We may need to have a conversation soon, Liam. You're showing up here an awful lot lately.
It's good to see you, my friend.
I hope you can feel that.
I'm going to start to have basketball practice at 7.30, and so I'm going to need to stream before that.
Let's not tell November, but we're trying to already shift.
Ladies and gentlemen, this is number 42, number 42 in a row, just in case you're keeping track.
42 in a row.
We scheduled for 60 minutes next.
It's going on French, British, Italian, Japanese television.
We've only got 15 people watching. Maybe somebody should tweet this out.
I always forget to do that. I'm not very good at this.
Kids deserve a lot of credit. This town's been flooded with phony 20s for weeks.
Oh, it was nothing, really. But old Mr. Pietro posing as the doorman sure had us fooled for a while.
He really gave himself away when he put on his little puppet show for us.
The real hero was Scooby-Doo. And by the way, where is he?
Oh, no. Look at him.
Like I said before, what a ham.
Whoa, whoa, whoa, whoa.
Good evening, ladies and gentlemen.
Oh, God, and my voice still hurts like hell, but you know what?
It's the 17th of October, and this is, as I said earlier, 42 in a row.
I'm going to break that streak for a little sore throat.
We're not going to get all the way through this.
I forgot that this is a little slow.
Let's see if I can fix this.
Oh, there we go. That fixed it.
That fixed it.
Ladies and gentlemen, there was no spread in New York City.
Infectious clones are the only real threat as far as R&A goes.
The SIBO batches were likely distributed to make things probable,
and transfection and healthy animals is dumb.
Protocols were murdered, gain of function is a mythology.
The Scooby-Doo mystery that you think you're solving is real.
We've got to save our family and friends from it, because these players are committed to lies.
And that'll keep everybody solving this mystery and the mysteries of the future
if we don't expose their lies.
Good evening, ladies and gentlemen.
This is Giga Home Biological, a high resistance low noise information brief
brought to you by a biologist.
It is the 17th of October, 2023. My name is Jonathan Cooley.
I'm coming to you live from Pittsburgh, Pennsylvania, in the great state of Pennsylvania
in the United States of America.
It often sounds like I'm on a starship because, in fact, I am.
In the back of my garage, I also have a mock-up starship enterprise
which I can shift to with a click of my mouse.
Oh, wait, I have to also push this button.
See, I'm not very good at this. I told you that a million times.
The starship enterprise that I'm trapped on is a starship enterprise
which has fallen out of orbit, so to speak, because of a rupture in time.
And I'm going to try and explain that on Halloween over the course of a whole day on YouTube.
So mark that on your calendar that once the workday is done on Halloween,
JC on a bike is going to start streaming live and it's going to be a Halloween spectacular.
And that's why I've been using this Star Trek background for a while
because I've had this idea in my head like burning a hole in my brain for almost two years now.
And it's never quite felt like the right time.
But now it's definitely the right time.
We don't need you in here. You can go back.
So that's where we are.
We don't want to be taking the bait on social media.
We don't want to be taking the bait on TV, but I understand that it's hard not to turn it on.
It's hard not to pay attention.
But the show will go on.
And the Scooby-Doo mystery is still being shoved down our throats.
I showed you yesterday that there's a new book coming up by Rand Paul.
And it is called the great COVID cover up. There's even a masked bad guy on the front cover.
So if you think that the Scooby-Doo mystery is a joke, I hate to say it, but
a few people have had a more apt analogy for what has been done to us.
Because in order to describe what has been done to us, you need to adequately
codify or describe what it is that happened.
And you and me and all the members of drastic and everybody that wrote blog posts and medium posts and
subsets about the potential that this was a lab leak in 2020 were all fooled into that behavior.
We're all enchanted.
Not by what was said on TV, but what was not said.
What was said on social media, but was not said.
What was not reported, but was not reported.
In other words, it was a combination of what was said on TV and what didn't make sense.
And also what wasn't said on TV and what made sense.
And having enough prerequisite knowledge and enough
skills with regard to learning new things when it needed to be learned,
especially in the context of biology, there were very few people in a position to do that.
A few hundred thousand on every continent all around the world that were currently engaged in the study of biology for a career.
Reading every day, asking questions and finding the answers every day.
Gee, I wonder how that receptor reacts or interacts with that receptor.
I'm going to go and look it up.
I'm going to see if anyone's asked this question or question related to it.
And in order to be clever enough to answer those questions and to find those answers,
you have to understand how those questions are asked, how they're formulated,
how to use search engines, how to follow bibliographies,
and you need to hold a whole host of terminology should be second nature to you
so that you can read into these different fields of biology and bring together
a cohesive concept of what's happening.
And so not everybody that has their own business as a plumber is capable of doing that.
Not everybody who teaches for a living is capable of doing that.
Everybody who's a lawyer is capable of doing that in the context of biology.
But it should have done, Ben, everybody working in a biology degree, academic setting,
be it as a faculty member or a postdoc or a PhD student or a master's student
or a senior in undergraduate biology.
Anybody that had immunology 101 and had learned it, anybody that had a few years of biology
so that the context of viral replication, the context of DNA and RNA,
transcription and translation wouldn't be something that you also needed to learn.
And at that stage, you had all of the tools necessary to be enchanted by the idea that
you were covering up a lab leak and it would make sense.
And so with the help of Jordan Peterson and Ben Shapiro and the Weinstein brothers
and all the other people on this and elsewhere,
a consensus that the mystery to be solved was where did this virus come from
to be a solution according to Sam Harris, is it was an accidental lab leak
or something from Mother Nature?
Obvious solution for Brett Weinstein, it was, well, it was a lab leak or a gain of function virus.
The obvious solution to everyone, whether they watched Brock's News or CNN,
is that it's probably a lab leak and even if it wasn't a lab leak, they sure covered it up like it was.
And so the beauty of this is not who they bamboozled but how we bamboozled each other.
By their obvious reaction, by our obvious reaction, by those two positions being taken
and so vehemently defended, it's not so different than the way one defends or doesn't defend abortion,
the way that one defends or doesn't defend Israel,
the way that one does defend or doesn't defend religion or Islam or the freedom of religion
or the freedom of speech, the way that one does or doesn't use racism as a way of dividing people,
a way of identifying a way that the world works.
These divisions are all on the same line, they are dividing all the same people from one another
and it's becoming increasingly clear that that is the goal, increasingly clear over decades that that's the goal.
And these people have been put in place to control that narrative early on about a dangerous novel virus
that we had to do something like lock down masks and make a vaccine for,
that natural immunity might not work, that masks and bandanas and bushmeat,
these people are responsible for it and I'm on this page right here.
All of us are responsible for it, but at some moment in 2020 some people started to wake up.
And so we can find some of those people, we can eliminate them from this illusion of consensus,
we can see that they weren't part of it and not intentionally.
More importantly, we can see that none of the people that are currently and listen carefully to this,
please, none of the people that are currently out in front of the dissonant movement
were out in front of the dissonant movement in 2020, none of them,
not Robert Malone, not Steve Kirsch, not here at funded bush, no, not none.
Michael Eden's not in front of us anymore, but you could call he was very out early
and then canceled, canoe with Kowski, gone, Wolfgang Wodach, gone.
The people that are currently leading the dissonant movement didn't even speak up until 2021,
and meaningfully until the end of 2021 and that concludes Brett Weinstein and Steve Kirsch
and Robert Malone and here at funded bush.
All of these big names, none of them were speaking in Germany like Bobby was in 2020,
none of them were talking about natural immunity like Ryan Cole was in 2020,
none of them were coming out about hydroxychloroquine, not increasing the size of hearts and being ridiculous,
Peter McCullough was, nobody was complaining about ventilating people that didn't need to be ventilated,
none of these people, what Pierre Corey was,
and so some of these people are real dissidents that saw the animal in the early stages,
and when you see the animal in the early stages you get co-opted,
because the animal in the early stages was a natural security priority,
it involved special phone calls, it involved dudes with suits,
it involved a national security protocol that was enacted by DHS employees,
people from the military, people from homeland security, people from health and human services were all around the United States,
and so when Pierre Corey went from Wisconsin to New York, he didn't just meet other doctors in New York City,
he met the government, he met the military,
this illusion of consensus has been created on purpose for us to solve this mystery of lab leak or natural virus,
and in accepting the challenge, we have also accepted the premises of the challenge,
which is that there is indeed a novel virus,
and then we're always going to be trapped, our kids will always be trapped,
and so as we move these people around the board,
and people like Peter McCullough come out against the vaccine schedule,
and Nick Hudson makes a nice presentation that Thomas Binder keeps crushing it,
Denny is still doing amazing work,
Jessica Hockett is still doing amazing work,
Professor Martin Neal, and of course my friend Mark Yousatonic,
Mark Yousatonic has been single-handedly
I mean, the kinds of information that he's bringing together,
the kind of backstory that he's put together is not some kind of piecemeal house of cards.
It becomes very clear that this has been a long-standing plan.
It becomes very clear that some of these people have been involved in this long-standing plan for a long time,
Thursday, 5 o'clock Eastern, please be there.
And so we need to rally around these people,
rally around these people to help them, rally around them to get their message out,
and to share it.
This is the main message.
The main message is the intramuscular injection of any combination of substances with the intent of augmenting the immune system is likely very dumb,
and the transfection is not immunization.
So you know the show must go on and the narrative must be kept alive,
and in this quest to understand why we have been listening a lot to the words of Robert Malone,
and in his rather recent objection, or let me say critique of the awarding of the Nobel Prize to Caracao and Weismann,
as I recall, on the Vay John Health interview, which we covered a few weeks ago, which I highly recommend,
he mentioned a name, Peter Colis, as being integral to the development of the COVID vaccines,
and particularly the lipid nanoparticle that is being used for them.
His intellectual property is held by Canada and in Germany, I think,
and I thought it would be really cool to find a lecture by him, and it turns out,
it turns out that Peter Colis actually got awarded the, I think it's the Gardener Award,
which is one of these awards.
It usually comes like a year or two before the Nobel Prize for some people,
not all the people that get this award get a Nobel Prize,
but a lot of the Nobel Prize winners have gotten, most of them have gotten this award before they get the Nobel Prize.
And so luckily for us, it looks like Canada in an attempt to, you know,
make sure that the Nobel Prize committee knew that it was these three awarded Weismann, Caracao, and Colis,
the Gardener Award in 2022.
And so in so doing, then Peter Colis has given some talks around Canada,
and I thought we'd listen to one of those if you don't mind.
Big head move, play.
So I think we'll get going, everyone.
It's a pleasure today that we're going to be welcoming Dr. Peter Colis to the University of Manitoba as our Gardener Lecture.
Before I start, I just want to acknowledge that the University of Manitoba campuses are located on the original lands
in Avis, and on the new land of the Métis Nation.
We respect the treaties that were made on these territories and acknowledge the harms and mistakes of the past
and we dedicate ourselves to move forward in partnership of Indigenous communities with a spirit of reconciliation and collaboration.
That was striking.
I'm not sure what to say about that, because as a multiracial American with more ethnicities in me that I care to count
and I've frankly cared to do research,
I don't really, I don't really know what happened in Canada, I know it must have happened in Canada, pretty similar to what happened down here in some respects and so they want to be respectful to the cultures that came before the modern Canadian culture, but it's a little striking if that's the way that they start every single
I find that very impressive and I'm not sure, I'm not sure it's bad or good, I don't know what it means, it's just something that strikes me as pretty impressive
Rewards Lecture celebrates the world's best biomedical and global health researchers. The Garener Foundation was established in 1957 with the main goal of recognizing and rewarding international excellence in fundamental research that impacts human health.
Today there's been 402 awards that have been bestowed on laureates from over 40 countries and of those awardees, 96 have gone on to receive Nobel prizes, in fact many of the Garener Lectures, it's been seen now as almost like a pre-noble award.
Today our speaker is the recipient of a Canadian Garener International Award, there are five awarded annually to outstanding biomedical scientists who have made original contributions to medicine resulting in an increased understanding of human biology and disease.
Dr. Peter Collis is Director of the Nanomedicine Research Group and Professor of Biochemistry and Molecular Biology at the University of British Columbia.
He and his co-workers have been responsible for fundamental advances in the development of nanomedicines employing lipid nanoparticles, technology, and he'll be talking about that today.
He's co-founded 11 biotechnology companies published more than 350 scientific articles and is an inventor of over 60 patents.
He's also co-founded three not-for-profit enterprises including the Center for Drug Research and Development and the Nanomedicines Innovation Network.
The two drugs enabled by lipid nanopore technology, delivery systems devised by Dr. Collis and members of his UBC lab and colleagues in the companies he has co-founded have recently been approved.
So with this I want to also just highlight Dr. Collis' numerous awards including the Order of Canada in 2021 and the Vin Future Prize and Prince Mojito Award in 2022.
Peter, please give a warm up.
Okay, thanks for that introduction, Peter.
Okay, and what I'm going to talk to you about today is how accidental the way science actually is as opposed to the linear way that we often see it being portrayed.
And so that's why I entitled it science and serendipity.
There's a lot of good luck that's part of this and that relates to the phenomenon of particles that enable the COVID-19 vaccines.
And I could also entitle it 50 years of lipids because that's pretty much what it is.
So I've really been involved in this field for a while and there's been a long time.
Now how do I get these to advance? That's the next thing.
I'm just going to press a space bar here and maybe that'll work. There we go.
So you've seen various public announcements about the analyses of the vaccine, the mRNA vaccines.
And in some cases you see it's coming inside what people term as being tiny bubbles of past.
This is a headline from Bloomberg.
And so this is where the mRNA is coded in lipids.
And so what I'm going to talk about is really these tiny bubbles of past.
I'm not going to say that they're not really tiny bubbles of that, but anyway.
So what are they?
They're already tiny.
We're talking about systems that are 100 nanometers or less in diameter.
So 100 times smaller than a cell.
But they're not really bubbles of past.
They're nanoparticles made of membrane lipids.
They've really taken my whole career 50 years to develop.
So it goes way back to 1972 when I was involved in, I mean for 30 years I've been doing basic studies on membrane lipids.
Starting about 1985 we started to apply some of that knowledge to development of lipidase systems.
This dude is old because if he's been working on stuff since 1972, I was born in 1972.
That's some impressive shit.
Wow.
And he didn't get the Nobel.
These things aren't going to me.
To development of systems that deliver cancer drugs, which is what we started to do.
We started off trying to cure cancer and quite managed that with a few other things.
And then starting in 1995, applying the knowledge, our basic knowledge, to deliver nucleic acid based drugs.
Now, just going back to the beginning, this is, I got my PhD in solid state physics in using magnetic resonance in 1972.
And I was looking at semiconductors at 40 degrees Kelvin, like transistors on the moon.
Anyway, I decided after doing this that I really had to do something different.
Most of the interesting problems that I could see were outside the field of physics, particularly in the life sciences.
And so I got interested in applying NMR in the life sciences.
And I got a fellowship to go to the biochemistry department in Oxford in 1973.
And I knew absolutely nothing about biochemistry.
So this was quite an introduction by fire.
Now, I knew a bit about NMR.
I published my last physics paper in 1976, consisted of about 96 equations.
But anyway, that's pointing out that when you learn something as a physicist, you learn it in some depth.
And there's other things that you learn as a physicist.
You get the feeling that this guy is already like a Tyrannosaurus Rex compared to the salamander that Weisman was.
I mean, I already know that I would not want to sit at a table with this guy and open my mouth.
I would want to sit at this table and listen.
And it is completely the opposite feeling that you have when listening to Drew Weisman.
And I'm not trying to be a creep.
This guy clearly, I mean, wow, I don't even know what to say.
For a mentalist, when you need an instrument that isn't available, you build it.
And of course, going after basic problems is another aspect.
But what I got started in 1973, they had a mag, big mag.
I guarantee you, there's no pictures like that of Drew Weisman.
And so, some of them were powerful ones in the world at the time, actually.
They had no electronics to go with it.
So, we had to build me and a graduate student.
So, we built all the electronics to go with the sent-
Holy shit.
So, that's why I spent my first year there.
That's impressive.
Otherwise, it would have been a bit tricky.
But it was a bit tricky as it was.
And then I used the Edamar machine to-
See, it's not to be underestimated.
And I'll put myself in the same shoes or the same boxes, everybody else.
It's not to be underestimated how amazing it is that in the 70s and the 80s,
if you were doing science, you made everything yourself.
It's really very similar to this.
Let me show you another example of what I think is so extraordinary about
where we are in human time and how ridiculous it is.
When I was a child, there was a place that we would drive past on the highway.
We were about 30 minutes away from where the mall was and where all the stores were
because we lived in a super-tidy town in northern Wisconsin.
And so on this drive, we would go past this place where a lot of times
there were dudes playing with model airplanes.
And so you would drive past and then you would suddenly catch this super-tiny airplane
flying really fast and like, you know, doing loops or whatever.
And you immediately realized that it was a model airplane.
And we also occasionally would see a helicopter there.
But the helicopter didn't do anything.
The helicopter just flew.
But that was pretty unbelievable.
Now in those days, those guys were making almost everything that they did.
You know, even the servos, and they certainly had to be able to repair them.
They certainly had to customize them.
And so you couldn't go on Amazon and buy a kit for a helicopter.
And if you did buy a kit for a helicopter, it might be $2,000.
Now you can go on Amazon and you can get a helicopter that should cost $2,000 for about $200.
And the crazy thing is, is that the amount of skill that I need to build this is zero
because it comes built.
So you get it out, you put the battery in, you put it on the ground.
You can fly it.
And there's no building.
There's no tweaking.
I don't have to adjust the pitch and the way that the swash plate interacts with.
There's no, and I know how to do all that because I've been playing with helicopters for quite so many years.
But what I'm suggesting to you is, is that there is a whole generation of biologists that's growing up
going into the lab, going into graduate school, and rather than being required to build the helicopter
that they're going to use for their experiments, they order one.
And so they're not even really sure if the person who designed what they ordered knows what they're doing,
or whether it meets the specs, or whether it meets the fidelity measurements of the specificity that's required.
Science almost has to be done on the product now.
Let's evaluate this helicopter for its attributes before we can realize if we can use it for the experiment.
And so so much of science is spent looking for the product that you're going to use to do your measuring.
Looking for the apparatus and then making up an experiment rather than coming up with the experiment and building an apparatus like they still do some places.
The most cutting edge neuroscientists are making their own apparatus still.
But what I need you to understand is molecular biology used to be like that.
And it's clear that this guy cut his teeth during a time when science was real.
And has worked with people who know how to do real science.
From the ground up, from the dirt up.
We need to measure X. Well we don't have one of those in the catalog, so I'm going to make one that can measure X.
That's what he did.
There are almost, I would go out to say, there are almost no scientists to do this anymore.
And the worst is that there are almost no geneticists that do this anymore.
No molecular biologists that do this anymore.
The market is literally flooded with products that do it for you.
With pre-made reagents.
And it's not to say that accuracy can't be achieved with products, but it is to say that the mastery.
That the understanding.
That the in-depth grasp.
The question that you're asking and the limitations of it.
Are kind of lost if you can order the helicopter online.
And it comes already set up.
So that you don't have to program the electronic speed controller.
You don't have to bind it to the radio.
You don't have to program the radio.
You don't have to program the swash angle.
And so what the hell do you really know about how a helicopter works if you can order it online
and put it on the ground plug in the battery and fly it away?
And what do you really know about the genome if you can buy a mini prep kit,
amplify your DNA, sequence it, and then you get a piece of paperback.
Never having known what went into that aluminum product that you combined with your Abbott product.
And you combined with your bio-rad product and then put it back in your aluminum product.
Okay, I'm getting a little crazy here, but anyway.
Well, it was a bit tricky as it was.
And then I used the Edamar machine to study eulipins in biological memory.
So really basic stuff.
But it's going after basic problems. And so this is a model of biological memory,
which is a synchronical model, which is still quite relevant today,
showing the various components proteins and lipids that were all good.
No, I'm going to toot my own horn for a little bit, though.
Because I have a little invention that I invented for my work.
Which is a very, maybe I can use this camera.
It's a very hand sensitive air adjustment.
You can't even roll it now. This is probably a little rusty, but you put an air hose on this end.
And if you put an air hose on this end.
When you're making electronic electrical recordings from neurons under a microscope,
you need to be able to control the air pressure inside of the electrode.
Because you use the subtle change in pressure to actually make contact with the cell.
And in the old days, these patch climbers would use a hose in their mouth.
And they would blow in it a little bit or they'd suck in it a little bit.
And so when people were making these recordings for eight or nine hours a day when they were really obsessed,
they would be the whole day with this tube in their mouth.
And later on, people started using syringes and I didn't like it.
So I made this thing, I asked this machine, machinist student at the, the Erasmus University.
I hope George Webel here this.
And this summer student machined me this thing that you can roll with your hand and it moves the piston down.
And you can push this button and it makes it neutral.
And so just like taking it out of your mouth or blowing or sucking, you can essentially roll this knob,
you can blow and you can suck and you can also go neutral.
And you can do it with your hand and it's really, really small amount with your, with this roll.
You know, really small amount.
And it made my, it made all of the quality of my recordings just go out the roof.
And so I made lots of different varieties and versions of it and gave some to people.
And for a while, it was a really cool thing and it was something I was really proud of.
Because it really made me more efficient and it was really something that, you know,
after all this time of all these people contributing all this stuff to this one methodology,
it was cool after 15 years of doing it to finally make something that was really mine that actually made it better.
You know, and, and nobody cares about this stuff.
But I'm just saying that like, that's really where, where good, honest science is done.
It's done at that level where, where you've got to invent something in order to measure.
You've got to invent something in order to perform the experiment.
You've got to, you've got to solve a problem via invention in order to get to your goal is a very rare thing.
In academic science anymore and even more rare, it's rare in biology.
Because biological science has been inundated, completely inundated by products.
And even in neuroscience where you would think if you're designing a behavioral experiment for a monkey,
you're going to have to build your own custom setup, but you'd be wrong.
If you just take what Kevin McCarran does, for example, what he used to do when he was a neuroscientist
and actively working with monkeys, although he may have built his own apparatuses,
my guess is, is that if he were to start his own lab now,
there would be some product out there that would be better than anything he could build.
And if he had the grant money, he would choose to buy that because it's much faster and better and whatever.
My point is, is that these products are everywhere all over the place.
They're at every conference. Science isn't this going into the shop,
going into the, you know, wood shop, invention shop, metal shop,
using a lathe that's not like that anymore.
And in molecular biology, I know I'm beating a dead horse, but I really want you to hear it.
In molecular biology, it's like bakery where you don't have any recipes anymore.
It would be really like if all the bakeries were just boxed cakes
and you never went to the store and bought flour and sugar anymore,
you just bought boxed cakes from all these different companies.
And they came in all different sizes. You want to make a wedding cake?
Well, you can order a wedding cake from thermal scientific,
or you can order a wedding cake from Sigma.
But if you want cupcakes, I think, I think that, you know,
molyneau labs makes the best cupcakes you should order their product.
And it would come in a little box and all the, all the ingredients would be separate
and then there would be instructions on how to mix them.
And it might just say put two one and tube two and add four liters of distilled water,
stir for 30 minutes and then put it on at a temperature for an hour and there it is.
And because you were completely not involved in any part of the baking,
you don't understand anything.
You don't even know what was in tube one and tube two.
You just know that tube one and tube two couldn't be combined in transport.
In fact, hostess might not even tell you what's in tube one and tube
because it's proprietary information.
The buffers are secret.
Do you see my point?
These people don't know what they're doing when they sequence a reaction.
When they sequence a virus, they don't know what they're doing
when they do a PCR reaction. They're using a product,
reading the directions and interpreting the product's outcome based on the directions.
That's it.
And a lot of molecular biologists are so disconnected from the molecular biology
that they purport to do that they can't even explain what parts of the products they use
are responsible for what parts of the reaction they purport to be exhibiting.
So I'm trying to say, with a ridiculously long rant,
that this guy seems to be a PIMP.
A real deal.
And I really like that.
But you can see it because you could hear it from the very beginning.
This guy had to build electronics in order to do stuff.
He's the real deal.
Now, all biological membranes rely on a bilayer.
A little bit bilayer as a structural element.
So this is taking out the proteins. This is what you're going to see.
And the membrane lipid, of course, are amphicathic.
I mean, they have a polar head. They're self-assembling, which is a wonderful quality.
They have one end who likes to be in their water and the other end
who likes to be sequestered away from water.
So the basic questions I got interested in were two falls.
One of them was, well, positive memories contain a lot of lipids
that if you pull them out and then put them in water, they don't adopt bylars.
So what are they doing there? And what's their roles?
So what are these non-biler lipids there? It's called lipid polymorphism.
Along way from vaccines, what we actually used, the knowledge that we gained
studying with the polymorphism to develop more effective delivery systems for mRNA.
And the other question that we looked at was lipid asymmetry.
So the lipid composition on one side of a biological membrane is different than the lipid composition on the other side.
And so we asked the question, well, can this be related to our ingredients?
You know, they're present across membranes, whether they're sodium potassium
or proton or pH gradients.
And so this is, I spent a lot of time and still do spend time actually on investigating those properties.
And what we discovered.
One of the things I would hope, if you would pay attention to, if anybody has
listened to Christine Grace, this person that we covered one time on a V John Health lecture,
she seems to be quite the expert on nanoparticles and lipid nanoparticles.
It would be interesting if you're listening and you notice anything that she said
that's the same as what he said, or if you've noticed any contradictions
between what he's saying and she's saying.
What I guess is going to happen is, is you're going to hear almost no overlap in terms whatsoever.
No overlap in concepts whatsoever.
But maybe I'm wrong. I'm optimistic.
It was that we could use NMR, phosphorus NMR.
I mean, phosphorus have a phosphorus in them.
So we could use a phosphorus NMR to study these different structures that lipids a dot.
The misad water in these civil form bilayers are these other structures.
They form a bilayer, then their main emotional characteristic is rotation around the long axis.
And so this gives rise due to the phosphorus and the phosphate.
So this kind of characteristic line shape with a low field shoulder and high field peak.
So it's quite diagnostic of a lipid bilayer.
On the other hand, if they adopt these strange structures such as exactly the H2 phase,
it consists of long tubes of water surrounded by lipids on the outside.
These are about, say, ten animes or so on, or less in diameter.
Then they can, additional emotional averaging, they can rotate, they can go around these
so it gets very rapidly.
It ends up giving you a different line shape with a low field peak and high field shoulder.
So really quite, and if they have total emotional averaging, then you see a very narrow line shape.
And so this allowed us to study the properties of many lipids in terms of their face preferences.
Are you understanding that he's using NMR to look at the structure of lipids
that he uses the NMR signal to identify the organization of the lipid.
And so this NMR signal spectrum across frequencies is different than this one,
the reflection or the light or the energy that comes off of it.
As long as you understand that much, it's okay.
I don't know if I can even explain the particulars of NMR.
It's magnetic resonance, which basically means how do the molecules resonate
and the resonance across frequencies.
So I think they do a frequency sweep.
And when you see a frequency sweep and then the amount of resonance that you get,
and it's different in the different structures here.
So they can start to probe how lipids arrange themselves using NMR.
And the NMR machine is what he had to build by scratch.
And if they had total emotional averaging, then we can see a very narrow line shape.
And so this allowed us to study the properties of many lipids in terms of their face preferences
and have a good shift between one or the other.
This has been the crowd.
I worked on a lot of this with him in the late 70s, early 80s.
And just pointing out that we could rationalize this by, and this will come in back in,
when we talk about the vaccines.
The lipids and the biler structure have more of a cylindrical shape.
The Herion head group region can be more or less the same as in the isyl chain region.
Whereas if it's like the structure of this, such as these hexagonal phases,
have a cone structure where the area for a molecule in the head group is somewhat less
than the area is attended by the isyl chains.
So very simplistic thinking that them went on and saying,
okay, well, what are the function roles?
Can you hear that though?
Again, maybe I'm playing it too fast.
I can hear it, but maybe you don't.
So the way that they organize seems to be the way that the head, the phosphate head,
is related to the chain on the bottom.
If the molecular shape is the phosphate head on the top is bigger than the tail,
then you will get a micellar.
My cell micellars are these things that we talked about with Robert Malone a few weeks ago.
If the lipids on the bottom are related to the phosphate head are about the same size
and they're cylindrical, then you get this bilayer.
And if they're conical, meaning that the tails coming off the bottom,
I think those are fatty acids, but I'm not sure.
It's like a phospholipid head and then fatty acids on the bottom.
But the fatty acids are spreading out like that in a cone shape,
then they will make that hexagonal arrangement.
And so they're trying to study how lipids assemble.
Obviously, this will then allow them to make different assemblies of lipids
and understand why they assemble the way that they do.
It's really cool.
You would not be opposed to it being slower.
I'll put it one notch slower then.
By the acyl chains.
So very simplistic thinking that them went on saying,
okay, well, what are the function roles of these lipids?
Now, in order to investigate these roles, it's very difficult to do anything in the intact membrane.
There are hundreds of different lipids species there,
and trying to pick out the properties of one lipid versus others is pretty much impossible.
And so you have to use very simple model membrane or less termed liposomal systems.
Now, at the time, there was not really a good way of making these systems.
You wanted to make these systems with one bilayer of an inside and an outside, et cetera.
So we devised a high pressure extrusion technique
where we basically took larger lipid bilayer systems
and rammed them through a polycarbonate filter with a 100 nanometer pore size.
And so out of the other end, you get these unital amount of systems just like this.
So this is where building an apparatus should be formed a company on this that serves this very well.
But anyway, we can use these liposomes to show that membrane fusion depends on,
you know, if we have non-biodar lipids and we add them,
we put a certain small proportion in with these bilayer forming vesicles.
Then we'll see, we've been in dander fusion between them, and we'll see.
So definitely, this is much other evidence indicates that the membrane fusion
is really dependent on these lipids, of course, membrane fusion and vital to life in many ways.
Now, we also use these.
The subtitles are not getting that.
It keeps saying membrane fusion.
It's like saying remembering fusion just in case you're reading.
We use liposomes to demonstrate the consequences of lipidase symmetry.
And I'm going into this a bit because it points out the importance of doing quite basic research
on how you can use the inside of your game, from basic research,
to inform your and give you tools that you can use for more therapeutic or...
I think he said he formed a company that made those little lipids.
So it's forcing them through the carbon filter to make them a little tiny.
That was a company all by itself.
Patients.
So we synthesize this ionizable cation lipid called dodap.
And the thinking here was that this lipid has a property as a tertiary amine
that can exist in a protonated state, which is positively charged,
and that's at low pH, whereas it's a neutral pH that becomes repropenated
on the other net neutral molecule.
And the net neutral molecule can diffuse across the membrane really quickly.
But it becomes to the inside and gets protonated.
It becomes positively charged, but it can't get back out again.
Because charge molecules don't get through lipid bylars very easily.
And so we can drive lipidase symmetry in response to this pH gradient,
and we can look at various consequences of having more lipid on one side of the membrane
compared to the other.
And the sheet change is in order to more flow.
There's some huge changes that result from it.
I mean, think about how elegant that is.
Think about how basic of biology this is.
That he's got a system with nothing.
He's just looking at cell membrane.
He's looking how charge can cause molecules to flip from one side of the membrane to the other,
and that charge can keep them there.
And then looking at this charge asymmetry, I think it's really interesting.
And I think it's really amazing that people
were able to come up with these stepwise investigations to break down
and understand how these complex chemical systems work.
It's extraordinary, isn't it?
Again, real biology here.
No.
But we got distracted.
As we also found, we could load cancer drugs into these liposomes,
into the pH gradients.
And so these are the weak-based drugs that can exist in a protonated form or a neutral form.
Well, that neutral form can go across the bilayer.
If you have a low pH on the inside, it gets protonated in traps.
And so this shows where Dr. Ribison, which is a common anti-cancer drug,
that we could get so much drug in there that we'd pass the solubility product
and they would get these nanocrystals forming inside our...
This is 100 nanometer bar here inside these vesicles.
So we immediately thought, well, wow, this is going to be a good way
of delivering cancer drugs more specifically to where you want them.
This is an enormous problem.
Of course, I mean, cancer drugs go everywhere in your body cause really nasty.
Wait, did I miss something?
I'll actually get to where you want to go.
I'm distracted very easily.
And so we could drive...
Now, I see a little bit of critique here.
And I just want to be sure that everybody understands.
When I say that this is real biology,
yeah, you might want to say that this is more like biophysics.
But it's investigation of the basic properties of lipid bilayers,
which are fundamental to most living systems on Earth.
So in that sense, it's a very fundamental biology.
Yes, it's still a theory or a hypothesis about how these lipid bilayers work.
But I'm impressed with the fact that at least we're investigating that with the idea.
But I don't know where we just...
We just really crossed into delivering cancer drugs all of a sudden.
So I missed some transition there.
That's why I wanted to go back.
Drive-lividase symmetry in response to this pH gradient.
And we can look at various consequences of having more lipid on one side of the membrane
compared to the other.
And the shape changes in order to more...
There's some huge changes that result from that.
But we got distracted.
So we also found that we could load cancer drugs into these liposomes,
into the pH gradients.
And so these are the weak-based drugs that consist of a protonated form
or a net-neutral form.
Well, that neutral form can go across the bilayer.
If you have a low pH on the inside, it gets protonated in traps.
And so this is shows for Doxaribacin, which is a polynomial cancer drug,
that we could get so much drug in there that we'd pass the solubility products
and they would get these nanocrystals forming inside our...
This is 100 nanometer bar here inside these vesicles.
So we immediately thought, well, wow, this is going to be a good way
delivering cancer drugs more specifically to where you want them.
This is an enormous problem.
Of course, cancer drugs go everywhere in your body cause really nasty.
Only 0.01% will actually get to where you want it or less.
And so if you could deliver these more specifically,
it'd be a huge benefit.
So we started a company in 1992 called, this is me and four postdocs in the lab,
called Inik's Pharmaceuticals to use these systems to improve the delivery
of cancer drugs to tumors.
I have to say, this is a great way of keeping a team together.
We're still working together one way or another, some 40 years later.
And we've had some success.
Tom Haddon is now CEO of Acuitus, which supplied the banana particle
for the Pfizer biotech COVID-19 vaccine as an example.
But it's been quite a ride over the years.
We started this for cancer drugs, but we started working on gene therapies.
We hired a CEO, Jim Miller, and Monday about the middle 90s,
he came to me and said, well, I can't raise money for the company
putting these old drugs in liposomes.
I mean, if you're doing gene therapy, it has much more sex appeal.
That's exactly what he said.
In other words, sex appeal for investors.
And so this risk really started us off on a whole new path of reading.
I got to say, I completely and totally agree when they say you got distracted.
It means we got a shit ton of money.
And we went for the money.
Wow.
This is a great little talk here.
And gene therapy, you know, is a much more sex appeal.
Great.
Instead of delivering cancer drugs, I'm trying to deliver nucleic acid-based drugs.
So let's get back a little bit.
So what does gene therapy, what did the Miller mean?
If you go to Wikipedia, you can find a very general definition.
It's not, there's other definitions.
But one version of gene therapy is the therapeutic delivery of nucleic acids
into a patient cells as a drug to treat disease.
But delivery is really the operative word.
These approaches really require delivery systems.
Excuse me.
I'm modified nucleic acid-pombers.
They're really degraded very rapidly in the, I've got to sort of got some more here.
They're rapidly degraded in biological fluids.
But they don't go to where you want them to go if you inject them.
And if they get there, they can't do anything because they can't get across cell membranes.
So, you know, delivery systems are kind of important.
Now what we focused on was the delivery of RNA-based molecules to either inhibit gene expression
or promote gene expression.
So as you're all aware, DNA goes to mRNA, goes to protein.
So the sRNA interferes with translation by degrading mRNA for a very specific protein
according to the sequence in the sRNA.
A messenger RNA, of course, if you get that inside a cell, then it'll be taken up into the ribosomes
to produce any proteins we want.
And I think this is really important.
This is something that I mentioned yesterday as part of my little rant about what the RNA can and can't do.
I understand that there's DNA in the shots and that's real bad.
But there was RNA in the shots and RNA can be really bad too.
And one aspect of RNA and the insertion of foreign RNA into our system,
that hasn't been discussed at all, is this short interfering RNA potential.
The short interfering RNA potential is there from a nefarious perspective.
It's there from an erroneous perspective.
It's there from a quality control perspective.
And it's something that we haven't really at all talked about, even with the greatest molecular binds on the
incidence side, none of them have ever mentioned this as a potential danger.
But especially, and I say this with great trepidation, but especially with injecting mRNAs into pregnant women,
those mRNAs, if they are the smear on the gel that they showed to the FDA,
then there are lots of small RNAs that have this potential that may have overlap with human transcripts.
If you put this in a pregnant woman and then use accidentally interfere with RNA expression in the developing embryo,
that's not going to be really good.
And the potential for that interference is very, very high if the RNA is in pure.
If the RNA has a lot of overlap, if they haven't been adequately,
and you know that they haven't, if they haven't adequately investigated the potential for interference to occur.
Interference happens when this shorter RNA sequence binds to an existing transcript
and that double strand of RNA then gets degraded, because the body doesn't tolerate double-stranded RNA.
We know that this is a thing because we've used it in academia to stop or lower the expression of a protein temporarily
in order to study its effects.
We have already used it as a way of trying to treat diseases when it comes to the inhibition of a production of a pathogenic protein, for example.
And so as he talks about the delivery of RNA, he's talking about the whole spectrum of products that could be used in academia
because there's billions of dollars from the welcome trust in the NIH and all these other non-governmental organizations for academic bench research.
And academic bench research uses transfection and transformation all the time.
So you don't even really have to think about curing disease or changing the world of childhood diseases.
You can just think about delivering RNA in the context of academic biology and look to make millions.
And again, here we're talking about the throwing of money at academic biology has created a whole gigantic multinational industry of chemical production
and chemical apparatus, biological apparatus, molecular biological tools, kits, methodologies, machines.
And all of these industries have moved scientists, biologists, chemists, behavioral neuroscientists, everybody farther away from understanding the biology that they think they're studying
because they don't understand how their measuring tool works because their measuring tool is just a product
that they follow the directions for like a cake that comes out of a box with tube A and tube B and sac A and B.
And you combine tube A with sac A in a bowl and then you add B and B and you stir it up and put it in a oven and then you have your cake, you don't know what you did.
And you wouldn't know anything about how to tweak it.
You wouldn't know how to make a variation or an adjustment to it.
And so as we talk about this, understand how long this guy started in 1972 and got distracted in the early 80s to deliver RNA.
It ain't a new thing.
So as a remarkable statement that comes out of this, if you can do this, you can potentially treat most diseases, most human diseases, which is really a remarkable statement.
If you think about it, all diseases rely on their cause by proteins either being overexpressed or not being available.
So both SRNA and mRNA require delivery systems to reach the interior of target cells.
So we spent the last 27 years, I guess, developing these lipid nanoparticles to deliver SRNA and mRNA into cells in vivo.
So I was going to go through three aspects of that which is the design for encapsulation of these nucleic acid polymers, which is still going on today
and we're still improving these systems.
The patocerian or on-patriole story, which is to treat a particular disorder known as trans- thyristin-induced amylidosis.
And then I'll briefly mention the vaccine application.
So our aim in 95 was to develop a delivery system to try and silence a gene in the liver.
We started off with any sense of the nucleotides and then switched to SRNA in the early 2000s.
But this is actually one heck of a problem.
When you think about it, we're challenged.
Packaging it up, first of all, on lipid nanoparticle, and it has a circulator round after an IV injection.
Let's say if we're targeting a gene in the liver, then it has to extrapolate in the liver.
So I got a message here which says,
Intradidum was a biotechnology company that develops gene therapy technology based on RNA interference.
Intradidum merged with silence technologies in 2009, and the merged company is now publicly traded.
Silence technologies is involved in developmental research of targeted RNAi therapeutics for the treatment of serious diseases.
RNAi being RNA interference.
And this is just a different way of abbreviating short interfering RNA as the same as RNAi, RNA interference.
Dr. Robert Malone co-founded and helped secure the 2.3 million in venture capital funding, including monies from the Norvargis Vester Fund,
ETP Venture Capital Fund, and the state of Maryland.
He also performed facility setup, infrastructure setup, and intellectual property development business and technology development planning,
including in-depth business and scientific plan.
So we know that Robert Malone knows what SIRNA is.
We know that he knows that RNAi can interfere with the regulation of endogenous RNA.
And so he has to know then that the injection of active lipid nanoparticles filled with less than optimal quality controlled RNAs into a pregnant woman would be absurd.
He has to know that, otherwise he couldn't have helped a company like silent technologies back in 2009.
I'll give you a big guess as to who just sent me that message, but he's in the chat now and he's a beast.
SIRNA has to get taken up by hepatocytes, has to then get out of the endosome and into the cytoplasm.
And so really building up that capability.
Am I too quiet?
I feel like I'm talking a lot.
And also, of course, you've got the immune system fighting you every inch of the way.
This certainly doesn't want foreign genetic material getting into cells in your body.
So the first problem that we hit, and this is where the serendipity, some of the serendipity aspects comes in,
was that in order to encapsulate negatively charged polymers such as nucleic acid and RNA DNA.
I don't know if you can see it already, but for me, what I see there is the start of an Ebola virus.
That's what I see.
You can see the start of an Ebola virus.
It is a double-stranded molecule with a lipid nanocode around it, and so it's going to become a long snake.
Into a lipid nanoparticle, we had to use the positively charged lipids.
You can see that the associate with the negative charge, and we can see the potential then for getting a hydrophobic entity
that we could then encapsulate as the lipid nanoparticle.
Now, there's a huge problem here, and that is that there's no permanently-positive charge,
and that is in nature.
There are really toxic molecules.
There's only net-neutral lipids or negatively-charged lipids.
And so we thought, wow, well, how do we get past this one?
Because the toxicity if you're developing a drug, now that's always what's going to get you in the end.
And so what we did was we tried the lipid that we developed for the lipid asymmetry studies,
where we knew that at pH 4, say, when we're below the pKa of this tertiary amine,
it's going to become proteinated, so it's positively charged,
whereas that neutral pH is not going to be charged, and so, therefore, presumably, it's going to be much less toxic.
And so we asked the question then, well, can we load these polymers?
Can we load antisense, or SRNA, at pH 4, where the dodap or other ionous lipids is positively charged?
And is it retained when we raise the pH, 2 pH 7.4?
And the answer is obviously yes, otherwise we wouldn't be giving this talk.
So what we developed, a rapid mixing procedure for formulating these systems,
and, again, one of the lights they're working with lipids as I mentioned is their self-assembling.
And so we dissolved the lipids in ethanol, and then, through a rapid mixing process,
let's say, the SRNA, or antisense, or whatever else we want to get in there.
And these are all...
One of the first things to fall out of the solution is the...
This is most...
You take acid polymer, it's surrounded by the positively charged lipid.
This is most certainly patentable.
Oh, I didn't know I had that on.
This is most certainly patentable.
The whole process is patentable.
All of these things, because lipids are self-assembling,
all these processes are patentable.
That's why I have so many patents.
That's clear now to me.
Now, if you do this fast enough, then other things will fall out of solution, such as this peg lipid here.
And you can trap these systems in what we turn on limit-sized vesicles, in other words,
the smallest size that's compatible with the molecular components.
And that when we took the pH back up to pH 7.4,
the contents were retained in these systems.
And so this really got us past the toxicity issue.
And also, you can see intuitively how it is that we could get, you know,
encapsulation efficiencies that might approach 100%.
So it turns out to be a pretty useful technique.
But it's basically dependent on that basic research where we were playing around with the ionizable cationic lipid,
and then we had a tool that we could use in the...
You know, for making these nanoparticle systems,
these are relatively non-toxic.
They have a hydrophobic core.
This is a cryo-TM picture.
Certainly, any negatively charged macromolecule, we can encapsulate it 100% shopping efficiency scalable.
We can change the size to all the size just by changing the surface lipid to core lipid ratio.
All kinds of advantages to this process.
So we know we had things that were formulated in lipid nanoparticles.
You know, could they actually do anything?
At least we had something that was basically not too toxic,
and that was a prime criterion before we even went near animals.
So after a conference that I attended in London,
this was 2004, I was pursued by...
Well, this term is a mad Russian, because it kind of is.
The guy named Victor Katellianski, who at that point was the vice president research.
He had a company in Boston called online on pharmaceuticals.
Now, an island was founded in 2002 to develop the small interfering RNA as a therapeutic,
and when it's silenced to particular genes in the liver,
to inhibit production of proteins or causing problems.
And he had a statement, was we have a delivery problem?
How did we get our S RNA into the liver, into hepatocytes in vivo?
And so this stimulated a seven-year collaboration that went on from 2005 to 2012.
We had teams in Vancouver and in Boston, and we synthesized many different lipid nanoparticle formulations.
But it resulted in a formulation that we could silence a gene in the liver
with a therapeutic index approaching 1,000.
In other words, give 1,000 times higher dose than that,
which we received some biological effect before we saw toxic side effects.
So we started off with a question.
Can these lipid nanoparticle systems, silence genes in the liver following an IV injection?
So there's really no targeting information on the outside here.
I could go into other forms of serendipity.
They actually turned out they do target quite well for reasons maybe we can discuss the question period.
But so they have a very simple, I mean, it's complicated in many drug terms,
but we've encapsulated, say, 1,000 of these oligonucleotides in 100 nanometer or 89 nanoparticle,
and we were injecting them IV.
So what's going to be the process whereby they actually have some biological effect?
Now, lipid nanoparticles get into cells by a process.
You're all familiar with the endocytosis of cell-eating process.
And so this means that we don't want things to go on to the lysosomes.
We're saying, you know, nucleic acids would get degraded.
We have to break out of the end zone at some point so that the oligonucleotide is really delivered
into the cytoplasm.
And so they just hand-wave that.
It's a little bit like the infectious cycle, right?
That's it.
That's what you're just going to say.
It just opens up and they leak out and that's all good or what?
This is really wrong.
And we shouldn't let him get away with this, but they're letting him get away with it.
I think that this is a lot of hand-waving here, and I don't think that they know exactly what happens.
They just assume a lot like the infectious cycle of viruses.
The oligonucleotide is really delivered into the cytoplasm.
And so how can these ionizable lipids destabilize an end zone?
What we found was that if we took positively charged lipids and added them to negatively charged lipids,
just those lipids you find in endosomes and other biological membranes,
it will flip the lipid from a bio-organization.
This is the phosphorous NMR signal that I showed at the beginning.
They'll flip it straight over into these non-biodar structures.
Let me describe this to an electrostatic interaction changing the shape as it were of this molecule
and flipping it from a bio-organization.
But anyway, certainly very membrane destabilizing.
And so this took us back to the polymorphism.
They really basically, again, basic studies, but it gave us a way forward for designing better and better ionizable
and counting on lipids.
And so we needed to design them so they interact with the components of the endosome
at some vulnerable part of the endosome maturation process.
And so this is our model for saying, okay, what we're trying to do here is to destabilize it
by introducing these non-biodar structures.
Now we assessed the invivial potency of the systems using factor seven mouse model.
This is going to point out some of the amazing advantages of gene therapy approaches.
If we can get it to work for factor seven, which is the clotting protein as you're all aware,
then if we can silence that gene, we can silence any other gene in the hepatocytes.
And so we're used to this as a model.
We had factor seven, that's SRNA to silence factor seven.
Packaged that in a lipid nanoparticle, introduce that into the intravenously,
and then assay for factor seven in the blood 24 hours later.
So we know that factor seven is made in the hepatocytes,
and so if we are inhibiting the production of factor seven,
then we're going to see less factor seven in the blood subsequently.
So I could do two experiments a week, it wasn't high throughput,
but we could certainly run through quite a number of formulations.
I should say for nanomedicines in general, screening in vitro doesn't really tell you much,
you really have to get to the invivial circumstance.
So we found that the potency of these systems was really sensitive to the species
of the cationic lipid, the ionizable cationic lipid that we employed.
And so this is just going through a sequence of, you know, we started off with DODAP and KDM-A,
KC2, MC3, et cetera. They're all pretty similar.
I mean, linoleic acid chains, we've got tertiary amine.
So why, but, you know, there's a huge difference in terms of their potency.
And we found that the potency was really very, very sensitive to the PKA,
a point at which these ionizable lipids became positively charged.
So this is a graph of the potency, now potency is one over the effect of those
where we could basically knock down factor seven by 50%.
And it's a function of the PKA. This is a log plot here.
So you can see, I mean, a PKA was as little as half a unit away from some optimum.
We could decrease the activity by two orders of magnitude.
So that's really quite a, quite a pronounced dependence on the PKA of the ionizable lipids.
And so as a result of this, we were able to take effective dose from 10 migs per gig
where we would see some deans silencing down to five micrograms without increasing the toxicity.
If anything, we decreased the toxicity.
So this is where this therapeutic index of a thousand came from.
Anyway, so at this point, the clinicians, or at least we said,
we think this is ready to go into the clinic.
And so the clinicians at Onalam said, okay.
I'm kind of annoyed because he keeps using this therapeutic index,
which he says is a thousand,
and the dose that they're using is a thousand times higher than what they need
to create an effect, and they still don't see toxicity,
or the toxicity occurs only when they increase from
an effective dose a thousand times.
What is the toxicity that he measures?
What is this, that, it's sort of hand waving here,
but again, I get that he's given this general talk, so he can't explain everything,
but it's a little, yeah, anyway.
We think this is ready to go into the clinic.
And so the clinicians at Onalam said, okay, what disease should we go after,
and the disease that was chosen,
and that was the disease that I'd never heard of before,
called trans-theritin-induced amylodosis, a hereditary disorder.
As I mentioned at the beginning, by science and factor 7,
we knew we could start as any gene in the parasite,
so all we had to do was put in a different SRNA
that was going to silence our particular target.
So this was work that then went on at Onalam.
HATTR is actually a pretty nasty disorder.
So the trans-theritin, it's a protein that's made primarily in the liver.
If there's a mutation, and there are ways of number of mutations,
it's a big protein, can cause a formation of fibrils,
which presumably deposit everywhere in your body,
but they have really nasty effects in nervous tissue and in cardiac tissue,
so it's no effective therapy.
They usually fail a little bit in five years of diagnosis.
It's kind of a nasty disease, which is indicated here.
It's a wasting disorder that goes through the stages.
It's indicated here.
Kind of particularly nasty because it's hereditary,
and so if you find you're stumbling in your thirties,
you sort of know what's in store for you,
because you're likely to see in a relative go through the similar process.
So this is where the simplicity of gene therapy approaches comes in.
So, okay, well, this is caused by the protein trans-theritin.
Well, this has stopped it being produced.
And so this is taking a, I've been at a particle now,
containing SRNA to silence trans-theritin,
and the idea is, if we shut that down,
then we're going to reduce the circulating tetramers,
the deposition of the fibrils,
and perhaps we might even get some clearance
if there's very little in the blood.
So potentially a simple solution to what is really a devastating disease.
This is the results of the phase three study,
which came out in 2017.
So there was 148 patients who got to the drug
in the dose of .3 mics per gig, IV every three weeks,
or they got sterile saline as a placebo.
And the neural impairment score was a primary endpoint,
quality of life, weakness, et cetera,
over secondary endpoints, ability to walk, and so on.
Now, so these were some of the top line results
for the save for the neural impairment score.
So over the course of the 18 months,
the patients that were on the sterile saline
or the control were getting steadily worse.
Their neural impairment score was getting higher,
whereas those patients that were being treated with this.
Okay, so we're treating a hereditary disease that I'll go back
so you can see what it was called.
Hatter amyloidosis
that is going to kill people in a pretty awful way,
and it's hereditary.
Usually fatal within five years of being diagnosed.
It looks like it hits you when you're an adult.
But giving mRNA in a lipid nanoparticle
to a person who's going to go through this in five years
is very different than giving it to your four-year-old.
It's so different, it shouldn't even be discussed.
But vaccines are given to kids.
Vaccines are given to healthy adults.
This is not a healthy adult.
This is a guy who has a five-year death ahead of him
after diagnosis, and so it's fine to give him mRNA
in a lipid nanoparticle. Why not?
And it doesn't even work that well as you see.
It does stop it, but I mean, it's not curing him.
Since they were being treated with a drug
to silence a transliteration in the liver,
if anything, we're getting better.
So, really, you're improving the status of these people
suffering from a hereditary disease.
So, it's quite a remarkable thing.
So, the Phase III trial results were announced in 2017.
As I said, I also refer to the p-value for the
neural impairment story.
This is 10th of the minus 24,
one over Avogadro's number.
They're absolutely sure that this drug works,
but it's equally convincing for self-reported quality of life,
muscle strength, ability to walk, nutritional status, etc., etc.
So, it's certainly one of the most,
why that's the most impressive clinical trial result
I've ever seen.
It really points out how these genetic drugs, you know, are...
So, if you talk, you start with a dude who's really dying.
You can use mRNA to briefly fix him.
I don't think this returns them to normal.
I don't think it means that he's going to live for 50 more years.
And I bet if he's really honest about it,
the guy probably still died two years later,
but at least he didn't feel bad while he died.
At least he didn't deteriorate anymore.
Because my guess is that therapy won't work forever.
That's the tricky part.
That's the part he doesn't have to tell you right now.
They really work.
Because we're going right after the root cause of things.
So, this was approved by the FDA, the trade name is on Petro,
and by the FDA in 2018, for treatments,
the first FDA approval of an SRNA-based drug,
and a clinical validation, obviously,
for the, depending on a particle delivery approach,
really dramatically demonstrates the power of the gene therapy approaches.
Okay, I'm just going to go on now to the vaccine story,
which really took place between 2012 and 2020
for the COVID-19 vaccine.
Now, this is, when the, when on Patrick went into the clinic in 2012,
there was nothing you can do as a scientist that has that point.
I mean, it's all the clinical trial.
You can't change things in the middle of a clinical trial.
And so, we said, well, okay, if we can deliver SRNA
and get that to silence the gene in the liver,
it's a pretty big molecule.
It's not as big as an mRNA,
but maybe if we package mRNA in the same way,
we'll get some gene expression.
And so, that's what we did.
And the, what we found was that we could use the,
depending on a particle approach to use the liver as a biorat
to produce any protein we want.
So, think about that.
If you want to win the Tour de France, this is the...
So, is that where we're making spike protein in our liver?
Probably some of it.
Injecting mRNA, including for erythropolietin,
and you get, this is a big model.
Now, you get super physiological levels of EPO
and the corresponding increase in the metacritic cetera in these,
in these animals.
So, this points out to the, there's, so this, this got,
this, this was our whole focus was, why?
There's, there's just an enormous number of diseases,
rare diseases, et cetera, that one can go after using this,
using this, this approach.
But we, again, had another serendipitous event
because we were approached in 2014 by Drew Weissman
of the University of Pennsylvania.
He'd been working with Katie Currico and Drew and,
Drew Weissman and Katie Currico are co-winners with me of the
Geradner Award.
So, they've been working for many years to try and get,
reduce the toxicity of messenger RNA, the immunotoxicity,
and that, so they come up with, you know, they show them by
modifying mRNA, they could, that problem.
So, in a way, right, this is exactly what I was talking about
earlier with too many words.
Currico and Weissman couldn't have done anything that they did
without the products and patents and proprietary
preparation methodologies for the lipid nanoparticles that this
guy came up with.
And they just decided not to give them the Nobel, him the Nobel
Prize for that, instead gave them the Nobel Prize for the
adjustment to the mRNA that they made.
Seems pretty random, also seems pretty useless because they
don't even know what they're doing because they don't understand
the chemistry of the lipid nanoparticles this guy does.
They just bought him.
They just added him to the team, right?
His 30 years of biochemistry and NMR research on how lipids
stick together.
But still, they had a delivery problem.
How do we get mRNA coding for viral proteins into muscle
and immune cells in vivo?
And so, they needed a lipid nanoparticle, obviously, enough
to get the mRNA coding for vaccine into the cytoplasm of both,
say, muscle cells and antigen presenting cells to get a
vigorous MHC1 or MHC2 class immune response.
So, the first thing that we looked at was, or the drew looked
at, was Zika virus.
So, the lipid nanoparticle in this case contained messenger
RNA coding for a surface protein on the supreme membrane
and envelope biker protein on Zika virus.
And so, this was in the mouse model, and just showing that this
is interdermally injected with nanoparticles containing mRNA.
I didn't see the question, but amyloidosis is the process
that leads to amyloid plaques.
Amyloid plaques is just a consequence of amyloidosis.
So, here we are at Zika.
Here we are at Zika.
And I don't know what to say other than here we are at Zika.
It's all the same.
It's all the same stunts.
It's all the same theaters.
It's all the same targets.
It's all the same nonsense.
Are they going to talk about antibodies to the envelope
glycoprotein and antibodies to the premembrane?
I would be willing to bet they are.
For the Zika virus, the premembrane and envelope biker protein,
a bit of the mouthful, and then challenging it two weeks
or 20 weeks with Zika virus itself.
Did they show?
Oh my gosh, they showed microencephaly.
We had Randall Bach on our show, and he's also been on Mark's
useatonic live.
And in his book, he describes in detail how it's pretty sure
that microencephaly is actually not really associated with Zika virus.
That was kind of baloney.
So, that's really interesting.
We are in A-quoting for the Zika virus, the premembrane and envelope
lycoprotein, a bit of the mouthful.
And then challenging it two weeks or 20 weeks with the Zika virus itself.
And the quite remarkable results, and as much as was published in Nature
in 2017, complete protection both at two weeks and 20 weeks
against the Zika virus challenge.
So, this is looking at the viral copy numbers per milliliter.
Nature paper.
Wow.
This is not a direction we were going in at all.
It was only, we were trying to say, express proteins in the liver,
and you got a phone call, and then things change.
Now, in this cause, cutus, it causes to start working with the biointech
to develop an influenza vaccine.
Obviously, that's from a commercial point of view of huge interest.
Now, it turned out that biointech had also been working Pfizer on this.
From a commercial point of view is of a huge interest.
Not from a public health perspective, because we don't need flu vaccines.
This is so stupid.
The vaccine.
And so, in January, February of 2020, all those efforts were switched,
using the liver nanoparticle that we've been supplying to developing a COVID-19 vaccine.
And you all know the results of this, that in November of 2020,
the vaccine was demonstrated to be 95% effective against COVID-19,
independent of age or gender, race, et cetera,
and was reasonably well tolerated across all populations.
This is 43,000 participants.
So, this is certainly one of the larger clinical trials you're ever going to see
from a vaccine, remarkably convincing results.
They expected to produce 1.3 billion doses by the end of 2021.
They were much closer to 3 billion, I think,
and obviously, has been approved in many jurisdictions.
And so, that's really what the, as to say,
we spent 27 years developing these systems.
It's been a pretty amazing journey.
I hope I pointed out how that journey has really depended on some very basic research
and also some good luck, the serendipity.
It's really quite remarkable.
But the point is, it's just beginning.
I often refer to mRNA systems as really being, you know,
the third generation of pharmaceuticals where the first generation,
small molecule drugs, second generation, biologics, monoclonal antibodies, et cetera.
And then third generation, these gene therapies for protein replacement,
you know, you don't have a protein being made, okay, well, let's make it.
Those vaccines, this is obvious.
Gene editing is another approach that we can use to alter gene expression.
So, quite remarkable how these are the broad applicability.
And the other thing that's kind of mind-boggling is we're used to, you know,
developing a drug that might take 15 years and a billion dollars.
Once we've identified the protein that we want to express or silence
or edit or whatever, we can reduce the S RNA or the mRNA
and it's time on the order of say a month or so.
And we can package it in a day or so.
And so you have this really highly targeted personalized medicine available
and it's time on the order of weeks.
So this changes the paradigm of medicine as far as I'm concerned.
It just makes a huge, it's a huge leap.
He's making the same argument that they've been making for a long time
because all you have to do is change the RNA
that you don't need to do any therapeutic trials on it anymore
because it's just like a cassette.
It doesn't matter what cassette you put in the cassette player.
It's not going to hurt the cassette player.
Put Van Halen in there or if you put Miles Davis in there, it doesn't matter.
And that is the dumbest thing that you could ever possibly hear out of these people's heads.
But this is, maybe this guy's more of a chemist.
He believes that the clinical trials are the most remarkable thing ever.
And now we're going to kill Alzheimer's disease and Huntington's and cystic fibrosis,
cancer, heart disease, Alzheimer's.
It's all going away.
All going away thanks to this guy's many patents on how to make small soap bubbles.
Holy crap.
What happened here?
I muted it somehow.
They do that.
So the next few years, obviously other vaccines are certainly in the cards.
Universal flu vaccine, for example, HIV is looking promising.
The chronic diseases, for example, heart diseases.
There's just a paper published basically for heart failure.
I'm sure we can eliminate fibrosis fibrotic lesions in the liver and the heart gets better
using a protein cell approach actually.
Inherited diseases, the obviously replacing a protein that's not being made.
Anyway, the list goes on and on.
And so it's a very exciting time to be in medicine when we're suddenly enabling all of our
understanding of microbiology in a very direct therapeutic manner.
So it's changing the game.
Clearly he doesn't deserve a Nobel Prize for this work.
It might be very creative from a chemical perspective and a right might be quite creative
from a product development perspective, from a methodological development perspective,
from a mathematical therapeutic perspective, from a biological insight perspective,
and I mean if there's anything that you can take from this, the idea that Robert Malone
said this guy should have gotten the prize before them is really
That to me makes Robert Malone sound like a cloud.
Because I was ranting at the beginning, this guy's a real scientist, a real chemist.
He did this, these experiments.
He made these measurements.
The insights that he's gained in terms of how to put these things inside of stuff,
to put RNA and DNA inside of these things and then make changes in animals.
It all works great.
But that is so very different.
Augmenting a pattern integrity that's about to self-destruct, like a man with
head or amyloidosis, is not the same as augmenting a pattern integrity that is currently
operating perfectly with exquisite precision and has the momentum to operate with that
exquisite precision for another 90 years.
Let me explain that again.
It's very different to augment the system.
A pattern integrity that is within five years of self-destruction.
A man with head or amyloidosis, who has less than five years to live and is a
wasting disease.
Augmenting that pattern integrity for it to last longer or to become more stable is
not the same ethical, biological, chemical or temporal problem of augmentation that
augmenting a four-year-old perfect child's immune system is.
It's not the same.
It's not even the same ballgame.
It's not even the same sport.
And this kind of representation that the anecdotal Jesse Gelsinger that didn't
die is evidence that we can use this technology to augment the perfect children
of the world.
It's just so wrong and so ridiculous, arrogant and naive.
As somebody in the chat said, this guy really likes to be bought.
He loves selling his stuff.
He's very proud of it.
But he's no, he's no, I guess I would say he's no genius.
The talk started out amazing and it ended really weak.
Because after all that, all that pomp and circumstance in the beginning there was
really nothing left.
It's just a bunch of soap bubbles and he got distracted by therapies and products and
processes that he could patent and charge people money for.
And his understanding of lipids and his understanding of how lipids are used in
biology, how they're used in cells, how they're used in exosomes, how they're used in
endosomes became secondary even tertiary to the objective of delivering nucleic
acids to cells in animals and people.
That's what I see.
And I agree with the person in the chat.
I think it was Jason M. who said that he likes to be bought.
That's what's very obvious here.
In a fundamental way.
Now, I can't stop without acknowledging all of the people I've worked with for literally 40 years
as I pointed out, as well as many as Mick Hope Tom Madden.
As many such as Steve Ansel, Ying Tam, Barbooie, Paul Lynn, 20 years or more.
And the people that are beautists.
Ian McLaughlin, James Hayes, O'Mileham.
This is a hugely successful collaboration.
Mark Tracy, akin to King Martin Mayor, Madam Madam Heron.
Marcus Ifloni in the chemistry department at UBC who really played a big role in breaking
the whole problem of the ionized lipids.
Now, I think these things work in the brain.
I haven't discussed that, but it's in my own group.
And of course, rewisement at the University of Pennsylvania.
So with that, I'll close and take any questions that's rewisement at the University of
Pennsylvania.
So he didn't thank Carrico at all?
Just Weismann?
That's kind of shit.
He isn't it?
I don't know.
I mean, I know she was on the slide earlier, but I mean Weismann and not her.
Maybe she's not at Penn anymore.
She's at BioNTech, so he doesn't have Doug in here.
Maybe, but he's got other people here.
So with that, I'll close and take any questions that people may have.
Thanks, Peter.
That was a fantastic talk.
And if there's anybody who has any questions, please raise your hand.
But maybe I'll start with.
So silencing a protein is one thing, putting one in that's going to be upregulated.
How do you control that regulation?
How do you know you don't over-expressing a protein?
Have you even talked to that?
Yeah.
I mean, one of the things about this approach course is titradable.
So you can start low and work it up.
The other is that it's not like you're inducing production for protein forever.
You know, you're going to get it going from maybe a week or two.
But that's about it.
And so it's self-limiting in that extent too.
So if you're causing nasty side effects, then no case stop giving it and then things will.
So that would do.
Things will go back to normal.
If it's not autoimmunity, you see how naive they are?
If you're getting bad side effects, just don't give anymore.
And it'll go back to normal.
That's not how...
It's not all of this works.
I mean, it might work that way in a mouse if you don't look very hard.
But that's not how it works in a four-year-old girl.
That's not how it worked in Jesse Gelsinger.
Holy crap.
I mean, holy crap.
That is extraordinary.
My next question.
How often do you think you'd have to give something if you were dosing?
It depends on the length of time that you want.
And also the stability of the protein that you're producing.
Like antibodies, we can make those in the liver.
Say if you put the heavy-like gene mRNA in.
And they'll circulate around for, say, a week or so because they're fairly stable.
Other molecules, you know, might be a matter of a night.
He just said they can make antibodies in the liver.
Have you ever thought about that possibility that they can give you mRNA that would just make antibodies?
Then you're cells that express antibodies in the liver, I guess.
Do they just excrete them then or what?
That's incredible.
I mean, I'm sure it's fine if you make other cells other than the immune system cells make antibodies, right?
I mean, what difference does it make?
B cells, liver cells, who cares?
Anybody's or anybody's, right?
An hour or so.
So it's going to, this is where you're going to see improvements in the technology itself.
You know, a more of a depot effect to have things play out over a longer time.
There's a long way to go in the ways in which we can manipulate things.
And in your delivery system, do you think there's going to be a way to actually target it to different tissues?
So right now you've been talking about getting it into the liver, but how do you, can we actually restrict which tissues?
It's going to be tricky.
That's going to be tricky.
People have been trying to target these lipid or many nanomedicine actually.
That's going to be tricky.
I thought it stayed in the muscle right now.
I thought the COVID-19 vaccine stayed in the muscle.
Is he actually admitting that it doesn't?
In 2022 at a University of Manitoba Gardener Lecture.
He's admitting it's tricky to target it to a tissue.
I thought it just stayed in the muscle.
Oh, wait, it goes all over the body.
And they're admitting it now.
Do you hear it?
It's kind of funny.
It's like they don't even care.
Holy shit.
Being into the liver, but how do you, can we actually restrict which tissues?
It's going to be tricky.
That's going to be tricky.
People have been trying to target these lipid or many nanomedicine actually.
More specifically to where you want it from than to cancer cells.
It's an obvious choice without any success over 40 years of trying.
And that put points out how difficult it is.
You tend to raise an immune response or you put it on the outside.
And you get aggregation and the difficulty of the manning.
But the list goes on and on.
I've worn out five graduate students.
You get aggregation.
I mean, he wore out five grad students.
Holy crap.
And that put points out how difficult it is.
40 years of trying and they still haven't gotten into work.
You tend to raise an immune response or any problem on the outside.
And you get aggregation and difficulty of the manning.
But the list goes on and on.
I've worn out five graduate students on that project.
The last one refused to go on.
That's why I changed your projects.
Okay.
I did that.
But the points.
But there are other ways to go.
The microbiology, you can start to say, okay, one of the expressed in a particular cell.
That requires very sophisticated microbiology.
But I think it's doable.
Oh, there he's talking about cree recombinase or something like that where it's independent.
The mRNA is dependent.
It's expression won't happen unless there's a gene present or a protein.
You could use that too.
That could work.
Then the mRNA'd go a bunch of places and just sit there and you never know what it would do until...
He just admitted it.
He just admitted they don't have a clue where it goes.
They can't control where it goes.
He wasted five grad students on it.
The last one said, if you don't change my project, I'm going to quit.
And his solution is that we can make the molecular biology of the molecule that we're carrying
in the lipid nanoparticle dependent on the cell type.
But that's some pretty sophisticated biology, but I think it's doable.
I'm hurting my tongue now.
He completely admitted it.
The other approach is that things are activated by external stimulation.
One of the nice things you can do with the nanoparticles, we can incorporate things like iron oxide
nanoparticles or golden up.
And then laser or RF or whatever other stimulation you can see.
Oh, we can use radio frequencies or electricity to open them.
Oh, walk in, Robert Malone, please.
Why don't we just bring in Robert Malone from the right side of the stage with his electroporation gun?
They say, OK, turn something on here, but not here.
So there's going to be approaches that will achieve that.
There's going to be approaches that will achieve specificity in the targeting of lipid nanoparticles,
but we don't have it yet.
We're sorry, but all you people that took the lipid nanoparticle and thought we had it.
Sorry, we didn't really have it yet.
But we're going to get there.
It's coming just over the next hill.
Any questions from the audience?
A question here and then a question way at the back and up there.
So we'll start here.
I'll go up there.
So please, loudly.
All right.
Very nice computer.
So I mean, it's sort of alluded to that open, but with mRNA, our ability is obviously a kind of limited expression
so that works well for an acute disease or a vaccine.
But any work on DNA, the research then says it's going to come back
and we'll be able to see if it's an integration or say an internal coming to be where you don't have that.
Yeah, we worked on it without any success.
I mean, it's commonly used in cell culture for context.
Absolutely.
I mean, in cell culture, you've got rapidly dividing cells.
He said it's got to be used in cell culture for transfection.
But the problem is that for cells that are not rapidly dividing,
and so therefore the nucleus isn't, you know, you can't get things into the nucleus as readily,
then these systems don't work.
And so that's a, which is, you know, we certainly haven't beaten that one.
Jason M, you're totally correct, but we had already busted that.
There's no frickin' way that Robert Malone didn't know that they hadn't solved this problem.
There's no frickin' way that he didn't know that.
And him saying that is just a bald-faced lie, but they're liars.
They are liars.
Remember, Robert Malone gave a talk in front of the who about flu vaccines
and flu vaccine fill-and-finish technologies.
And after he finished that talk in 2011, he was thanked by Rick Bright.
Robert Malone has been in this space.
A vaccine technology and brokering of vaccine technologies
between non-governmental organizations and governmental organizations
for more than three decades.
Robert Malone has been in this space of gene delivery
and RNA delivery for three decades.
And there's no way on God's green earth that he didn't know
that lipid nanoparticles had no means of mechanistically targeting a tissue.
Never mind that it could stay where you put it.
He knew it was exactly the opposite, and he's a liar every time he said that he thought that they had solved it.
And he and other people are responsible for all of the damage
that has been done by this horrible, poor excuse for a medical product.
They're all responsible because they all knew.
He also knew.
He knows that they can't make it stay in the shoulder.
He knows that they lied about it.
Every time he's heard someone talk about it, he knows they're lying.
Yeah, we're feeling pretty good about having God's power if he's gotten,
but yes, there's other barriers to get through for sure.
Yeah, yeah, and there's no doubt we can get DNA into the cytoplasm
in the same way that we can, or that messenger RNA,
but to get it into the nucleus.
At least for non-dividing cells, we haven't achieved that.
Oh, yeah, no, we're fiddling around with every possible...
Well, we really haven't figured out.
I mean, it's coming to light now a little bit,
but are the structure-activity relationships between the structure of the lipid nanoparticle
and the actual activity in vitro and in vivo.
Well, those things are starting to become elucidated.
It's quite remarkable.
You have a very successful medicine,
and we still don't understand some of the basics of how it actually works.
We have a very successful medicine,
but we still don't understand how it works.
Actually, I think you're unaware that it doesn't work.
I think you have been misled to believe that it works, but it don't work.
Holy shit, I can't believe it.
So, you know, those things are becoming pure.
A lot of it has to do with manipulating the various components that we have in there.
I'm sorry, I can't hear the question anymore.
I don't know if it's worth listening anymore.
We've already caught him on the worst one.
We've already caught him on the worst possible thing he could have said.
And that is that we don't know how to target places.
Yeah, we can't make it go anywhere.
We don't know how to do that.
So, it goes to the liver because it goes to the liver because that's what the liver does.
It cleans stuff out.
So, a lot of it will go to the liver.
It could go to the bone marrow.
It goes wherever we said it goes.
And it goes random because he doesn't know how to control it at all.
He burnt five post-docs on that project.
The last one threatened to quit.
We're trying all kinds of stuff.
But it's crazy.
We have a working medicine.
We don't know how it works.
We have been completely and totally bamboozled.
Even this guy has been completely and totally bamboozled.
That his bullshit works.
It's extraordinary.
You want to link to this video?
It's just extraordinary.
I just can't believe it.
I thought it was going to be kind of a fun video at the start.
I thought we were going to hear some really intelligent guy.
Real smart dude.
Tell us all about the limitations of his work.
It turns out it's just, you know, serendipitous that they were able to make something that ended up saving the world.
That's how science works.
I guess it's just serendipity.
Although we still don't know how it works.
We still don't know why it works.
We're still not really, I mean, wow, I'm just, I'm a loss for words.
I'm fumbling really bad here.
But obviously these guys believe in pandemic potential because they think their technology saved us from it.
And they're Canadian.
So it sounds like they're pretty down with the inversion of individual rights to community privileges.
If you don't take these highly effective.
What an illusion of consensus we have to fight my friends.
What a terrible place we live right now.
Where the who can invert our understanding of respiratory disease can invert the way that we treat respiratory disease to lead to a higher cause, all cause mortality.
But the TV and social media could lead us to believe that an RNA molecule did it.
And RNA molecule did it.
And it was a RNA molecule that's been pretty consistent all around the world for like four years now, except for one part of it.
And this lie is going to, it's going to deceive our children and our grandchildren.
And if we don't dispel this lie, our grandchildren will be enslaved by it.
This illusion of consensus will enslave our children if we don't break it now.
And we don't have that much time.
We got about a year.
Bobby's book is coming out in December 5th.
And from that point on, we have about a year to break it and break the illusion we must.
Because people are still solving the mystery.
People are still believing that we had to change our mind about these things because it was a novel virus.
And people have still not taken into account how many people were killed by these protocols.
And how many people were killed by some novel thing, RNA.
People are not talking about this stuff anymore, ladies and gentlemen.
It's me and Mark and crickets.
And it shouldn't be this way.
This illusion of consensus about a laboratory leak needs to be broken.
We need people to understand that they have taken a natural phenomenon, a natural noise signal and turned it into a consensus about a laboratory leak.
By fooling us into believing that something was covered up.
I'll tell you what was covered up, that the PCR test is bogus.
I'll tell you what was covered up, that there are coronavirus signals everywhere that we can't really track and follow with any fidelity.
And so we make shit up and we use infectious clones to try and approximate them in a laboratory.
Nobody's talking about that.
Protocols were murder and transfection is not medicine.
It might have been an infectious clone. It could have been a transfection agent.
I don't care what you call it, it wasn't no viruses.
Because we can make infectious clones and we can make exosomes and we can make self replicating RNA.
And we can package that in little tiny, little tiny vesicles.
You don't want to call them viruses, don't call them viruses, but transfection works.
Transformation works.
And these things can be sprayed.
That's it.
The protocols were murder and transfection is not medicine.
The players will continue not to address the PCR as fraud.
These players will continue to address the variants as real and unquestionable.
They're not going to talk about death certificate fraud or whether the RNA is pure or not.
They're going to focus exclusively on our DNA contamination.
They're not going to talk about protein folding and how that impacts the potential epitopes that are generated by a codon optimized pseudo-uridine substituted version of a viral protein.
Not going to talk about transfection in general and the fact that it doesn't really work except for in limited circumstances where a biological pattern integrity is about to be destroyed.
By cancer or had or amyloidosis.
And all of these same people are not talking about natural immunity at all.
They never have.
They've never given you an immuno 101 lecture.
Never mind a six hour one.
That's how I see through all these liars.
If somebody says they're an immunologist by training and they've never done an immunology lecture online in three years of being a dissident, they're a liar.
They are trying to invert our sovereignty to permissions because they want our data.
More importantly, they want our children's data.
Most importantly, they want our children's children's data.
This is a long game for all the marbles.
And it starts here, intramuscular injection of any combination of substances with the intent of augmenting the immune system is dumb.
And transfection is not immunization.
We need to teach our grandparents this, our parents this, and our children this.
Or they will be enslaved by this mythology for the rest of their lives.
Ladies and gentlemen, stop all transfections in humans because they are trying to eliminate the control group by any means necessary.
I'm just going to keep pushing through.
Either I'm going to completely lose my voice or it's coming back soon.
I like my new hat.
Bessel Park Black Hawks.
Pittsburgh.
Thanks for joining me, guys. I'll see you tomorrow.
42, 42, 42 in a row, baby.
Thanks for being here, guys. Good to see you, Jeff from Earth.
Good to see you again, Christie.
Grace Southwick. I haven't seen you here in a while, but thank you for being here tonight, Andy Rock.
And Madarina, thank you very much, sir, for being here and being the doubter in the group or the critic in the group.
I really appreciate you being here and still keeping it real.
Lisa Simon says, good night.
Sue Spider.
Welcome to Eagle.
You want to be a guest on the show?
You want to be a guest on the show sometime? Welcome to Eagle.
There's a lot of people at the Defender that are interested in hearing about your bears reporting.
And they would like you to be on the show, so maybe you need to send me an email.
See you, guys.