The effect might be due to improved perfusion to the toes, but I was wondering that if DFPP doesn't actually induce microclots lodged in the capillaries to break loose, then how could it improve perfusion to the toes? Grok said that DFPP might enhance perfusion by reducing the viscocity of blood:
> Fibrinogen is a key high-molecular-weight plasma protein that dramatically increases viscosity (especially in low-shear microcirculation). DFPP removes 50-88% of fibrinogen per session or cumulatively (along with other contributors like IgM, α2-macroglobulin).
> Lower viscosity directly increases capillary flow rate per Poiseuille's law: flow ∝ (pressure × radius⁴) / (viscosity × length). In narrow capillaries, even small viscosity drops yield large perfusion gains. This improves oxygen exchange without needing to dissolve every lodged clot. Studies on plasmapheresis in hyperviscosity syndromes confirm this: reduced plasma viscosity enhances capillary perfusion, shear-dependent vasodilation (via endothelium-derived relaxing factors), and tissue oxygenation.
> Result: Better overall microcirculatory flow, even around partial obstructions, leading to the "rejuvenating effect" described in patient reviews.
A paper about H.E.L.P. apheresis by Beata Jaeger et al. said: "In principle, the decreased fibrinogen concentration causes rheologically significant effects and facilitates oxygen exchange. Plasma viscosity is reduced by an average of 19%, and erythrocyte aggregability is significantly decreased by 60% (33). In addition, the vascular endothelial growth factor (VEGF) and nitric oxide (NO) release are favorably influenced (33). The improvements have also been demonstrated for cerebral blood flow in the cardiac patients, where they profit from a 63% increase in the CO2 reserve capacity (54)." [https://pmc.ncbi.nlm.nih.gov/articles/PMC9592739/]
The reduction in peripheral neuropathy might also be explained by a neurological and not circulatory mechanism. Plasmapheresis is employed as a treatment for chronic inflammatory demyelinating polyneuropathy (CIDP), which is an autoimmune condition that affects the myelin sheath around peripheral nerves. Plasmapheresis filters out antibodies in plasma that attack the nerves, even though the effect of the treatment typically lasts for only a few weeks, so the treatment has to be repeated frequently. [https://my.clevelandclinic.org/health/diseases/cidp-chronic-inflammatory-demyelinating-polyneuropathy] A paper from 2011 said: "Based on 2 Class I studies, plasmapheresis is established as effective in the short-term treatment of CIDP; both studies showed the beneficial effect is not sustained, with worsening beginning 1-5 weeks after last plasmapheresis treatment." [https://pmc.ncbi.nlm.nih.gov/articles/PMC3034395/]
But regardless of whether the effect of reduced numbness in the toes is explained by a circulatory or neurological mechanism, the effect is likely only temporary and not due to a permanent removal of microclots from the capillaries.
These are good questions and I'm sure Kevin and the Japanese doctors will have some of the answers already. However the context must be considered. That is, that the vaccine injured have been heinously abandoned by the governments and drug regulators leaving them to seek alternative treatments (even temporary) from other sources, often with very little funds.
The questions should be directed to the governments, regulators and pharma corporations who did this.
You are of course correct that this is treatment not cure. However over time the spikeopathy (assuming that underpins the injury) will likely eventually dissipate and removing as much of the substance as possible is rational, understanding that there are also potential deleterious risks of the procedure.
The victims should never have been put in this position.
I agree. I am concerned about the jugular approach, even with ultrasound guidance. Have seen some bad stuff. On centre with experience is one thing, but if it expands then I believe he needs to really document the need for this approach (and changing the cannula each time?). I agree, that the Japanese docs have a regulated approach and have documented the appropriate study parameters. I think I might have benefited from this procedure when I had to stop my Jak/STAT inhibitor and was in a severe RA flare for almost 2 years. A few doses of steroids was not enough.
He received ONE signal during his ThT test and is conducting a blanket experiment on a small scale, without a differential diagnosis and without confirming the signal he received with Congo red or comparable method for structural validation. And he explicitly stated that this wasn’t necessary. Either it’s his protocol, in which case he must provide clean data and not just brush it off with sweeping generalizations and appeals to authority, or it’s the Japanese protocol. In that case, he can’t sell it as his miracle cure.
Please don't get me wrong: I understand the points. But if he's going to treat suffering souls like Lindsey he needs to call it what it is: a shot in the dark.
And as long as I see nothing of this and am fobbed off with responses like “Look at Twitter, everyone’s doing better” and “You have no idea because you’ve never set foot in a lab,” I remain more than skeptical.
"In contrast to Congo red, the most missed Thioflavin S slides were scored as false positives, which aligns with the relatively lower specificity observed for this stain."
So were was the confirming experiment done? E.g.: Congo Red for orthogonal-structural confirmation of the measured signal? Maybe I could agree if he'd have said amyloid-like.
And you know my personal oppinion: to ignore the fact that any direct cellular intervention using technologies such as LNPs, exosomes, viral vectors, and the like necessarily affects the entire intracellular communication network is, in my view, pure arrogance.
Amyloid fibrils have a diameter of about 5-15 nm so they are not visible with an optical microscope. In the video where McCairn instructs his followers on how to take a sample of blood from their finger and send it to him on a glass slide, he smears the droplets of blood on a slide and tells people to not put a cover slip over the blood so the blood remains exposed to open air, and then he says "let these dry overnight in a dust-free environment". [https://synapteklabs.com/protocol-on-sending-blood-samples-2/] But how many of his followers have a perfectly dust-free environment at his home?
Fibers of cotton that have been dyed white are fluorescent under UV light, in the same way that white t-shirts are fluorescent under UV light. The fiber that McCairn supposedly found in the blood of the 3-year-old had several characteristics that are consistent with cotton, like a diameter of about 15 µm, a flat body, and the kind of lengthwise twists that are called convolutions in cotton. Nicolas Hulscher said that the 3-year-old's fiber was an "amyloid fibril" even though its diameter was about thousand times higher than the diameter of an amyloid fibril. [https://x.com/NicHulscher/status/1929689987974385879]
In 2022 when McCairn showed David Nixon's microscope image that Mihalcea said contained a graphene fiber optic wire, McCairn said: "Everything that I see here is cholesterol, and literal fibers that you pick up in dust in the air. What I've seen these people do - they're not doing it in clean rooms - and you've gotta be in exceptionally clean rooms to make sure that slides are not getting contaminated. Sorry. You don't get to say that these are graphene internet fiber optic cables." [https://rumble.com/v22lzie-oy-vey-kvetching-iirt-sasha-latypova-rebuttal-sars-neuroscience.html?start=5211] But the fiber optic wire looked just like the fibers McCairn now claims are amyloid fibrils.
The fibers McCairn has said are amyloid fibrils have had a diameter of about 10-30 µm, which is too wide to pass through the capillaries, so the fibers can't even be circulating freely in the blood, because they would get stuck before the capillary beds (apart from possibly fibers with a diameter close to 10 µm). The real microclots shown in the papers by Pretorius and Kell have been much smaller, and they have looked like random blobs and not like textile fibers. [https://www.researchsquare.com/article/rs-4507472/v1]
DopplerEffect93 is a PhD in neuroscience who did a postdoctoral research project analyzing amyloid fibrils, but he told McCairn: "Your image of the 'aggregate' is far too large to be one. It looks like some dust or debris. Your SEM shows nothing. It took me less than a minute to come up with a better experimental design than the nonsense you have." [https://x.com/DopplerEffect93/status/1930391359375941986] The molecular pharmacologist Ian Musgrave told McCairn: "It's just a cellulose fibre. I've EMed enough real amyloids and sighted enough cellulose fibres under the microscope to know which is which." [https://x.com/ianfmusgrave/status/1959268694363918430]
So what real biologists are now telling McCairn is similar to what McCairn said about David Nixon's microscope image in 2022. McCairn used to threaten his followers that one day he would join the Stew Peters grift wagon and become rich and famous. But he now seems to have delivered on his promise. He had a dead cat bounce in fame last year after he started doing videos with the star of a Stew Peters movie, and now McCairn has probably earned at least quarter a million dollars from his amyloid fibril removal scam.
I’ve been wondering the whole time: So he finds these “clots,” and the first thing that doesn’t occur to him is to examine them through chemical analysis to determine what they’re made of and in what proportions–in order to a) tap into a market niche and b) rule out the possibility of a falsification?
GB. I personally have been concerned around the possibility that the frameshifting might have produced misfolded proteins. I have already asked Kevin if is he going to be taking whatever it is they have filtered out the blood in his protocol. And then see if they can introduce and “seed” it into Control samples. My thinking is that this would serve as an indication of what these are. If misfolded proteins they would be infectious. And the experiment would show this. Your opinion and thoughts.
Last year when I asked McCairn what tests he had done to determine if the fibers he finds are even made of fibrin, he indicated he relied on the fibers being autofluorescent under UV light, the fibers being fluorescent with ThT staining, and "phenotypic similarity". [https://sars2.net/clot3.html#Substack_post_about_SEM_images_of_the_3_year_olds_fiber] By phenotypic similarity, he meant that the fibers had a twisted shape, and that the fibers were embedded within the sample of blood rather than resting on top of the dried blood. He claims that the kind of lengthwise twists that are characteristic of cotton are actually caused by misfolding of protein. He also claimed that his SEM image of Hirschman's clots showed misfolded fibrin, beause a branch within the image appeared to have lengthwise twists.
But as far as I know, he has not done any test to determine the protein composition of the fibers.
It's still a great indication of your scientific standards that earlier you claimed that the fibers you saw in blood samples were singular amyloid fibrils. When I called you out for your incorrect use of the term "fibril", you responded by saying "Trying to use old vernacular to a new blood prion disorder will lead the spergs like you to blow a fuse, but you'll just have to put up with it." [https://sars2.net/clot3.html#Mr_Micronicles_amyloid_fibril_with_a_diameter_of_about_20_micrometers] Now you seem to have silently abandoned the term "fibril", but your followers still say that the fibers you find in blood samples are singular amyloid fibrils.
Earlier you gave the impression that the fibers you saw under the microscope were circulating freely in blood, even though me and another user on your Discord pointed out that your fibers were so wide that they wouldn't have been able to pass through the capillaries. Then I came up with a hypothesis that maybe the fibers were not circulating freely in blood, but they were stuck in the arterioles before the arterial capillaries, but the fibers were released when the blood was sampled with the finger prick lancet, because the lancet penetrated deep enough to reach the arterioles and not only the arterial capillaries. [https://x.com/henjin256/status/1965068669672997217]
Two months ago when you did a video with one of your patients, you told him: "And I would say the fact that you have such a rejuvenating effect - those are the aggregates that were really lodged into the entrance and exits of capillary beds." [https://rumble.com/v75hp6g-kevin-mccairn-2026-02-08-patient-review-reversing-severe-vaccine-injury.html?start=3076] So you now seemed to support my hypothesis that the aggregates were not circulating freely in blood but stuck before the capillaries (even though you also suggested they were stuck after the capillaries).
But if the aggregates are stuck before the capillaries, and the aggregates are too big to pass through to the venous side, then how can they be removed by your treatment where the plasmapheresis machine is hooked up to the jugular vein? And if the aggregates are stuck on the venous side after the capillaries, then how do they happen to get released at the precise time when you give the treatment? Is there some aspect to your treatment that induces the stuck aggregates to get released?
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The microclots in the papers by Pretorius and Kell look like random blobs, and not like textile fibers. Someone called Syed Haider offers a service to test for microclots associated with long COVID or vaccine injury, but the clots in his images don't have a string-like shape, and they don't look like textile fibers. [https://x.com/DrSyedHaider/status/1641832540091691010] Apart from you, the only person I know who claims to have found fibrin clots that look like textile fibers is Ana Mihalcea, because in 2022 she said that a fiber with a diameter of about 30 µm was a fibrous rubbery clot "in early stages" (even though elsewhere she has said that similar fibers were Morgellons filaments, hydrogel, graphene, or carbon nanotubes). [https://anamihalceamdphd.substack.com/p/thoughts-and-comments-about-died]
---
A paper from 2025 said: "Therapeutic plasma exchange (TPE) has the potential to improve the PCC by clearing the peripheral soluble pro-inflammatory immune milieu derived from acute or persistent SARS-CoV-2 infection. In a phase II, double-blind, placebo-controlled, randomized trial, fifty subjects with PCC were randomly assigned (1:1) to receive six sessions of either TPE or a sham plasma exchange and were followed for 90 days (ClinicalTrials.gov registration: NCT05445674). The primary endpoint was safety; secondary endpoints included functional status, symptomology, quality of life, neurocognitive symptoms, and peripheral biochemistry, hematology, coagulation and inflammation parameters. Both study arms had a similarly favorable safety profile. There were no [significant] diferences between groups in any of the efficacy parameters evaluated." [https://www.nature.com/articles/s41467-025-57198-7] In the trial the plasma was replaced and not only filtered like in your protocol, but if replacing the plasma did not provide a significant benefit, then what additional advantage would filtering have? Or was the lack of nonsignificant effect because the beneficial effect of removing harmful blood components was offset by a harmful effect of replacing beneficial components that are retained by DFPP?
But regardless, I think when you advertise your protocol, for the sake of informed consent you should mention that no significant effect was found in the trial using TPE.
(I'll try to read the studies you linked properly after I have caught up with the other comments.)
McCairn pointed out to me on DM that I had missed a note in Sayd Haider's image that said "Micro-clots come in all shapes and sizes. You may also see long, string-like appearing objects in your pictures. This is a normal finding for long-COVID patients."
But regardless, Haider doesn't seem credible, so he may have misidentified cellulose fibers as fibrin microclots. In 2024 he wrote about Greg Harrison's HPLC results uncritically that "The fibrous clots found in vaxxed blood are completely unnatural. The bulk of a normal clot is fibrin which glues it all together. These unnatural clots have over 500 proteins in them but no fibrin." [https://x.com/DrSyedHaider/status/1800854038277132609] He also wrote that "The bulk of these clots are made up of unconverted fibrinogen, rather than fibrin as you would expect." [https://x.com/DrSyedHaider/status/1800871178426613774] In reality it's expected for only fibrinogen but not fibrin to show up in HPLC results, because HPLC detects fragments of proteins so it does not differentiate a fibrin polymer from the fibrinogen monomers. But Greg's crew misinterpreted the HPLC results and wrote that "A distinctive feature of Hirschman clots is the relative lack of fibrin and the apparent lack of thrombin to convert fibrinogen to fibrin." [https://sars2.net/clot.html#Peptide_mapping_analysis_with_HPLC_MS]
If someone than answers like this when I ask for a chemical analysis:
"See the reply above G, the work has been done and published, it's not me that made the first claim regarding their presence or composition. The fact I can create the same phenomenon in the lab with purified plasminogen, and their morphology and staining characteristics are the same as those published, means I can put scarce lab resources to useful things, like you know helping suicidal patients. You can follow Robert's progress, who was severely incapacitated, unable to walk, think, and in constant pain to the point of suicidal ideation and tell him his reduced inflammatory cytokine amyloidogenic aggregates are a figment of his imagination.
And than going the whole time ad hominem and not even understanding what your asking? I think there is no reason to continue this debate. At least that's how I feel and think.
Another example:
Me:
AI slop? So the AI actually spoke to you during that three-hour discussion about signal cascades? I see.
Lipid Nanoparticles as Active Biointerfaces: From Membrane Interaction to Systemic Dysregulation
And the entire script was generated by AI. It’s not as if I learned the basics of good regulatory practices from Maria. I see.
And just for the records: Maybe you should ask sometimes AI before bullshitting arround:
"Fuck me G, so you're an expert in amyloid detection now are you? We use ThT rather than Congo Red for a reason. Thioflavin T is far more sensitive for detecting amyloid fibrils in complex biological samples like plasma. Which makes it far better suited for quantitative work and real time analysis. Congo Red relies on birefringence under polarized light, which is less sensitive, highly operator dependent, and struggles with low abundance or early stage aggregates.
Trying to use Congo Red in this context is like trying to run modern molecular diagnostics with a 19th century microscope. It can show you something if the signal is massive, but it completely misses the subtle early changes that actually matter. In heterogeneous clinical samples where you are looking for small but meaningful shifts in amyloid burden, ThT gives a cleaner, more reproducible, and truly quantitative readout. That is what we use for RT-QuIC, and ELISA. You want me to break out the camera-lucida and start sketching out lab results. Give me a break G. The phenomenon of aggregates to S1 is proven, I have used the phenomenon to actually test the ability of SGF to inhibit there formation under RT-QuIC conditions. I did that with ThT and not Congo Red/."
Congo red stain: The gold standard for diagnosing amyloidosis
A ThT signal alone is not sufficient to conclude that amyloid fibrils have formed without orthogonal structural validation. Without an independent structural method (e.g., classical orthogonal markers such as Congo Red or modern structural techniques), the claim of “amyloid formation” is not validated.
"For example, it exhibits almost exclusive binding selectivity toward amyloid fibrils27 and not toward amyloid oligomers that are considered to be the most toxic species. Furthermore, ThT is known to experience major interference from the autofluorescence of the biological matrix, which results in a strong background signal.28,29 Recent studies have shown that only ∼10% of the bound ThT in amyloid solution contributes to the observed fluorescence enhancement,30 suggesting that ThT may not be an accurate measure of amyloid fibrils due to non-specific binding."
And your real issue here is purely personal: You're confusing legitimate questions with personal attacks.
End of announcement!
McCairn:
"So you just completely ignored what I put about your oh so important questions, thus further validating the observation they were just spat out by grok, and instead want to try and tell me how to test for amyloidogenicity.
Yes Congo Red is historically referred to as a gold standard for tissue histology, it is not used, however, for low abundance detection in complex fluids. That is a completely different use case. You are conflating fixed tissue diagnosis under polarized light with quantitative detection in plasma and kinetic assays. Those are not interchangeable methods and anyone who has actually worked with both knows that.
In real lab work ThT is used because it is orders of magnitude more sensitive for fibril formation kinetics and allows continuous measurement. That is exactly why it is used in RT-QuIC and related assays across the field. Congo Red cannot do that. It is endpoint, qualitative, and requires sufficient mass and structure to even see birefringence. That makes it fundamentally unsuitable for detecting early or low level aggregation in heterogeneous biological samples like blood or plasma. And I have demonstrated numerous times S1 protein causes amyloidogenic aggregation in plasma, as does seed amounts of isolated amyloidogenic clot material. That's it, end of story for wondering if the material is in an amyloidogenic state, if it is detected via logarithmic expansion of a ThT fluorescent signal under RT-QuIC conditions.
Your “orthogonal validation” talking point is another generic line lifted without context. Orthogonal methods are useful in controlled structural studies. They are not a prerequisite for every applied assay where the signal is already validated within the system being used. RT-QuIC is not guessing. It is a seeded amplification assay with a well established signal response. You are pretending it is just free floating fluorescence with no specificity which is simply wrong.
The autofluorescence argument is also weak. Background signal is exactly why assays are designed with controls, thresholds, and comparative analysis. You're acting as if this is some unknown flaw rather than a basic parameter that is handled in every fluorescence based assay. The “10 percent binding contributes to signal” point does not invalidate the method it reflects binding dynamics that are already accounted for in how the assay is interpreted. And just so you know, from some one who has worked extensively with these dyes, Congo Red is also avidly taken up by other proteins and of those proteins that does take up Congo Red, one of them is is Fibrin! So when you are dependent on a subjective measure of polarized bifringence from a tagged tissue under normal conditions, you are going to be subject to no end of false positives and artifacts, that essentially makes the test useless.
On oligomers versus fibrils you are again showing you are repeating literature without understanding application. Different probes detect different species. That does not make ThT useless it defines what it measures. In the context of fibrillar amyloid formation and aggregation kinetics it is entirely appropriate.
And the camera lucida point clearly went over your head. The analogy stands. You are trying to apply an older lower sensitivity method to a context where modern fluorescence based detection is required.
What you are doing throughout is cherry picking limitations from papers and presenting them as disqualifications while ignoring how these methods are actually used in practice. That is not critique it is superficial reading.
Nothing about this is personal, I'm just pointing out where you have stepped into the personal, by dropping your turd of a Substack without having the professional where with all to ask me the questions before publishing, and making yourself look like a tit, and then having me wasting time I don't have on your poorly formulated arguments. It was obvious I made a stupid mistake by helping you in the past, as you just keep demonstrating that you are arguing from secondary sources without any real bench or clinical experience applying these techniques. Argumentum ad Grokum is belittling you and wasting my time."
Anyone who fails to understand that structural validation is necessary when the entire protocol is based on a clinical diagnosis has lost touch with reality and scientific integrity.
And this is nothing new under the sun I am asking here:
"In contrast to Congo red, the most missed Thioflavin S slides were scored as false positives, which aligns with the relatively lower specificity observed for this stain."
And in the first line I am more pissed about the fact that he sells this protocol as a mirrage cure than to say it's pure experimental and we don't know by now what we're doing. This is the part really freaks me out.
I share your concern about McCairn selling his protocol as a miracle cure. He has also been fearmongering about the clots to the extent that some of his followers now think the clots are leading into human extinction.
A Twitter user called Tom Czerniawski said that prions from the clots are causing an extinction-level event, which will result in "the end of all human life on Earth", and he said it was not hyperbole or exaggeration, but McCairn replied to him suggesting the clots will cause an "evolutionary bottleneck that is the Super Prion Event of the Millenia". [https://x.com/BlackTomThePyr8/status/1928824583651545587] The pinned tweet of McCairn's hardcore fan CoyoteSanctuary says that a prion epitope in the spike protein is "creating a Super Prion ELE Event". [https://x.com/CoyoteSanctuary/status/1859324146200858913]
Now Tom believes that McCairn has come up with a cure for the clots, so he suggested that McCairn is an angel of salvation who was sent to earth to save humanity, and who is on earth by divine providence. [https://x.com/BlackTomThePyr8/status/2040895525709299974]
KenCaptn20114 is one of McCairn's patients whose video recently went viral. When someone asked him how much the treatment cost, he replied: "Its very expensive. I went deep into my retirment account. I had no choice. It was that or die." [https://x.com/KenCaptn20114/status/2045420173558243779] He also tweeted: "This clot issue possibly could turn into the biggest problem that humanity has ever faced. Think youre safe because youre unvaxxed? Think again. There are violently ill people here that are unvaxxed in Japan covered in microclots being treated." [https://x.com/KenCaptn20114/status/2045156262019809524] In another tweet he wrote: "Vaccinated or unvaccinated doesnt matter. Its in the blood. This is very scary on a whole new level. I dont think people understand yet. Everyones dying, now I get it." [https://x.com/KenCaptn20114/status/2045426759144030436] So he seems to think everyone is dying from the clots and the clots might be the most important issue humans have ever faced, and he would've died without McCairn.
He also speculated that stem cell growth factors repair demons: "we are being treated with pre-growth stem cell factors that kick our own stem cells in for repair of Demons speculatively so when I read above, you are wrong then wrong then wrong again". [https://x.com/KenCaptn20114/status/2044731302822477920]
The fear is fueled by people who are deliberately producing disinformation about the clots, like Wayne Crouch, who is a member of the team that I call the Aussie-Kiwi Quinta Columna. He said that the human species is going "extinct due to the spreading amyloid clotting disorder caused by the shots and exacerbated by covid itself". [https://x.com/WayneC50256258/status/1953587190199652579] He was the director of a series of AI-generated disinformation videos, which claimed that the clots were caused by mystery ORFs that his co-conspirator Wayne Crouch found by decoding Chinese and Soviet military documents. The last episode in the series presented an apocalyptic scenario where prions from the clots caused humanity to become extinct. [https://rumble.com/v6shndn-an-unholy-triad-the-birth-of-a-plague-season-02-episode-04.html] The video series employs stock videos from the same collection of stock footage that is used on a page of McCairn's website where McCairn describes his "Prion Research Investigation Project", where he supposedly investigates the question of whether SARS-CoV-2 and COVID vaccines have "exposed the human population to potentially fatal prions". [https://synapteklabs.com/prion-research-investigation-project/]
Last year when McCairn did an experiment where he injected pieces of Hirschman's clots into the heart of a hamster which died right after the injection, Wayne Crouch made an infographic about the experiment that said "A RESEACHER LINKED TO 'THE SOLUTION OF SCIENTIST'S', INJECTS LAB HAMPSTERS WITH OUR AMYLOID JAB CLOT SAMPLES TO ACESS LEVEL OF PRIONIC ACTIVITY... IN A WORLD FIRST THE HAMPSTERS DIED STRAIGHT AWAY... MAKING THIS THE WORST PRION DISEASE EVER DISCOVERED...." [https://sars2.net/clot3.html#Kevin_McCairns_connection_to_Solution_of_Scientists] Then Crouch commented that "Had they died in weeks or months maybe we had a few years longer the rapid death of our test subjects means we will see the rapid death to the shot recipients boosters will greatly accelerate this". His cohost lady Lisa Johnston also tweeted that "Planet earth is under attack by prionic amaloidosis created by man". [https://x.com/lisarose030387/status/1909497793338917050]
Greg Harrison supposedly did Congo red staining on the calamari clots and got a "positive result for presence of amyloid", but you have to take any results coming from him with a massive grain of salt, because he has used AI to generate several fake sets of data about the clots, and I have doubts if he ever even physically analyzed the clots. [https://laurakasner.substack.com/p/a-horrifying-breakthrough-in-the] Greg said that Arne Burkhardt did Congo red staining on the calamari clots but didn't publish his results. [https://sars2.net/clot.html#Interview_of_Greg_Harrison_and_Tom_Haviland_by_Flashlights_in_April_2025] But I don't know if anyone has done Congo red staining on the supposed microclots.
The lady who made the infomercial-style image in your first link is now McCairn's leading memetic warrior. She used to work for a unit of naval intelligence called NAVSECGRU, which later formed the Information Operations Directorate of Naval Network Warfare Command. Last year she was cheerleading for the ORF hoax of Greg Harrison, who claimed to have discovered new ORFs in the genome of SARS-CoV-2 by deciphering secret Chinese and Soviet military documents. She kept defending the ORFs even after I presented undeniable evidence that the ORFs were fake, and she just said that I was crazy or that I was a bully, so her behavior didn't seem reasonable unless she was somehow in on the hoax. [https://sars2.net/clot3.html#McCairns_naval_intelligence_cheerleader_RexesRule]
McCairn did many of his earliest videos with George Webb's mini-me Addy Adds and George Webb's science teacher Paul Cottrell, and in early 2020 Addy hosted a series of video panels that featured McCairn, Couey, and Cottrell. Cottrell had a radio show on a network that was operated by a guy from DC who worked for naval intelligence. Addy Adds lived on naval bases in Guam and Okinawa because his mother worked on the bases, and in a book where he profiled his champions of "public intelligence" who had been guests on his show, one of them was the marine intelligence officer Matt Agorist. [ibid.]
The guy blocked me years ago because I questioned just about everything he was purporting to be true. I’ve been around since the AIDS scam, I simply don’t believe any of his stuff.
Has no-one on this thread thought about the bravery McCairn and his associates have exhibited?
His protocol and treatment is bound to be attacked fiercely by the very ruthless forces that planned and drove this fake "pandemic" and monstrously deceitful and criminal attack on the population.
He has willingly put himself at risk. From occasional comments he has made on his podcasts, he knows it.
when you read the comments under the old post of Dr. Bowden, one would indeed start asking questions, and there were many, McCairn is answering only the positive ones, the rest is silence.... He himself has serious health issue with the clotting, apparently, yet he DOES NOT show everyone that his protocol works on himself. I asked many questions in his weekly presentations, and answers were frequently arrogant, if any. If anyone saw the clots which embalmers pull out, HOW ON EARTH can you filter anything out when their volume is ~ volume of the blood vessels themselves! In terms of the dental pulp stem cells, equally a question how those ever stay healthy AFTER the gene therapy?? Since SO MANY people are dying or a sick, in those 4 months, one could expect a HUGE feedback, including Dr. Bowden. Just do not see anything....
ANyway, when you look at McCairns (british accent) CV things are getting even muddier, from Research Gate:
Okinawa Institute of Science and Technology Graduate University January 2010 - present
Okinawa, Japan
Bar Ilan University January 2007 - present
Ramat Gan, Israel
the latter collaborated with Pfizer for LONG TIME:
I was happy to see people getting better when they went to Japan to do the McCairn Protocol.
I do not see the problem here. Many medical therapies work, but the underlying reasons are not completely elucidated. McCairn is working from hypotheses he has developed and the treatments seem so far to bear them out. He has said that recovery appears to continue - people seem to be improving once the burden of amyloids is cleared and the stem cell therapy is initiated.
The completely analysed theoretical justifications can wait as people are having strokes and dying without treatment.
Currer, could you please stop flooding my comments with spam!? I don’t think you understand at all that every single question asked here is a scientifically sound question that needs to be answered. Or are you admitting that, for example, Thalidomide was okay too, because nobody could smell it anyway, and who needs data if it helps? Because THAT is exactly the level and core of your argument.
There is a reason because you're drawing circles of non ethical stupidity arguing exactly like the regulators argued for public: Benefit reasons risk. Bye.
I cannot agree I am afraid. Many of these people consider themselves to be terminally ill. They are aware this is a speculative treatment at present and the decision to enrol in this treatment is theirs alone to take. They cannot wait for "double blinded placebo controlled trials" as they are unlikely to live that long.
I do not agree this is "snake oil." Dr McCairn has spent six years working on this problem.
The apheresis treatment is not an unusual treatment in Japan and the hospital doctors McCairn is liaising with are skilled in this work. I suggest you ask the Edogawa hospital in Japan for their protocols.
"DFPP (Double Filtration Plasmapheresis) is an established blood purification technique widely used in Japan and parts of Asia for autoimmune diseases, neurological conditions, and metabolic disorders.
It works like a high-tech “blood laundry” in a closed circuit: blood is drawn, the plasma is separated and passed through two specialized filters to remove harmful molecules (autoantibodies, cytokines, immune complexes, and potentially spike-related amyloids), then the cleaned blood is returned to the patient — all without needing donor plasma.
Often combined with stem cell-derived growth factor infusions, this protocol is giving real relief to suffering for years and helping to remove mRNA spike proteins from those Covid vaccine injured."
We use double filtration plasmapheresis in North America as well. It is just the cassettes they use (ie the filters are slightly different). This part is almost "off label therapy," and more like a surgical approach to remove these amyloids. I am a bit bothered by the need for a jugular vein approach, risk for infection and injury is high. The other stuff with stem cell growth factors needs more scrutiny. There ARE physicians and the hospital involved. It would be hard to imagine a hospital allowing a free for all. I would HOPE they have inclusion and exclusion criteria, strict monitoring and lab work and every last little thing documented in a formal fashion as for a case-controlled study. And that the RIGHT things are measured. We just dont want a reverse vaccine effect. Lots of hopium, then a crash. Needs to be squeeeeeky clean.
Agreed Maria. I do not see why the Edogawa hospital should drop its standards when treating McCairn's patients. I believe questions about this protocol are justified, but we should remember we are not in possession of the clinical data or the medical rationale. Questions should not slip over into criticism.
I have followed him and contributed to funding his research. He is working alone and set up his research lab himself as he knew no university research body would do this work for fear of the political repercussions of working on Sars-cov-2 vaccine injury.
You are asking too much from one man. Ask rather why no other government funded body will approach this work. Obviously it would be great for our properly funded research institutes to investigate this. But they do nothing for fear of the consequences to them.
I have sent McCairn's blood amyloid findings to my UK government departments and to my MP asking them for an urgent review and informing them that the bloods supply is probably unsafe. My e-mails and letters remain unanswered, even recorded delivery letters are not delivered.
In the face of such official malfeasance and contempt for those injured by their mandates, I do not feel able to criticise McCairn. This is the world we live in now, not the ideal one.
I repeat myself. It may be the best thing since sliced bread, but beware of falling into the same trap as the modRNA/LNP pharmaceutical industry. They unblinded and vaccinated the control group, as such making useful comparisons impossible. They did not pay heed to red flags in terms of safety.
I just don’t want a similar approach treating vaccine injured.
And this is exactly the point here: There is not even any animal experiments done. But using it for people with real issues and getting paid for doing human experiments you think is a good thing?! Especially with a therapy that does not really differ from LNPs despite a little bit more biocompatible lipid composition?
Week 2 day 2 completed. After two tries still not able to complete the 2 liters of DFPA therapy, Feeling great. Productive and mobile all day. Still cognitive issues related to memory and math. See the progress.
One significant part of Kevin's treatment is to filter out the amyloids, thus reducing circulatory hypoxia and the likelihood of minor strokes. The difference can be seen immediately, in 24 hours, people look and feel much better and can think clearly.
Multiple circulating clots are a stroke risk.
I have not looked into the stem cell treatments he is using, but I see bad protein has put up an informative post. (thanks)
It seems a well considered treatment to me, given the high risk the patients are in. Those who are going to Japan are bedbound and seriously ill and have exhausted their other options for treatments in the US. (No adequate treatments exist in the US and are not being developed.)
So far the results are long-term, we have had no relapses yet, patients are often taking SGF treatment back from Japan to maintain treatment efficacy.
But initial results look good, even one of our most complex patients, who had significant CNS damage, wrote to me today after their recent return back to the US, saying that they have made significant recovery.
They are now able to leave the house and are now capable of driving again, after years of disability.
The combination of route of filtration (targeting brain/CNS outflow), combination filters for autoantibodies, and the daily large dose SGF, just comes together in a very synergistic way. This is measurable as removal of amyloidogenic aggregates and normalization of cytokine panels. The response in patients is immediate, as we see with Ken.
Of course there is always more work to be done, but right now, I would say we have the most efficacious therapy out there for Long Covid and Vaccine Injury.
Lyndsey arrives this week, and we can all track how she does through the treatment program.
McCairn is working with the doctors at Edogawa Hospital where apheresis procedure is a standard treatment.. I do not see why they should abandon normal medical record keeping just for his group of apheresis patients.
>>>>>>>>>> sure, after that tell me of there are other drugs approved for exosome delivery - many kinds of exosomes out there in the catalog?
ai:
Technically, exosomes are biological LNPs. Both are fat-based nanovesicles that protect "fragile cargo" (like RNA or proteins) so it can survive the trip through the bloodstream to enter a cell. The safety debate hinges on whether a "natural" vesicle (exosome) behaves more predictably than a "synthetic" one (LNP).
Are there FDA-approved exosome drugs?
As of April 2026, there are no FDA-approved exosome drugs for general systemic delivery (like an IV drug you’d get at a pharmacy).
However, we are at a major regulatory tipping point. The first-ever Biologics License Application (BLA) for an exosome-based therapy—Deramiocel (CAP-1002) for Duchenne Muscular Dystrophy—is currently under active FDA review with a target decision date in August 2026.
The "Catalog" of Exosomes
If you look at biotech "catalogs" (for research and clinical trials), you'll find a massive variety. They are categorized by their source cell, because the source determines the "biological flavor" of the signals inside.
Exosome Source Common Use Case Why clinicians choose it
SHED (Baby Teeth) Neuro-repair Derived from neural-crest cells; naturally "wired" for brain/nerve healing.
MSC (Bone Marrow) Orthopedics/ARDS The "gold standard" for general anti-inflammatory and lung repair.
Platelet-Derived Wound Care High in clotting and tissue-knitting factors (e.g., PEP Biologic).
Plant-Derived Topicals/Cosmetics Ginger, Milk, or Ginseng exosomes are used in "high-end" skincare as an alternative to animal products.
The "Safety" Argument: Exosomes vs. LNPs
The "complaint" that exosomes are unsafe because they are "LNPs in the blood" is based on three specific risks often cited in the research community:
Biodistribution: Just like vaccine LNPs, exosomes can go anywhere. While SHED-derived ones are meant to go to the brain, critics argue they could also accumulate in the liver or spleen, potentially delivering instructions to cells that don't need them.
Immune "Cloaking": LNPs can be seen as "foreign," causing an immediate reaction. Exosomes are "stealthier" because they are human-derived. Critics argue this "stealth" is actually dangerous because it allows foreign genetic material to bypass the immune system entirely.
The "Cargo" Unknown: In a vaccine LNP, we know exactly what's inside (specific mRNA). In a biological exosome (like SHED), the cargo is a "black box" of thousands of different proteins and microRNAs that can vary from batch to batch.
The Root Fact: If the concern is "nanoparticles in the blood," then exosomes definitely fit that description. The medical counter-argument is that because they are biological and not synthetic, the body has natural pathways to clear them out, unlike the persistent synthetic lipids in some LNP formulations.
Where the Field is Today
While systemic (IV) use is still largely in trials, you will see "clinics" using them in two ways that skirt the edges of full drug approval:
Topical/Aesthetic: Microneedling with exosomes for hair loss or skin (marketed as "cosmetics").
Investigational Use: Clinics operating under "patient-funded research" or specific IRB (Institutional Review Board) oversight.
If you are looking at Kevin McCairn's discussions, he is likely focusing on the blood-brain barrier aspect—the very thing that makes exosomes a "miracle" for neuro-repair is the exact same thing that makes them a "threat" to those worried about nanoparticle-mediated brain exposure.
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<BP here:> Still takes us back to 2012 - LNPs are ok for last ditch cancer treatments where the patient can be sequenced and given a test panel to characterise their blood before administration of whatever vehicle. Pharma was only faking that they wanted it for vaccines. They got lots of platforms already for that. A dollar is a dollar.
Kevin is targeting the brain which i imagine is why the tube goes in the neck.
I would consider it 'attempted local administration'
But Helsinki does not apply to the aphoresis. Standard stuff
You can complain he is mad scientisting by confounding 2 treatments. And would be correct if he was a big company or university or hospital doing research. This is not that.
The patient will not find a competing treatment offered. Once there is no menu at the restaurant, or chef, you turn on the stove and open the fridge.
The patient could get the stem cells at some other boutique.
He developed an idea and the patient accepted it. Could be a good idea or terrible, sure, doing any secondary treatment will confound a research project.
The person paying the hospital is just buying a service.
If you want better oversight, ask Pfizer or Moderna to take over her care lol.
They have all the answers and the microtweezers.
<BP ends>
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doi: 10.2174/1574888X16666201221151512.
Stem Cells Derived from Human Exfoliated Deciduous Teeth (SHED) in Neuronal Disorders: A Review
Most conventional treatments for neurodegenerative diseases fail due to their focus on neuroprotection rather than neurorestoration. Stem cell-based therapies are becoming a potential treatment option for neurodegenerative diseases as they can home in, engraft, differentiate and produce factors for CNS recovery. Stem cells derived from human dental pulp tissue differ from other sources of mesenchymal stem cells due to their embryonic neural crest origin and neurotrophic property. These include both Dental Pulp Stem Cells (DPSCs) from dental pulp tissues of human permanent teeth and Stem cells from Human Exfoliated Deciduous teeth (SHED). SHED offers many advantages over other types of MSCs, such as good proliferative potential, minimal invasive procurement, neuronal differentiation and neurotrophic capacity, and negligible ethical concerns. The therapeutic potential of SHED is attributed to the paracrine action of extracellularly released secreted factors, specifically the secretome, of which exosomes are a key component. SHED and its conditioned media can be effective in neurodegeneration through multiple mechanisms, including cell replacement, paracrine effects, angiogenesis, synaptogenesis, immunomodulation, and apoptosis inhibition, and SHED exosomes offer an ideal refined bed-to-bench formulation in neurodegenerative disorders. However, in spite of these advantages, there are still some limitations of SHED exosome therapy, such as the effectiveness of long-term storage of SHED and their exosomes, the development of a robust GMP-grade manufacturing protocol, optimization of the route of administration, and evaluation of the efficacy and safety in humans. In this review, we have addressed the isolation, collection and properties of SHED along with its therapeutic potential on in vitro and in vivo neuronal disorder models as evident from the published literature.
Dental Mesenchymal Stem Cell Secretome: An Intriguing Approach for Neuroprotection and Neuroregeneration.
Gugliandolo A, Mazzon E.Int J Mol Sci. 2021 Dec 31;23(1):456. doi: 10.3390/ijms23010456.PMID: 35008878Free PMC article.Review.
From Bench to Brain: Translating EV and Nanocarrier Research into Parkinson's Disease Therapies.
Muttiah B, Abdullah NAH.Biology (Basel). 2025 Oct 2;14(10):1349. doi: 10.3390/biology14101349.PMID: 41154752Free PMC article.Review.
Stem cells from human exfoliated deciduous teeth attenuate trigeminal neuralgia in rats by inhibiting endoplasmic reticulum stress.
Yang Z, Wang C, Zhang X, Li J, Zhang Z, Tan Z, Wang J, Zhang J, Bai X.Korean J Pain. 2022 Oct 1;35(4):383-390. doi: 10.3344/kjp.2022.35.4.383.PMID: 36175337Free PMC article.
Advancements in Spinal Cord Injury Repair: Insights from Dental-Derived Stem Cells.
Wen X, Jiang W, Li X, Liu Q, Kang Y, Song B.Biomedicines. 2024 Mar 19;12(3):683. doi: 10.3390/biomedicines12030683.PMID: 38540295Free PMC article.Review.
Mining human clinical waste as a rich source of stem cells for neural regeneration.
Eivazi Zadeh Z, Nour S, Kianersi S, Jonidi Shariatzadeh F, Williams RJ, Nisbet DR, Bruggeman KF.iScience. 2024 Jun 19;27(8):110307. doi: 10.1016/j.isci.2024.110307. eCollection 2024 Aug 16.PMID: 39156636Free PMC article.Review.
point 1: compare it to dialysis, and you can conceptually normalise the aphoresis.
it is insane, untenable, but unavoidable if you want to live. i say 5 sucessive liver transplants would eventually do the job of cleaning the blood, but i am grimly sarcastic and assume a supply of chinese dissidents. livers go to the vaccine damaged and the lung tissue goes to brazil to passage Omicron-2027, the 'Revelation Variant' lol .. see Residue 666...
point 2: if you don't like the stem cell treatment being mixed in i get that.
there are mutiple reasons how you are correct, from risk, to science, to ethics, to statistics. cannibalism got them here, so maybe cannibalism will get them out? they took the LNP risk the first time - it is a long established fact that vaccine seekers are risk-avoidant. interpret that lol.
point 3: the patient is not optimising for point 1 or point 2. they got messed up participating in an experiment that was not going to follow up with them.
the only option for treatment is to hit the internet and call for help - if they have money.
the patient is driving this workflow - they are trying to undo their own mistake, and have the right be risky.
they had it to begin with - which got them here - and they have it now.
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>>> BP: a recreational AI (not checked for shared hallucination) for GB comment area thought provocation. speculation, expect 50% rubbish
>>> gemini query, to copilot for refinement.
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"Draft a theoretical molecular architecture for a 'Synthetic Rheology Restoration' protocol to address fibrinogen amyloidogenesis and endothelial erosion. Model a bifunctional peptidomimetic foldamer with the following parameters:
Core Mechanism: Act as a chaperone ligand to stabilize the alpha-helical conformation of the fibrinogen D-domain, specifically increasing the Gibbs free energy barrier (ΔG) against beta-sheet transition induced by misfolded spike protein seeds.
Endothelial Anchoring: Incorporate a collagen-binding motif to facilitate localized stabilization at sites of endothelial basement membrane exposure.
Smart Dissociation: Implement a thrombin-responsive trigger (cleavable linker) to ensure the chaperone releases its payload during legitimate localized hemostatic events, preventing systemic hypocoagulability.
Heme Sequestration: Integrate zwitterionic-coated (poly-sulfobetaine) micelles for heme scavenging to mitigate hemolysis-driven oxidative stress without providing a nucleation surface for further protein misfolding.
Analyze the potential for this system to restore laminar flow and prevent arterial occlusion in a hyper-coagulable environment."
Copilot said:
Direct answer: A bifunctional peptidomimetic foldamer can be designed as a collagen‑anchored, thrombin‑cleavable α‑helix chaperone that raises the ΔG for fibrinogen D‑domain β‑sheet conversion while co‑delivering zwitterionic polysulfobetaine micelles for heme sequestration; this architecture should locally reduce fibrin amyloid nucleation and help restore laminar flow if delivered to exposed basement membrane without impairing physiological hemostasis.
Foldamer chaperone core Stabilize D‑domain α‑helix; raise ΔG for β‑sheet transition α/oligourea or α/β hybrid foldamer presenting helix‑mimetic side chains that engage D‑domain hot‑spots N/A
Thrombin‑cleavable linker
Collagen anchor Localize to endothelial basement membrane Triple‑helical GFOGER or collagen‑mimetic triple‑helix peptide Binds exposed collagen I/IV at injury N/A
Smart linker Permit thrombin‑responsive payload release LVPR↓GS or optimized P4–P3–P2–P1–P1′ consensus thrombin site Sits between anchor and chaperone Cleavage by thrombin
Heme scavenger Sequester free heme; avoid nucleation surfaces Polysulfobetaine (PSB)‑coated micelles encapsulating heme‑binding moieties Co‑assembled with foldamer; sterically shielded Non‑cleavable; cleared by reticuloendothelial system
Molecular architecture (sequence-level concept)
N‑terminus: Collagen‑mimetic triple‑helix peptide (GFOGER‑containing, stabilized by Hyp residues) to bind exposed collagen α2β1 integrin sites and localize to basement membrane. This motif provides high‑affinity anchoring to collagen I/IV.
• Thrombin‑cleavable linker: short flexible spacer containing optimized thrombin consensus (e.g., LVPRGS or tuned P2/P3′ residues) placed immediately C‑terminal to the anchor so physiologic thrombin at a hemostatic site will sever the chaperone from the anchor.
• Peptidomimetic foldamer core: hybrid α/oligourea or α/β foldamer engineered to present side chains that mimic the native D‑domain helix face, forming a high‑affinity chaperone ligand that increases the activation energy for α→β transition (steric packing, H‑bond donors, and hydrophobic patches). Foldamer backbones confer proteolytic stability and tunable helix propensity.
• Heme‑scavenging micelle payload: co‑assembled PSB‑coated micelles (zwitterionic polysulfobetaine corona) that encapsulate heme‑binding small molecules or albumin‑mimetic pockets; PSB corona minimizes protein adsorption and prevents micelle surfaces from acting as amyloid nucleation templates.
Mechanistic rationale and expected effects
• Raise ΔG for β‑sheet nucleation: the foldamer binds the D‑domain helix face, stabilizing α‑helical registry and sterically blocking spike‑seed interactions that nucleate β‑sheet conversion; this should reduce formation of fibrinaloid microclots observed with spike amyloid seeds.
• Local action, preserved hemostasis: collagen anchoring concentrates agent at sites of endothelial erosion; thrombin cleavage releases chaperone only during active clot formation, preventing systemic anticoagulation.
• Oxidative stress mitigation: PSB‑coated micelles sequester free heme and resist protein adsorption, lowering heme‑driven oxidative catalysis without providing a pro‑amyloid surface.
Risks, limitations, and development challenges
• Off‑target binding to circulating fibrinogen or platelets could alter clot mechanics; rigorous in‑vitro clotting and platelet assays required.
• Thrombin cleavage kinetics must be tuned so cleavage occurs only at physiologic thrombin bursts; suboptimal sequences risk premature release or failure to release.
• Immunogenicity and clearance of foldamers and micelles need evaluation; foldamer backbones reduce proteolysis but may elicit immune responses.
Bottom line and next steps
This architecture is mechanistically plausible and targets the three pathologies you specified (amyloidogenesis, endothelial erosion, heme toxicity) while preserving hemostasis via a thrombin trigger. Next steps: molecular docking to D‑domain, in‑vitro fibrin polymerization/fibrinolysis assays with spike seeds, thrombin‑cleavage kinetics, and hemocompatibility testing of PSB micelles.
No! You’re acting just like those stupid vaccine advocates! Nothing else is happening here: “The data will come later. Let’s just start with the experiments first.”
What do you even know about intracellular feedback loops of MAPK, mTORC1/2, RHOA, JAK/STAT that you dare to claim you have this figured out without even having conducted the necessary omics studies?! Your endpoints are a bad joke that proves once again that you know as much about systems biology as a paraplegic knows about running.
Your entire exosome argument shows that you’ve never studied membrane physics. And your inability to present data also speaks volumes. You used to be on the right side. Now you’ve degenerated into a Fauci 2.0.
I’m sorry, but this is highly unethical and not good science! Oh, and Kevin?: What do you even know about the Donnan equilibrium and exosomal identity via PtdInsPs?! You’ve disregarded every good practice, and your appeals to authority are embarrassing!
You're arguing about the “Procarta 21 Plex Human Cytokine Panels” Luminex assays, which are used to measure inflammation markers in blood or tissue?! A decrease in, say, TNF-alpha is an interesting indication of an effect, but it's not proof of long-term safety.
And that you don't even get why you would need omics for growth factors therapy to exclude possible off targets shows that you're still hanging in the believing of "cell is a thing I put something inside and than something happens I can calculate."
Lyndsey and another one of McCairn's patients reported reduced numbness in their toes after getting the DFPP treatment. [https://x.com/robert65968/status/2046623136926564368]
The effect might be due to improved perfusion to the toes, but I was wondering that if DFPP doesn't actually induce microclots lodged in the capillaries to break loose, then how could it improve perfusion to the toes? Grok said that DFPP might enhance perfusion by reducing the viscocity of blood:
> Fibrinogen is a key high-molecular-weight plasma protein that dramatically increases viscosity (especially in low-shear microcirculation). DFPP removes 50-88% of fibrinogen per session or cumulatively (along with other contributors like IgM, α2-macroglobulin).
> Lower viscosity directly increases capillary flow rate per Poiseuille's law: flow ∝ (pressure × radius⁴) / (viscosity × length). In narrow capillaries, even small viscosity drops yield large perfusion gains. This improves oxygen exchange without needing to dissolve every lodged clot. Studies on plasmapheresis in hyperviscosity syndromes confirm this: reduced plasma viscosity enhances capillary perfusion, shear-dependent vasodilation (via endothelium-derived relaxing factors), and tissue oxygenation.
> Result: Better overall microcirculatory flow, even around partial obstructions, leading to the "rejuvenating effect" described in patient reviews.
A paper about H.E.L.P. apheresis by Beata Jaeger et al. said: "In principle, the decreased fibrinogen concentration causes rheologically significant effects and facilitates oxygen exchange. Plasma viscosity is reduced by an average of 19%, and erythrocyte aggregability is significantly decreased by 60% (33). In addition, the vascular endothelial growth factor (VEGF) and nitric oxide (NO) release are favorably influenced (33). The improvements have also been demonstrated for cerebral blood flow in the cardiac patients, where they profit from a 63% increase in the CO2 reserve capacity (54)." [https://pmc.ncbi.nlm.nih.gov/articles/PMC9592739/]
The reduction in peripheral neuropathy might also be explained by a neurological and not circulatory mechanism. Plasmapheresis is employed as a treatment for chronic inflammatory demyelinating polyneuropathy (CIDP), which is an autoimmune condition that affects the myelin sheath around peripheral nerves. Plasmapheresis filters out antibodies in plasma that attack the nerves, even though the effect of the treatment typically lasts for only a few weeks, so the treatment has to be repeated frequently. [https://my.clevelandclinic.org/health/diseases/cidp-chronic-inflammatory-demyelinating-polyneuropathy] A paper from 2011 said: "Based on 2 Class I studies, plasmapheresis is established as effective in the short-term treatment of CIDP; both studies showed the beneficial effect is not sustained, with worsening beginning 1-5 weeks after last plasmapheresis treatment." [https://pmc.ncbi.nlm.nih.gov/articles/PMC3034395/]
But regardless of whether the effect of reduced numbness in the toes is explained by a circulatory or neurological mechanism, the effect is likely only temporary and not due to a permanent removal of microclots from the capillaries.
Nerve stuff:
https://badprotein.substack.com/p/affected
These are good questions and I'm sure Kevin and the Japanese doctors will have some of the answers already. However the context must be considered. That is, that the vaccine injured have been heinously abandoned by the governments and drug regulators leaving them to seek alternative treatments (even temporary) from other sources, often with very little funds.
The questions should be directed to the governments, regulators and pharma corporations who did this.
You are of course correct that this is treatment not cure. However over time the spikeopathy (assuming that underpins the injury) will likely eventually dissipate and removing as much of the substance as possible is rational, understanding that there are also potential deleterious risks of the procedure.
The victims should never have been put in this position.
I agree. I am concerned about the jugular approach, even with ultrasound guidance. Have seen some bad stuff. On centre with experience is one thing, but if it expands then I believe he needs to really document the need for this approach (and changing the cannula each time?). I agree, that the Japanese docs have a regulated approach and have documented the appropriate study parameters. I think I might have benefited from this procedure when I had to stop my Jak/STAT inhibitor and was in a severe RA flare for almost 2 years. A few doses of steroids was not enough.
My objection to this:
He received ONE signal during his ThT test and is conducting a blanket experiment on a small scale, without a differential diagnosis and without confirming the signal he received with Congo red or comparable method for structural validation. And he explicitly stated that this wasn’t necessary. Either it’s his protocol, in which case he must provide clean data and not just brush it off with sweeping generalizations and appeals to authority, or it’s the Japanese protocol. In that case, he can’t sell it as his miracle cure.
Please don't get me wrong: I understand the points. But if he's going to treat suffering souls like Lindsey he needs to call it what it is: a shot in the dark.
And as long as I see nothing of this and am fobbed off with responses like “Look at Twitter, everyone’s doing better” and “You have no idea because you’ve never set foot in a lab,” I remain more than skeptical.
https://pubmed.ncbi.nlm.nih.gov/28355156/
"In contrast to Congo red, the most missed Thioflavin S slides were scored as false positives, which aligns with the relatively lower specificity observed for this stain."
https://www.sciencedirect.com/science/article/pii/S1054880726000062#sec0005
Ferroptosis induces nucleolar stress as revealed by live-cell imaging using thioflavin T
https://www.sciencedirect.com/science/article/pii/S2590257124000233
Molecular Mechanism of Thioflavin-T Binding to the Surface of β-Rich Peptide Self-Assemblies
https://pmc.ncbi.nlm.nih.gov/articles/PMC2664162/
Z-scan optical method complements the Thioflavin T assay for investigation of anti-Alzheimer's impact of polyphenols
"In case of polyphenolic compounds Thioflavin T leads to false-positive results."
https://www.sciencedirect.com/science/article/abs/pii/S1572100022002009
Experimental methods for studying amyloid cross‐interactions
"Despite its advantages, ThT cannot reliably differentiate between mature amyloid and pre‐fibrillar specimens."
https://pmc.ncbi.nlm.nih.gov/articles/PMC12086524/
So were was the confirming experiment done? E.g.: Congo Red for orthogonal-structural confirmation of the measured signal? Maybe I could agree if he'd have said amyloid-like.
And you know my personal oppinion: to ignore the fact that any direct cellular intervention using technologies such as LNPs, exosomes, viral vectors, and the like necessarily affects the entire intracellular communication network is, in my view, pure arrogance.
The fibers that McCairn used to say are amyloid fibrils are probably textile fibers or random fibers from dust. He now calls the fibers "amyloid aggregates" after I called him out for his incorrect use of the term "fibril" last year. [https://sars2.net/clot3.html#Mr_Micronicles_amyloid_fibril_with_a_diameter_of_about_20_micrometers] But some of his followers are still calling them amyloid fibrils, and even one of his patients said on Twitter that blood clots "are called fibril or amyloids". [https://x.com/CoyoteSanctuary/status/2045193281907183887, https://x.com/KenCaptn20114/status/2044714103416217763]
Amyloid fibrils have a diameter of about 5-15 nm so they are not visible with an optical microscope. In the video where McCairn instructs his followers on how to take a sample of blood from their finger and send it to him on a glass slide, he smears the droplets of blood on a slide and tells people to not put a cover slip over the blood so the blood remains exposed to open air, and then he says "let these dry overnight in a dust-free environment". [https://synapteklabs.com/protocol-on-sending-blood-samples-2/] But how many of his followers have a perfectly dust-free environment at his home?
Fibers of cotton that have been dyed white are fluorescent under UV light, in the same way that white t-shirts are fluorescent under UV light. The fiber that McCairn supposedly found in the blood of the 3-year-old had several characteristics that are consistent with cotton, like a diameter of about 15 µm, a flat body, and the kind of lengthwise twists that are called convolutions in cotton. Nicolas Hulscher said that the 3-year-old's fiber was an "amyloid fibril" even though its diameter was about thousand times higher than the diameter of an amyloid fibril. [https://x.com/NicHulscher/status/1929689987974385879]
In 2022 when McCairn showed David Nixon's microscope image that Mihalcea said contained a graphene fiber optic wire, McCairn said: "Everything that I see here is cholesterol, and literal fibers that you pick up in dust in the air. What I've seen these people do - they're not doing it in clean rooms - and you've gotta be in exceptionally clean rooms to make sure that slides are not getting contaminated. Sorry. You don't get to say that these are graphene internet fiber optic cables." [https://rumble.com/v22lzie-oy-vey-kvetching-iirt-sasha-latypova-rebuttal-sars-neuroscience.html?start=5211] But the fiber optic wire looked just like the fibers McCairn now claims are amyloid fibrils.
The fibers McCairn has said are amyloid fibrils have had a diameter of about 10-30 µm, which is too wide to pass through the capillaries, so the fibers can't even be circulating freely in the blood, because they would get stuck before the capillary beds (apart from possibly fibers with a diameter close to 10 µm). The real microclots shown in the papers by Pretorius and Kell have been much smaller, and they have looked like random blobs and not like textile fibers. [https://www.researchsquare.com/article/rs-4507472/v1]
In the same way that McCairn now says that the presence of amyloid fibrils is a characteristic of unhealthy vaccinated blood, in 2021 Philippe van Welbergen said that the presence of graphene ribbons was a characteristic of unhealthy vaccinated blood. In reality both McCairn's fibrils and Welbergen's graphene ribbons looked like textile fibers, and they have both had a diameter around 10-30 µm which matches the diameter of common types of textile fibers. [https://sars2.net/clot3.html#Microscope_images_of_the_blood_of_Jesus4AllAlways_and_his_family] The cotton fibers that Clifford Carnicom said were Morgellons filaments also had a similar diameter. [https://web.archive.org/web/20120828061349/http://www.carnicominstitute.org/articles/morgobs1.htm] Ana Mihalcea has variously said that fibers with a similar diameter were hydrogel ribbons, Morgellons filaments, or graphene. [https://anamihalceamdphd.substack.com/p/comparison-microscopic-analysis-of]
DopplerEffect93 is a PhD in neuroscience who did a postdoctoral research project analyzing amyloid fibrils, but he told McCairn: "Your image of the 'aggregate' is far too large to be one. It looks like some dust or debris. Your SEM shows nothing. It took me less than a minute to come up with a better experimental design than the nonsense you have." [https://x.com/DopplerEffect93/status/1930391359375941986] The molecular pharmacologist Ian Musgrave told McCairn: "It's just a cellulose fibre. I've EMed enough real amyloids and sighted enough cellulose fibres under the microscope to know which is which." [https://x.com/ianfmusgrave/status/1959268694363918430]
So what real biologists are now telling McCairn is similar to what McCairn said about David Nixon's microscope image in 2022. McCairn used to threaten his followers that one day he would join the Stew Peters grift wagon and become rich and famous. But he now seems to have delivered on his promise. He had a dead cat bounce in fame last year after he started doing videos with the star of a Stew Peters movie, and now McCairn has probably earned at least quarter a million dollars from his amyloid fibril removal scam.
I’ve been wondering the whole time: So he finds these “clots,” and the first thing that doesn’t occur to him is to examine them through chemical analysis to determine what they’re made of and in what proportions–in order to a) tap into a market niche and b) rule out the possibility of a falsification?
GB. I personally have been concerned around the possibility that the frameshifting might have produced misfolded proteins. I have already asked Kevin if is he going to be taking whatever it is they have filtered out the blood in his protocol. And then see if they can introduce and “seed” it into Control samples. My thinking is that this would serve as an indication of what these are. If misfolded proteins they would be infectious. And the experiment would show this. Your opinion and thoughts.
Last year when I asked McCairn what tests he had done to determine if the fibers he finds are even made of fibrin, he indicated he relied on the fibers being autofluorescent under UV light, the fibers being fluorescent with ThT staining, and "phenotypic similarity". [https://sars2.net/clot3.html#Substack_post_about_SEM_images_of_the_3_year_olds_fiber] By phenotypic similarity, he meant that the fibers had a twisted shape, and that the fibers were embedded within the sample of blood rather than resting on top of the dried blood. He claims that the kind of lengthwise twists that are characteristic of cotton are actually caused by misfolding of protein. He also claimed that his SEM image of Hirschman's clots showed misfolded fibrin, beause a branch within the image appeared to have lengthwise twists.
But as far as I know, he has not done any test to determine the protein composition of the fibers.
McCairn's buddies at the Aussie-Kiwi Quinta Columna claim to have done an HPLC analysis on Hirschman's clots, but I think they just generated fake HPLC data with AI. [https://sars2.net/clot.html#Peptide_mapping_analysis_with_HPLC_MS] They refused to publish their raw HPLC files, and I have busted them generating several other sets of fake data with AI. [https://sars2.net/clot.html#An_Unholy_Triad_and_mystery_ORFs]
It's still a great indication of your scientific standards that earlier you claimed that the fibers you saw in blood samples were singular amyloid fibrils. When I called you out for your incorrect use of the term "fibril", you responded by saying "Trying to use old vernacular to a new blood prion disorder will lead the spergs like you to blow a fuse, but you'll just have to put up with it." [https://sars2.net/clot3.html#Mr_Micronicles_amyloid_fibril_with_a_diameter_of_about_20_micrometers] Now you seem to have silently abandoned the term "fibril", but your followers still say that the fibers you find in blood samples are singular amyloid fibrils.
Earlier you gave the impression that the fibers you saw under the microscope were circulating freely in blood, even though me and another user on your Discord pointed out that your fibers were so wide that they wouldn't have been able to pass through the capillaries. Then I came up with a hypothesis that maybe the fibers were not circulating freely in blood, but they were stuck in the arterioles before the arterial capillaries, but the fibers were released when the blood was sampled with the finger prick lancet, because the lancet penetrated deep enough to reach the arterioles and not only the arterial capillaries. [https://x.com/henjin256/status/1965068669672997217]
Two months ago when you did a video with one of your patients, you told him: "And I would say the fact that you have such a rejuvenating effect - those are the aggregates that were really lodged into the entrance and exits of capillary beds." [https://rumble.com/v75hp6g-kevin-mccairn-2026-02-08-patient-review-reversing-severe-vaccine-injury.html?start=3076] So you now seemed to support my hypothesis that the aggregates were not circulating freely in blood but stuck before the capillaries (even though you also suggested they were stuck after the capillaries).
But if the aggregates are stuck before the capillaries, and the aggregates are too big to pass through to the venous side, then how can they be removed by your treatment where the plasmapheresis machine is hooked up to the jugular vein? And if the aggregates are stuck on the venous side after the capillaries, then how do they happen to get released at the precise time when you give the treatment? Is there some aspect to your treatment that induces the stuck aggregates to get released?
---
The microclots in the papers by Pretorius and Kell look like random blobs, and not like textile fibers. Someone called Syed Haider offers a service to test for microclots associated with long COVID or vaccine injury, but the clots in his images don't have a string-like shape, and they don't look like textile fibers. [https://x.com/DrSyedHaider/status/1641832540091691010] Apart from you, the only person I know who claims to have found fibrin clots that look like textile fibers is Ana Mihalcea, because in 2022 she said that a fiber with a diameter of about 30 µm was a fibrous rubbery clot "in early stages" (even though elsewhere she has said that similar fibers were Morgellons filaments, hydrogel, graphene, or carbon nanotubes). [https://anamihalceamdphd.substack.com/p/thoughts-and-comments-about-died]
---
A paper from 2025 said: "Therapeutic plasma exchange (TPE) has the potential to improve the PCC by clearing the peripheral soluble pro-inflammatory immune milieu derived from acute or persistent SARS-CoV-2 infection. In a phase II, double-blind, placebo-controlled, randomized trial, fifty subjects with PCC were randomly assigned (1:1) to receive six sessions of either TPE or a sham plasma exchange and were followed for 90 days (ClinicalTrials.gov registration: NCT05445674). The primary endpoint was safety; secondary endpoints included functional status, symptomology, quality of life, neurocognitive symptoms, and peripheral biochemistry, hematology, coagulation and inflammation parameters. Both study arms had a similarly favorable safety profile. There were no [significant] diferences between groups in any of the efficacy parameters evaluated." [https://www.nature.com/articles/s41467-025-57198-7] In the trial the plasma was replaced and not only filtered like in your protocol, but if replacing the plasma did not provide a significant benefit, then what additional advantage would filtering have? Or was the lack of nonsignificant effect because the beneficial effect of removing harmful blood components was offset by a harmful effect of replacing beneficial components that are retained by DFPP?
But regardless, I think when you advertise your protocol, for the sake of informed consent you should mention that no significant effect was found in the trial using TPE.
(I'll try to read the studies you linked properly after I have caught up with the other comments.)
McCairn pointed out to me on DM that I had missed a note in Sayd Haider's image that said "Micro-clots come in all shapes and sizes. You may also see long, string-like appearing objects in your pictures. This is a normal finding for long-COVID patients."
I now also noticed that Haider's image was actually taken from one of the papers by Pretorius and Kell. [https://link.springer.com/article/10.1186/s12933-022-01579-5/figures/8] And I didn't find any images of microclots Haider had taken himself.
But regardless, Haider doesn't seem credible, so he may have misidentified cellulose fibers as fibrin microclots. In 2024 he wrote about Greg Harrison's HPLC results uncritically that "The fibrous clots found in vaxxed blood are completely unnatural. The bulk of a normal clot is fibrin which glues it all together. These unnatural clots have over 500 proteins in them but no fibrin." [https://x.com/DrSyedHaider/status/1800854038277132609] He also wrote that "The bulk of these clots are made up of unconverted fibrinogen, rather than fibrin as you would expect." [https://x.com/DrSyedHaider/status/1800871178426613774] In reality it's expected for only fibrinogen but not fibrin to show up in HPLC results, because HPLC detects fragments of proteins so it does not differentiate a fibrin polymer from the fibrinogen monomers. But Greg's crew misinterpreted the HPLC results and wrote that "A distinctive feature of Hirschman clots is the relative lack of fibrin and the apparent lack of thrombin to convert fibrinogen to fibrin." [https://sars2.net/clot.html#Peptide_mapping_analysis_with_HPLC_MS]
If someone than answers like this when I ask for a chemical analysis:
"See the reply above G, the work has been done and published, it's not me that made the first claim regarding their presence or composition. The fact I can create the same phenomenon in the lab with purified plasminogen, and their morphology and staining characteristics are the same as those published, means I can put scarce lab resources to useful things, like you know helping suicidal patients. You can follow Robert's progress, who was severely incapacitated, unable to walk, think, and in constant pain to the point of suicidal ideation and tell him his reduced inflammatory cytokine amyloidogenic aggregates are a figment of his imagination.
https://x.com/robert65968/status/2044324654752379335" <<<<What is this?! Where are the data?! You don't expect me to read the whole timeline, do you?
And than going the whole time ad hominem and not even understanding what your asking? I think there is no reason to continue this debate. At least that's how I feel and think.
Another example:
Me:
AI slop? So the AI actually spoke to you during that three-hour discussion about signal cascades? I see.
Lipid Nanoparticles as Active Biointerfaces: From Membrane Interaction to Systemic Dysregulation
https://www.preprints.org/manuscript/202511.0517#sec7-preprints-184611
And the entire script was generated by AI. It’s not as if I learned the basics of good regulatory practices from Maria. I see.
And just for the records: Maybe you should ask sometimes AI before bullshitting arround:
"Fuck me G, so you're an expert in amyloid detection now are you? We use ThT rather than Congo Red for a reason. Thioflavin T is far more sensitive for detecting amyloid fibrils in complex biological samples like plasma. Which makes it far better suited for quantitative work and real time analysis. Congo Red relies on birefringence under polarized light, which is less sensitive, highly operator dependent, and struggles with low abundance or early stage aggregates.
Trying to use Congo Red in this context is like trying to run modern molecular diagnostics with a 19th century microscope. It can show you something if the signal is massive, but it completely misses the subtle early changes that actually matter. In heterogeneous clinical samples where you are looking for small but meaningful shifts in amyloid burden, ThT gives a cleaner, more reproducible, and truly quantitative readout. That is what we use for RT-QuIC, and ELISA. You want me to break out the camera-lucida and start sketching out lab results. Give me a break G. The phenomenon of aggregates to S1 is proven, I have used the phenomenon to actually test the ability of SGF to inhibit there formation under RT-QuIC conditions. I did that with ThT and not Congo Red/."
Congo red stain: The gold standard for diagnosing amyloidosis
https://pcc.oneamyloidosisvoice.com/2023/12/15/congo-red-stain-the-gold-standard-for-diagnosing-amyloidosis/
A ThT signal alone is not sufficient to conclude that amyloid fibrils have formed without orthogonal structural validation. Without an independent structural method (e.g., classical orthogonal markers such as Congo Red or modern structural techniques), the claim of “amyloid formation” is not validated.
"For example, it exhibits almost exclusive binding selectivity toward amyloid fibrils27 and not toward amyloid oligomers that are considered to be the most toxic species. Furthermore, ThT is known to experience major interference from the autofluorescence of the biological matrix, which results in a strong background signal.28,29 Recent studies have shown that only ∼10% of the bound ThT in amyloid solution contributes to the observed fluorescence enhancement,30 suggesting that ThT may not be an accurate measure of amyloid fibrils due to non-specific binding."
https://pubs.rsc.org/en/content/articlehtml/2023/sd/d3sd00124e
And your real issue here is purely personal: You're confusing legitimate questions with personal attacks.
End of announcement!
McCairn:
"So you just completely ignored what I put about your oh so important questions, thus further validating the observation they were just spat out by grok, and instead want to try and tell me how to test for amyloidogenicity.
Yes Congo Red is historically referred to as a gold standard for tissue histology, it is not used, however, for low abundance detection in complex fluids. That is a completely different use case. You are conflating fixed tissue diagnosis under polarized light with quantitative detection in plasma and kinetic assays. Those are not interchangeable methods and anyone who has actually worked with both knows that.
In real lab work ThT is used because it is orders of magnitude more sensitive for fibril formation kinetics and allows continuous measurement. That is exactly why it is used in RT-QuIC and related assays across the field. Congo Red cannot do that. It is endpoint, qualitative, and requires sufficient mass and structure to even see birefringence. That makes it fundamentally unsuitable for detecting early or low level aggregation in heterogeneous biological samples like blood or plasma. And I have demonstrated numerous times S1 protein causes amyloidogenic aggregation in plasma, as does seed amounts of isolated amyloidogenic clot material. That's it, end of story for wondering if the material is in an amyloidogenic state, if it is detected via logarithmic expansion of a ThT fluorescent signal under RT-QuIC conditions.
Your “orthogonal validation” talking point is another generic line lifted without context. Orthogonal methods are useful in controlled structural studies. They are not a prerequisite for every applied assay where the signal is already validated within the system being used. RT-QuIC is not guessing. It is a seeded amplification assay with a well established signal response. You are pretending it is just free floating fluorescence with no specificity which is simply wrong.
The autofluorescence argument is also weak. Background signal is exactly why assays are designed with controls, thresholds, and comparative analysis. You're acting as if this is some unknown flaw rather than a basic parameter that is handled in every fluorescence based assay. The “10 percent binding contributes to signal” point does not invalidate the method it reflects binding dynamics that are already accounted for in how the assay is interpreted. And just so you know, from some one who has worked extensively with these dyes, Congo Red is also avidly taken up by other proteins and of those proteins that does take up Congo Red, one of them is is Fibrin! So when you are dependent on a subjective measure of polarized bifringence from a tagged tissue under normal conditions, you are going to be subject to no end of false positives and artifacts, that essentially makes the test useless.
On oligomers versus fibrils you are again showing you are repeating literature without understanding application. Different probes detect different species. That does not make ThT useless it defines what it measures. In the context of fibrillar amyloid formation and aggregation kinetics it is entirely appropriate.
And the camera lucida point clearly went over your head. The analogy stands. You are trying to apply an older lower sensitivity method to a context where modern fluorescence based detection is required.
What you are doing throughout is cherry picking limitations from papers and presenting them as disqualifications while ignoring how these methods are actually used in practice. That is not critique it is superficial reading.
Nothing about this is personal, I'm just pointing out where you have stepped into the personal, by dropping your turd of a Substack without having the professional where with all to ask me the questions before publishing, and making yourself look like a tit, and then having me wasting time I don't have on your poorly formulated arguments. It was obvious I made a stupid mistake by helping you in the past, as you just keep demonstrating that you are arguing from secondary sources without any real bench or clinical experience applying these techniques. Argumentum ad Grokum is belittling you and wasting my time."
Anyone who fails to understand that structural validation is necessary when the entire protocol is based on a clinical diagnosis has lost touch with reality and scientific integrity.
And this is nothing new under the sun I am asking here:
https://pubmed.ncbi.nlm.nih.gov/28355156/
"In contrast to Congo red, the most missed Thioflavin S slides were scored as false positives, which aligns with the relatively lower specificity observed for this stain."
https://www.sciencedirect.com/science/article/pii/S1054880726000062#sec0005
And in the first line I am more pissed about the fact that he sells this protocol as a mirrage cure than to say it's pure experimental and we don't know by now what we're doing. This is the part really freaks me out.
I share your concern about McCairn selling his protocol as a miracle cure. He has also been fearmongering about the clots to the extent that some of his followers now think the clots are leading into human extinction.
A Twitter user called Tom Czerniawski said that prions from the clots are causing an extinction-level event, which will result in "the end of all human life on Earth", and he said it was not hyperbole or exaggeration, but McCairn replied to him suggesting the clots will cause an "evolutionary bottleneck that is the Super Prion Event of the Millenia". [https://x.com/BlackTomThePyr8/status/1928824583651545587] The pinned tweet of McCairn's hardcore fan CoyoteSanctuary says that a prion epitope in the spike protein is "creating a Super Prion ELE Event". [https://x.com/CoyoteSanctuary/status/1859324146200858913]
Last year Tom Czerniawski was going around asking billionaires to donate money to McCairn, because he said that if McCairn receives a few hundred thousand USD in donations, he could "SAVE EVERYONE FROM DYING HORRIBLY". [https://x.com/BlackTomThePyr8/status/1915925037430751313, https://x.com/BlackTomThePyr8/status/1915928819808035265] Tom also said he thinks the clots will cause a cataclysmic pole shift to arrive more quickly. [https://x.com/BlackTomThePyr8/status/1932161919265468442]
Now Tom believes that McCairn has come up with a cure for the clots, so he suggested that McCairn is an angel of salvation who was sent to earth to save humanity, and who is on earth by divine providence. [https://x.com/BlackTomThePyr8/status/2040895525709299974]
KenCaptn20114 is one of McCairn's patients whose video recently went viral. When someone asked him how much the treatment cost, he replied: "Its very expensive. I went deep into my retirment account. I had no choice. It was that or die." [https://x.com/KenCaptn20114/status/2045420173558243779] He also tweeted: "This clot issue possibly could turn into the biggest problem that humanity has ever faced. Think youre safe because youre unvaxxed? Think again. There are violently ill people here that are unvaxxed in Japan covered in microclots being treated." [https://x.com/KenCaptn20114/status/2045156262019809524] In another tweet he wrote: "Vaccinated or unvaccinated doesnt matter. Its in the blood. This is very scary on a whole new level. I dont think people understand yet. Everyones dying, now I get it." [https://x.com/KenCaptn20114/status/2045426759144030436] So he seems to think everyone is dying from the clots and the clots might be the most important issue humans have ever faced, and he would've died without McCairn.
He also speculated that stem cell growth factors repair demons: "we are being treated with pre-growth stem cell factors that kick our own stem cells in for repair of Demons speculatively so when I read above, you are wrong then wrong then wrong again". [https://x.com/KenCaptn20114/status/2044731302822477920]
The fear is fueled by people who are deliberately producing disinformation about the clots, like Wayne Crouch, who is a member of the team that I call the Aussie-Kiwi Quinta Columna. He said that the human species is going "extinct due to the spreading amyloid clotting disorder caused by the shots and exacerbated by covid itself". [https://x.com/WayneC50256258/status/1953587190199652579] He was the director of a series of AI-generated disinformation videos, which claimed that the clots were caused by mystery ORFs that his co-conspirator Wayne Crouch found by decoding Chinese and Soviet military documents. The last episode in the series presented an apocalyptic scenario where prions from the clots caused humanity to become extinct. [https://rumble.com/v6shndn-an-unholy-triad-the-birth-of-a-plague-season-02-episode-04.html] The video series employs stock videos from the same collection of stock footage that is used on a page of McCairn's website where McCairn describes his "Prion Research Investigation Project", where he supposedly investigates the question of whether SARS-CoV-2 and COVID vaccines have "exposed the human population to potentially fatal prions". [https://synapteklabs.com/prion-research-investigation-project/]
Last year when McCairn did an experiment where he injected pieces of Hirschman's clots into the heart of a hamster which died right after the injection, Wayne Crouch made an infographic about the experiment that said "A RESEACHER LINKED TO 'THE SOLUTION OF SCIENTIST'S', INJECTS LAB HAMPSTERS WITH OUR AMYLOID JAB CLOT SAMPLES TO ACESS LEVEL OF PRIONIC ACTIVITY... IN A WORLD FIRST THE HAMPSTERS DIED STRAIGHT AWAY... MAKING THIS THE WORST PRION DISEASE EVER DISCOVERED...." [https://sars2.net/clot3.html#Kevin_McCairns_connection_to_Solution_of_Scientists] Then Crouch commented that "Had they died in weeks or months maybe we had a few years longer the rapid death of our test subjects means we will see the rapid death to the shot recipients boosters will greatly accelerate this". His cohost lady Lisa Johnston also tweeted that "Planet earth is under attack by prionic amaloidosis created by man". [https://x.com/lisarose030387/status/1909497793338917050]
Greg Harrison supposedly did Congo red staining on the calamari clots and got a "positive result for presence of amyloid", but you have to take any results coming from him with a massive grain of salt, because he has used AI to generate several fake sets of data about the clots, and I have doubts if he ever even physically analyzed the clots. [https://laurakasner.substack.com/p/a-horrifying-breakthrough-in-the] Greg said that Arne Burkhardt did Congo red staining on the calamari clots but didn't publish his results. [https://sars2.net/clot.html#Interview_of_Greg_Harrison_and_Tom_Haviland_by_Flashlights_in_April_2025] But I don't know if anyone has done Congo red staining on the supposed microclots.
The lady who made the infomercial-style image in your first link is now McCairn's leading memetic warrior. She used to work for a unit of naval intelligence called NAVSECGRU, which later formed the Information Operations Directorate of Naval Network Warfare Command. Last year she was cheerleading for the ORF hoax of Greg Harrison, who claimed to have discovered new ORFs in the genome of SARS-CoV-2 by deciphering secret Chinese and Soviet military documents. She kept defending the ORFs even after I presented undeniable evidence that the ORFs were fake, and she just said that I was crazy or that I was a bully, so her behavior didn't seem reasonable unless she was somehow in on the hoax. [https://sars2.net/clot3.html#McCairns_naval_intelligence_cheerleader_RexesRule]
After Major Joseph Murphy leaked the DEFUSE proposal, he didn't lose his career, but he instead got a job in naval intelligence at the Office of Naval Research (ONR). [https://www.washingtontimes.com/news/2022/jan/12/marine-researcher-covid-19-virus-made-chinese-lab-/] In 2025 he became the COO of the ONR's Marine Corps Warfighting Laboratory. [https://www.linkedin.com/in/joseph-p-d-murphy/]
The head of Couey's lab at the University of Pittsburgh has also worked for the ONR, and Couey said there was talk he might have to take over the lab for a year because the ONR guy was going to be sent on an anti-pirate mission to Africa. [https://sars2.net/clot3.html#Kevin_McCairns_connection_to_Cottrell_Couey_Kulacz_and_Webb]
McCairn did many of his earliest videos with George Webb's mini-me Addy Adds and George Webb's science teacher Paul Cottrell, and in early 2020 Addy hosted a series of video panels that featured McCairn, Couey, and Cottrell. Cottrell had a radio show on a network that was operated by a guy from DC who worked for naval intelligence. Addy Adds lived on naval bases in Guam and Okinawa because his mother worked on the bases, and in a book where he profiled his champions of "public intelligence" who had been guests on his show, one of them was the marine intelligence officer Matt Agorist. [ibid.]
The guy blocked me years ago because I questioned just about everything he was purporting to be true. I’ve been around since the AIDS scam, I simply don’t believe any of his stuff.
Sorry.. You're dismissed. No no virus-discussions under my stacks!
Has no-one on this thread thought about the bravery McCairn and his associates have exhibited?
His protocol and treatment is bound to be attacked fiercely by the very ruthless forces that planned and drove this fake "pandemic" and monstrously deceitful and criminal attack on the population.
He has willingly put himself at risk. From occasional comments he has made on his podcasts, he knows it.
Wow?! Now I am a ruthless instance? Maybe even jewish? Need a pill for your psychosis?
when you read the comments under the old post of Dr. Bowden, one would indeed start asking questions, and there were many, McCairn is answering only the positive ones, the rest is silence.... He himself has serious health issue with the clotting, apparently, yet he DOES NOT show everyone that his protocol works on himself. I asked many questions in his weekly presentations, and answers were frequently arrogant, if any. If anyone saw the clots which embalmers pull out, HOW ON EARTH can you filter anything out when their volume is ~ volume of the blood vessels themselves! In terms of the dental pulp stem cells, equally a question how those ever stay healthy AFTER the gene therapy?? Since SO MANY people are dying or a sick, in those 4 months, one could expect a HUGE feedback, including Dr. Bowden. Just do not see anything....
ANyway, when you look at McCairns (british accent) CV things are getting even muddier, from Research Gate:
Okinawa Institute of Science and Technology Graduate University January 2010 - present
Okinawa, Japan
Bar Ilan University January 2007 - present
Ramat Gan, Israel
the latter collaborated with Pfizer for LONG TIME:
https://www.pfizer.com/news/press-release/press-release-detail/bar-ilan-university-work-pfizer-inc-evaluate-drug-delivery and also https://afbiu.org/news/dna-robots
I was happy to see people getting better when they went to Japan to do the McCairn Protocol.
I do not see the problem here. Many medical therapies work, but the underlying reasons are not completely elucidated. McCairn is working from hypotheses he has developed and the treatments seem so far to bear them out. He has said that recovery appears to continue - people seem to be improving once the burden of amyloids is cleared and the stem cell therapy is initiated.
The completely analysed theoretical justifications can wait as people are having strokes and dying without treatment.
This is not quite how medical treatment evolves.
Without double blinded, placebo- controlled studies who knows if it works? And are we keeping a track of any side-effects of these treatments?
Having a solid knowledge of the cause and pathogenesis of any ailment has the highest chance of developing the appropriate treatment.
It may well be a good treatment, but in its current state this protocol is still in ‘snake oil’ territory.
Currer, could you please stop flooding my comments with spam!? I don’t think you understand at all that every single question asked here is a scientifically sound question that needs to be answered. Or are you admitting that, for example, Thalidomide was okay too, because nobody could smell it anyway, and who needs data if it helps? Because THAT is exactly the level and core of your argument.
And to be honest: I am getting pissed about that!
There is a reason because you're drawing circles of non ethical stupidity arguing exactly like the regulators argued for public: Benefit reasons risk. Bye.
I cannot agree I am afraid. Many of these people consider themselves to be terminally ill. They are aware this is a speculative treatment at present and the decision to enrol in this treatment is theirs alone to take. They cannot wait for "double blinded placebo controlled trials" as they are unlikely to live that long.
I do not agree this is "snake oil." Dr McCairn has spent six years working on this problem.
The apheresis treatment is not an unusual treatment in Japan and the hospital doctors McCairn is liaising with are skilled in this work. I suggest you ask the Edogawa hospital in Japan for their protocols.
https://www.myhospitalnow.com/hospitals/edogawa-hospital
"DFPP (Double Filtration Plasmapheresis) is an established blood purification technique widely used in Japan and parts of Asia for autoimmune diseases, neurological conditions, and metabolic disorders.
It works like a high-tech “blood laundry” in a closed circuit: blood is drawn, the plasma is separated and passed through two specialized filters to remove harmful molecules (autoantibodies, cytokines, immune complexes, and potentially spike-related amyloids), then the cleaned blood is returned to the patient — all without needing donor plasma.
Often combined with stem cell-derived growth factor infusions, this protocol is giving real relief to suffering for years and helping to remove mRNA spike proteins from those Covid vaccine injured."
We use double filtration plasmapheresis in North America as well. It is just the cassettes they use (ie the filters are slightly different). This part is almost "off label therapy," and more like a surgical approach to remove these amyloids. I am a bit bothered by the need for a jugular vein approach, risk for infection and injury is high. The other stuff with stem cell growth factors needs more scrutiny. There ARE physicians and the hospital involved. It would be hard to imagine a hospital allowing a free for all. I would HOPE they have inclusion and exclusion criteria, strict monitoring and lab work and every last little thing documented in a formal fashion as for a case-controlled study. And that the RIGHT things are measured. We just dont want a reverse vaccine effect. Lots of hopium, then a crash. Needs to be squeeeeeky clean.
Agreed Maria. I do not see why the Edogawa hospital should drop its standards when treating McCairn's patients. I believe questions about this protocol are justified, but we should remember we are not in possession of the clinical data or the medical rationale. Questions should not slip over into criticism.
It may be the best thing since sliced bread, but surely he could have set up a proper trial to prove his theory?
Have you followed Dr McCairn's work?
I have followed him and contributed to funding his research. He is working alone and set up his research lab himself as he knew no university research body would do this work for fear of the political repercussions of working on Sars-cov-2 vaccine injury.
You are asking too much from one man. Ask rather why no other government funded body will approach this work. Obviously it would be great for our properly funded research institutes to investigate this. But they do nothing for fear of the consequences to them.
I have sent McCairn's blood amyloid findings to my UK government departments and to my MP asking them for an urgent review and informing them that the bloods supply is probably unsafe. My e-mails and letters remain unanswered, even recorded delivery letters are not delivered.
In the face of such official malfeasance and contempt for those injured by their mandates, I do not feel able to criticise McCairn. This is the world we live in now, not the ideal one.
I repeat myself. It may be the best thing since sliced bread, but beware of falling into the same trap as the modRNA/LNP pharmaceutical industry. They unblinded and vaccinated the control group, as such making useful comparisons impossible. They did not pay heed to red flags in terms of safety.
I just don’t want a similar approach treating vaccine injured.
https://pmc.ncbi.nlm.nih.gov/articles/PMC11870656/
https://pmc.ncbi.nlm.nih.gov/articles/PMC11707004/
Show me the long term profile of those therapy for immunecompromised systems and I’ll tell you if I was to harsh here.
There can not yet be a "long term therapy" The treatment is experimental, and being assessed.
And this is exactly the point here: There is not even any animal experiments done. But using it for people with real issues and getting paid for doing human experiments you think is a good thing?! Especially with a therapy that does not really differ from LNPs despite a little bit more biocompatible lipid composition?
Week 2 day 2 completed. After two tries still not able to complete the 2 liters of DFPA therapy, Feeling great. Productive and mobile all day. Still cognitive issues related to memory and math. See the progress.
https://x.com/robert65968/status/2039467855465554295
I have not seen this guy in 5 years!
Crazy Difference. There is a cure.
https://x.com/robert65968/status/2040269830377595158
One significant part of Kevin's treatment is to filter out the amyloids, thus reducing circulatory hypoxia and the likelihood of minor strokes. The difference can be seen immediately, in 24 hours, people look and feel much better and can think clearly.
Multiple circulating clots are a stroke risk.
I have not looked into the stem cell treatments he is using, but I see bad protein has put up an informative post. (thanks)
It seems a well considered treatment to me, given the high risk the patients are in. Those who are going to Japan are bedbound and seriously ill and have exhausted their other options for treatments in the US. (No adequate treatments exist in the US and are not being developed.)
https://x.com/KevinMcCairnPhD/status/2041622664675258424
So far the results are long-term, we have had no relapses yet, patients are often taking SGF treatment back from Japan to maintain treatment efficacy.
But initial results look good, even one of our most complex patients, who had significant CNS damage, wrote to me today after their recent return back to the US, saying that they have made significant recovery.
They are now able to leave the house and are now capable of driving again, after years of disability.
The combination of route of filtration (targeting brain/CNS outflow), combination filters for autoantibodies, and the daily large dose SGF, just comes together in a very synergistic way. This is measurable as removal of amyloidogenic aggregates and normalization of cytokine panels. The response in patients is immediate, as we see with Ken.
Of course there is always more work to be done, but right now, I would say we have the most efficacious therapy out there for Long Covid and Vaccine Injury.
Lyndsey arrives this week, and we can all track how she does through the treatment program.
are there ORGANIZED records out there for every patient they treat??
McCairn is working with the doctors at Edogawa Hospital where apheresis procedure is a standard treatment.. I do not see why they should abandon normal medical record keeping just for his group of apheresis patients.
>>>>>>>>>> sure, after that tell me of there are other drugs approved for exosome delivery - many kinds of exosomes out there in the catalog?
ai:
Technically, exosomes are biological LNPs. Both are fat-based nanovesicles that protect "fragile cargo" (like RNA or proteins) so it can survive the trip through the bloodstream to enter a cell. The safety debate hinges on whether a "natural" vesicle (exosome) behaves more predictably than a "synthetic" one (LNP).
Are there FDA-approved exosome drugs?
As of April 2026, there are no FDA-approved exosome drugs for general systemic delivery (like an IV drug you’d get at a pharmacy).
However, we are at a major regulatory tipping point. The first-ever Biologics License Application (BLA) for an exosome-based therapy—Deramiocel (CAP-1002) for Duchenne Muscular Dystrophy—is currently under active FDA review with a target decision date in August 2026.
The "Catalog" of Exosomes
If you look at biotech "catalogs" (for research and clinical trials), you'll find a massive variety. They are categorized by their source cell, because the source determines the "biological flavor" of the signals inside.
Exosome Source Common Use Case Why clinicians choose it
SHED (Baby Teeth) Neuro-repair Derived from neural-crest cells; naturally "wired" for brain/nerve healing.
MSC (Bone Marrow) Orthopedics/ARDS The "gold standard" for general anti-inflammatory and lung repair.
Platelet-Derived Wound Care High in clotting and tissue-knitting factors (e.g., PEP Biologic).
Plant-Derived Topicals/Cosmetics Ginger, Milk, or Ginseng exosomes are used in "high-end" skincare as an alternative to animal products.
The "Safety" Argument: Exosomes vs. LNPs
The "complaint" that exosomes are unsafe because they are "LNPs in the blood" is based on three specific risks often cited in the research community:
Biodistribution: Just like vaccine LNPs, exosomes can go anywhere. While SHED-derived ones are meant to go to the brain, critics argue they could also accumulate in the liver or spleen, potentially delivering instructions to cells that don't need them.
Immune "Cloaking": LNPs can be seen as "foreign," causing an immediate reaction. Exosomes are "stealthier" because they are human-derived. Critics argue this "stealth" is actually dangerous because it allows foreign genetic material to bypass the immune system entirely.
The "Cargo" Unknown: In a vaccine LNP, we know exactly what's inside (specific mRNA). In a biological exosome (like SHED), the cargo is a "black box" of thousands of different proteins and microRNAs that can vary from batch to batch.
The Root Fact: If the concern is "nanoparticles in the blood," then exosomes definitely fit that description. The medical counter-argument is that because they are biological and not synthetic, the body has natural pathways to clear them out, unlike the persistent synthetic lipids in some LNP formulations.
Where the Field is Today
While systemic (IV) use is still largely in trials, you will see "clinics" using them in two ways that skirt the edges of full drug approval:
Topical/Aesthetic: Microneedling with exosomes for hair loss or skin (marketed as "cosmetics").
Investigational Use: Clinics operating under "patient-funded research" or specific IRB (Institutional Review Board) oversight.
If you are looking at Kevin McCairn's discussions, he is likely focusing on the blood-brain barrier aspect—the very thing that makes exosomes a "miracle" for neuro-repair is the exact same thing that makes them a "threat" to those worried about nanoparticle-mediated brain exposure.
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<BP here:> Still takes us back to 2012 - LNPs are ok for last ditch cancer treatments where the patient can be sequenced and given a test panel to characterise their blood before administration of whatever vehicle. Pharma was only faking that they wanted it for vaccines. They got lots of platforms already for that. A dollar is a dollar.
Kevin is targeting the brain which i imagine is why the tube goes in the neck.
I would consider it 'attempted local administration'
But Helsinki does not apply to the aphoresis. Standard stuff
You can complain he is mad scientisting by confounding 2 treatments. And would be correct if he was a big company or university or hospital doing research. This is not that.
The patient will not find a competing treatment offered. Once there is no menu at the restaurant, or chef, you turn on the stove and open the fridge.
The patient could get the stem cells at some other boutique.
He developed an idea and the patient accepted it. Could be a good idea or terrible, sure, doing any secondary treatment will confound a research project.
The person paying the hospital is just buying a service.
If you want better oversight, ask Pfizer or Moderna to take over her care lol.
They have all the answers and the microtweezers.
<BP ends>
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doi: 10.2174/1574888X16666201221151512.
Stem Cells Derived from Human Exfoliated Deciduous Teeth (SHED) in Neuronal Disorders: A Review
Minu Anoop 1 , Indrani Datta 1
Affiliations
PMID: 33349220 DOI: 10.2174/1574888X16666201221151512
Abstract
Most conventional treatments for neurodegenerative diseases fail due to their focus on neuroprotection rather than neurorestoration. Stem cell-based therapies are becoming a potential treatment option for neurodegenerative diseases as they can home in, engraft, differentiate and produce factors for CNS recovery. Stem cells derived from human dental pulp tissue differ from other sources of mesenchymal stem cells due to their embryonic neural crest origin and neurotrophic property. These include both Dental Pulp Stem Cells (DPSCs) from dental pulp tissues of human permanent teeth and Stem cells from Human Exfoliated Deciduous teeth (SHED). SHED offers many advantages over other types of MSCs, such as good proliferative potential, minimal invasive procurement, neuronal differentiation and neurotrophic capacity, and negligible ethical concerns. The therapeutic potential of SHED is attributed to the paracrine action of extracellularly released secreted factors, specifically the secretome, of which exosomes are a key component. SHED and its conditioned media can be effective in neurodegeneration through multiple mechanisms, including cell replacement, paracrine effects, angiogenesis, synaptogenesis, immunomodulation, and apoptosis inhibition, and SHED exosomes offer an ideal refined bed-to-bench formulation in neurodegenerative disorders. However, in spite of these advantages, there are still some limitations of SHED exosome therapy, such as the effectiveness of long-term storage of SHED and their exosomes, the development of a robust GMP-grade manufacturing protocol, optimization of the route of administration, and evaluation of the efficacy and safety in humans. In this review, we have addressed the isolation, collection and properties of SHED along with its therapeutic potential on in vitro and in vivo neuronal disorder models as evident from the published literature.
Keywords: Mesenchymal stem cells; Parkinsonœs disease.; SHED; dental pulp stem cells; exosome; secretome.
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
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Sadly: It is not even a scientific argumentation: "BUT they look and feel great." I feel also great smoking crack or taking steroids.
Dr McCairn can write elegant papers. I feel sure he is assembling his findings and we will hear more once the scientific results are all in.
point 1: compare it to dialysis, and you can conceptually normalise the aphoresis.
it is insane, untenable, but unavoidable if you want to live. i say 5 sucessive liver transplants would eventually do the job of cleaning the blood, but i am grimly sarcastic and assume a supply of chinese dissidents. livers go to the vaccine damaged and the lung tissue goes to brazil to passage Omicron-2027, the 'Revelation Variant' lol .. see Residue 666...
point 2: if you don't like the stem cell treatment being mixed in i get that.
there are mutiple reasons how you are correct, from risk, to science, to ethics, to statistics. cannibalism got them here, so maybe cannibalism will get them out? they took the LNP risk the first time - it is a long established fact that vaccine seekers are risk-avoidant. interpret that lol.
point 3: the patient is not optimising for point 1 or point 2. they got messed up participating in an experiment that was not going to follow up with them.
the only option for treatment is to hit the internet and call for help - if they have money.
the patient is driving this workflow - they are trying to undo their own mistake, and have the right be risky.
they had it to begin with - which got them here - and they have it now.
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>>> BP: a recreational AI (not checked for shared hallucination) for GB comment area thought provocation. speculation, expect 50% rubbish
>>> gemini query, to copilot for refinement.
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"Draft a theoretical molecular architecture for a 'Synthetic Rheology Restoration' protocol to address fibrinogen amyloidogenesis and endothelial erosion. Model a bifunctional peptidomimetic foldamer with the following parameters:
Core Mechanism: Act as a chaperone ligand to stabilize the alpha-helical conformation of the fibrinogen D-domain, specifically increasing the Gibbs free energy barrier (ΔG) against beta-sheet transition induced by misfolded spike protein seeds.
Endothelial Anchoring: Incorporate a collagen-binding motif to facilitate localized stabilization at sites of endothelial basement membrane exposure.
Smart Dissociation: Implement a thrombin-responsive trigger (cleavable linker) to ensure the chaperone releases its payload during legitimate localized hemostatic events, preventing systemic hypocoagulability.
Heme Sequestration: Integrate zwitterionic-coated (poly-sulfobetaine) micelles for heme scavenging to mitigate hemolysis-driven oxidative stress without providing a nucleation surface for further protein misfolding.
Analyze the potential for this system to restore laminar flow and prevent arterial occlusion in a hyper-coagulable environment."
Copilot said:
Direct answer: A bifunctional peptidomimetic foldamer can be designed as a collagen‑anchored, thrombin‑cleavable α‑helix chaperone that raises the ΔG for fibrinogen D‑domain β‑sheet conversion while co‑delivering zwitterionic polysulfobetaine micelles for heme sequestration; this architecture should locally reduce fibrin amyloid nucleation and help restore laminar flow if delivered to exposed basement membrane without impairing physiological hemostasis.
Design overview
Module Primary function Key motif / chemistry Localization cue Release trigger
Foldamer chaperone core Stabilize D‑domain α‑helix; raise ΔG for β‑sheet transition α/oligourea or α/β hybrid foldamer presenting helix‑mimetic side chains that engage D‑domain hot‑spots N/A
Thrombin‑cleavable linker
Collagen anchor Localize to endothelial basement membrane Triple‑helical GFOGER or collagen‑mimetic triple‑helix peptide Binds exposed collagen I/IV at injury N/A
Smart linker Permit thrombin‑responsive payload release LVPR↓GS or optimized P4–P3–P2–P1–P1′ consensus thrombin site Sits between anchor and chaperone Cleavage by thrombin
Heme scavenger Sequester free heme; avoid nucleation surfaces Polysulfobetaine (PSB)‑coated micelles encapsulating heme‑binding moieties Co‑assembled with foldamer; sterically shielded Non‑cleavable; cleared by reticuloendothelial system
Molecular architecture (sequence-level concept)
N‑terminus: Collagen‑mimetic triple‑helix peptide (GFOGER‑containing, stabilized by Hyp residues) to bind exposed collagen α2β1 integrin sites and localize to basement membrane. This motif provides high‑affinity anchoring to collagen I/IV.
• Thrombin‑cleavable linker: short flexible spacer containing optimized thrombin consensus (e.g., LVPRGS or tuned P2/P3′ residues) placed immediately C‑terminal to the anchor so physiologic thrombin at a hemostatic site will sever the chaperone from the anchor.
• Peptidomimetic foldamer core: hybrid α/oligourea or α/β foldamer engineered to present side chains that mimic the native D‑domain helix face, forming a high‑affinity chaperone ligand that increases the activation energy for α→β transition (steric packing, H‑bond donors, and hydrophobic patches). Foldamer backbones confer proteolytic stability and tunable helix propensity.
• Heme‑scavenging micelle payload: co‑assembled PSB‑coated micelles (zwitterionic polysulfobetaine corona) that encapsulate heme‑binding small molecules or albumin‑mimetic pockets; PSB corona minimizes protein adsorption and prevents micelle surfaces from acting as amyloid nucleation templates.
Mechanistic rationale and expected effects
• Raise ΔG for β‑sheet nucleation: the foldamer binds the D‑domain helix face, stabilizing α‑helical registry and sterically blocking spike‑seed interactions that nucleate β‑sheet conversion; this should reduce formation of fibrinaloid microclots observed with spike amyloid seeds.
• Local action, preserved hemostasis: collagen anchoring concentrates agent at sites of endothelial erosion; thrombin cleavage releases chaperone only during active clot formation, preventing systemic anticoagulation.
• Oxidative stress mitigation: PSB‑coated micelles sequester free heme and resist protein adsorption, lowering heme‑driven oxidative catalysis without providing a pro‑amyloid surface.
Risks, limitations, and development challenges
• Off‑target binding to circulating fibrinogen or platelets could alter clot mechanics; rigorous in‑vitro clotting and platelet assays required.
• Thrombin cleavage kinetics must be tuned so cleavage occurs only at physiologic thrombin bursts; suboptimal sequences risk premature release or failure to release.
• Immunogenicity and clearance of foldamers and micelles need evaluation; foldamer backbones reduce proteolysis but may elicit immune responses.
Bottom line and next steps
This architecture is mechanistically plausible and targets the three pathologies you specified (amyloidogenesis, endothelial erosion, heme toxicity) while preserving hemostasis via a thrombin trigger. Next steps: molecular docking to D‑domain, in‑vitro fibrin polymerization/fibrinolysis assays with spike seeds, thrombin‑cleavage kinetics, and hemocompatibility testing of PSB micelles.
No! You’re acting just like those stupid vaccine advocates! Nothing else is happening here: “The data will come later. Let’s just start with the experiments first.”
What do you even know about intracellular feedback loops of MAPK, mTORC1/2, RHOA, JAK/STAT that you dare to claim you have this figured out without even having conducted the necessary omics studies?! Your endpoints are a bad joke that proves once again that you know as much about systems biology as a paraplegic knows about running.
Your entire exosome argument shows that you’ve never studied membrane physics. And your inability to present data also speaks volumes. You used to be on the right side. Now you’ve degenerated into a Fauci 2.0.
I’m sorry, but this is highly unethical and not good science! Oh, and Kevin?: What do you even know about the Donnan equilibrium and exosomal identity via PtdInsPs?! You’ve disregarded every good practice, and your appeals to authority are embarrassing!
LOL?! You're really crazy, bro:
You're arguing about the “Procarta 21 Plex Human Cytokine Panels” Luminex assays, which are used to measure inflammation markers in blood or tissue?! A decrease in, say, TNF-alpha is an interesting indication of an effect, but it's not proof of long-term safety.
And that you don't even get why you would need omics for growth factors therapy to exclude possible off targets shows that you're still hanging in the believing of "cell is a thing I put something inside and than something happens I can calculate."