Dean Cheramie

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Dean Cheramie

Dean Cheramie

@DysautoDad

POTS Advocate | “Realize that people expend tremendous energy merely to be normal” - from Camus

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Dean Cheramie
Dean Cheramie@DysautoDad·
It's happening! My daughter Annelise (Li) will be treated in Japan in August for debilitating POTS, dizziness, neuropathy, headaches, brain fog, GI disruption, and crushing exhaustion, with a long history of hEDS and MCAS issues. DFPA filtration for removal of amyloidogenic clotting, and restorative treatment for the vascular system, and heart, brain, and organ tissue. Bravest and strongest person I know (other than her Mom). Bless the McCairn-Edogawa team. 🙏
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Dean Cheramie
Dean Cheramie@DysautoDad·
@VNoelte12 Hi Victoria if you go down my timeline, I have posted some very good summaries and video discussions about the treatment in Japan. Or research McCairn Edogawa Protocol.
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Victoria
Victoria@VNoelte12·
@DysautoDad Hi, can you point me to research for this treatment? Name of the clinic? How did you hear about it? What are the usual results?
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Dean Cheramie
Dean Cheramie@DysautoDad·
It's happening! My daughter Annelise (Li) will be treated in Japan in August for debilitating POTS, dizziness, neuropathy, headaches, brain fog, GI disruption, and crushing exhaustion, with a long history of hEDS and MCAS issues. DFPA filtration for removal of amyloidogenic clotting, and restorative treatment for the vascular system, and heart, brain, and organ tissue. Bravest and strongest person I know (other than her Mom). Bless the McCairn-Edogawa team. 🙏
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Dean Cheramie
Dean Cheramie@DysautoDad·
@emuntonmay Thank you Emily I will share this with her. It is very close to her current diet.
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Emily Munton
Emily Munton@emuntonmay·
@DysautoDad I don’t know if this will help at all but these interventions have helped our son with MCAS. Wishing your daughter all the best.
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Dean Cheramie
Dean Cheramie@DysautoDad·
Thanks for responding. I saw your response also to Kelsey. You will be interested that Annelise has had POTS and MCAS for a long time, it just got much worse under the blood clotting condition. Her hEDS has always been pretty bad with frequent disclocations. We are of course hoping for any improvement, but anxious about whether this could even address the underlying conditions that she had long before Covid came to this party. Thank you for following and we will issue more updates.
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Granny
Granny@JustClockIt·
@DysautoDad This is amazing news. Will you please update us in the treatment and how she’s doing? I would imagine Japan is light years ahead of the U.S. with treatments. Wishing her much healing.❤️‍🩹
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Dean Cheramie
Dean Cheramie@DysautoDad·
Thank you for responding. In her specific case, timing does not point to one or the other. The blood clotting disorder occurs in the vaccinated and the unvaccinated, sometime quickly after a vaccine or Covid infection, sometimes more slowly. Since in her case, we do not know, we do no conjecture.
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Dean Cheramie
Dean Cheramie@DysautoDad·
@redpavement Hello Jorge, the blood clotting condition is caused by Covid or the vaccine, or both. In her specific case as the symptoms evolved slowly, we do not know which. She did not take SSRI's. Thank you for being interested.
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Dean Cheramie
Dean Cheramie@DysautoDad·
@jeffreytee Thank you, Jeffrey. Currently this approach for this specific is available in Japan and a couple of EU countries. Is not available in the U.S. or Mexico. That will probably change, but due to her condition and the risks, timing is important.
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Dean Cheramie
Dean Cheramie@DysautoDad·
@bjornfri2020 Yes, I have been quite anxious to get her on their schedule before U.S. and UK pharma find a way to undermine it.
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Dean Cheramie
Dean Cheramie@DysautoDad·
Following up on Captain Ken’s challenge to the medical profession, here is the primer on how to evaluate patients for amyloidic fibrinogen aggregates, aka micro-clots.
Resia Pretorius@resiapretorius

There has been a discussion on X lately about biomarkers for #LongCOVID, so I thought I would share some blood markers available that might point to immune, clotting and endothelial dysfunction. Encouragingly, all of them are available at specialised pathology labs worldwide. These are also the molecules we keep finding trapped in fibrinaloid microclot complexes across our various (proteomics) analyses: fibrinogen, von Willebrand factor, Factor VIII, serum amyloid A, complement proteins (C3, C4, C5, C1q, factor B), platelet factor 4, P-selectin, myeloperoxidase, neutrophil elastase, transforming growth factor beta-1, endothelin-1, vascular endothelial growth factor, Serum Amyloid A, and many more. We also know that many of our collaborators have also find these molecules in the soluble fraction of plasma, when when they have done proteomics and ELISA tests. We have known for a while that these proteins are present in both the soluble and the insoluble fraction of plasma, mostly, we have just been searching inside the insoluble fraction of blood plasma for possible dysregulated inflammatory molecules that might in future, be targeted by treatment regimens. What is new in our approach, is that we have only recently started looking at post-translational modifications (PTMs), on proteins and we have found that some are extensively modified: glycated, oxidised, deamidated, citrullinated. What is PTMs? A post-translational modification (PTM) is a small chemical change made to a protein after it has been built, that slightly alters the protein without changing its underlying identity. A simple way to picture it: the protein is the basic product, and PTMs are the stickers, tags and add-ons attached to it afterwards. The item is still the same item, but the additions can change how it looks and behaves, whether other things can grab onto it, and how long it lasts. In the body, these tags get added in response to conditions like inflammation, high blood sugar or oxidative stress. Common examples are sugar molecules stuck on (glycation), oxygen damage (oxidation), or other small chemical groups. The protein's amount in the blood can look completely normal, while these tags quietly change how it works, which is exactly why a routine test can read "normal" and still miss the problem. Also note that much earlier work by well-known researchers in the fibrinogen field has found post-translational modifications on fibrinogen in various inflammatory diseases. More to come from our research group! Please, in the mean time see a the table below. These might be some valuable biomarkers that might to used in clinical investigations and might assist clinicians to target some symptoms. @dbkell and I have also discussed possible devices like capillaroscopy for detecting vascular damage. @ImmunoFever has recently discussed the applications in numerous posts. Lastly, this is in no way suggesting that these are the only biomarkers, it is just a small snapshot molecules our lab is finding and studying. There are numerous more biomarkers that can be looked at for neuro-immunology, muscle and many more systems.

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Dean Cheramie
Dean Cheramie@DysautoDad·
@resiapretorius @BlackTomThePyr8 Following up on Captain Ken’s challenge to the medical profession, here is the primer on how to evaluate for amyloidic fibrinogen aggregates.
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Resia Pretorius
Resia Pretorius@resiapretorius·
There has been a discussion on X lately about biomarkers for #LongCOVID, so I thought I would share some blood markers available that might point to immune, clotting and endothelial dysfunction. Encouragingly, all of them are available at specialised pathology labs worldwide. These are also the molecules we keep finding trapped in fibrinaloid microclot complexes across our various (proteomics) analyses: fibrinogen, von Willebrand factor, Factor VIII, serum amyloid A, complement proteins (C3, C4, C5, C1q, factor B), platelet factor 4, P-selectin, myeloperoxidase, neutrophil elastase, transforming growth factor beta-1, endothelin-1, vascular endothelial growth factor, Serum Amyloid A, and many more. We also know that many of our collaborators have also find these molecules in the soluble fraction of plasma, when when they have done proteomics and ELISA tests. We have known for a while that these proteins are present in both the soluble and the insoluble fraction of plasma, mostly, we have just been searching inside the insoluble fraction of blood plasma for possible dysregulated inflammatory molecules that might in future, be targeted by treatment regimens. What is new in our approach, is that we have only recently started looking at post-translational modifications (PTMs), on proteins and we have found that some are extensively modified: glycated, oxidised, deamidated, citrullinated. What is PTMs? A post-translational modification (PTM) is a small chemical change made to a protein after it has been built, that slightly alters the protein without changing its underlying identity. A simple way to picture it: the protein is the basic product, and PTMs are the stickers, tags and add-ons attached to it afterwards. The item is still the same item, but the additions can change how it looks and behaves, whether other things can grab onto it, and how long it lasts. In the body, these tags get added in response to conditions like inflammation, high blood sugar or oxidative stress. Common examples are sugar molecules stuck on (glycation), oxygen damage (oxidation), or other small chemical groups. The protein's amount in the blood can look completely normal, while these tags quietly change how it works, which is exactly why a routine test can read "normal" and still miss the problem. Also note that much earlier work by well-known researchers in the fibrinogen field has found post-translational modifications on fibrinogen in various inflammatory diseases. More to come from our research group! Please, in the mean time see a the table below. These might be some valuable biomarkers that might to used in clinical investigations and might assist clinicians to target some symptoms. @dbkell and I have also discussed possible devices like capillaroscopy for detecting vascular damage. @ImmunoFever has recently discussed the applications in numerous posts. Lastly, this is in no way suggesting that these are the only biomarkers, it is just a small snapshot molecules our lab is finding and studying. There are numerous more biomarkers that can be looked at for neuro-immunology, muscle and many more systems.
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Dean Cheramie
Dean Cheramie@DysautoDad·
Celebrate with EmileeJustice as she reports good results from her early treatments in Japan. Even small gains can be overwhelming, when you have been so injured for so long.
AventJustice@EmAdJustice

@CatsRule2023 @KevinMcCairnPhD I feel really good right now. I’m waiting for them to let me walk home. I can feel my toes - for the first time in almost 4 years my toes aren’t numb and my legs aren’t heavy. Positive beginning 🙏

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Dean Cheramie
Dean Cheramie@DysautoDad·
Those who do serious and unparalleled research on the devastating injury and death caused by amyloidic fibrinogen aggregates are harrassed and intimidated. Because they are over the target. Thank you Resia we owe you our lives.
Resia Pretorius@resiapretorius

To my X followers, including the fake and catfish accounts: For some time I have been the target of sustained personal harassment on this platform, much of it from anonymous and impersonating accounts. I have stayed quiet and kept working. I am addressing it now, once, and then returning to the science. I am not the only one. A number of researchers working on the biological basis of this illness, including collaborators of mine, have faced the same pattern of harassment. Much of it appears coordinated and comes from a small number of accounts whose interest is clearly not the science: their aim is not scientific debate; it is to intimidate people for doing research they do not like. Targeting scientists for studying a disease is not scepticism; it is intimidation. On the facts: the claim that our work "has not been replicated" is untrue. Independent groups have confirmed or applied these findings: - the same aggregates were confirmed in pulmonary embolism (Baker et al., Communications Medicine, 2023); - amyloid-fibrinogen aggregates predicted disseminated intravascular coagulation and mortality in sepsis (Schofield/Toh et al., Blood Advances, 2024); -increased fibrinaloid microclots were found in Long COVID by an independent UK group (Dalton et al., Sheffield Hallam, preprint, 2024); - and the methods have been taken up in paediatric Long COVID (Steifman, Yonker et al., Pediatric Research, 2026). This is now a field with dozens of independent papers. One thing to make very clear: I have no involvement in any apheresis or plasmapheresis treatment for these conditions. Why? It is simply not my field of expertise. I cannot control how others use published methods, and it is wrong to attribute their choices to me. On Biocode, our start-up company: public universities have a clear responsibility to translate research into public benefit, and commercialising discoveries through spin-out companies is a core part of that mandate. That is precisely what Biocode was created to do. It is an early-stage university spin-out, it is not profitable, and repeated insinuations that I am personally enriching myself are false. I welcome robust scientific criticism; that is how science works, and II have actively reached out to colleagues who see the field differently. Harassment, account stalking, impersonation and personal attacks are not criticism. I am documenting it, I am taking advice on my options, and I will not be engaging with it further. Just because biological researchers are targeted in this way does not mean we will stop. If anything, it strengthens our resolve to understand diseases and to serve the millions of patients who are waiting for answers.

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Dean Cheramie
Dean Cheramie@DysautoDad·
The McCairn-Edogawa protocol treats patients with debilitating POTS, dizziness, nausea, neuropathy, pain, brutal headaches, brain fog, crushing exhaustion, and other injuries by removing amyloidogenic microclots and larger blood clots, and treating damaged vascular, heart, brain, and organ tissue.
Lyndsey, RN 💜🐭@HouseLyndseyRN

A Thread: ~THE MCCAIRN-EDOGAWA HOSPITAL CLINICAL RESEARCH PROGRAM~ • Dual Filtration Plasmapheresis/Apheresis Adsorption Therapy
& Stem Cell Growth Factor Treatment • A hospital-led pathway for long COVID & vaccine injury presentations, pairing DFPA blood purification with cytokine analytics, amyloid detection, live blood analysis, & SHED-derived regenerative growth factor support @KevinMcCairnPhD @CharlesRixey @shonyan @edogawa_PA

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Dean Cheramie
Dean Cheramie@DysautoDad·
Excellent summary of Systemic Capillary Leak Syndrome.
Dr. Lynn Fynn-derella (ret)@Fynnderella1

Systemic capillary leak syndrome (SCLS) is absolutely a recognized adverse event from the COVID shots. This isn't fringe speculation — it's documented in the medical literature and acknowledged by regulatory bodies, even if they've downplayed the scope. What the Evidence Shows The mechanism isn't mysterious. The spike protein — whether from the virus or from the shots — is vasculotoxic. It binds to ACE2 receptors which are abundant in endothelial cells lining your blood vessels. When those cells get damaged, the tight junctions between them loosen, and plasma starts leaking into surrounding tissues. That's SCLS in a nutshell. Case reports started appearing in the literature within months of the rollout. Patients presenting with the classic triad: hypotension, hemoconcentration, and hypoalbuminemia — blood pressure crashing, blood thickening because the fluid component is leaking out, and albumin levels dropping for the same reason. Some had no prior history. Others had pre-existing monoclonal gammopathy of undetermined significance (MGUS), which is a known risk factor for SCLS, and the shot appears to have triggered a full-blown episode. What VAERS Shows VAERS, for all its limitations, captures the signal. Searching for capillary leak reports post-vaccination returns a non-trivial number of cases — many in people with no prior SCLS history. The CDC's own passive surveillance picked this up. But passive surveillance systems miss the vast majority of adverse events, so what we're seeing is almost certainly the tip of an iceberg. The Spike-Endothelial Interface The core problem is that the shots deliver instructions for your own cells to manufacture spike protein, and there's no way to control where it goes or how much is produced. Spike protein has direct cytotoxic effects on endothelial cells. This isn't theoretical — perfusion studies and in vitro work have demonstrated endothelial barrier disruption from spike exposure. When capillary beds become permeable, in severe cases you get compartment syndrome, limb ischemia, multi-organ failure. Several deaths have been attributed to post-vaccination SCLS. Bottom Line Yes, COVID shots can cause systemic capillary leak syndrome. The question isn't whether — it's how often, and the answer is almost certainly more often than the official numbers suggest. The same institutions that spent two years calling myocarditis "mild and self-limiting" before quietly admitting it's a real problem are doing the same thing here. The pattern is identical: acknowledge a few cases, call them "rare," and move on without investigating the true scope.

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Dean Cheramie
Dean Cheramie@DysautoDad·
@MaryBowdenMD Outstanding discussion of the McCairn Edogawa treatment protocol. SPOILER ALERT: This is best for people that have following closely. If you are new to the topic, you may need also need some background.
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Dean Cheramie retweetledi
Mary Talley Bowden MD
Mary Talley Bowden MD@MaryBowdenMD·
40 patients severely injured by the COVID mRNA shots have flown to Japan to have amyloid microclots filtered from their blood + stem cell growth factors. Their response has exceeded expectations and brings hope to the injured. youtube.com/live/LVKaQhfgF…
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Dr. Lynn Fynn-derella (ret)
Systemic capillary leak syndrome (SCLS) is absolutely a recognized adverse event from the COVID shots. This isn't fringe speculation — it's documented in the medical literature and acknowledged by regulatory bodies, even if they've downplayed the scope. What the Evidence Shows The mechanism isn't mysterious. The spike protein — whether from the virus or from the shots — is vasculotoxic. It binds to ACE2 receptors which are abundant in endothelial cells lining your blood vessels. When those cells get damaged, the tight junctions between them loosen, and plasma starts leaking into surrounding tissues. That's SCLS in a nutshell. Case reports started appearing in the literature within months of the rollout. Patients presenting with the classic triad: hypotension, hemoconcentration, and hypoalbuminemia — blood pressure crashing, blood thickening because the fluid component is leaking out, and albumin levels dropping for the same reason. Some had no prior history. Others had pre-existing monoclonal gammopathy of undetermined significance (MGUS), which is a known risk factor for SCLS, and the shot appears to have triggered a full-blown episode. What VAERS Shows VAERS, for all its limitations, captures the signal. Searching for capillary leak reports post-vaccination returns a non-trivial number of cases — many in people with no prior SCLS history. The CDC's own passive surveillance picked this up. But passive surveillance systems miss the vast majority of adverse events, so what we're seeing is almost certainly the tip of an iceberg. The Spike-Endothelial Interface The core problem is that the shots deliver instructions for your own cells to manufacture spike protein, and there's no way to control where it goes or how much is produced. Spike protein has direct cytotoxic effects on endothelial cells. This isn't theoretical — perfusion studies and in vitro work have demonstrated endothelial barrier disruption from spike exposure. When capillary beds become permeable, in severe cases you get compartment syndrome, limb ischemia, multi-organ failure. Several deaths have been attributed to post-vaccination SCLS. Bottom Line Yes, COVID shots can cause systemic capillary leak syndrome. The question isn't whether — it's how often, and the answer is almost certainly more often than the official numbers suggest. The same institutions that spent two years calling myocarditis "mild and self-limiting" before quietly admitting it's a real problem are doing the same thing here. The pattern is identical: acknowledge a few cases, call them "rare," and move on without investigating the true scope.
Dr. Lynn Fynn-derella (ret) tweet media
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