REFERENCE

Well, now, as you may or may not know, we have been struck from YouTube and I am making the decision that I'm just not going to go back on on that platform because I have been holding my tongue and basically editor, not editorializing, being selective in the stories that I would report on, particularly those surrounding vaccines, adverse events to vaccines, etc. So that's the way it's got to be. I'm going to be speaking with Walter in hopefully a couple of minutes. Let me just email him the chat. Oh, my computer's glitching like crazy. Copy invite link. Let me just, I've got to just send the email and get the, wow, is that my camera that's glitching out? It is, isn't it? Huh? Fucking nothing works! God damn tapio boys! I can use my button now. I can use my button now. Shut it. Isn't that not working? They always, they always come through, but we will, we will keep soldiering on and do our best. So let me just find my email. Do this, do this. Send invite link. All right, let's, let's do that. So whilst, whilst I'm waiting for, why is it? Oh dear, oh dear. Do this. OK, let me keep that on the screen whilst I wait for Walter.

Look, this, this is the, I hate the word now, the terrain that we have to navigate. And the, the simple, the simple fact is, this is what I've been telling you since forever, right? You cannot trust these corporate platforms, especially in the age of covert moral bio enhancement. That includes psychological warfare against you. And they will do anything to shut down people who are calling out, well, essential war crimes. OK? And it would be naive to think that staying on a platform like YouTube and calling out the deep state for crimes against humanity, their incessant pursuit of bio warfare agents and medical countermeasures is anything but a losing strategy. So, like I say, people that are listening, please, please, please spread the word. You know, there's 66 watching on Rumble. That's pretty good. We've got 80 people watching so far. So that's, that's not so bad, considering we're highly, highly dependent on, or we were highly dependent on YouTube to sort of send out alerts. But folks, this is not stopping the totalitarian, globalist, technocratic bankathon that they've got. Lined it up for you isn't going to stop. And you've got to, you've got to adapt. You've got to, you've, you've got to stop being creatures of convenience. OK? And it means that you're going to have to seek out other places. Get a, get a, I don't know, does Rumble have an app for the phone that does alerts? I don't even know how it works on Rumble, if it works. Rumble have an app for the phone that does alerts. I don't even know how it works on Rumble, if it sends out alerts or not. But the, it's not going to get better. OK? And, you know, when you've, you know, just, just to go off on, Simon says, free speech video site, Rumble now has Peter Thiel as a shareholder, his company, Palantir Technologies, helps buy agencies, makes sense. Yeah, yeah, yeah, of course.

Of course. Of course. Don't expect Rumble to be there. And literally, the last readout that we have is maybe Twitter and our own streaming platform. But, you know, that streaming platform is very, very costly. And, you know, I was talking with Simon yesterday. The numbers that are using it, I'm not sure warrant the expense at the moment. I'm not sure I can maintain the expense to keep running it because it is very, very expensive to do. I'm not, of course, I want to pursue it, but unless it really starts gaining traction in the first few months, I'm just not, I'm not going to have the funds to be able to do it. I've got to be able to eat and feed my kids.

So I'm still waiting for Walter. Did I send that email? Let me just check. Yeah, should do. I'm still waiting for Walter. I need to just get Walter in my contacts for the most free site is Bitchute, but even they remove murder killing videos. Look, man, you know, gore videos. Look, if you want gore, go to chaotic.com, OK?

This isn't about gore. This is this is about talking about government programs that have spun out of control. No, I wouldn't even say spun out of control have been being deliberately maneuvered to make sure that they're controlling every aspect of your life. The COVID-19 pandemic has laid the groundwork for their total surveillance state. And it's state is the wrong word. It's just transnational public private partnership that's going to be run by weffers, basically. And woe betide you, should you should you want to speak up against it? Now, we may be living in more enlightened times where you're not going to get shipped off to deepest Siberia to be put into the gulag. But the. They're just your home becomes your gulag that they'll just restrict your access to these digital services and, you know, any of the corporate platforms are essentially going to be. Don't trust them. Don't trust them. You've got you've got one one platform which we're trying to build out and barely anyone is using it. And I get it. It's easy. It's easier to go to YouTube or to rumble to to switch on their app and do the recording. But unless unless the facilities are being used, it's going to be very, very hard to just maintain it going into the future. And it's you know, it's not just it's not just the hardware itself. You know, I like to try and you know, the little I can do is help the people that are running it as well. And, you know, I'm not sitting here on piles of gold trying to do this. This is this is literal activist streaming, trying to find our way through the political nonsense, the scientific gaslighting that they're engaged in and they still know Walter.

And what can I do for that? Well, whilst whilst we're waiting, whilst we're waiting for Walter, what I'll do is I'll just remind everyone where they can find me. Go to McCairnDojo. Okay. And, you know, we'll do a bit of housekeeping here. Okay. This site keeps us alive. This keeps us being able to stream and give me the space to be able to look at papers and break them down for you and give you my thoughts and opinion on them.

And maybe you don't agree with my opinions about everything. But, you know, I do think we're over the target a lot of the time. And I would, again, encourage everyone to, you know, if you want this available to you and you don't just want to be fed a plate of vanilla scented dogshite via the likes of YouTube, you must you must support this project. And if if we can't get the support, it'll go down in flames and another bar on the prison will be placed in front of you. So, you know, if you're not already become a member of the Discord, right? Do it. Do it through McCann Dojo. Okay. And we'll let you in. I'm still trying to pass a Midwestern doctors theory for clot formation.

That doctor is just laying out exactly what I've been telling you that these are amyloidogenic clots. Right. We can argue about the minutiae of the details, but 99.99 percent that amyloidogenic.

Okay. Also, you can get an email. Okay. Go to register to be notified and I will give an email when I go live. Okay. If you're not signed up for that, you just put your email in, click agree and you can unsubscribe at any time. But I do try to use this as a way to get word out that I am streaming and we're going to be doing something of interest, I hope. And well, I'm still still waiting on Walter. So Did I, I sent it to him. It sent him the link. I am.

Zoom link. They're with me, folks. Anyway, Email notifications work really well. I mean, it should do. It's bloody expensive. This is, this is the world in which we find ourselves. You know, that's why these platforms are so seductive. YouTube has all the alert systems built into it. Again, I don't know about Rumble. So if it's, if it does an alert, I don't, I should probably spend more. I just know that it does do the stream and people are going to it and using it and the getting occasional buffering per minute or so on WTYL. So let, let Simon know or I'll let Simon know. And what we're going to do with the WTYL platform is set up and I'm no expert on this, but it's this Content delivery around something called Kubernetes that basically sort of automatically stands up resources as you need them for people who are as people sort of log in to watch and rumble. No buffering yet.

Simon's putting a link to another, I don't know, we talk, you listen. Again, this is, can I get Neapolitan dog shite? Yeah, I don't even think you'll get that, I'm afraid. Like I say, if you can't see the accelerationism that is happening right now, and I don't know what to tell you. Okay, all those that applauded the rollout and mandating of gene transfection technologies have laid the groundwork. I would, I would say that those who have, well, if you want to give me cryptocurrency, I'm happy to take it. But you know, that's, that was them sort of trialing the infrastructure needed for central bank digital currencies. That's all coming. There are protests happening right now in, I want to say it was Amsterdam and London, where people are actively showing their displeasure about the idea of central bank digital currencies. I think the executive decision has already been made that they're going to be rolling this type of stuff out. And, you know, why, why would that be? Yes, there's probably an element of, hang on a second. Something about vaping. JM, I actually bought a vape yesterday, and it was bloody hard, actually. Every vape that I tried to get was, they wouldn't, they wouldn't ship it to me, but I got one, some batteries, some juice, and it wasn't cheap. It was, I want to say, it was like 200 Canadian dollars to get like the whole kit and caboodle. And I don't know how long that juice lasts, but I've been informed that my vaping, vaping system is in, in the post. And we will, I will be blowing big clouds of vapour on stream when I get it. And let me just do this, go back to the live stream chat.

And yeah, right now I'm just waiting for Walter to join the link. He was ready to go sort of at 8.30. I said I've got a bunch of set up to do, but nothing, nothing since, no response. I hope he's okay.

Okay. So as we're on Rumble and I had a, oh no, I don't have them. I don't have them set up anymore. There's a whole bunch of Shaheed's that we could go through. I feel free to do that comedy skit now of looking at Shaheed's, but as I thought I was going to have Walter on, and I was trying, I was trying to be a good boy for YouTube, just to try to stay on YouTube, just to give people the option. I have, I haven't been doing that. So, but I do have, there's a whole bunch of people who have sequestered their carbon and we can, we can poke fun at them now and have a good laugh.

Take those honk pills with the black ones. Let's see. Maybe it went to spam. Redudable RDA MTL deck is for men. Pens are for girly men. Let me just show you. I'll show off my vape that I did get here. And the colour choice was not mine. It was the only one that I could get that would, oh, there's Walter. There's Walter. Here we go. Pink. Just wait for him to get in. Admit. Oh, come on. Admit. My computer's really laggy. It hasn't been reset for over a month.

Walter, how are you, sir? Hello. Hang on. Let me, let me just switch, switch screens so people can see your chiseled…

You got the, you got the monkey juice.

Yes. Sorry. But we're on Rumble now. I'm, I'm not going back to YouTube. I'm, I'm going to cut loose with all sorts of anti-social outrageous sound, sound clips and sound drops. Let me just switch off my other camera. There we go. That should be us on the screen. And Jig says, Walter trying to save me. I don't know if you were listening to the, the stream just prior to joining, but.

No, I was not. I'm, I'm, I'm sold on vaping after my last trip to the U S and, um, I bought, I bought like these little, um, disposable ones and, um, they're, they're, they're too, uh, well they run out real quick and I've invested. I've invested, I've invested it. It's about 200 Canadian dollars to get, uh, it's called a geek vape Aegis legend two with cerebrous 200 watt starter kit, whatever that means.

I'm, I, I was finishing my daily cigars. I was doing, I smoke a cigar after dinner every night.

Oh, you do? Uh, any particular brand that's, uh, you're a Monte Cristo man? Uh, I do like Monte Cristo. Um, I like Upman. Um, I like CAO. I like the Monterey Excalibur black.

So there's the variety that I smoke, but I think, um, Monte Cristo and Upman are my favorites at the moment. Yeah. I used to like, uh, the odd cigar now and again, but, um, I could, I could never maintain the discipline of just keeping it in my mouth. I would inhale.

Oh, I never inhale it ever, ever, ever. I mean, I, I did when I was younger and it made, yeah, it just does not make my, does not make me feel good. No, unless someone takes a Thrillo pad to your, right. Exactly. Exactly. So I make sure to, I never inhale it. I just love the taste and I love the, the, the, the, the, the, the Valdanshan of being under the spell of a good cigar is just magical.

So I applaud you for your discipline because I, thank you. I'm always, uh, I'll suck that right down. down. You know, I thought I, back when I was on Twitter, I thought I had some pretty good cigars and then a doctor in Florida sent me a picture of his humidor and it was just loaded with like $60 Cubans. It was like, Oh my God. Do you have a humidor? Are you that into it? I have a small humidor. It keeps about 20 cigars and I never keep, I have to live on myself to one a day. So I do not keep more than 20 on hand. What's the price of one of your cigars? What's the, they write about 10 bucks a stick. I get them, I get them from a Jr cigars or a Mike cigars. Um, I, that way I avoid the, uh, the tax situation and they're there. Otherwise it'd be 20 or $30 a stick if I got them. Yeah. That's the thing that put me off a surprise. It's ridiculously expensive. And, um, yeah, it's, I would be a chain smoker dude. Um, if it wasn't, would you really? Oh, Oh God. Yeah. Yeah. I mean, I, I, I quit smoking in my twenties. Um, but I've always, always, I've never stopped nick tea. Right. And I can't break that habit. Um, well that's good because it, it takes up the NaChR receptors and the spike can get to it. Yes. So it's actually good. Any excuse. That's my excuse. Because the nicotine has a greater affinity than the spike for the NaChR receptors. So that's my, that's my medical excuse to smoke cigars. Yeah. That's, uh, any excuse to get nicotine in, I'll, um, I'll justify it. It's good for you. It staves off Parkinson's. That was, uh, that's true. Well, you know, there's, I, I don't know how true that is. It's one of those sort of large epidemiological observations. Well, let's hope it's true. I can leave it at that. Well, I don't think it's worked in my case.

Um, my, my last MRI wasn't looking good, bro. Oh, really? Oh yeah. Um, hypo intense all through my, um, globus pallidus externus, which is the indirect pathway, which is what goes wrong. Um, when you get Parkinson's and, um, nice morning. Oh, I'm sorry to hear that. It is what it is. Look, man, I'm 50 and, um, you know, looking at it, you could probably say, yeah, you've got five, 10 years of, um, normal activity that puts me in sixes and then another 10 years is just sort of, that's it. You're, you're, you're heading down, right? And you know, my grandfather had it. Um, so it's, it's obviously in the family. We just, we just have the medical technologies now to be able to, um, to, to peer into the brain. Um, it doesn't, yeah, I'm not sort of concerned beyond the just, oh, I'm just slow moving in the morning. And it's what it is. Get out for a walk. Yes.

It was interesting because that MRI, uh, paper study that came out, I think it was last week that I referenced in my substack shows the, uh, the brain stem, um, lesions due to, uh, the spike protein. And it's, and what I also find interesting is that it's the, as I hypothesized and the MRIs are proving true, it's the immune complexes, the spike doesn't actually even have to be able to enter the, uh, the brain to cause the damage. It's the immune complexes of the spike, which leads me to a couple of big discoveries that I've made over the past day. Um, one of them I've realized is that it really isn't the spike per se that is the problem. The problem is that if the spike is cleaved and then proteolysis occurs, it's the peptides of this, the cleavage and the peptides of the spike that are the danger. So it's like the spike in and of itself as a fully formed intact spike. And the studies have shown that it doesn't actually do anything. It's the full spike by itself, but when it's cleaned and proteolyzed, that's when it causes all the pathology. So it's, when it's broken apart, that's the danger. Cluster munition of, um, amyloidogenic peptides. I don't know if you've seen my, um, recent streams, uh, but someone sent me a useful software called Waltz. Um, maybe does this work? Is that working? Do you see my screen? Uh, I see. Yes, I do. Yes.

So, um, this is the amyloidogenic, um, analysis of Delta. Oh, wow. And this is Omicron. This is wait, this is Moderna. This is, uh, I can't remember what this was. This is H1N1, flu. And just for shits and giggles, we, I ran OC43, the sort of, um, ancestral beta coronavirus. Um, and that's highly amyloidogenic as well. Yes, it is. It's the common, common cold now. But, um, after, so after the stream, people, people were asking, are we, are we getting all concerned because, you know, all many viruses are going to be containing these amyloidogenic sequences? Um, well, maybe. So I looked into the, the history of OC 43 and it's, they think it's responsible for the, uh, a pandemic in the 1890s. And, um, even though it's considered mild now, I mean, as good as sort of clinical reports are from, um, over a hundred years ago, apparently it was much, much more severe, um, during the actual pandemic itself. And, you know, I made, I made the point yesterday that, um, it doesn't, it doesn't have the furin cleavage site that is the problem in, um, uh, the current SARS sort of iteration.

But, um, you know, these are, these are things that, you know, people should be aware of, they, we shouldn't be sort of, well, under normal circumstances, were it just a natural virus, et cetera, I would just bin it with other viruses and hope that the immune system does its best. And I would consider that the best way to proceed forward. But, um, we live in an age where they've decided to take these amyloidogenic sequences and gene transfect them into, into people. And we, we don't know the consequences of that. And I think we're seeing that. Yes, yes. So, you know, the, um, the obvious question that I can ask freely is, uh, we're not being, um, pared down upon by the YouTube I've saw on, um, what's…

What's your opinion on, what's it called? Died Suddenly? Well, I, that's exactly what I wanted to talk about. You mean, you mean the movie? Yeah. Yeah. I think I'm not a big fan of, of, uh, I haven't watched it, but I don't think the movie is really as much of the point as, um, the mechanisms behind it. And we all know about, okay, so what I've discovered in the last 24 hours is the, died suddenly, the sudden deaths. It looks like there are at least three roads that are leading to a sudden cardiac death. One of course is myocarditis. The other is brainstem malfunction leading to probably a central apnea and, or a fatal arrhythmia, which is why people are dying in their sleep. And if you look at my most recent post, the study they did of severe COVID, it was a limited number of people, but five of them died in their sleep suddenly. So I think that again, is it a very fast mechanism or is it the same mechanism that is taking more time in some people rather than being that the path is, is more, um, more accelerated in some than others, but it's still the same path.

And if you look at this, I found this paper, um, if you could please bring this up, I put it in the chat. And I think this is a very, very interesting paper, which shows, so we have myocarditis, we have the brainstem, and then we have amyloidosis as the third path. They all converge on sudden cardiac death. Um, I don't know if you can share the screen and look at this paper, but I'm, I'm very curious. And if you look all the cardiac sudden deaths, none of them had arthrosclerosis. I think maybe one did, but the point is, is that the vast majority of them, none of them, the vast majority of them did not have arthrosclerosis. So if you just go through this paper, yes, thank you.

So amyloid deposition of improperly folded insoluble proteins may affect one organ or maybe systemic, this we know, although plasma cell dyscrasia, that's a new one. By the way, that's another thing I addressed is, is the, the, uh, the malformed B cells. That's another thing I discussed in a previous post on, so I predicted that as well. So that's the dyscrasia? Yes, that's a dyscrasia. Is frequently implicated in etiology and is due to immunoglobulin light chain production, amyloidosis, age-related amyloidosis, believed to be secondary to transetherine production. Chronic inflammation-related amyloidosis is fought due to acute phase reactants and dozens of others are also described. Clinical presentation is dependent upon the organs involved and those associated with unexpected death are expected to involve the cardiovascular system. Here we are. Yeah. All cases received for forensic post-mortem examination, blah, blah, South Carolina, were searched to identify any in which amyloidosis was listed as final diagnosis. Seven cases were identified that met the criteria and were previewed for demographic information, presentation cause and manner of death, an assessment of pertinence of the diagnosis of amyloidosis to the cause and manner of death. Interestingly, gross examination of the heart was suggestive of amyloidosis or other infiltrative process. In only two of the cases reviewed and the history of myeloma was only noted in one individual. Interesting.

And if you scroll down through the cases, you can skip through all this and look at the cases. Here we go, like case one. So a 70 year old black, 74 year old, sorry, black male presented to the hospital following a fall down three stairs, multiple rib fractures. Ouch, that hurts. I know from personal experience. Had elevated troponin 1, decreased urinary output and then elevated creatinine of 2.3 megs per DL were noted upon evaluation, respiratory distress and arrest and ensued and he died on the hospital day three despite resuscitation attempts. Medical history was significant for congestive heart failure with an ejection fraction of 30%, mitral regurgitation, systemic and pulmonary hypertension and chronic obstructive pulmonary disease. Well, the COPD is a killer. That took my father out and it was his heart that gave out in the end. Findings at autopsy included a calculated body mass index of 26.0, it was fatty as well, with chamber dilation and diffuse pale brown coloration and increased ventricular wall thickness. No significant coronary artery arthrosclerosis was present. Interesting. The last weighed 660 grams to gather and bilateral pleural effusions were noted. Microscopy demonstrated cardiac myocyte hypertrophy and patchy amorphous pink material in the myocardial interstitium. This material stained positively with Congo red. There's that stain folks. That's what we have to do.

I was teeing off yesterday just Karen Kingston was one of these individuals, some doctor woman who's in tune with the great spirit of Ramphen, apparently. That's a, I don't know, medical framework, a 30,000 year old demiurge. Anyway, but they were, they're looking at these live blood samples from people where they can see these ribbon like occlusions insoluble. And I think you would agree with me that there's a high probability that those ribbons that they're seeing in these, not only vaccinated, but people who have had COVID are likely the amyloid occlusions building up. Absolutely. But none of them are doing the stain for Congo Red. And they need to. Yeah. It's critical. It's incredibly infuriating.

Well, that's one of the issues brought up in this paper is the incredible cost of doing that. And that's why it's not done at autopsy because of the incredible cost involved in doing that. Well, Congo red isn't expensive. What's expensive is the tissue preparation. Right, right. It's getting to that point that the process is prohibitively expensive. Yeah. So you need a pathologist. You need to extract out your organs of interest. And even taking the heart out of a monkey or the brain out of a monkey, that's a half day effort, right? Just to chip away at the bone. It's sort of like getting the rear main seal fixed on your car. The parts $5, but you have to take it out. And then there's the time sink with just processing the tissue, right? So you've got to perfuse it properly and then you've got to slice it. And then you've got to mount it onto slides. Then it needs dehydrating.

And then you do your stains and it's, well, it's somewhat automated now, but yeah, it's not easy, right? But, and this is something I'm sure you'll agree on as well. It's incredibly disturbing the lack of autopsy data we're receiving from people who are quote unquote dying suddenly. And if you continue with it, I'd like to look at a few of these cases because as you can see, that's, that's amyloid rich. Yeah. And if you keep looking down like the next one, systemic amyloidosis. Yes. And then if you look for the one that fell, it looks like the precipitating event, someone fell from their balcony, but it looks like it was a arrhythmia from amyloidosis that caused the fall and they fell off their balcony.

Yes. In one of these cases, but they, they, they believe that the amyloidosis of the heart precipitated an arrhythmia that caused it. But yeah, this is nice. Again, interestingly, the queen died of multiple myeloma, just for a very interesting. Yeah. I'm not, not a royal fan either. But again, myeloma is something that the spike protein can cause, but that's a whole another discussion. But if you keep scrolling down. And she did have, she did have a case of COVID. And she did have a case of COVID. Exactly. So what's this? This is actually interesting that Congo red is showing up so well under polarized light and makes my job much, much easier in the coming weeks. Okay, see people died in there right here.

Another, these are all people that are found dead. What I would say they're all at that 70 year old. But the point is, is that, is that this is being accelerated by an, by a, you know, we're getting the heart to 70 year olds and much younger people do to the amyloidosis, which is far premature than what it should be. That's the point is that you're getting your people are developing the heart of a 70 year old, even though they might have a 20 year old body. That's the point. Yes. Yes. Is that before COVID this, we didn't see this, but now we're seeing this. And the point is that it's giving people 70 year old hearts in 20 year old bodies. That's the point. Yeah. And you know, we do, we don't know the, how much it's sort of penetrated in into the population, right? We can look at the excess deaths. We can look at the actuarial data. There's a signal there. Absolutely. But, you know, I wonder how many people will just sort of limp along, especially if they're not sort of exerting themselves.

Well, if you notice the people who are like that, there was a financier that died at 30 like just yesterday, a country singer, the pro athletes and others, we're seeing people with high stress profiles being taken out first. As you astutely pointed out, what if you just live along? What if you just take your walk? What if you don't actually do or have a stressful life? Is this just going to cause it to happen later? Yeah. Well, you know, even if it takes you out in your forties, fifties, that's still, it's still significant years lost. Absolutely. You're looking at what, a 40% reduction in lifespan at that point.

But this paper is, thank you very much for this paper because this paper is phenomenal. And if you scroll down, see another found dead. This is after, this one, the 81 year old, but they, if you scroll down, they see after review of the being in a circumstances, cardiac amyloidosis is considered contributory that are presumably precipitated in arrhythmia resulting in the fall. So death was blunt force trauma to the head. Right. But, but that was due to, they believe in arrhythmia caused by the cardiac amyloidosis. Yeah. So my point is that we're seeing parts of 70 year olds, octogenarians in those who are under 40. And this is my point that the amyloidosis is being accelerated in young and healthy individuals that are having old and unhealthy hearts. This is the problem. Now the other point is, how do I get out of, okay.

The other point is the cancer that we're seeing. Now I think please look at, if you can pull up one more paper, please let me put this in the chat. I think the cancer is secondary. So if you can please bring up this paper. So I think the main point is just sharing the screen to bring up the chat. So I think the accelerated cancers is secondary to the primary problem is sudden cardiac death. And through three routes, I see myocarditis, brainstem compromise, and amyloidosis. And then I'll wait for you to bring this paper up. Cause this is another very interesting paper and I think extremely relevant and important. Here we are. Oh, old P53. Yep. There you go. There you go. Good old P53.

“Oncogenic gain of function due to P53 amyloids occurs through aberrant alteration of cell cycle and proliferation”. So I think it all comes back. I think the main goal of the spike protein is to induce sudden cardiac death. And the surging cancers is secondary because of perhaps this.

Well, maybe I might tune that statement because not all people are the same, right? And you know, the best analogy that I have is hay fever. And you know, some people are allergic to pollen. Some people can be allergic to cats. Some people could be allergic to peanuts. And one doesn't necessarily translate to the other. And so, you know, my overarching theme is that we need to be concerned about amyloidosis as a condition generally. And how that manifests in different people is, like I say, it's going to depend on their genetics, their environment, their general toxic load, their age, you know, all the contributing factors.

Hi, Dr. Richard Fleming in the chat. Good to see you, sir. I hope you're well.

And let me just go through this abstract real quick. So transcription factor. Right. So I think this is incredibly important. So transcription factor P53 also has been shown to aggregate into cytoplasmic and nuclear inclusions, compromising its native tumor-suppressive functions. Oh, so it's misfolding. Interesting. Finally, P53 has been shown to form amyloids, which play a role in conferring cancerous properties to cells, leading to tumorigenesis. However, the exact pathways involved in P53 amyloid-mediated cellular transformations are unknown. Here, using an in-cellular model of full-length P53 amyloid formation, we demonstrate the mechanism of loss of P53 tumor-suppressive function with concomitant oncogenic gain of functions. Global gene expression profiling of cells suggests that P53 amyloid formation dysregulates genes associated with the cell cycle, proliferation, apoptosis, and senescence, along with major signaling pathways. This is further supported by proteome analysis, showing a significant alteration in levels of P53 target proteins and enhanced metabolism, which enables the survival of cells. Our data indicate that specifically targeting the key molecules in pathways affected by P53 amyloid formation, such as cycling-dependent kinase 1, leads to loss of the oncogenic phenotype and induces apoptosis of cells. Overall, our work establishes the mechanism of the transformation of cells due to P53 amyloids leading to cancer pathogenesis. This article has an associated first-person interview. Oh, okay.

That's not necessary for the paper. But I've just learned something new. I had no idea that P53 could become amyloidogenic. Right. And I think that the reason why we're seeing the surge in cancer, I think the sudden cardiac deaths are just one, of course, of the many manifestations of the amyloiddosis. But I think sudden cardiac death is sort of the main quote unquote goal of the spike protein. And this is a secondary effect of it. I think that one can make that case. The other thing we need to know is, well, yes, there are people dying of sudden cardiac, but how many people are having sudden kidney failure, sudden liver failure? You know, how many people are having other sudden organ failures due to amyloidosis? Because I do not believe it is simply the heart. I believe it can be systemic and it can be other organs other than the heart. Clearly, it can be the brain as well, obviously. So, the question is, what other sudden failures are people experiencing? And I believe that there has been a great rise in sudden kidney failure as well.

So, you know, I've been looking at the CDC and shout out to Richard for this because he turned me on to this data. But the CDC data shows three primary areas where we're seeing excess deaths. Dementia, cardiovascular, cancer. And this is what you would predict if the environment is being seeded with these amyloidogenic peptides. Absolutely. Which goes back to what I said earlier, that it's not the spike protein per se. It's when it's cleaved and proteolyzed. That's the danger. When it is broken down. It's like setting up a pool table and the balls are all together. That's the spike. It's when it's broken apart. That's what's causing all the problems. Because one of the papers that I put up showed that the spike itself, the full spike, isn't causing these things when they expose cells to the full spike, it's when it's cleaved and broken apart. That's what's causing all the problems. And of course, you know, spike is cleaved. I have to assume that through mRNA, the spikes being expressed on the cell surface are being cleaved and broken down. I would assume that they have to be. Well, that was their selling point. Right. Of course. Yeah. Yeah, of course.

That's what they sell people. Your body would just break it down and present it. Well, that's the problem. Yeah. Yeah, exactly. That's the problem. I have a huge, huge problem with that. And it just shows the lack of insight into the biology that the mass injectors have with respect to long term consequences. And look, even if you gave them the fact that maybe there's a reduction in acute hospitalization and death, it in no way addresses these sort of longer term issues. And the Of course, it's all poppycock. It's insanity. You know, it's like, you know, it's like you save one dollar to spend 20. It doesn't.

I'm always doing that, dude. I'm not one to comment. And wow, we've got 125 people watching on Rumble. Shout out to Rumble, man. And 100 and wow, we've got 159 watching live. Good show. You need to come on more often, dude. Well, thank you. I would I you know, I love to talk on anything regarding research.

Well, so the I did a paper not not very well, I'm afraid it was, you know, it was a sort of letter. So everything was sort of compacted and, you know, a lot of the sort of genes that they're mentioning and what have you. You know, I don't claim to have any any sort of expertise in. But the the conclusions of the paper were that the S2 subunit is amyloidogenic as well through modulation of an enzyme called gamma secretease and gamma secretease is enzyme of interest in Alzheimer's and it's miss, how should we say, misprocessing of amyloid precursor protein. And and you know, that's that's what these Waltz analysis would show. It's it's studied all through the sequence itself, all through the spike itself. And, you know, just talking about the cleavage aspect, I think it was the Nyström and I don't know how you pronounce that second name, Sørenström {Hammarström}, I think. Sørenström. Sørenström. Yeah. Sørenström, yes. Goddamn Scandinavian names. The umlauts, yes. Right tongue twisters. But they, you know, quite disturbingly showed that the the flanking sequences around part of where neutrophil elastase makes its cleavage had been increased relative to the original SARS, I guess, or other, I'm trying to think back to the paper. I think they compare to SARS and maybe I should pull it up. Let me just see if I can pull that up real quick. Just just so just so we're scientifically accurate. Nyström. I just have the preprint. Let's bring this up.

While you're doing that, I think the I think the big takeaway and the big picture of all of this is what the spike protein is doing is sort of I liken it to taking a car engine where you have all of the systems running smoothly. You have the coolant running smoothly through. You have engine oil running smoothly through. And what is happening is that the components of the engine are being clogged up and the tubing destroyed. And it's slowly you know, you know, like peine dure et forte, you know, the the French that you know, they would lay stone on top of stone on someone until they were crushed to death. And it's slowly doing that to the microvascular and to the organ to slowly deleting the micro microvasculature and it is slowly clogging up the organs. And that is what is happening now. What is interesting is why does it happen in some people with lightning alacrity and others? It takes time and hopefully in some it doesn't happen at all. So these are the questions that I have.

Yeah, I'm trying to look through the paper right now. Was it part of the supplementary data? Basically what it's doing is giving 20 and 30 year olds the blood vessels and organs of someone who's in their 80s. Yeah, right. Why can't I get to the yes. Now, I swear to God there was a supporting information is available free at charge. Open link. It just takes me back to how dare you. This one, maybe. Well, if it if it's not this, this paper. Yeah, I think I think this is it. So if we go down, what we'll find is them making the comparison to other other coronaviruses and flanking sequences being tuned, I would argue for. Yes, this. I believe it's this. So this flanking sequence, I believe. Let me just make on it. Here it is. Yes. So MERS, SARS… MERS, SARS and SARS-CoV-2. And what's identified in red there is these sequences which allow it to be cleaved easier by the neutrophil elastase. And it's not there in other related viruses. And again, this to me is just another indicator that someone with very, very sophisticated understanding of the amyloidogenic pathways has put this in there. It makes no sense to me that that should just emerge spontaneously. And, you know, people people don't talk about this. They focus on the furin cleavage site. I've been corrected on open reading frame six, as I was under the presumption that that was completely novel. But it's it is there in in the original SARS, but its reactivity is increased with respect to amyloidogenic activity and ORF10 is novel to SARS-CoV-2 as being amyloidogenic inducing peptide accessory protein.

And everything to me points to this weaponization of the disease process that just isn't on most people's radar, right? Epidemiologists are going to be not familiar with amyloidosis. It's a niche area of medicine. It's not it's not that common as a disorder generally within the population. Yeah, you can argue that the neurodegenerative component is but then you're looking at end of life. And people just sort of take that as well. You know, you've got to be you got to check out somehow, right? You know, if you survive the cancer and the cardiovascular disease, the neurodegeneration will get you, right? And… Right. And what we're seeing here is, again, I would argue that someone has and it's it's it's not like this isn't known biology. And so they've taken this opportunity to seed the environment, not only with the virus itself, but also the the mass gene transfection and constantly loading people with these with these peptides of concern.

It's not just… if you could please bring up the the paper I just put in the chat. Because it's not just amyloidosis. There's also very direct damage to the brainstem. And yes, right here. Now, they say they if you read the paper, they wonder what antigen could be causing it. I think we all know what antigen is causing it. Take a stab in the dark, right? Take a guess. All right. Let me let me let me. Yes, if you look at this, it's abstract. Okay, so the underlying mechanisms mechanisms by which severe acute respiratory syndrome leads to acute and long term neurological manifestations remains obscure. I'm not so sure about that. I'm not sure about that either. We aim to characterize the neuropathological changes in patients with SARS and determine their underlying pathophysiological mechanisms. In this autopsy study of the brain, we characterize the vascular pathology, the neuro inflammatory changes and cellular and humoral immune responses by immunohistochemistry. All patients died during the first wave of the pandemic from March to July 2020. All patients were adults who died after a short duration of the infection.

Some had died suddenly with minimal respiratory involvement. And this is the important key. This is where they've gaslit the public into thinking that just SARS is respiratory pneumonia. Not at all. It's very, very frustrating. And if I can say one thing before we continue what you'll see, and I think the most interesting thing, well, a lot is all interesting, but it is the immune complexes are activating the glial cells, which are then literally eating the rhonophagy, the brain stem. So that's, I think also, I'm sorry, I'll let you continue.

No, no, no. It's a critical point. And, you know, one, when I'm not doing the comedy routines and I, you know, present the papers, there was a very early paper in virology where there's a an account from a Chinese medical resident. Okay. And she said that she had to consciously stay awake to think about breathing. I read that. And, you know, that's, that's an indicator to me that these, you know, Bötzinger complex {earlier streams} and the other respiratory complexes, which are all very, very close to each other in the brain stem are under assault. Now, you know, the nature of that assault, you know, I think, you know, microglial activation, I think the evidence is sort of really sort of piling in on that. You know, how much is viral expression within these regions? Oh, there was none. This is all from the immune complexes. They found no viral expression in the brain.

Well, there's a new paper from, I want to say, Scripps Institute, and they do find, and well, I think the data is mixed. Okay, it is mixed. Yes, that is true. And they mentioned that in the paper. Yeah. So some studies say, yeah, but we're finding evidence of viral replication. Others say not so much, but you know, that there's many, many factors which would sort of lead up to that, which is, you know, how, how leaky the blood brain barrier is becoming. And, you know, there's, I don't think I can emphasize enough just how intricate the vasculature of the brain is, right? When you, when you, so, you know, people have a sort of comprehension of the lungs, right? And you, you'll sort of see the vasculature of that. It's orders of magnitude more dense and complex in the brain than it is the lungs, because actually alveoli are generally, you know, macroscopic in size. In the brain, you've got to think of each functional neural unit, which includes the neuron itself, the astrocyte, the microglia, the oligodendrocytes, all need to be close to blood supply, right? And so, and when you think how, you know, how much packing of active tissue, because it's multiple cell types in the brain, obviously, but they all need immediate access to oxygen, because their activity can ramp up and down so quickly. And so, like I say, the vasculature is highly complex. It's, you know, the blood-blame barrier itself is, you know, it's a consequence of the knexin, I think, is the protein. So, it's very, very tight gap junctions that just are responsible for making sure that only certain molecules are transferred easily into the brain. But, you know, we know that that's breaking down. And did you see the presentation from Professor Arnaud Burkhardt recently? No, I have not. Oh, God, it's… I've seen references to it. I've just been so busy, I haven't had time to watch it. So it's in German, unfortunately. I can understand most German when I hear it, so I can probably get through it. But the slides are self-explanatory. And in his slides, what they show is that in the brain vasculature, they see expression of spike protein. The epithelia is breaking down. You've got infiltrate, obviously, breaking into the parenchyma of the brain. And no, and there's good evidence that it's just from the vaccine, because there's no nucleocapsid present when they… Of course, yes. That I did see. Yes, that I did see. There's no end protein, right. And in… I'm probably looking… If I put you here, now I can talk to the camera. I've got you over here. Try to make some eye contact with you. The interesting part of that was that they get a positive hit with Congo Red, and also iron deposition, right. And these are pathophysiological traits that both yourself and myself have been focusing on for a number of years now. And to see it, to see the predictions theory coming out and being demonstrated in the pathophysiology, I would argue is sort of fair complex, for sure. But it's not having the impact that I would hope it would. My hope was get some rodents, expose the brain to active vaccine, and see if we get a hit for amyloid, Congo Red staining, et cetera. But it's been done already in humans and nary a blip on the radar with respect to top-down diktats from bureaucrats who, for sure, don't understand this pathophysiology. And I would add this caveat to that data, that it was in an elder, right. But I would make the presumption that that's happening in, the same thing is happening in younger people. Absolutely. That's the, I would argue that that would be the pathophysiological footprint of brain fog, right? Yes. But again, I think it's systemic. I don't think it's just the brain, right. I think that, you know, I mean, there's infertility, it's, you know, I think another good analogy is sort of, you know, the big plastic island in the Pacific. It's sort of view the plastic as the amyloids in the Pacific as the organ. It's basically slowly filling up the organs with trash. If we call the amyloids trash, it's slowly, but surely over and over with every exposure, slowly filling in the organs, rendering them more and more dysfunctional. That is what needs to be looked for. I am certain it will be found, but it is slowly happening. The only question I have is why is it happening very quickly in some, slowly in others, and perhaps hopefully not at all in some, if not many. Now, this is the main question. Why is this amyloidosis on a curve? Why is it happening? You know, there must be a genetic factor. That's a driving question in research since forever. Of course. Why? Well, what's causing it this time? Why? I want to know why. I'm looking and I'm looking and I'm looking and I cannot find why is this happening. Obviously, upon initial infection in an unfortunate very few, it happens. If you notice, I think the most amazing thing about this is that if you scroll down, if you can scroll down, keep going all the way down to the discussion. This is what really threw me with this paper, that this made me go, this is one of the most important papers. I keep going all the way down to the, we can come back, we can go all the way down to the. I'm just taking a quick look. Yeah, I know. But yeah, if you go down to the discussion. Oh, wait, my clear lacrimation, right? Yeah, well, we can get to that. But what I want to show is, is if you, what I think is very, very important. All right, keep going, please. Where it gets to the brain stem. And if you can keep going and keep going. So we also found multifocal loss of neurons in the hindbrain using the cerebellum. This pattern of neuronal loss cannot be attributed to hypoxia. Right, not attributed to hypoxia. The damaged neurons were often in close vicinity of actuated macrophages or microglia. And there was evidence of neuronophagia. Yes, yes, yes. Suggesting neuronal. And if you scroll down, just one more, you can come back. I've got to find the sentence. Let's see. Do I need to read that paragraph? Interestingly, when it begins, interestingly. The paragraph begins interesting. Keep going down when it begins. Interestingly, that's that paragraph. Please read that one. I think it's the next one. Yes, this paragraph. Interestingly, several of the pathological findings were more prominent in the hindbrain, which is consistent with other studies, although the cause remains unclear. It's been hypothesized that the virus may reach the brainstem via the olfactory pathways of the vagus nerve that innervates the respiratory and gastrointestinal tanks. I was shouting that from the beginning, Wola. Exactly. However, we were unable to confirm the infection in the brainstem. Involvement of the brainstem could have dire consequences since many vital functions are controlled by this region. It may also explain many of the acute and persistent manifestations seen in patients with COVID-19. Importantly, five patients in our study died suddenly most while sleeping. While sleeping. Here it is. Hence, the possibility of central apnea needs to be considered, although cardiac arrhythmia of dysautonomia could be contributory. This paper, everyone needs to read this paper. It is seminal. I want to scroll up and look at those, Mike. Please, let's go back and look. I wanted to get to that, but please, let's look at what you wanted to look at. I apologize for that. Yeah, I'm a sucker for I was I was railing yesterday about, you know, I want to I want to see pictures of biology, right, because these silly bints on this podcast that we were trashing, you know, they were they were making all claims about how gene information was transferred via laser light from chickens to duck eggs and vice versa, such that chickens were born with duck bills and webbed feet. And I was like, where's the pictures? Right. I mean, it's a it's a it's a stunning claim, if true. Can we can we not just know where's the some data? But you see this. But what this shows is what I said from the very beginning. SARS-CoV-2 doesn't kill you, SARS-CoV-2 causes you to kill you. In other words, it causes your your glial cells to eat your brainstem. There was no infection found in the in the brainstem. This is all caused by a reaction to the immune complexes of the spike protein. That's the point. And I'll just add the so the cerebellar regions that they're pointing at here. These are some of the most metabolically active cells. And yes, right. Yes. They fire a hundred spikes per second. They're very big cells. And yeah, it doesn't it doesn't surprise me to to see this. Now, the question becomes, what's the what's the precipitating agent that's getting in there that would cause the neuronephagy, right? They talk about that. It's the it's the it's the uptake from the immune complexes. The deposition compliment deposition. That's what's causing it. And they talk about that in the paper that's called the neuronephagy.

I'm just trying to parse that. So, yeah, which complexes and they go through the mechanism if you go if you go into the paper, if you look for the it was done in the discussion and they talk about that. Let's see if we can find that. OK. We investigate whether the vascular comprise could be related to endothelial cell dysfunction. Well, I think that's what do you call it? PEDS? SPED. Spiked Protein Endothelial Disease. Correct. And that's this. Another study showed damage to endothelial cells and brain resulting in empty basement membranes known as string blood vessels. We found increased levels of PCAM1 on endothelial cells. Again, as I said, destruction of the microvasculature. Contrast in vitro study showed a decrease in PCAM1. I'm not sure what PCAM1 is. That's the mechanism of increased PCAM levels. I'm trying to find neuronephagy. You just keep going down and discuss it. To determine whether the compromise of endothelial cells may be an immune mediated phenomenon. Yes. We look for the deposition of immunoglobulins. Aggregates of IgG and IgM were found on endothelial cells and platelet aggregates that co-localized with several members of the complement cascade. Presence of C1Q, C4D and C5B9 suggests activation of the classical complement pathway. We also found deposition of C1Q and C3 in macrophages and endothelial cells, which has been sown to be induced by CS-CoV-2 spike protein. Deposition of complement cascade and immunoglobulin suggests an immune mediated injury to the endothelial cells. The antigen against which this immune response is targeted remains unknown. Yeah, that's my question. Right. Really? Okay. Possibly the antibodies are directed against an antigen on the endothelium. See, I wonder if this is the, what are they called? Oh, it says anti-antideotypic. Right, but I think it's the alternatively immune complexes formed by the antibodies in the spike protein. There it is right there. That's what I believe it is. Alternatively, immune complexes formed by the antibodies in spike protein that may bind to ACE-2 receptor. That's what it is, I believe. But that would, I wonder if they're sort of becoming free form and translocating into the brain parenchyma then. We'll keep going because I believe that's what they discuss. Okay. I believe that's exactly what they discuss. I'm on the right track. You're on the right track. Yes, to compromise the blood pressure. Right there. Then we found the cellular, next paragraph. We found cellular infiltrates of macrophages, CD4 T cells and CD8 T cells in COVID-19 patients. Let's not forget, there's evidence out there that SARS will replicate in CD, I want to say CD4 T cells. Mirroring these observations, the results of our spatial transcriptomics data demonstrate that the signaling pathways involved in the migration or trafficking of these cells were enhanced in regions rich in PCAM1. I need to know what PCAM1 is. This is the problem with all these complement cascades and transcriptions. Well, I'm too well to commit it to memory. That's what the internet for. Platelet endothelial seal cell adhesion molecules. Oh, so NCAM, similar to NCAM. Right. Okay. That makes sense. These included, again, it's just whatever these pathways are. Rho, GDI, P10, G, alpha, I, signaling pathways, and cellular infiltrates were predominantly in the perivascular regions. Yeah, so parasites, I think. So we know that there's data which shows that parasites are the sort of pathway, can be a pathway into the brain. So transfection of parasites, parasites into astrocytes, and then possibly from astrocytes into neurons. Okay. So although there were a few T cells, CD8 cells, outnumbered CD4 cells, and there were only rare B cells, this suggests that the inflammatory infiltrate was secondary to the leakage of serum proteins into the perivascular regions as macrophages act as scavengers and help with the repair process. This is consistent with other studies that have found activated monocytes and macrophage markers in CSF and brain. In one study, CD8 positive T cells were further characterized to show that they have both cytotoxic and exhaustion markers. Hardly surprising. We observed that the serum proteins such as fibrinogen and conflux were taken up by glia and neurons. There it is. Astrocytosis was also most prominent in the perivascular regions, suggesting that this was secondary to the vascular. And the next paragraph continues the mechanism. We also found multifocal loss of neurons in the hindbrain, including the cerebellum. Didn't we just read this one? Yeah, we read this one. We didn't get to the part, if you go back to the, we stopped before the neuronephagia. We did. Yeah, the damaged neurons were often closer to the activated macrophages and microglia. There was evidence. Yeah, we didn't get to that. So the damaged neurons were often in close vicinity of the activated macrophages and microglia. There was evidence of neuronephagia suggesting the neuronal injury was second to glial cell. The glial cell activation, which is secondary to the vascular injury. Yeah. So, you know, it makes sense because, you know, you've got, you can't just leap into the brain, right? You've got to, you've got to sort of degrade that blood brain barrier and, you know, well, there's multiple, there's multiple pathways. There's the sort of axonal transport mechanisms, which, you know, I think, I think that there's enough evidence to suggest that that is a pathway. But, you know, when you're, when you're sort of dealing with this systemic assault, this inflammatory, Rich is in the chat, so we'll say, inflammothrombotic response. The, all of that is going to impact on the, on the ability of the blood brain barrier to maintain integrity. And, you know, that's, and, you know, that's not only Professor Burkhardt's work, but, I'm trying to think of the paper now, but they literally show parasites sort of peeling away within the blood vessels and that sort of basement membrane breaking down. So, yeah, this is, yeah. And then the next sentence, neuronephagia in the brain stem of patients with COVID-19 has been described previously. So, I think this is how the spike protein in SPED, going back to SPED, is causing the destruction of the brain stem, which is then causing the sudden deaths, particularly when people are sleeping. I don't know if anyone saw yesterday, 37-year-old country music star just got married this weekend, died in his sleep, Sunday and Monday night. Perfectly healthy. A few hours after getting married. I was gonna say, I always said marriage bad for your health. So the question is, is how can we, we need to look at, oh, this is interesting. Sorry to interrupt. For example, APD has shown to be upregulated in the brain following HCOV OC43. As you were saying earlier. Yeah. And well, Spartacus, if he's listening, there's your peroxidated lipids as well. So, you know, going back to this. What we started with. Yeah. So this is the OC43 spike protein. So here's the issue that we have, you know, with the canonical beta coronavirus infections, they don't have the furin cleavage site. And it's the furin cleavage site, which just allows it to disseminate and target so many more tissues. And then once it's targeting all those tissues, you, of course it's going to be proteolyzed. And as doing so, again, the best analogy is just a cluster munition of these toxic peptides. It's carpet bombing. Yeah. Yeah. It's carpet, it's peptide carpet bombing. Yeah. Yeah. And, you know, this, and my, my concern has always, always been that those, those who are interested in weaponization have keyed into this mechanism, right? Because very few people are going to, can make the conceptual jump to it, right? Most people just struggle with viruses in general, right? But in this instance, we've basically got a aerosolized pre-energic agent hopping from person to person. And, well, we get down to your question, which is why some are more susceptible than others to the, to the outcome. And yeah, that's just- And worse yet, is it happening in all of us slowly? And the mRNA injection is just accelerating it exponentially, something that is inevitable over 20. I mean, this is, I'm sorry, but we have to think about this. Yes. Yeah. I'm sorry. And we can think about it and talk about it freely as we're not on, that's not on YouTube. Right. So that's- I mean, is it happening to me? Is it happening to you? I mean, we need, we need large scale surveys with MRIs of people's brain stems to see what is going on. Well, maybe a better approach is PET, right? Because there are- That would work too. There are Liggins now, which I'm presuming they've moved on since 10 years ago when I was involved using them, that are specific for amyloid. And, but then, you know, how many PET machines are available? How many people do you put in? Exactly. At least, at least those who are long, PASC, long haulers, at least they should be being examined in this manner. Absolutely. And, you know, I had this, you know, there's this jabber, you know, vaccine lovers on Twitter. They're always getting me banned, but- What is with Graham Botley? I just don't understand that individual. I don't know, someone who's somehow achieved a little bit of clout on Twitter and drunk with power that there was a report button that enabled him to flag anything that would question the orthodox narrative that was being put out by governments. But look, bureaucrats who have zero understanding of these mechanisms- They don't know what's going on. Most doctors don't, dude. Right, most doctors have no idea what's going on. An ER doctor lived across the street from me and he just, all he did was just parrot, I go, have you thought about this? And he went, no, I never thought. It's like, no, of course, they don't think about these things. It's like, I would mention the endothelial issues, the amyloid issues, the, you know, the P53 issues, and they'd never heard of it. And this is an ER doctor. He had never heard of any of it. So is anyone reading anything? Well, that's a good question. And most people were, but look, what do I read? I tend to still focus around the neuroscience and neurology. You know, I listen to you when I find out about all these other mechanisms, you know, it needs many, many people to sort of come and tackle this problem. So, you know, one person can't be all things. But yeah, it's in the current environment in which we find ourselves, particularly one that's so politically dangerous where they're looking to leverage, quote unquote, pandemics as a means of population control. It's incumbent upon you to, if you're not doing the reading, at least doing the listening to those that are doing the reading. And it's a good chance to plug your substack, to follow up with the substack and stay up to date. Because like I say, you're going in and pulling out papers that I wouldn't come across. It takes a lot of work to find this. I mean, I spent hours and hours reading, reading, driving, delving, just searching. And it's a lot of work. But I don't regret a second of it. And, you know, just getting back to that, the mutton wankers, the... Yes. Right. So, you know, I'm sort of jousting with them on, you know, I'm my own worst enemy just because I get, I just find it funny, dude. It's entertaining. But like one of their responses was, well, oh, the free spike protein in the plasma is only around for seven days. Well, I'm like, well, hang on a minute. It doesn't matter if you've cleared it within seven days, if you're kicking off these prion cascades. Correct. And they just can't compute that there would be this lower substrate of disease that you need to take into account. And so I'm talking about this amyloidogenic risk. And their rebuttal was sending me a CDC link for people with amyloidosis that says, you should go and get your vaccines. Yeah, you'll need a wrecking ball in front of your house for 10 minutes to have your house destroyed. So, I mean, it's... Right. And, you know, who in the CDC has thought about the studies? And are they aware of these amyloidogenic sequences? I would say obviously not. And, you know, Botley will just always block me because I just nailed him on the neutrophil elastase, chewing up the spike protein, and basically causing this cluster munition carpet bombing like effect within organs. And, you know, once you nail them on one thing, they'll block you. But he's just profoundly stupid is my takeaway. He just, he thinks he knows so much and he knows absolutely nothing. What is he, a flow cytometrist? Yeah, yeah. And he dared to write a paper on his experience. And I mean, he's clearly a malignant narcissist. That's my unofficial psychiatric diagnosis of Mr. Botley. Well, he's not a scientist. He's a part-time sheep farmer and RPG nerd, right? He doesn't have the scientific experience or the lab experience to be talking about this type of pathology. That doesn't even bother me if he'll be willing to discuss anything. And to me, that's his cardinal sin is the inability to discuss anything. I mean, I really don't care what his opinions are if he's willing to discuss them. But the fact that he's not willing to discuss anything means that his opinions are worthless. And you know, so my, I guess, point is that we've never been in a situation where with gene trans, transfected amyloidogenic sequences, we don't know. I hope we never are again. Well, I'm not so sure that that's going to be the case because flu vaccines are going to be this mRNA platform as well. And, you know, we can look at H1N1. You know, it's got amyloid. And it's less, but... Well, I mean, it's a shorter spike sequence. It's half the size of the SARS spike. But there's no precedent or any preclinical research looking into these long-term effects. And these, these are generally long-term disorders. Now, yes, we're seeing what appeared to be acute responses or responses is wrong. Acute manifestations of pathology in some individuals. But again, I would sort of use the hay fever or allergy type. That's a very good analogy. Yes. Some people are just going to be exquisitely sensitive to this. And, you know, there's just the issue around the variability in how much RNA is being delivered. You know, this is another thing that sort of bothered me is the, I don't remember his name, Gerardo, something like that. It's this French dude who's going around and saying that all the adverse events are a consequence of the lipid nanoparticle. Well, you know, we know the lipid nanoparticle is inflammatory, but there's too much overlapping pathology that matches up with these amyloid-like disorders for us to dismiss that. And Professor Burkhart's work shows that the spike protein is being expressed and presumably proteolized at the endothelial barrier. And if that's the case, that trumps any theory that you would have by trying to lay everything at the doorstep of the lipid nanoparticle. And I would extend that further by saying the lipid nanoparticle has been put into billions of people now. The cardiac, the cancer, the dementia, it's not all of them, right? And so I would, my suspicion would be looking at how much active mRNA that they received, where it's deposited around the body, because that's going to be highly variable as well. As well, yeah. And we just, I'm just very suspicious of people who would just take a very binary approach to this problem and say, it must be this, right? Just one thing. And why can't it be all of those things? Absolutely. Absolutely. Yes, of course. As I said to people, I have no doubt that there may be a robust immune response, but at what cost? CDC, WHO, all of them, robust immune response. Yes, but what is the cost of that robust immune response? If those complexes are seeding endothelium, it's insanity. How could you stop at one thing and not look, that would be like a chess player looking one move ahead and saying, oh, I know what to do. I'm safe. That would be the same. If I were to play a game of chess and make one move, look one move ahead and say, oh, I'm not getting checkmated if I make this move and not looking at what happens three moves later when I am checkmated. That's how stupid this is to just look at a robust immune response and end the conversation there. When I first read that, it struck terror in me when I read the robust immune response. That struck absolute terror in me because it was like, well, let's end the conversation there. No need to look further. As I say, my night is safe on D4. Wonderful. You have to put this in the context of that the vaccines have been shown to, I'm calling it gene transfections, have been shown not to stop viral replication. They're holding high levels of virus. Maybe you can make arguments that it's slightly less days. But again, how long does it have to be there to trigger these underlying more subtle, no, not subtle, subtle is the wrong word, pernicious disease mechanisms of prion cascades? That goes back to what you said with the hay fever. I don't know, but there is some mechanism which is putting this, I assume on a bell curve. Well, is it a bell curve? I mean, the data I've seen, we see a peak early, it goes down and then potentially sort of three to four months later, we're seeing another uptick in mortality. I think that there's two different mortality curves you have to look at. I think there's a mortality curve when there's active infection, there's a mortality curve of the fallout of the long-term issues. I think there are two mortality curves that we have to, and I think that's why it's confusing everybody. I think everyone's trying to look at a mortality curve and it's two. There is a mortality curve of the acute infections and then there is a mortality curve of the underlying pathologies caused by the acute infections and that's the problem. Very eloquently put. Thank you, sir. It's incredibly frustrating to see the health freedom movement. I hate that term. What about just critical thinking? That should be an unnecessary term. If you told someone 20 years ago that we would be discussing health freedom, someone told me that I would have laughed in their face and saying you're crazy. I would have said that three years ago, bro. That's the fact that you have to say that. Three years ago, I would have said that. There were so many things three years ago that I would have just taken as granted and figured that we had these ethics and moral frameworks tied down. We did Nuremberg, we did Helsinki. Most institutes would have an ethics board for experimentation, but all of that's just been soaked in gasoline and hit with a flame thrower. It goes back. I have a friend, obviously I'm not going to mention his name, but he's a world famous MD, PhD. He told me, he was Walter, nobody can fight the WEF. I'm coming to that conclusion. You are. You're not picking up a rifle and going and storming their chateaus, right? No, the barricades with students at the French Revolution are never happening again. Yes, correct. No. The solution that I'm honing in on is to build a clan, a community that has a talent stack that enables us to watch what they're doing so we can make the adjustments to behavior. The thing I object to and what I find abhorrent is why is an economic organization dictating medical discussion? That's all I want to talk about. Why is an economic organization dictating medical discourse? Why? Because it's a way to monetize and commoditize behavior. That's what I would put forward. Medical discourse should not, of course, involve that in the slightest. Medical discourse is medical discourse. Why is it being politicized? Why are there two viruses? Why is there a virus that doesn't exist? The whole thing is I'm being facetious, of course, but politically, why is someone's medical opinion based upon their political affiliation? I'm not talking about educated people in the matter. I'm talking about the general populace here. That terrifies me that someone's medical opinion is aligned with their political belief. That is absolutely terrifying. Yeah. That cuts both ways. How does it fall? It's generally those on the left who are falling in line with the diktats of the state apparatus. But on the other side of the spectrum, there's a degree of denial. Right, which is equally dangerous. Yeah. We don't know the long-term consequences of that sequence on the screen, right? Oh, I think we do. Unfortunately. As I said, I wish I was wrong. I wish I did not see what I see. But I see what I see. I was making a point yesterday that that documentary died suddenly. I have not seen it. I have no opinion on it. I have read everything from it's a piece of junk to it's got something. But I don't know what to think because I haven't watched it yet. Have you watched it? I watched it. What are your thoughts? Because I will respect your opinion and will not need to watch it. There were some important data points in it. So interestingly, they showed in real time them where they're perfusing a corpse and basically they start pulling out these, I'm making the presumption, they're just amyloidogenic occlusions or aggregations. And that of itself is an important data point that needs to be honed in on and we need to have proper autopsy and pathology investigations done to definitively define what it is. My problem is when they're just saying it's only the vaccine that's doing it. I don't buy that. My scientific heckles rise when again someone would engage in that type of binary thinking. Well then it goes back, oh if you get COVID it's just a flu and you have nothing to worry about. See that's very dangerous because I do not believe that to be true. No, but to sort of steel man the other side, many people do just get the initial infection and it's essentially mild and they shrug it off. The problem is how many people that we're seeing keel over, is that a consequence of prior infection six months ago? For some absolutely, I'm certain it is. And again then you have the confounding factor that they've gone and mass jabbed people with these amyloidogenic sequences that are going to disperse through the body and into organs that are incredibly sensitive to this type of pathology. Do you know Joseph Trito? No. He wrote a book. I actually translated it from Italian into English to read it. He published it in the summer of tweed. He speaks Italian as well. I can read it, I can't speak it. So I translated it myself. I can send you the translation if you want to read it. It's fascinating. He talks about the, obviously it's absolutely from Wuhan. He lays out a case that makes it unmistakable and he quotes a British virologist, he won't say who it is, but who said that what the problem is with SARS-CoV-2 is that it never lets its victim go. And that's been in here. This virologist said it in February of 2020 that he didn't want to cause alarm, but that SARS-CoV-2 never lets its victim go. And I've been wondering, well, if that's true, then how? Well, I can think of multiple mechanisms. And now we can see, I didn't know what he meant by that. There's just the issue around that some people very obviously have viral reservoirs because they keep finding spike protein in the plasma, in the blood. But not end protein. In long COVID, they're finding the S protein, but not the end protein, which to me means, yes, there's a paper in long COVID is just the spike protein they're finding, not the end protein. So what that tells me is that, and this happens, there is a section of the RNA that creates the spike that is being preserved and replicated in cells. It's not the entire virion that's being reproduced. It is just the spike. Yes. I wonder if it's being reverse transcriptase into the nucleus. It could be. And that is simply the spike, because that's all they're finding in those long COVID is just a spike protein. It's not the end protein. So therefore the entire virus is not being replicated. I'd love to see that paper. Huh? I'd love to see that paper. Let me see if I can find it. I would have made the presumption that somewhere like the gut or a sort of immunoprivileged region is acting as a reservoir, and it's kind of spitting out virions at a sort of low rate, and that's what's causing the issues. But if they're not finding it... That is. If you'd like to bring this up, let me get back to Zoom. It's just a spike protein. Let's see. Can we get the study? Persistence circulate in SARS-CoV-2. There it is. That's it. Diagnosis and management of PASC poses an ongoing medical challenging. Identifying biomarkers with PASC would... Yeah, yeah, yeah. We analyze PASC from samples collected from a cohort of PASC and COVID-19 patients to quantify circulating viral antigens and inflammatory markers. Strikingly, we detect SARS-CoV-2 spike antigen in a majority of PASC patients up to 12 months post diagnosis. Okay. Furthermore, the temporal antigen profiles for many patients show the presence of spike at multiple time points. It doesn't mention anything about n-protein. Here we go. You've seen previously developed and optimized ultrasound. Yeah, yeah, yeah, yeah, yeah. Including S1 subunit, full-length spike nucleocapsid in the collected plant, figure 1. And of course, we're going to have to hunt through the paper. For the diagram. Yeah. I love the pre-prints, but it's always a mess. So, let's see. So, look, there's no N, it's just S. God, why would that be? Well, for what I'm saying, that it is being transcribed only. And probably in the endothelium. Other places too, most likely. That presumes that you've got a leader sequence just on the spike genome that's enabling its transcription. Well, could you insert that? Well, I think it would be reported that it is there already. I'm unaware of any paper that's... I am also unaware of any paper. The most plausible mechanism that I can think of is that somehow just the spike genome is being incorporated into the chromosomal... Well, that's very bad, if true. Yeah, because that has multiple implications for germ lines and whatnot. But I don't want to say I doubt these authors' findings. I don't either. But it is a head scratcher. Yes, I've been trying to figure it out for weeks. And the only thing I can come up with is that that particular sequence, maybe it's in the cytosome, maybe that particular sequence is in the cytosome, and the ribosomes are only translating that particular sequence. But why would that mRNA survive? And what's replicating that RNA? Why is that mRNA being transcribed? Why? And how? And there has to be a leading sequence, a poly-A... No, not poly-A tail. But there has to be a mechanism for it to latch into the ribosome, and I would make the presumption that someone would have pointed that out right now, or by now. Well, maybe no one's looked for it. I don't know. I would presume it would just come from the sequencing data. I mean, I remember... Can it be modified post-transcriptionally? I don't have enough knowledge. I don't have enough knowledge either. But this is... It's a thought. It is possible that it could be post-transcriptionally. That's a tongue twister. Well, you know what? I remember that there was a paper that was basically saying that there was overlapping reading frames within the spike protein. Oh, really? Yeah. And... When was that paper? That was a long, long time ago. And, you know, my... I wish Eric Topol was in the chat. We could ask him. I wonder if they ever watch, but... I wonder. Hang on. So, Doc Kek is saying fragmentary mRNA transcription, yes, in the ribosome. Methyl pseudo-uridines preserve the clone nature. Yeah, but this isn't synthetic spike in this case. These are people who have had the natural... Right. ...infection. Why, and do they distinguish? Well, for the gene transfection, it must have the leader sequence for ribosomal attachment. It's got to be there, right? Otherwise, it wouldn't work as a therapy. And I would make the presumption that that would be added. So, are they adding it? It would be added as part of the genetic material. Again, I don't like to guess, so I'm not going to venture further until I know more, because I don't like to guess. Yeah. I mean, well, I mean, there's nothing wrong with sort of hypothesizing and... True. Wait, people are saying the stream has gone? Really? Can't even stream on Rumble now. We were shut off? Yeah, it's offline. We got shut down, dude. You've got to be kidding. Yeah, got everything shut down. How long ago? Well, I'm guessing within the last few minutes. I can try...