1/ 🚨🚨 Varma is Chief Tech/Sci/R&D Officer at SIGA TECH
🚨Detected/Suspected Collaborations w/ Evidence of SIGA TECH:
1. Biomedical Advanced Research and Development Authority (BARDA)
2. U.S. Department of Defense
3. CDC, WHO, NIAID, and academic institutions.

Details (receipts with archives in posts below in the thread):

🚨Biomedical Advanced Research and Development Authority (BARDA)
Approximate dates:
Contracts initiated in 2014, w/ subsequent modifications through 2024 and continuing:
Development and procurement of TPOXX (tecovirimat) for public health preparedness against smallpox and other orthopoxvirus.

🚨U.S. Department of Defense (DoD)
Collaborations began around 2014 and continue to the present. Research and development initiatives focusing on antiviral efficacy against biological agents, "enhancing national security".

🚨Centers for Disease Control and Prevention (CDC)
Ongoing partnerships since at least 2014. Purpose: Public health initiatives aimed at preparedness and response strategies for infectious disease outbreaks, including public awareness regarding antiviral treatments.

World Health Organization (WHO)
🚨Discussions and potential collaborations initiated in 2020.
Addressing global health threats and improving access to antiviral therapies, especially in low-resource settings.

🚨National Institute of Allergy and Infectious Diseases (NIAID)
Collaborative research started around 2016 and is ongoing. Purpose: Joint research projects to develop therapeutics for viral infections and evaluate antiviral compounds.

Academic Institutions (specific collaborations may vary)

(see attached posts for details. these might need editing/updating with more information or corrections) 2./ Jay Kumar Varma
Chief Tech/Sci/R&D Officer at SIGA TECHNOLOGIES, INC.
Net worth: 156 201 $ as of 2024-08-30

Archive: archive.ph/WN41j#selectio…

1/ 👀🚨⚕️⚕️Happy Sunday! How I sped up the healing of my torn hip that I was told I needed surgical intervention on (I have not had any surgery on it!!!):

I was told I needed medical intervention on my hip after imaging showed tear of the anterosuperior labrum from 12:00 to 3:00, an additional partial tear of the distal left gluteus medius tendon, and suspected occult fracture of the femur.

I do some pretty serious trail running and I jump over downed trees and I go very quickly. I make tracks fast. However I'm getting older and I have EDS confirmed by an actual EDS doctor so I am prone to these injuries. I work out anyways because it is the best protection for someone with EDS. Lift weights and workout. Joint tears are a thing for me--I am no stranger to them, and I HAVE had several joint reconstructions because of sports injuries, but not this time.

I do not drink or do drugs and I have not been one to do those things--I am not in recovery. I have eaten a primary whole food diet since I was a baby. We grew up with gardens and I have continued that. I am a long time martial artist, I have played in sports in school, and I am a distance runner cross-country ultra runner and I am 49 years old. I have to believe this is why I don't have any wrinkles at age 49 even though I only use soap on my face, and why I heal faster even though I can get injured a bit easier.

I've been doing some research on the injection injuries and those with lingering viral symptoms. I've been looking at macrophages and I know our friend doorless carp has too.

Macrophages exist on a spectrum. They are part of your immune system and the cleanup process. There are macrophages called m1 and M2. You have an inflammatory type and an anti-inflammatory type but there are subtypes and they are very adjustable and they are known to have what is called plasticity.

It's not like an on/off switch and I think that's where a lot of people even doctors and scientists will get confused thinking you can just flip things. They can actually exist in both states at the same time and you do not want to have just an entire mess of your macrophages to be in an anti-inflammatory state because you need the ones that attack not just heal. M1 macrophages are pro-inflammatory and M2 are anti-inflammatory.

Knowing that I don't drink soda or juice and I also primarily just drink water, green tea, and black coffee with whole foods mostly I started a couple of supplements that are known to shift macrophages from the pro-inflammatory type that are activated by cytokines to the m 2 type which are anti-inflammatory.

When I went for my initial MRI of my hip I was placed on a stronger MRI machine compared to the regular one people usually go on which is 15 times stronger than a regular MRI. I noticed the next day my hip felt a little better and I wondered why and I thought holy smokes did the strong magnets of the MRI just flip my macrophages (I've been doing other writing on a different paper involving macrophages I also plan to submit to publication).

So I searched journals and I found a study really quickly that shows when mice were subjected to different strengths of MRI they had a strong correlation in their macrophages flipping from the inflammatory type to the anti-inflammatory type and the stronger the MRI the stronger that response was. The researchers also found that the mitochondria shifted in the cells and a few other things happened.

I'm not suggesting anyone do this. This is not medical advice. Always check with your doctor.
So I thought I should do what any smart person would do because the MRI is targeting the area--find a way to get them to do it again!!!!
So I hopped up on that stronger version of the Tesla 3 MRI to get my hip scanned again.

I know that I'm not completely healed but I am now walking faster about 3 to 5 mi a day out hiking now and I know that I'm going to jog very soon.

I'm taking it easy so I don't accidentally re-injure myself.

My doctors are baffled.

I sent them this study in the second tweet. 2/ "The Effect of Magnetic Field Gradient and Gadolinium-Based MRI Contrast Agent Dotarem on Mouse Macrophages"

ncbi.nlm.nih.gov/pmc/articles/P…

1/ Study: Ivermectin Promotes Peripheral Nerve Regeneration during Wound Healing.
I am uncertain if anyone has spoken about nerve healing with Ivermectin
I wondered if people w/ burning pain were getting better w/ ivermectin because it was healing nerves, not spike related. 2/ here is the study and my substack reviewing the study:



pubs.acs.org/doi/10.1021/ac…
christiegrace.substack.com/p/study-iverme…

1/ 🚨 👀 This is very concerning and it requires additional posting.

"Right now in the US, Lockheed Martin is close to completing a prototype that will analyze media to “detect and defeat disinformation.”

And by media, those commissioning the tool – called the Semantic Forensics (SemaFor) program – mean everything: news, the internet, and even entertainment media. Text, audio, images, and video that are part of what’s considered “large-scale automated disinformation attacks” are supposed to be detected and labeled as false by the tool."

"The development process is almost over, and the prototype is used by the US Defense Department’s Defense Advanced Research Projects Agency (DARPA)."

Maybe some of you can chime in on the implications of this, if they aren't obvious enough. 2/ reclaimthenet.org/darpa-system-c…

Timeframe for possible cancer risk (growth formula included at end). We will use calculations AND LOVE CANAL CHEMICAL EXPOSURE example (something I wrote about in undergrad). These are just my concerns. Cancer is not a mathematical calculation, it is exponential when it comes to onset and exposure of populations to a genotoxin.

The cancer experts who have been interviewed SHOULD have told you that. Maybe a cancer expert can chime in (and do not give the "bad luck" hypothesis):

The obvious scenario is a known genotoxic/mutagenic substance was injected into billions of people on the planet, some of them, more than once, and there is serious concern that this known harm can cause genetic instability and worse.

If we do not even look at pseudouridine content in the modified RNA or spike protein, from what I have read and my knowledge working in industry and education is the following:

If we introduced just the linearized DNA plasmid pieces alone inside of a lipid nanoparticle and injected them into people, this will vary depending on how many exposures have occurred--each exposure meaning a single injection (discount RNA or anything else in there--this is just hypothetical for DNA):
Time frames (we are working off March 2021 as that as when general population was getting the first of the "series"):

1. First Window of Time for Cancer Risk: 0-2 Years out from initial exposure
0-2 years out will see the LOWEST number of cancers. We would see acute reactions--the immediate toxicity or inflammation.
Cancer rates should be the lowest during the first two years (that is the time we are now exiting, we are entering the next window of time), but aggressive hematological cancers ( acute leukemias, lymphomas) are the ones that are showing up with pancreatic. However, there are other genetic and environmental factors. We add in spike and pseudouridine, so these timelines might be speeding up. This timeline is just DNA plasmid pieces.
Existing polyps with mutations might show accelerated growth or progression to dysplastic lesions or early-stage cancer during the first two years out. The immediate effects of plasmid-induced genomic instability or inflammation could speed up the malignant transformation. We are primarily speaking to colon polyps, although there are endometrial polyps, etc and those are less likely to turn with a lower incidence.

2. Second window of time is 2. 2 to 5 Years after initial exposure.
DNA plasmids have either caused significant genomic instability through cGAS STING, or other mechanisms, or integration, causing increase in cancer. Chronic hematological cancers and early solid tumors should be appearing. This window would show a peak in cancer development if the genotoxic effects are significant but not immediate, meaning, it took time.

Polyps with pre-existing mutations, if changed by DNA plasmids inside of an LNP, might progress to more advanced stages of cancer, FASTER. We would see progression from polyps to cancerous tumors.

3. Third window of time should be the highest we see, which is within 3. 5 to 10 Years since initial exposure

The largest number of cancers SHOULD be seen during this window of time. Solid tumors in the liver, pancreas, or lungs, and hematological cancers should be exploding now in the rates that will be seen The delayed nature of these cancers reflects the cumulative impact of long-term genomic instability, inflammation, and mutagenesis induced by the DNA plasmids and LNPs.

This is also should be the peak time for poylps now showing cancer progression if exposure to DNA plasmids inside of an LNP were correlated. The largest number of cancers related to mutated polyps might be detected during this period.
Dr. Harvey Risch I believe to be one of the more respectable people who has spoken out, and he has stated at the three year mark is when we should start seeing more. However, that is just the beginning, because we go exponential, not mathematical.

Numbers game/probability:
Cancer numbers should be exponential cancer risk by time frame/windows after first exposure of injection because in biological systems, cancer incidence often shows exponential growth, not linear, due to accumulation of genetic mutations and interactions of multiple factors contributing to tumor progression.

Arbitrary numbers (I am just throwing numbers in here for math's sake so you can see scales of progression) might look like:
Quantification
If we were to model this mathematically:

Linear increase model using arbitrary numbers:
If we observed 5 cancers in the first 3 years, and the incidence rate increases linearly, we might expect an additional 5 cancers in the next 3.5 to 10 years, resulting in a total of 10 cancers.

Cancer rates go exponential:
If the increase is exponential, the number of cancers should grow faster.

Let's take the starting point of five cancers as example. Of COURSE there are other factors like total number of mutations already present, environment, predisposition, female versus male, lifestyle, age, etc, but if cancers double every year, starting from 5 cancers, you could expect a significantly larger number of cancers in the later period.

For example, if the rate of increase is such that the number of cancers doubles every 2 years, then by 7 years (from the initial 3), you could see approximately 40 cancers (based on doubling).

Real Math:
Exponential Growth Formula:

The general formula for exponential growth is:
N9t)=N0​×e(rt)--that is N nought times e and then (rt) is an exponent.

N(t) is the number of cancers at time t
N (0)​ is the initial number of cancers
e is the base of the natural logarithm (approximately 2.71828).
r is the growth rate
t is the time period

Ok, let's go back to the initial which we are saying is five cancers, that is it.

this is the calculation for growth rate, which we do not have at the moment:
Estimate Growth Rate (r): Calculate the growth rate r using:
r=ln(N(t)/N0​)​/t

If we started with five cancers and this is just all arbitrary, we had a growth rate of 0.2 (we do not know what this is!) then we say time is after ten years, we do the math and we land at 37.
N(10)=5×e(0.2×10) N(10)=5×e2N(10) = 5 \times e^{2}N(10)=5×e2 N(10)=5×7.389N(10) = 5 \times 7.389N(10)=5×7.389 (since e2≈7.389e^2 \approx 7.389e2≈7.389) N(10)≈36.945N(10) \approx 36.945N(10)≈36.945

Either way, we do not know the growth rate but we know cancer is exponential process.

Love Canal was a disturbing thing that happened years ago. Love Canal was a neighborhood in Niagara Falls, New York. The Hooker chemical company (this is all off the top of my head) had been dumping chemicals into the ground, buried chemical waste in an abandoned canal. This site was later used for residential development, and they sold the land for a dollar and this land was used to build houses on for families. A woman who was not a scientist by the name of Lois Gibbs did her OWN epidemiological investigation into the miscarriages and cancers that started to pop up in her community that would lead to a government investigation. It was terrible.

In the 1970s, residents reported high rates of cancer, birth defects, and other health problems, which were linked to the buried chemicals leaching into the environment.

In the Love Canal case, exposure to toxic chemicals did not immediately result in a large increase in cancer rates. The effects were observed over several years.

Epidemiological studies found elevated rates of cancer and other health issues among the residents, particularly in the years following their exposure.

In the lipid nanoparticles with the existence of DNA plasmids, where exposure to carcinogens is high and widespread, cancer incidence can increase exponentially. This was injected into billions of people.

Thinking back to those who have given their speeches, I am kind of horrified you did not mention this as cancer experts.

I am kind of alarmed.

I have no idea what the outcomes are going to be but if cancer increases exponentially and if a large portion of the population of the planet was subjected to genotoxic material SIMULTANEOUSLY within similar time frames starting in March of 2021, I cannot say what will happen, but we are now at September 1st of 2024, and I hope this is all incorrect and the people speaking out saying it is nothing or rare are correct. pubmed.ncbi.nlm.nih.gov/24283955/

🚨💉 For those not aware, if you go to Moderna's website that lists their clinical trials, you'll see they are in process of redevelopment of traditional vaccines and changing to RNA based with lipid nanoparticle. It is imperative to place political motivations and others to the side right now and focus on global public health and the ramifications.
Spike protein and DNA plasmid do not have to be present for this platform to cause harm. Those are just additional things which cause harm, and yes they are concerning beyond belief.
You do not need pseudoephedrine despite what anyone says anywhere with any credential to have a frame shift, junk proteins made, or misfolding resulting in aberrant protein creation by the human body by injecting RNA with a lipid. If you look in my highlighted tweets you will see a thread with over 100,000 views which details out a study that was done by Moderna scientists which was paid for by Moderna where they showed the positively charged lipids are binding through a covalent bond to any nucleic acid which they come in contact with.
Inside the lipid nanoparticle that is going to happen with the RNA and it's going to create what is called an adduct.

The fact that no podcaster ever mentioned this besides the ones I have been on despite the fact that I have tagged them all is alarming. Instead politicians and podcasters only focused on the pseudoeuridine, unless I went on that podcast and we had a talk otherwise it has been ignored and I'm pissed and you should be pissed too.
Another conversation to be had is why this is being ignored.

This is alarming. This is alarming on multiple fronts.

The positively charged lipids can also bind with other nucleic acids that have a negative charge. They will form what is called a covalent bond.

This will cause slippage in what is called the ribosome.

It does not matter if it is the spike protein or not. It does not matter if pseudoeuridine is present or not.

Molecular mimicry will also occur. To think this will not happen is outrageous.

Take the number of people who have died, those who have survived who have lasting harms, take the number of pregnant women who suffered, the miscarriages, all of it, and there is the very real potential of taking that number and multiplying it exponentially if all of these come to fruition.

This is not to discount anyone who has already been harmed or died.

The potential for harms are unimaginable.

We also know that the biodistribution impacts pregnant women differently.

We know that 8 times the amount of the lipid nanoparticle goes to the lymphatic system of pregnant women compared to women who are not pregnant who get these injections.

This isn't a mathematical calculation when we speak to risk. This isn't an addition. This isn't a plus or minus numbers game. This is exponential harms. 2/

https://x.com/_HeartofGrace_/status/1820648214036423042

🚨💉VERY IMPORTANT! THERE IS HIGH CONCERN OTHER CONTAMINATION HERE! THIS is what they do not want you to know!
Too long; didn't read: there are MANY other possible contaminants in the mod RNA COVID injections!

This data is NOT just important for gaining the DNA plasmid contamination levels that landed in the COVID injections that are correlated to myocarditis, autoimmune disorders, organ injury, clots, and worse. (the DNA plasmids that were used in E coli to make the modRNA injections)--no. Anyone who has worked biotech KNOWS (this is why you need to pull in real biotech people who designed this stuff to know what to look for) that there are many possibilities of other contaminants, that may have landed inside of these lipid nanoparticles ENTERING THE CELLS OF PEOPLE.

🚨1. If you look up ANY form 483 (this is a form that cites observations made by the FDA during an inspection of a company like a drug manufacturer or biotech company that indicates a product is in violation of FDA requirements. Often times you will not just find bacteria, you will see cited what is called CROSS CONTAMINATION. This is when other DNA product parts or other ingredients, even if in what is called a cGMP facility was where these things were made, have been routinely found, by very large companies and sites. We are talking about OTHER plasmids. WE are taking about REAGENTS.

🚨 2. Reagents are substances that are used in the production of many things, like RNA, DNA plasmids, etc. They can be introduced at ANY point during the manufacturing process. The enzymes used to break down the DNA plasmids in the modRNA LNP injections are ALSO reagents, like enzymes: proteases, kinases, and phosphatases for protein modification or degradation.

Reagents are used to make THE VARIOUS LIPIDS used in the LNP. REAGENTS are used to make the DNA plasmids that were used. REAGENTS were used even in the clinical trials in what people THINK is the SAFER version of these injections (process ONE). Process TWO used DNA plasmids, and what landed in BILLIONS of arms.

🚨☑️💉This is going to get sciencey and you might not be familiar with this stuff, but read the last part, and THEN you will understand (hopefully)

*********************************************

☑️Examples of REAGENTS:
DNA and RNA Reagents:
Nucleotides: dNTPs (deoxynucleotide triphosphates) for DNA synthesis, NTPs (nucleotide triphosphates) for RNA synthesis.
Enzymes:
Polymerases: Taq polymerase, Pfu polymerase for PCR.
Reverse Transcriptase:
For converting RNA into cDNA.
Ligases:
T4 DNA ligase for joining DNA fragments.
Restriction Enzymes: For cutting DNA at specific sequences.

Protein Reagents

🚨Enzymes: Proteases, kinases, and phosphatases for protein modification or degradation.

Chemical Reagents
Detergents:
SDS, Triton X-100 for lysing cells or solubilizing proteins.
Fixatives:
Formaldehyde, paraformaldehyde for preserving cells or tissues.
Reducing Agents:
DTT, β-mercaptoethanol for breaking disulfide bonds in proteins.
Denaturing Agents:
Urea, guanidine hydrochloride for denaturing proteins or nucleic acids.

Molecular Biology Reagents
PCR Reagents: DNA polymerase, dNTPs, primers, buffer systems for amplification of DNA.
Cloning Reagents:
Vector plasmids, ligase, competent cells for gene cloning.
Sequencing Reagents:
Dideoxynucleotides, sequencing primers, polymerases for Sanger sequencing.
CRISPR Reagents:
Guide RNA (gRNA), Cas9 nuclease, donor DNA for gene editing.

SOME of the chemicals YOU just read above, are used in the making of the modRNA injections.

This means, they are subject to contamination.

How do I know other than working in the industry and designing this stuff? Here is one of several studies showing contamination in REAGENTS. AND THESE contaminants if not filtered out, would ALSO EXIST IN THE FINAL PRODUCT:
This is just a few examples:

(heavy science time):

"Characterization of plasmid residues Of the 80 contigs with plasmid signatures, 41% (n = 33) had an origin of replication, 63% (n = 51) a selection marker and 52% (n = 42) an insert. Apart from the EIAV coding expression vector, three other artificial expression vectors could be identified by their inserts. Of these inserts, 19% included a chimera of a human-mouse chimera Bicaudal 1 gene (n = 8), 11% the UL-32 gene of the Cytomegalovirus (n = 5) and 5% the leukemia fusion protein AML1-MTG8 (n = 2). All contigs with a specific insert had been aligned and the consensus sequence displayed in SnapGene Viewer gave a predicted plasmid map (Fig. 5). The plasmids coding for Bicaudal 1 chimera and UL-32 genes were identical to those used for other studies in our laboratory and had, therefore, been identified as laboratory contaminants. BLAST of the 2268 bp long fragment of “Und_TR29_len2635”, found in the Und sample (Undetermined contigs), showed a 99% query coverage with homo sapiens mRNA for AML1-MTG8 fusion protein (GenBank: D13979.1). The source of this plasmid remains unknown.
Natural plasmids residues are derived from a variety of sources Besides the presence of artificial plasmids, natural occurring plasmids from different species were found in all twelve samples (n = 12). The most frequent plasmid was from Micrococcus spp. (92%) followed by Serratia spp. (50%), Burkholderia spp. (42%), Ralstonia spp. (25%), Acinetobacter spp. (25%), Mucilaginibacter spp. (17%), Streptococcus spp. (17%), Enterobacter spp. (8%) and Cupriavidus spp. (8%; Table 1). The plasmid sequences we found from Serratia maracesens pUO901 (ID: NG_047232.1) and Enterobacter cloacae pEC005 (ID: NG_050201.1) coded only for antibiotic resistances. The first one was identified as a aminoglycoside-(3)-N-acetyltransferase (AAC(3)s), whereas the latter coded for a Class A extended-spectrum beta lactamase TEM-157 (Table 1). These plasmids are likely from natural sources.

Analysis of metagenomics studies Finally, we analyzed previously published metagenomic data sets of human gut and plasma samples as well as a data set using different whole genome amplification kits50–52 for the presence of plasmid residues. Retrospective analysis of these data sets, natural plasmid residues had been found in most sets and most commonly Acinetobacter sp. and Escherichia sp. as source organisms (Table 1 and Table 2). The highest diversity of plasmids had been found in metagenomic data focusing on the fecal microbiome53. Especially metagenomic studies analyzing high bio mass samples such as microbiome studies are expected to contain a higher amount and diversity of natural plasmids compared to samples with low biomass (e.g. plasma). Remarkably, a plasmid highly similar to Xuhuaishuia manganoxidans strain DY6-4 had been detected in several samples of two unrelated metagenomics studies although this bacterium has been found only in the Pacific Clarion-Clipperton Fracture Zone51 (Table 3) so far." 2/ ncbi.nlm.nih.gov/pmc/articles/P…

1/ 🚨🚨💉FOIA UPDATE : CONTAMINATION RECORDS REQUEST FOR PFIZER AND MODERNA (CATALENT): SUBMITTING APPEAL AFTER DENIAL OF FOIA. DNA plasmid is not the only contaminant. There is ALWAYS a LIST of contaminants on the QA. I asked for help, but none came. Below is my response.

https://twitter.com/_HeartofGrace_/status/1798460071363420482

2/

1/If you haven't been paying attention, MANY social security numbers and full info were hacked and released. Everyone that I know had their social security number and information breached and their info landed on this list. Instructions on how to place a freeze on your credit👇🏻 2/ I've been helping my parents check and place freezes on their credit to protect what they have.

fortune.com/2024/08/19/soc…

1/ A 🧵combining a bunch of 🧵s on cGAS STING and modRNA and LNP harms, including peer reviewed studies, specific injuries, with substack and podcast at the end.
"BREAKING STUDY PUBLISHED 10/17/2023: Foreign dsDNA can cause strokes via cGAS STING":

https://x.com/_HeartofGrace_/status/1714482073149346299

2/ Length of the dsDNA plasmid drives strength of cGAs STING and the immune system. Cleaning it up and lowering amounts is a false statement.
Even in low amounts, longer pieces of dsDNA cause the most harm. 6/20
activatiohttps://x.com/_HeartofGrace_/status/1804274300255457685

🚨🚨💉💉Here's how lipid nanoparticles and the spike protein should theoretically cause birth defects and other harms, even if they never even tough the baby growing in the womb if the mother got a modRNA/LNP injection, with no DNA plasmid present:

Below is a screen shot from a Rumble presentation from the late Dr. Arne Burkhardt (rumble link and citations below). In this screenshot of Dr. Burkhardt's presentation, he obtained this tissue and saw that it contained spike protein expressed in the placenta, and this mother, had received at least one modRNA injection.

We know from multiple LNP studies that the LNP is indeed going to the placenta.

The trophoblast is part of the placenta and it is made up of layers contribute to the formation of the placental barrier, which separates maternal and fetal blood while allowing the transfer of nutrients, gases, and waste products.

This is important because many nutrients and hormones cross the placenta that are involved in fetal development.

The trophoblast also produces several hormones needed for pregnancy, including hCG, to maintain the corpus luteum for progesterone production, and hPL, which regulates maternal glucose metabolism. It also modulates the immune system to stop the mother's immune system form thinking that the placenta is foreign tissue to be attacked by her immune system.

If any abnormalities form in this area, this can impact trophoblast function and cause complications like preeclampsia, placental abruption, birth defects, and still birth.

Blood flow could also be disrupted.

Regarding the placenta there is a transporter "system" that regulates the passage of nutrients and hormones, among other things, and this transporter system can be compromised.

There are important hormones that need to cross the placenta to reach the growing baby that are vital to the development of a healthy baby.

The size and charge of the LNP may interact with this system, and compete for certain aspects of this transport system or simply block it.

The following are important hormones, glucose, amino acids, and other nutrients that are vital to fetal development:

Glucose transporter (SLC2A1 AKA GLUT1) transports glucose from the mother to the growing baby.
If LNPs accumulate in the placenta, they could obstruct or alter the function of GLUT1, reducing glucose supply to the fetus, causing intrauterine growth restriction and developmental delays in the baby in the womb.

There are a couple of amino acid transporters involved in getting amino acids to the growing baby.

SLC22A4 transports amino acids and other small molecules. LNPs could interfere with the transport of amino acids that could be detrimental to protein synthesis in the baby and could negatively impact fetal growth.

LC38A1 and SLC38A2 transport what are called neutral amino acids, and if these are disrupted this could also negatively impact fetal development and growth.

Thyroid Hormones

A BIG FACTOR is thyroid hormones.
SLC16A2 is paramount for of the thyroid hormones T3 and T4 into fetal tissues. LNPs blocking this could theoretically result in inadequate thyroid hormone delivery to the fetus, causing not only birth defects but concerns with the cognitive function of the baby.

Iron transport:
SLC11A2 regulates iron uptake and if this was impacted, it could cause anemia in the growing baby.
TFRC--this is the transferrin receptor which mediates uptake of the transferrin-bound iron, and if this is impacted we would see iron deficiency, impacting fetal brain development and overall growth.

Calcium channels:
CACNA1S and CACNA1C are what are called L-type calcium channels, and they are in charge of calcium transport from the mother and these are essential for bone development and other physiological processes, and if there are calcium imbalances as a result of LNP imbalances, we might see fetal bone growth and development impacted in the womb.

Water channels!
Yes, the placenta has what are called water channels. Water channels are pretty cool, these are called aquaporins--AQP1 and AQP3 and these are responsible for the transport of water across the placenta to the growing baby. If there was a pregnant mother who received a modRNA injection, and she suffered from oligohydramnios (low amniotic fluid), one might wonder if this was correlated.

Oligohydramnios can cause compression of the umbilical cord, promoting decreased oxygen, nutrient supply to the fetus, preterm labor, or what is called "potter's sequence," which includes limb deformities and facial deformities due to compression of the fetus.

**************************************************************************
If we tie this all together, then we might see LNP causing a disruption in the placenta without ever touching the growing baby, and interference with glucose, amino acid, and iron transport can result in nutrient deficiencies, impacting fetal growth, development, and health.

Insufficient thyroid hormones, glucose, or amino acids can lead to developmental delays, cognitive disabilities, and other congenital conditions.

Disruption in nutrient and hormone transport can cause intrauterine growth restriction, causing low birth weight and potential long-term health issues.

Disruption of calcium and water transport can result in metabolic imbalances, affecting bone health and fluid regulation.

Has anyone heard of any issues with pregnancies after modRNA injection with LNPs?

Asking for a friend.

^^^ Burkhardt's video

Some citations:








rumble.com/v4t7a59-dr.-ar…
pubmed.ncbi.nlm.nih.gov/17536998/
pubmed.ncbi.nlm.nih.gov/20415585/
pubmed.ncbi.nlm.nih.gov/19079273/
ncbi.nlm.nih.gov/pmc/articles/P…
ncbi.nlm.nih.gov/books/NBK53295…

🚨🚨🚨💉For those who lost loved ones, who never got a reason why, did you loved one experience the following? Septic like symptoms but no sepsis? (they could not figure it out?) Fever, chills, low blood pressure, rapid heart rate (Tachycardia), rapid breathing (Tachypnea), weakness, lactic acidosis, multiple organ dysfunction, darkening of skin under the eyes, and confusion? Did this happen before the death of your loved one but no doctor could explain why? Septic like symptoms but no bacteria present?

If this is you, YOUR LAWYER contacts me in full name on X only, and we have a call. If it was Pfizer or Moderna, I am almost certain can explain the EXACT mechanism in laymans terms and technical.

Anonymous accounts in DMs will be not be answered. @drcole12
@AaronSiriSG

I know why this happened if they had Pfizer or Moderna. I will not post it in some tweet. I will represent your client in court. I will bring in my evidence of where I worked, what i did, and I will explain this fully.

@Answers4Sean
I know how this happened. I am so sorry.

Have you docs who say they can explain it explain all of that?

I can.

🚨🚨💉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.