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Dr. Pretorius and a colleague discuss unusual clotting observed after COVID-19 vaccination, including embalmers reporting back pressure when introducing embalming fluid and the extraction of very long, congealed clots—six inches to several feet—as well as patients with long brachial clots. They note thousands of clotting reports in VAERS across all vaccine types, describing these clots as not normal. Some clots cause major emboli affecting circulation to the lungs, detected by scans and perfusion studies, while others are microclots with a branching pattern visible in imaging. A clinician also shared a photo of a clot with a complete branching pattern into medium and smaller vessels. Dr. Pretorius’ work is cited to explain the mechanism: spike protein can induce immediate clumping of proteins in platelet-poor plasma in the absence of platelets, a highly unusual clotting pathway not relying on the classical coagulation cascade. This is described as a proteinaceous, pseudo-amyloid–like clot. The spike protein is reported to circulate after vaccination, with studies in the Journal of Immunology showing spikes in circulation and exosomes up to four months after shots. Long-haul COVID data (Patterson’s study) reportedly shows S1 protein present in nonclassical monocytes in blood, suggesting persistence of spike protein, whether from infection or the vaccine, which can induce clotting pathways on its own. Dr. Pretorius discusses observations of upregulation of intercellular adhesion molecules (ICAMs) on leukocytes within clots, causing white blood cells to adhere in addition to fibrin, contributing to difficulty in dissolving these clots. Concerning treatment and detection, the speakers describe depletion of plasminogen, reducing the body’s ability to break down clots, and note that standard anticoagulants are less effective against these clots, which are described as amyloid-like and atypical. They emphasize that these are not the classical clotting pathways involving platelet activation and typical thrombin–fibrin cascades. They contrast this with expectations of standard clotting mechanisms and reference the unusual, non-classical pathway highlighted by Pretorius. The discussion also mentions the idea that spike protein in circulation can drive clotting without the usual platelet activation, and that some patients have continued to experience spike-related effects long after vaccination. They assert that vaccines were developed targeting the original Wuhan strain and may not cover Omicron; they suggest the shot’s risk-benefit balance is unfavorable given ongoing clotting, immune suppression, and cancer-inducing pathways, and they claim data indicate those who receive two or three shots may acquire Omicron at a higher rate than those unvaccinated. They conclude that the shot is expired for a virus that is no longer circulating in its original form and argue that vaccination induces dangerous pathologic processes with no protective benefit.

A viewer asks if the proteins from the vaccine enter the bloodstream. The speaker explains that the mRNA blueprint for the protein is given, which is then translated into the protein in the muscle cells. The protein may enter the tissue and possibly trace amounts may enter the blood, but it is not measurable. The reaction occurs in the muscle, the corresponding defense cells, lymph nodes, and minimally in the blood. The speaker concludes that they have reached an agreement on the topic.

Research conducted by Bruce Patterson at InCelDx reveals that spike proteins can remain in the body for extended periods. In severe COVID cases, the s one segment was found in white blood cells for up to 15 months after infection. Even after vaccination, the full-length spike protein, including the s one and s two segments, was detected in white blood cells for at least 9 months. Another study from Stanford, led by Roelkern and colleagues, discovered messenger RNA, the genetic code for the spike protein, in lymph nodes for up to 2 months. These findings suggest that both messenger RNA and spike proteins can persist in the human body for several months.

Speaker: A lot of the analysis techniques that were being employed now on the white clots. And about three years ago, there was one piece of analyses that I came across just by accident, which was a thing called an ICP analysis, which is an analysis that determines the elements present in white clots. It was done by a gentleman in The USA called Mike Adams, who presented the findings of his initial white clot analysis from samples that Richard had provided him some almost three years ago now. And it surprised me what the findings were, because I have used the ICP analysis. It’s called Inductively Coupled Plasma Mass Spectrometry. Don't worry about the name. It's just a very well known piece of analytical equipment that you can rely upon to tell you what elements are there in the white clot and in what abundance. And what surprised me was in the analysis that Mike presented was a very the highest element they found was phosphorus, followed by sodium, tin, and later on sulphur, and carbon. And we also found that there were no normal blood marker elements present in the white clots. So, we've actually employed two laboratories in Europe, and there's a long reason behind that because I'm associated with people in Europe who do this kind of work. Anyway, we sent clot samples, they all ran ICP analyses. They found exactly the same results that Mike Adams found. We found aberrantly high levels of phosphorus, we found aberrantly high levels of sulphur, tin, sodium, and carbon. And being an organic chemist, I know a little bit about tin chemistry, because I used to sell tin catalysts, believe it or not, for polymerisation reactions. So I had to study the chemistry of tin. And I wondered why tin would be present in a white clot. So, obviously, we could not believe this first series of results. It's set about replicating the results in two separate labs, and they came back and said, you're right, there's high levels of phosphorus, tin, sulfon, carbon. So the next thing we did was to do an analysis called HPLC, High Performance Liquid Chromatography. And what this does is actually pulls apart the white clots and tells you what the protein components are. And surprisingly, we found that the highest level of proteins we found was fibrinogen. But the HPLC analysis actually will determine what kinds of fibrinogen chains are there. In a normal red blood clot, there's normally one to one to one ratio of the alpha chain, beta chain and gamma chain. We found in our white clots that the beta chain far exceeded the alpha chain and the gamma chain. And in fact, it was beta gamma alpha. So the alpha was the lowest proportion. Now, we're not biochemists, and we're not medically qualified in any way. But we can do simple research to find out why the fibrinogen content was so high. Fibrinogen forms fibrils. This is exactly why when John O'Learny first described the white clots as being calamari like, he is exactly correct. That's exactly the texture that fibrin will bring into a white clot. Okay, so from then on, we then ran some amino analysis results. My colleagues ran an amino acid analysis, and they found a high level of Praline, Aspartic acid, Lysine, a whole range of about 18 amino acids, all that have a phosphorus affinity. And as we said in the white clot, the element that has the highest concentration that we could confirm is porpoise. If you take time then to research the aberrant pathways that what they call excess phosphorylation will cause, it causes a whole range of problems in the human body. So we have determined, we think, the pathway to the formation of these white clots. We have three separate pieces of analysis, all confirming our findings. So we've now pieced together the formation of the white clots, and I'll come back to the very beginning. When we administer the injections, there is a lipid nanoparticle carrier, it's called a phospholipid. We found by our analysis that when the phospholipid releases the mRNA core of the lipid nanoparticle, at the very moment that it releases the core, it actually exposes a phosphorus head of the phosphorus lipid. The phosphor lipid reacts within the bloodstream naturally formed fibrinogen, and that's what's nucleating the white clot formation. Now we can prove all this. We've actually got over 200 peer reviewed papers confirming the pathway that I'm describing. And more importantly, once that initiation of the DSPC now the actual phospholipid that is encapsulating the lipid nanoparticle is a phospholipid called DSPC. I won't go into the name of it, but what it means is that that particular phospholipid we found, again through research, that it will liberate 80 to 90% of raw phosphorus heads as it releases the mRNA core. Those phosphorus heads all react with the fibrinogen in the bloodstream and they cause sandy blood. The reason you guys are seeing sandy blood and coffee grounds is that's the nucleation pathway to the final white clot formation. The other factor we found and proved the spike protein bonds to the phosphorylated fibrinogen. The body is generating methylcetiopridine generated spike, that spike in the bloodstream then starts to coagulate with the phosphorylated fibrinogen, and that feeds what we call a monomeric reaction that continues to grow. Those particles are free flowing in the blood and they find an anchor point. The anchor points they find are in fact the damaged endothelial layers. When an endothelial layer of the vascular system is damaged via inflammation and the cytokine storm that the spike protein generates, That opens up the natural phospholipid layer of the endothelial layer, and that forms anchor points for these nuclei. From these anchor points, that's when the clots begin to grow. So, I'm trying to encapsulate this in a very simple term. It's quite a complex number. Very

A viewer asks if the proteins from the vaccine enter the bloodstream. The speaker explains that the mRNA blueprint for the protein is given, which is then translated into the protein in the muscle cells. The protein may enter the tissue and possibly trace amounts may enter the blood, but it is not measurable. The reaction occurs in the muscle, the corresponding defense cells, lymph nodes, and minimally in the blood. The speaker concludes that they have reached the desired agreement.

The clots being formed, we've run mass spectrometry on these clots. They don't look like normal clots. They don't have the same composition. They don't have fibrin. They don't have thrombin, which are normal things you would see in a normal coagulation cascade. They have, instead, all the fibrinogen chains—alpha, beta, and gamma. They have them in a strange differential where it's not one-to-one-to-one; it's about 36 to 16 to 4 by ratios. They're aberrantly cross-linked by sulfide bonds. There's a ton of tin for some reason. I don't know why there's tin in there, but there's a ton of tin in there and a ton of phosphorus. And the spike protein is actually coated in GLIKNAK, which is a phosphate donor. So that might explain all the phosphorus if it's providing the energetics or in some way by cleaving or creating phosphate bonds. So I think that that's a big problem because that's a slow progression of coagulopathy that's, I think, narrowing the lumens of the vascular system, which is contributing to some of the organ failure that we're seeing, some of the neurological symptomatology that we're seeing, some of the fatigue, and things of that nature. And then finally, the spike protein is shown to produce—it’s shown to induce misfolding of proteins and actually

The coronavirus spike protein's shape before interacting with our cells is key to triggering an antibody response. To study this, we create the spike protein in the lab, maintaining its precise shape. This is achieved using a "clamp"—a small fragment of HIV protein—that holds the spike protein in its natural, pre-interaction conformation. This ensures the lab-made protein accurately reflects the virus's structure, allowing for effective antibody response studies.

Speaker 0 lays out a numerical comparison between vaccine versus infection to determine which creates more spike proteins, according to the source material. First, the infection scenario. The unit counted is the virion (one complete virus particle). At the peak of infection, the body could be fighting off somewhere between one to 100,000,000,000 virions. Each virion has spike proteins on its surface, counted as between twenty five and fifty spikes per virion. The calculation multiplies the range of virions by the spikes per virion, giving a peak infection spike protein load of two to 10,000,000,000,000 spike proteins. Next, the vaccination scenario. The math starts with modified messenger RNA (modRNA) molecules in a vaccine dose. A single vaccine dose contains somewhere between 14 to 42,000,000,000,000 modRNA molecules. Each of these trillions of modRNA molecules can produce multiple spike proteins, ranging from 10 to 1,000 each. When the numbers are multiplied, the source calculates a potential total of up to 100,000,000,000,000,000 spike proteins (up to 10^17, i.e., up to one hundred quadrillion). Speaker 0 then contrasts the two scenarios. In a side-by-side view, the initial particles are billions of virions versus trillions of modRNA molecules. The timing differs as well: a natural infection builds up over about a week, whereas the vaccine dose is delivered all at once, in just a few seconds. The final totals are two to 10,000,000,000,000 spikes from infection versus a potential of up to one hundred quadrillion from vaccination. Visually, this difference is stark, with the infection spike protein bar being far smaller than the vaccine spike protein bar, illustrating an order-of-magnitude difference. The discussion then moves to the distribution and persistence of spike proteins. The source describes the virus's spread as more localized or comparatively narrow, while vaccine components are said to travel throughout the entire body, with accumulation in areas including major organs like the heart and the brain, and the potential to cross barriers such as the blood-brain barrier and the placental barrier. Regarding duration, spike mRNA was reportedly detected in cerebral arteries after seventeen months, and some vaccinated individuals were reportedly still spike positive for up to sixteen hundred days. The source concludes, “Your spike load is orders of magnitude higher via injection.” Speaker 0 notes that the numbers show trillions versus quadrillions and emphasizes the presented math and its implications as the core of the comparison, while acknowledging the source’s look at spike proteins’ distribution and persistence.

Speaker 0 lays out a detailed critique of how the transition from process one to process two allegedly occurred, arguing that process one was deliberately structured to “cook the books” so that regulators would see nothing in their assays, while the real material of concern—DNA contaminants, including plasmids and RNA/DNA hybrids—would only be detectable in process two. Key points - The shift from process one to process two is alleged to be planned from the start. The assays used were designed “not to find things,” and the trial was set up in process one with the expectation that process two would ultimately be used, exposing a premeditated sequence of actions. - Ten nanogram limit and copy number. The ten nanogram figure is framed as a limited hangout: the real concern is molarity and copy number of DNA molecules, not weight. Naked-DNA half-lives are short, but lipid nanoparticles (LNPs) protect DNA, altering degradation and persistence. The origin of the 10 ng limit traces to Sheng Fowler and Keith Patten’s work, which emphasized copy number (molarity) rather than weight, particularly for small fragments and plasmids. The argument is that 10 ng can correspond to vastly different copy numbers depending on fragment size; smaller fragments dramatically increase copy number and potential integration ends. - Spike vs. CAN gene targeting. In process one, spike sequences are amplified, then RNA is generated via IVT, and residual DNA is monitored using a CAN gene target. The CAN assay is described as a decoy that would not detect post-amplification products; spike post-amplification would be abundant, but the CAN assay would show little or nothing. In process two, E. coli replication of the entire plasmid would introduce CAN sequences, yet regulators were still steered to look at CAN rather than spike, masking true residual DNA. - Assay design and regulatory deception. The EMA/EMAs documents and related papers show an RT-PCR setup that amplifies spike RNA to confirm expression while also using CAN primers that would not detect post-amplification plasmid content. A key accusation is that the regulators were given an assay that cannot detect the relevant post-amplification material, while an assay for spike exists but is not reported or used. - DNA vs. RNA measurement challenges. qPCR is argued to be ill-suited for this purpose due to fragmentation and the mismatch between input weight and actual molecule count. Fragmentation from DNase treatment is nonrandom: can (CAN) regions are hyper-fragmented, spike regions less so, causing disproportionate detectability depending on primer design and amplicon length. This yields underestimation of the true DNA content when relying on CAN-targeted PCR. - Enzymatic treatment and measurement implications. DNase I degrades CAN more efficiently than spike, particularly when DNA is in a DNA/RNA hybrid context post-IVT. Another enzyme (DNase XT) is claimed to better digest RNA-DNA hybrids, moving CT values for CAN and leaving spike detectable. This suggests the choice of enzymes was deliberate to obscure true residual DNA, while spike DNA remains more detectable under alternative assays. - Measurement methods and data interpretation. Fluorometry (e.g., PicoGreen or Ribogreen) is used to measure DNA or RNA doses, but crosstalk and fragmentation complicate interpretation. The speaker argues that fluorometry should be used in conjunction with RNase/DNase treatments and proper controls to distinguish DNA from RNA, and cautions that PCR-based extrapolations can massively overestimate or misrepresent actual DNA content due to fragmentation biases. - Consolidated claim. Across multiple studies and preparations, spike DNA is found at significantly higher levels than CAN DNA (e.g., a hundredfold difference in several datasets). The “can” assay is positioned as a decoy, while spike assays reveal the genuine DNA content and potential for integration, signaling intentional misdirection in regulator briefings. The speaker concludes that the “game of hide the ball” is ongoing: regulators have been misdirected to look for CAN DNA in process one, while the meaningful residual DNA relates to spike-containing sequences post-amplification—yet this is not consistently measured or reported. The overall thrust is that the design of assays and the choice of targets imply intentional deception to obscure true DNA contamination risks, particularly in the transition to process two.

Here's a shorter version of the transcript: We're examining fluorescent micrographs of plasma from healthy individuals. We're looking at a PPP smear, a smear with added spike protein, and plasma exposed to spike protein. The goal is to see if adding spike protein creates larger microclots than in healthy blood. We'll be conducting an experiment to investigate this. A question was raised about whether blood type matters, specifically if O positive individuals have fewer reactions to COVID. While I'm not certain, it's something to consider.

Our study investigates the impact of the SARS-CoV-2 spike protein on blood hypercoagulation. We used microscopy and mass spectrometry to examine the spike protein's interaction with platelets and fibrinogen. Results using platelet-poor plasma showed the spike protein may disrupt blood flow. Mass spectrometry revealed structural changes in beta and gamma fibrinogen, complement, and prothrombin after adding spike protein S1. These changes, similar to those observed in COVID-19 patient blood clots, showed resistance to trypsinization. We propose that the spike protein's presence in the bloodstream contributes to hypercoagulation in COVID-19 patients, potentially causing impaired fibrinolysis and persistent microclots. This finding has significant clinical implications. Our goal was to determine the spike protein's effects, as its interaction with these blood components warrants further investigation.

The spike protein on the surface of the coronavirus is crucial for its structure and interaction with our cells. To trigger a strong antibody response, Keith replicates the spike protein in the lab. He uses a small piece of HIV protein as a clamp to lock the spike protein into its original shape. This ensures that the spike protein maintains its structure and effectiveness.

In Goran, Neuquén, Argentina, we conducted analyses on COVID-19 vaccines, including CanSino, Pfizer, Covilock, and Sinopharm. Our first method was fluorescence microscopy, utilizing an optical microscope with various filters to observe different wavelengths. This study was performed in the presence of a public notary, Dr. Francisco Valdez, who verified the process and the sterility of the vials and materials used. The findings were documented in a notarial act certified by the College of Notaries of Neuquén.

We tested different vaccines on blood slides to observe their effects. Pfizer caused immediate cell clearing, J&J led to cell clumping, and the cells became nonfunctional. The changes were rapid and significant, raising questions about the vaccines' impact on blood cells. More research is needed to understand these findings.

Okay, let's get started. I need to find the right tools to draw blood, so please be patient. I'll put the scope back on so we can watch. Here are some micrographs: healthy predlopod plasma, then the same plasma with spike protein added. We want to see if adding spike protein directly to healthy blood creates larger microclots than we see in the samples with the spike protein already present. We'll compare the images to see the effects.

The spike protein of the coronavirus plays a crucial role in triggering a strong antibody response. To study it in the lab, Keith uses a small fragment of HIV as a clamp to lock the spike protein into its original shape. This helps maintain the structure of the virus on its surface.

I washed my slides and examined blood samples from everyone, including myself. I noticed some anomalies that I hadn't seen in unvaccinated individuals before. These anomalies appear when the blood starts breaking down, particularly during decomposition. Interestingly, while the blood changes, the anomalies do not decompose; instead, they morph into different forms. The red blood cells are present, but when they cluster together, they begin to evolve into something else. This transformation could happen at any moment.

The speaker explains that the spike protein on the coronavirus is crucial for its structure and interaction with our cells. To trigger a protective antibody response, Keith replicates the spike protein in the lab and locks it into the same shape using a clamp-like protein. Surprisingly, this clamp-like protein is a small fragment of HIV.

We take a blood sample from the patient and prepare a native blood spread. The sample is heated and dried, rendering the blood cells dead. After cooling, we mix a solution and apply it to the sample. Looking through a microscope, we observe the destroyed blood cells without movement. However, after a short time, the parasites inside the dead blood cells come back to life, swimming actively. These parasites are self-sufficient life forms, not apoptotic bodies. All human cell material in this sample is completely dead.

Speaker 0 describes an ICP analysis (Inductively Coupled Plasma Mass Spectrometry) of white clots, initially encountered about three years ago from samples provided by Richard. Mike Adams presented the initial findings. The ICP analysis showed the highest element in the white clots was phosphorus, followed by sodium, tin, then sulfur and carbon. They also found that there were no normal blood marker elements present in the white clots. Two laboratories in Europe were used to replicate the results; both reported aberrantly high levels of phosphorus, tin, sulfur, sodium, and carbon. To investigate further, they performed High Performance Liquid Chromatography (HPLC) to identify protein components. The highest level of protein found was fibrinogen. The HPLC analysis determined the kinds of fibrinogen chains present, and it showed that in the white clots the beta chain far exceeded the alpha and gamma chains, with a beta-gamma-alpha ratio. They noted they were not biochemists or medically qualified, but conducted simple research to understand why fibrinogen content was so high. Fibrinogen forms fibrils, which aligns with John O’Learny’s description of white clots as calamari-like in texture, matching the expected texture from fibrin. An amino acid analysis by colleagues revealed high levels of proline, aspartic acid, lysine, and about 18 other amino acids, all with phosphorus affinity. They reiterate that the element with the highest confirmed concentration in the white clot is phosphorus. They state that aberrant phosphorylation pathways can cause a range of problems in the human body. They claim three separate pieces of analysis confirm their findings, allowing them to piece together the pathway to the formation of white clots. They connect this to injections that use a lipid nanoparticle carrier, specifically a phospholipid. Their analysis indicates that when the phospholipid releases the mRNA core of the lipid nanoparticle, it exposes a phosphorus head of the phospholipid. The phospholipid reacts within the bloodstream with naturally formed fibrinogen, nucleating the white clot formation. They claim over 200 peer-reviewed papers confirm the pathway described. They specify that the DSPC phospholipid encapsulating the lipid nanoparticle liberates 80 to 90% of raw phosphorus heads as it releases the mRNA core. Those phosphorus heads react with fibrinogen in the bloodstream, causing the sandy blood and coffee-ground appearance as the nucleation pathway to final white clot formation. They add that the spike protein binds to phosphorylated fibrinogen; the body generates methylcetiopridine-generated spike protein in the bloodstream, which coagulates with phosphorylated fibrinogen, feeding a monomeric reaction that continues to grow. These particles are free-flowing in the blood and find anchor points on damaged endothelial layers. When endothelial layers are damaged via inflammation and the cytokine storm induced by the spike protein, the natural phospholipid layer of the endothelium opens up and forms anchor points for these nuclei. From these anchor points, the clots begin to grow. They acknowledge the complexity but describe this as a simple encapsulation of the process.

In the lab, it's easy to manipulate spike proteins, which play a significant role in the zoonotic risk of coronaviruses. By obtaining the sequence and constructing the protein, we collaborated with Ralph Barrick at UNC to insert it into another virus. This allows us to conduct experiments and enhance our ability to predict outcomes based on specific sequences.

A viewer asks if the proteins from the vaccine enter the bloodstream. The speaker explains that the mRNA blueprint for the protein is given, which is then translated into the protein in the muscle cells. The protein may enter the tissue and possibly trace amounts may enter the blood, but it is not measurable. The reaction occurs in the muscle, the corresponding defense cells, lymph nodes, and minimally in the blood. The speaker concludes that they have reached an agreement on the topic.

For those who appreciate science, here’s some insight. This image shows a normal cell, but after an injection, noticeable changes occur. White nanoparticles invade, altering the cells' appearance; they lose their round, normal shape. The final image illustrates blood cells that are no longer smooth and symmetrical, now covered with lumps and protrusions. This suggests a deliberate attack on human blood, as noted by experts like Dr. Sherry, Tim Penny, and Nobel laureate Luc Montagnier.

Italian scientists at Zero Spike developed augmented NAC and tested hundreds of chemicals to break the spike protein into pieces the body can clear. They found that NAC could do it a little bit—maybe 12% of the spike—but it would refold and didn’t get rid of it. A quantum physicist created coherence among NAC molecules so they were identical; when mixed with the spike protein it cuts up the spike into lots of bits and broke up 99.8% of it, enabling clearance through the liver and kidneys. The speaker started taking it—one capsule three times a day—and the next morning the tremor had gone. German labs measure spike protein in lymphocytes, exosomes, and serum; a urine spike test in Italy and America shows metabolites and whether spike comes from vaccine, infection, or gut. They say hundreds of thousands helped; a woman’s fits stopped within two days of starting augmented NAC.