatory Cytokines
Tumor Necrosis Factor-alpha (TNF-α)
Interleukin-6 (IL-6)
Interleukin-1 beta (IL-1β)
Interleukin-18 (IL-18)

Anti-inflammatory Cytokines
Interleukin-10 (IL-10)

Interferon-Stimulated Genes (ISGs)

ISG15
Mx1
OAS1
IFIT1
RSAD2 (Viperin)

PKR (Protein Kinase R)
IFI16
Other Proteins/ Markers
cGAS (Cyclic GMP-AMP Synthase)
cGAMP (Cyclic GMP-AMP)
STING (Stimulator of Interferon Genes)
TBK1 (TANK-binding Kinase 1)
IRF3 (Interferon Regulatory Factor 3)
NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells)
Progranulin
MAVS (Mitochondrial Antiviral Signaling Protein)
TRAF6 (TNF Receptor-associated Factor 6)
CYLD (Cylindromatosis)
Ddx41 (DEAD-Box Helicase 41)
IFI204 (Interferon-Inducible Protein 204)
Chemokines
CXCL10 (IP-10)
CCL5 (RANTES)
CXCL9 (MIG)
CCL2 (MCP-1)
Additional Markers
HMGB1 (High Mobility Group Box 1)
Lactate Dehydrogenase (LDH)
C-reactive Protein (CRP)

F. So then I looked at that list, and again, I heard there were some people with vaccine injuries that had pain, and that is NOT that it was not severe, or that this does not discount those who have died, those who are disabled, those who are dying, and in the worst pain of their lives--no. I was looking for something they all had in common:

PGRN/GRN: Progranulin.

Progranulin can show up when you are in pain without the other markers, but that does not mean that people do not also have cytokines, etc.

cGAS or STING is not a viable lab people can just have done.

BUT, PROGRANLIN, IS.

Then I looked at everything progranulin was implicated in, all the tissues of the body, the autoimmune, the cancer, the vasculitis, the heart disease--so many things.

I know people are trying hard to find solutions to those with injuries.

however, this single marker, has already been implicated, in the diseases I listed in the threads below, and these diseases, correlate to reported in literature, vaccine injury cases, which are including, but not limited to:
ANCA-Associated Vasculitis
Sjogren's
Progranulin Deficiency Induces Mitochondrial Dysfunction in Frontotemporal Lobar Degeneration
Cancer

There needs to be more testing done for those with injuries to help them.

This is but a start.

If you are a serious MD, and you want to start doing serology tests on vaccine injured with autoimmune and neuropathy, with or without inflammation markers, I am going to pin this thread.

Let other people do the politics, etc.

I do not have the time to get roped into individual conversations, chat groups, etc.

If you are a group of doctors, there might be solutions that can be worked on.

We cannot be stuck with nattokinase and prednisone.
These people need help.
And we have to start somewhere.

Thanks journals.sagepub.com/doi/10.1177/03…

🚨💉 Attention doctors, other medical staff, and vaccine injured (not meant to RX or DX)
PGRN/GRN: progranulin is a protein expressed by the GRN gene. Progranulin is known to be expressed in certain cancers, neuropathy, neurodegeneration, Alzheimer's, sjogrens, other autoimmune, autoimmune vasculitis--lots of implications. This is present in numerous types of disease.
I can't ask anyone to test for this. However, this might be something to look into. ncbi.nlm.nih.gov/pmc/articles/P…

1/ 🚨💉How Chronic inflammatory demyelinating polyneuropathy (CIDP) is caused by cGAS STING pathway interactions--Case Studies: patients experiencing AIDP after AstraZeneca COVID vaccine.
(case study discusses aberrant MHC class II expression, but that might not be the case). 2/ In CIDP, the immune system attacks the myelin sheath of peripheral nerves.
The chronic production of inflammatory cytokines can lead to demyelination, which is a hallmark of CIDP.

mdpi.com/2673-5601/2/1/9

1/ 🚨💉🦠🧬 It would be a terrible thing to introduce something into the colon, especially when a polyp is already present (which forms from mutations in the crypt), that would activate the cGAS STING pathway in the area (such as DNA plasmid/spike)

https://twitter.com/_HeartofGrace_/status/1790563365338644827

2/

1/🚨💉Reasons Why Women Suffer More Adverse Events From Vaccines and mRNA Injections Compared to Men: Revised Stack--Republished w/ cGAS STING Path and Genetics Edition.
TL;DR: Variations in cGAS STING pathway, immune system, hormones, and genes—XX versus XY--are the reasons. 2/ After menarche, the cyclic fluctuations of estrogen and progesterone during the menstrual cycle can affect the immune system. Estrogen has been associated with enhancing immune responses, promoting antibody production, and potentially exerting anti-inflammatory effects.

1/💉🚨 mRNA "vaccines" contain DNA plasmid, and spike protein, which can activate a pathway--cGAS STING, and drive ONCOGENE EXPRESSION and MUTATIONS W/OUT SV40!!
"cGAS-STING pathway expression correlates with genomic instability and immune cell infiltration in BREAST CANCER" 2/ The Study:
cGAS-STING pathway expression correlates with genomic instability and immune cell infiltration in breast cancer

nature.com/articles/s4152…