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Researchers examined tissues for spike and nucleocapsid proteins in a patient with COVID-19. Spike proteins are targeted by vaccines, while nucleocapsid proteins are not. In respiratory secretions, spike proteins were found, indicating the virus's presence. In the brain of a vaccinated patient who died, spike proteins were present, but nucleocapsid proteins were not. The absence of nucleocapsid proteins in the brain is puzzling.

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.

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

Tom Haviland, a retired major in the US Air Force and an experienced embalmer, discusses the presence of white fibrous clots found in the circulatory systems of deceased individuals. These clots, which have been observed in a high percentage of corpses over the past three years, are believed to be made of amyloid protein and fibrin. Embalmers have noticed an increase in the size and prevalence of these clots, as well as an increase in microclotting or "coffee ground" clots. The data collected from embalmers suggests that these clots may be linked to the spike protein produced by the COVID-19 vaccines.

There have been reports of blood clots in patients who have received the vaccine. These clots have been found in living patients and have also been observed in post-mortem examinations. The clots are made up of fibrous material and unusual combinations of proteins that make them difficult for the body to dissolve. However, it is important to note that not everyone who receives the vaccine will experience these clots. One possible solution is the use of an enzyme called Nattokinase, derived from fermented soy, which has been shown to break down fibrin and dissolve clots. Further research is needed to fully understand and address this issue.

We invited the staff of the Giovannini studio to discuss their study on the blood of over a thousand people, including those who were inoculated and those who were not. They found that the blood of inoculated individuals showed alterations in shape and arrangement of red blood cells when observed under dark field microscopy. In a normal blood sample, the red blood cells are spherical and well-oxygenated, with no foreign bodies present. However, in the blood of inoculated individuals, they observed the presence of nanotube-shaped inclusions that attracted red blood cells, leading to potential circulatory issues. This phenomenon, known as impelamento, can have thrombogenic effects. This occurs specifically in the blood of inoculated individuals.

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 speaker discusses the formation of white fibrous clots induced by the spike protein in the blood. These clots can lead to various health issues like heart attacks and strokes. The speaker mentions Nattokinase, an enzyme derived from fermented soy, which can break down fibrin and dissolve clots. They highlight that regions like Northern Japan, where fermented soy is consumed, have lower rates of heart disease and strokes. The speaker suggests trying Nattokinase as an enzymatic mechanism to break down clots before they worsen.

In a deceased patient, spike protein was found in the heart but not nucleocapsid protein. The autopsy revealed bronchopneumonia, Parkinson's disease, necrotic encephalitis, and myocarditis. The author suggests that the spike protein in affected tissues was likely from gene-based COVID-19 vaccines, not a SARS CoV-2 infection, as nucleocapsid protein was absent. Spike protein was found in areas with brain and heart inflammation, possibly contributing to the disease.

The data indicates that vaccinations have led to serious health issues, including blood clots, strokes, and amputations. A simple d-dimer test can reveal the presence of blood clots, yet the government has not mandated this test for vaccinated individuals. Studies by two cardiologists found that over 80% of vaccinated patients had elevated d-dimer levels, suggesting microemboli, which can cause gradual organ failure and increase the risk of severe thrombosis, particularly in the brain. Cases of thrombosis in young people are rising, likely due to microemboli and the spike protein from the vaccine affecting blood vessel walls. This connection has been established through clinical observations.

We purchased spike protein subunit MFC tag from Sino Biological and prepared it using doubly distilled water. A stock solution (0.25 mg/ml) was created by adding 400 µl of diluent to 100 µg of spike protein. This was diluted to working solutions. We assessed different spike protein concentrations in platelet-poor plasma using fluorescence microscopy. A healthy blood sample was divided into four tubes with varying spike protein concentrations (1000, 100, 50, and 1 ng/ml). Samples were incubated for 30 minutes at room temperature. We're replicating this experiment. I'll extract blood, add PBS buffer, and the spike protein. Then we'll look at the fluorescence.

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.

D-dimers are markers for thrombosis. When analyzing blood samples for suspected deep vein thrombosis or pulmonary embolism, the normal range should not exceed 500. However, there has been a significant increase in elevated d-dimers among vaccinated patients. Many patients have levels above 3000, leading to concerns about microthrombosis throughout the body. Despite further examinations, no embolism or thrombosis has been found. Fatigue is a common symptom among these patients. The risk is that these individuals may experience microthromboses, potentially leading to death in the future. This raises questions about the future health and insurability of those with high d-dimer levels. Investigations and studies should be conducted to understand these phenomena, including the occurrence of thrombosis in placentas during pregnancies.

There are real cases of blood clots in patients who have received the vaccine. These clots are thick and fibrous and can be seen in living patients. A tube of blood from a patient with cold-induced finger pain showed the same fibrils as the clots. The body has difficulty breaking down the material in the clots, including amyloid. Autopsies were discouraged early on, so these clots may not have been discovered. Morticians have noticed unusual back pressure when preserving bodies. The clots contain collected proteins and unusual combinations that are hard to dissolve. Nattokinase, an enzyme found in fermented soy, can break down fibrin and may be helpful in dissolving clots.

Protein misfolding is a recent phenomenon in the study of neurodegenerative disorders like Parkinson's and Alzheimer's. Other peptides besides the prion protein can also misfold and form toxic fibrils. Prions have been studied as potential biological warfare agents due to their robustness and toxicity. The transmission of prions is difficult, but recent research suggests that small epitopes on viruses and bacteria may also have amyloidogenic properties. Neuroinvasion and anosmia are independent phenomena caused by SARS-CoV-2 infection, indicating ongoing pathology at a fundamental level. The spike protein of SARS-CoV-2 has been found to cause amyloidogenic clots in the blood, potentially contributing to long-haul symptoms. There are also concerns about the homology between SARS-CoV-2 and HIV, as HIV epitopes have amyloidogenic properties and have been the focus of bioweapon research.

The spike protein, according to research in South Africa, induces fibrin from fibrinogen, forming the backbone of clotting in a way not previously seen. Unlike normal fibrin clots that are easily broken down, clots formed from COVID or the spike protein from the vaccine are difficult to break down, causing issues for many people. A cardiologist stated that in their decades of practice, they have never treated as many blood clots as in the last five years. These blood clots occur after the virus infection and the vaccine because the spike protein causes blood clots. Therefore, it is reckless to continue vaccinating people and loading the body with spike protein, causing more blood clots. According to a paper in Cell (July 2021), the nucleoprotein, not the spike protein, supplied broad and durable immunity for the prevention of infection. The speaker questions why the vaccine wasn't changed to target the nucleoprotein once this information came to light.

I recently conducted a survey of embalmers, and 73% of the 269 respondents reported finding white fibrous clots in corpses during 2023. These clots, which consist of fibrin, platelets, and amyloid-like material, are suspected to be a contributing factor in strokes and heart attacks. Embalmers are finding these clots are making it necessary to use multiple injection sites, lengthening the embalming process. While similar clots were observed in 2020, during the initial COVID outbreak, their prevalence exploded with the introduction of vaccines in 2021. The spike protein from the virus and vaccines may be responsible for the formation of these clots. Additionally, embalmers are reporting increases in microclotting and traditional grape jelly clots. One theory suggests "frame shifting," where ribosomes misread the modified RNA code from vaccines, creating aberrant proteins that form amyloid material. I can be contacted at thomashaveland@sbcglobal.net.

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.

White fibrous clots found in the living and dead recipients of mRNA vaccines are being ignored, but research reveals their composition and cause. The spike protein mutates fibrin into jagged, misfolded, insoluble amyloid, similar to prionic infections. Microclots form and align into large white clots, initiated by spike protein fragments like spike 601. Prolene, a "kinker protein" added to the spike protein, causes misfolding, with proline being prevalent in the clots. A 2021 paper showed the SARS CoV-2 spike induces abnormal blood clots due to the fibrinogen beta chain. Plasma exposed to the spike protein is imbalanced, with the fibrinogen beta chain being dominant. These clots contain four times the normal amount of phosphorus, released from lipid nanoparticles. Similar clots in 1988 were caused by sulfur-based heparin, which was resolved by reducing sulfur content. A 2017 paper showed altered phosphorus levels cause cancer. Thomas Havilland, who shares this information, is being ignored by mainstream and alternative media. Undertakers are seeing massive white fibrous clots at record levels.

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 speaker has been sequencing clots and found real human DNA, showing a signature of neutrophil extracellular traps, a reaction occurring in sepsis when the immune system clots around foreign entities. This process takes free-circulating DNA into clotting structures, leaving a specific signature. Sequencing reveals patient genome sequences that might predispose them to clotting. While billions received shots, not everyone clotted, suggesting a subset has a bad reaction. Genetic predispositions in the clotting cascade may increase risk. Initial analysis of two clots shows high-impact variants in genes involved in fibrin formation and clotting. Kevin McCarran's work demonstrates some clots bind thiophlavin, a marker for amyloid, suggesting a potential amyloidosis issue. Pathology needs careful examination as it may underlie clotting problems. This information is being suppressed, but citations are provided for reference.

The speaker discusses the formation of clots induced by the spike protein in the blood. These clots can be white and fibrous, and they can vary in size. The speaker mentions that these clots can lead to heart attacks or strokes if they block the flow of oxygen in the body. They also mention an enzyme called Nattokinase, derived from fermented soy, which can break down fibrin and dissolve clots. The speaker suggests that using enzymatic mechanisms to break down clots early can prevent the accumulation of amyloid proteins and the worsening of clots.

Bonjour à tous, Anaïs Bloqué, docteur en biologie santé, explique les impacts de la protéine Spike du SARS-CoV-2 sur le système immunitaire inné, basés sur son article récent. La Spike seule n'active pas complètement le TLR 4, un récepteur immunitaire, et ne produit pas d'interférons de type 1, essentiels pour la réponse antivirale. Pour une activation complète, la Spike doit s'associer au LPS (des bactéries Gram négatif). L'activation des interférons 1 augmente l'expression d'ACE2, le récepteur du virus, via les ISG, sensibilisant l'organisme à l'infection. Les ARN messagers des vaccins peuvent aussi lancer la production d'interférons 1 via MDA5. La Spike, protéine amyloïde, peut aussi déclencher le TLR 4 avec des fibres amyloïdes, entraînant un "double effet amyloïde". L'augmentation de NF-κB par les ISG peut bloquer la p53, potentiellement cancérigène. De plus, NF-κB induit le MIR-200c, qui bloque l'ACE2. Chez les individus avec comorbidités, une boucle d'amplification inflammatoire se crée : Spike-LPS-TLR4 induit interférons 1, ISG, surexpression d'ACE2, augmentation de NF-κB, MIR-200c, diminution d'ACE2 et augmentation d'angiotensine 2. La Spike persiste longtemps, et ses propriétés amyloïdes font craindre des pathologies dégénératives à long terme. --- Hello everyone, Anaïs Bloqué, PhD in health biology, explains the impacts of the SARS-CoV-2 Spike protein on the innate immune system, based on her recent article. Spike alone does not fully activate TLR 4, an immune receptor, and does not produce type 1 interferons, which are essential for the antiviral response. For complete activation, Spike must associate with LPS (from Gram-negative bacteria). Activation of interferon 1 increases the expression of ACE2, the virus's receptor, via ISGs, sensitizing the body to infection. Vaccine mRNAs can also trigger the production of interferon 1 via MDA5. Spike, an amyloid protein, can also trigger TLR 4 with amyloid fibers, leading to a "double amyloid effect." The increase in NF-κB by ISGs can block p53, which is potentially carcinogenic. In addition, NF-κB induces MIR-200c, which blocks ACE2. In individuals with comorbidities, an inflammatory amplification loop is created: Spike-LPS-TLR4 induces interferon 1, ISG, ACE2 overexpression, increased NF-κB, MIR-200c, decreased ACE2 and increased angiotensin 2. Spike persists for a long time, and its amyloid properties raise concerns about long-term degenerative pathologies.

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.