You
I
Guess I didn't update the stream. Yes, this is part two
I'll update the title later. I guess I thought I updated it here on my OBS
But I guess I didn't push the button done and so that it did not date my bad. This is part two. I
Shall do it
I'm afraid that the latest data tells us that we're dealing with essentially a worst case scenario
I
Think truth is good for kids. We're so busy lying. We don't even recognize the truth no more than society
We want everybody to feel good. That's not that's not the way life is
We should be okay here. I'm just gonna check this one. So I'm back from the gym
I thought I'd get part two done before tomorrow
We're eventually gonna be doing a show a day or two shows a day one at 10 10 and one at 13 13
So at 10 o'clock and one o'clock
But you know we got to roll slowly here and make sure that we we build this momentum
Intelligently and one of the things we're trying to build momentum around is this whole pre-on biology stuff
And there's a there's a lot to learn and so we were gonna finish the video that we started earlier
Thank you very much for being here. See you in a second
This episode is sponsored by mink that's moo plus like
Mm-hmm
This my point is that if if we were able to just like we're trying to get everybody to take the vaccine if we had
Put that into getting everybody to take hypermectin and fluvoxamine for for a month
If we and if we could accomplish that then COVID would be wiped out
We could do it and actually any municipality that could regulate its borders could clear the disease
But you can tell if someone's lying, you know, you can sort of feel it in people
And I have lied. I'm sure I'll lie again. I don't want to lie
You know, I don't think I'm a liar. I try not to be a liar. I don't want to be a liar
I think it's like really important not to be a liar
I mean that stands alone as like one of the best
Rapid fire statements made by anyone
Ever maybe in mainstream media
You
I
The meter this always looks like it's really soft, but it actually is always really really hard in my ears
Let's do it
Sweaty bombs, this is so crazy like these bumps. This is so crazy. I feel so nervous like what in the world man
Oh
Big-time brick
I'm glad somebody noticed that that was a big-time brick. I'm not trying to represent myself as some kind of baller here
That was the whole point of making it a real real clip one good shot one brick
That's about what I'm good for. I don't think that's that bad though
If you've been following along for a while you're here at the top of the wave
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Still trying to break the same illusion
Sometimes it's nice for having a little live Eric Johnson Evan root fever to try and help
Establish the mood that it's necessary in order to
Engage in United non-compliance is what you're really doing here
When you come here and try to discuss the flip side of the biology on TV the flip side of the biology on
Social media and so today we're going to keep up the good work
That needs to be done
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You
Thank you very much, this is giga ohm biological a high-resistance low noise information brief brought to you by a biologist
24th of April
2024 we're on our second stream of the day, but that shouldn't be something we should be applauded for
We need to do more and there is a lot of work to do
Sometimes it's just it's handy to be ready. We were ready for this
We've been preparing for this video for a long time and it's actually so far been incredibly revealing
And so I want to start first by kind of reframing where we are again
This is about a principle of informed consent
I'm gonna escape out of here for a second just to make sure that this is going where I want it to go
This is where I want it to be I'm gonna skip a couple of those slides
It's always smart to make sure you are where you need to be so we've talked about these TV scenarios where there's either a lab leak or a
Batcave virus, so maybe there's nothing at all
And how these things have generally
Hearded the vast majority of people in West Western civilization to accept a faith in
What is essentially a novel biology? It's not just a novel virus
But the whole story of a novel virus and how it has behaved in the last five years
constitutes a novel biology because first of all the precedents of a trackable gain of function
RNA because we need to be very honest with the people in our lives about what is essentially the story the story is not a virus
with lots of little gears and wheels and and
Enzymes and magnets and mitochondria inside
It is simply an RNA molecule wrapped around a
protein called the end protein and that is contained within what is essentially a cell membrane a
Lipi protein coat lipo protein coat
and
So coronaviruses as they are presented to us are nothing more
than a
nanoparticle with some RNA packaged inside of it, and so by the
The broad understanding of the rules of biology that
that model
then
dictates that whatever properties are
contained inside of an RNA pandemic are
emergent properties that are contained within the actual sequence of that RNA and indeed that is the story that many people have
been telling us from the very beginning that a fear and cleavage site that HIV inserts that
homology to a staphylococcan and teratoxin B protein could be partially
explanatory in terms of the severe COVID that we see in some places or the long COVID that we see in some places
And this mythology is extraordinary because at the heart of it again
I'm going to say it one more time is an RNA molecule that because of the actual content of its sequence the actual
Order in which the bases are found it is capable of doing something that otherwise all other RNA molecules
never even
Never even it doesn't cut it doesn't happen
Now the flu viruses is RNA molecules, but the crazy thing is is flu viruses are
Supposedly packaged with some enzymes
So even flu viruses have by definition even more gears and wheels and little motors in there
Then a coronavirus a coronavirus is actually just an
instruction module and
if that instruction module is read then
Apparently it makes copies of itself
But the point is is that if that instruction module has a fear and cleavage site or it has HIV inserts or it has
homology to to a
toxin protein
That now it can cause a pandemic
So the second part of this is that
Transfection was waiting in the wings for a very long time
Just waiting for the right opportunity to come and save mankind. I mean the whole species
and
Since we rushed it since we tried to make a lot of money and cut corners or whatever it is that we did
Or because we weren't liable. So since we weren't liable. We cut corners
That some people were injured because of the contamination found in some of these
And some of these countermeasures now keep in mind one of the major
Lawsuits that's currently moving through the courts is a lawsuit
To do with contamination of remdesivir vials so not even the use of remdesivir. Yes or no, but
Contaminated remdesivir and so you see
then when you realize that they've been talking since
2000
Wow a terrible weatherman 2020
About the spike protein being the center of this whole mystery
The spike proteins interaction with ACE 2 the spike proteins ability to cause multi-system inflammatory disease or whatever it's called
The spike proteins targeting of the heart muscle the spike protein being
amyloidogenic the spike protein being a pre-on or having pre-on-like sequences in it
Has been confounded from the very beginning
With the ability or the propensity for
transfection or transformation technologies to
result in
Pre-on-like disorders or whatever these things are like crowds felt the occub in the paper of Luke Montenier
The reason why the paper of Luke Montenier is so important is that it came out very early
and yet those people had been actually
They had been transformed with an adenovirus carrying the spike protein gene
So they had been transformed they had not been infected and
Of course right away the people were arguing. What were they arguing? What were they arguing?
They were arguing that maybe those people had been infected before they were
Before they were vaccinated
And so already they needed to clean the narrative already they had to cast out already
They had to speak up
Because the worst-case scenario was already under threat from the very beginning the worst-case scenario
Narrative centers always on the spike protein even though there are 29 or 30 other
Proteins that have various isoforms that can do all kinds of things most of which we don't know and
Yet we are hyper focused on the spike protein the spike protein is what's used to make the phylogenetic tree
The spike protein has defined all previous
Coronavirus variants in the past if you look for new SARS viruses
You don't look for new N proteins you look for new spike proteins
and
Part of the reason you look for new spike proteins is not because the spike protein is the most variable gene
It is because it's the most abundant
subgenomic RNA
and
We've looked at the infectious cycle since early sixties through the 70s 80s 90s
And now all the way up to now with nanopore sequencing and we keep finding the same weird ratio of almost no
full genomic RNAs, but
orders many multiple orders of magnitude more subgenomic RNAs
Predominated by spike protein e gene and gene
And so when you look for those subgenomic RNAs
You're looking for a signal that is expected to be there and many many many many many many orders of magnitude even in their
most honest appraisal of
the infectious cycle of their entity called coronavirus and
So so much of this biology is almost wholly based on the cartoons they draw rather than on the experimental results that they've obtained
So much of this biology is based on the cartoons
They draw rather than the data and the experimental results that they have actually obtained
And that is the reason why this story is so complicated and needs to be obfuscated by people who say well
There's just no viruses at all
None of the viruses exist
And
So it is a very very complicated trap that we find ourselves in and prions as part of that prions and
Understanding what they are and what they're what they aren't if they're anything at all is
Extremely important
And as with virology we would be very very
It would it was we're risking a very very big error if we assume that the biology that we've been given or told or led to assume
As it would be because none of us have studied this intentionally until recently
That we really understand to what extent any of this stands on firm ground and so let me switch over to the the desk here
One of the things that I would like to start out with with this with this second part is
Just to kind of review about what he said in the first part
One of the things that he said in the first part was in the beginning and I'll give you the example
I think I have it up already
Don't I have it up already?
If we go back to the beginning of this you can find that one of the
One of the things that they were doing first was trying to optimize the production of the disease
So first they couldn't find it
Right it was very hard to achieve some kind of enrichment of the disease
Agent and so he used two different graphs here to show you where the sucrose agent
He said well darn it
He said what you would expect to see is some kind of peak right some kind of peak over a certain place in
The sucrose gradient, but you instead you see all kinds of a smear now
Here's one of the things that I find already very interesting. Let's go back
to the other the other
Let's go back here
This is the the nature pre-on paper that we've we've referenced a couple times now and lead up to this discussion
And this is perhaps a little bit better drawing. It's a little more up to date
This is the pre-on protein, right?
Can you see oh sorry?
This is the pre-on protein the protein that is on the outside of the cell that we don't know very much about what it does
but it's for sure on the outside of the cell or on the inside of lysosomes and in the basal state
It does something but in the in the pre-onogenic
State or the prey I guess in this case it's PRPC
And then this is a pre-on. Sorry. I had that wrong. This is the regular
Pre-on protein and you see three alpha helis is there and then here you see the pre-on protein
And it's many of them all layered on top of each other. That's what you see there
And the implication is is that it's some kind of little fibro right there all layered on top of each other
So this is already several pre-on proteins that have folded incorrectly and then induced it on one another
And then this one can look induce the blue one to join them you see that
And so this concept implies a couple things if we believe that the sequence of a protein is very much
related to how it folds and
So the potential for it to fold
is related to its sequence means that it was should at least in this model and it appears also to imply that it's not able to
Able to make any other proteins fold like this
But it can make
proteins with the right sequence the the protein pre-on the pre-on protein
sequence
so what I find interesting about the
What I find interesting about this figure in the in the video that we watched earlier today is that this
Is still seeming to imply that there is one protein now if there's one protein that makes
Aggregates, what can we predict? What's the model right? That's what science is all about you have a model
And then it makes predictions about measurements in the future and those predictions if
If done cleverly or or or tested cleverly
can provide fruitful
Guidance to the experiments that should be done
So let me just take you over here and let's talk first about the the concept of pre-ons making more pre-ons
By
Coming together right pre-ons press pre-ons equals a fibrel
And that was also what he was talking about with regard to amyloidosis and
Amyloid I guess be in the same thing really just different sides of the same coin or something which I called out before as being nonsense
But I don't so I don't want to imply that I'm I'm saying it here
But let's just talk specifically now about this model and the idea that the actual profile that they measure in this sucrose gradient
is smeared across densities which means
Apparently not one thing and the argument that they might make is one where they would say
Sorry, they would say that that the
That the pre-on
protein is is
making
Fibrels in those fibrels because they're multiples of the the pre-on protein
Then they're going to be all across that sucrose gradient, but that's not entirely
accurate because if the pre-on protein weighs
X
then two pre-on proteins will weigh two X and the and the in a gel like that you're going to get
Lines or in a sucrose gradient you could get lines where okay
Well, then this is you know two and then this would be five and this would be eight or whatever right?
I mean you can actually count it because it would move up in increments by weight
because they move through these things by weight or by density and
So in a sucrose gradient if they don't separate by density there might be a way to do it by charge in a
In a gel, but there must be some way to show me
That these preons are working together because if they're if they're they're coming together in multiples
Then the multiples after digestion should become visible. They should be small fractions of the things that aren't digested
And yet somehow or another this part of the model which I can show you again is very clearly visible
Here
That's exactly what's implied by this nature paper from not too long ago
and in fact, I think a lot of what Stanley Prusner implies in his
Oops, sorry about that. I'm just losing my buttons here implies in his
In his slides and so that's what I'm a little
Frustrated with in regard to that, but we're gonna keep going because there's more we're gonna we're still reviewing this
So then he said that one of the best things that happened if I recall correctly is that they were able to get yet there it is
The mouse model took a really long time. It took like a year and 60 animals before you could I guess
Decide whether there was was scraping protein to analyze for but anyway, they got something to work much faster in hamsters
And I'm still I it's still homework for me to figure out exactly this what the story is on this slide
But the point would be that after this they now managed somehow this next slide suggests that they got the incubation time bio assay down low enough
So that you didn't have to waste a lifetime as he said made jokes and people laughed about
Waste a lifetime trying to wait for this stuff to happen so that you had something that you could use I guess to put in other animals heads
And try to make the disease move from animal to animal
So then he tries to purify using detergent extraction nuclei
Digestion and protonase K digestion and after all of that stuff there's still some
Pre-on protein present right because it's it's resistant to all of this stuff
And so then that helped develop this concept that even after they get rid of the the nucleic acids even after they use detergent
There's still something there that apparently causes this this
Well, this disease stayed at some point when they injected into the brains of animals
But already this this started to fall apart a little bit. It seemed already like
Hand-waving and so then he moves on farther
And he gets to this crucial point here where they're using knockout mice
and
In the well, they're using knockout mice and regular mice
But anyway, the point in this picture was supposedly we could let him say it I guess
Is that here you have the pre-on protein and then here is where you take that protein fraction and you digest it with
Protonasis enzymes to cut the protein up and then essentially everything's gone
but in the
Pre-anagenic state or in the in the scraping state
Then when you digest these proteins which are different proteins apparently then are in lane one even though
This is supposed to be the control and this is supposed to be the experimental group
And then you digest that fraction what you are left with is still a
Fraction, I guess it kind of a similar weight as this one and so then the argument is
that this represents the
Pre-anscrapey form that is
Undigestable by these protonasis that it's gone here because it wasn't present in this fraction in the healthy animal or in the
The un-un manipulated animal we could listen to see what he says there again if you want
Just to see exactly what anybody talks about destroy the protein we destroy the infectivity or every time we destroy the infectivity
the protein was removed or
destroyed and
when we
Eventually figured out what was going on we found that there was a normal form of the protein in all of us now
This is a gel and the proteins migrate and the smaller they are the faster they migrate through this gel this porous material
sort of like jello and
Then we can stain them with antibodies
And so what we found was that the protein was a protein in all of us
Which is a normal form of the pre-an protein and when we treat with enzymes that destroy proteins the protein was completely destroyed
But in the brains of these hamsters that became ill with Scrapey
What we found was that there was both a normal form of the protein and another form of the protein that when we treated with
The enzymes that destroy proteins there was a residual piece and here now this is funny
I didn't catch this the first time but he was using antibodies here
He gee he shows us later in the talk that there are antibodies that bind one and not the other so why do we know that the antibody
He's using here doesn't bind the fraction that's left here
Maybe there is a fraction here, but the antibody doesn't bind it whereas it does bind it in this form
There's lots of weird things happening here because we use antibodies so
The best word I guess I have is laxidazically at this time in science in 2002
we were still holy clueless to the bouquet of
Molecular variation that's found even in some of the best what were presumed monoclonal antibody preparations. It's a really interesting
Signal here too because you know if the resolution is
Like this with all this noise that he doesn't feel like he needs to explain
Then you can already see that something interesting is happening here. So then they say
Something about the structure of the pre-an protein and that then the normal form
it has these three alpha helices and then in the
Infectious not so good form. It has more beta pleated sheets or more beta helices in this region
And then they go on to say that when they digested these guys
They found these pre-an like rods or pre-an rods
According to the guy that he was working with after they cut the N-terminal off of
the pre-an protein in vitro and later this structure was apparently
Compared and considered homologous to amyloid protein
Plaques or or fibros that were found in the brain of amyloid disease or the hundreds many many many diseases
Apparently according to to Stanley that do the amyloid thing
Then he told us about this crystallization that happens when you make enough of it and how they used
x-ray crystallography
To start to study the formation that they make and what formations they can make with one another as subunits
Inside of that crystal and then that allowed them to kind of understand indeed that there was there were these three alpha helices
and confirm that and so
Then he showed us this picture which isn't very unlike the infectious cycle to tell us exactly how this happens
The pre-an protein gene is expressed
The protein is manufactured inside of the Golgi and expressed on the chant on the outside of the membrane and then it can also be
Taken in in some of these
Evaginations and then I don't know at some point. I guess it's something bad can happen
We don't know what it does
Which is really interesting
So then
He told us about this other gene that's in the family
He said that it was very much related to it and that it had the same three alpha helices
But these same three alpha helices only have about a 25% amino acid homology
With the pre-an protein alpha helices, so I met made the point that that doesn't seem very homologous to me
but
because again alpha helices beta pleated sheets and beta
Heloces are all general structures that can be made with chains of amino acids and one is
many different combinations of amino acids can form these these forms and so
the particular shape and form and
Hydrophobicity of each of these alpha helices might be very different depending on the combination, but the the general shape is not so
Decimilar and so it's it's that's the reason why you can go through a sequence and identify that this is an alpha
He was even though it's only 25% the same as this one
It's more of the what repeats when and that kind of thing
and
So that's another gene that they're that he's now kind of saying might be related to this stuff
then he starts talking about crowdsfeld yachob in in families and
sometimes it's
evidence of
preons getting into humans is 20 years or 40 years later
So we could still see the effects of eating preon infected meat 20 or 40 years later
which is very convenient in 2002 because that could actually be right now and and
timed perfectly with
Transfection to cover it up and we could just turn around and say well
We shouldn't have been eating meat for the last 20 years at least that's what he definitely implied
There was also in here some stuff where they were
Bovinizing mice, but it was a little bit of hand waving and nonsense and I still think it was probably over expression of protein rather than
Replacement thereof then he talked about that was where this there it is the bovine the bovine
the bovinized mice
So they over express a bovine
Probably under some kind of conditional promoter they over express the bovine preon protein and then they show that that
makes the mouse
susceptible to the bovine sponge of form encephalopathy, but not the other ones and so
Kinda demonstrates that there's some specificity
to the different agents, but the different agents are all basically coming from the same
Protein, so I'm not really sure, you know, we'd have to go through all these papers to see how
Biologically useful this model is or whether it's really just you know injecting junk in animals heads twice
and
Then we got to the yes
these are some more antibodies and whether they bind or not and this is just showing you that they they use antibodies as a way of
probing whether certain parts of a protein are present or not or whether they're
Available for antibody binding or not and to a certain extent. I think this makes some
Sense, but it would really requires very clever controls and very astute
Alternative experiments to support and so I feel like a lot of times in this talk. It has been used as kind of a hand-waving thing
Here I'm gonna prove to you that these things fold differently
And the way I'm gonna do that is use antibodies that bind and don't bind and I think that's a little bit of
Yeah, anyway, I think that's a little bit sketch then we might be right where we were wanting to be I
Think
Think we might be right where we wanted to be we stopped here because
we were looking at the regular prion protein of the protein in this great escapee form and
How degradation took longer in these neuroblastoma cells and I was kind of angry because I didn't understand how they were
Expressing the same protein that folds in two different ways in these
Separately in these cell lines it seemed to imply that they knew a sequence that was different or something and I didn't understand that
So I said this is a PRPC and defined what is called the house
So I said that we had I had to look into that
So I think that's where we are right now
So there's a few things that just don't really line up
But now we're gonna go into more of the chemistry and messing around and I think we're gonna see more of the same kind of
weird bridges being made that aren't really
supported by very much evidence just conjecture and cartoons, so let's see half life for formation very rapid and
David Borchardt working here in San Francisco
Confirmed that and then showed that the half-life time for degradation is about six hours and that PRP scrapie was made even more
Slowly with a half-time of formation of about three to ten hours now
I had thought that PRP scrapie was complete granite and that it was never degraded
But in the last slide that I showed you this is really represents the degradation of PRP scrapie
the loss of prions from the culture
And so we were able to calculate a number as I mentioned before where 50% of the PRP scrapie disappears of about 30 hours
This has important implications for thinking about all the general
You know it could be that they just stain with these different
Anybodies that they claim are selective for the proteins and when the stain goes away then they say the proteins are gone
If there's some indirect measurement we would have to look into it diseases
It tells us that cells are capable of degrading both PRPC and PRP scrapie
And it raises the question whether PRP scrapie is normally found at very low levels in normal cells and has a physiological function
And that is a very appealing way of thinking about all of this because it makes much more sense than thinking that PRP scrapie is something totally apparent
It raises the question of whether or not we really have an issue
It's a kinetic race between the formation of PRP scrapie and the cells ability to clear PRP scrapie and that when the cell can keep up with the
formation and clear it like it does with other protein all other proteins in fact that when that happens everything is functioning fine
But when the cell gets out of balance see you almost felt like you had to make that point
That all other proteins fold incorrectly and we have to do it
We have to get rid of we have to degrade all other proteins and we do I'm not saying we don't
I'll let I'll go back just so you can hear it again. I didn't interrupt
It's a kinetic race between the formation of PRP scrapie and the cells ability to clear PRP scrapie
And that when the cell can keep up with the formation and clear it like it does with other protein all other proteins
In fact that when that happens everything is functioning fine
See so that's that's the place where we stopped where really the model is and let's let's let's be clear
We want to do the model the model is that
the pre on protein and
Pre on protein folded incorrectly with the SC superscript
The scrapie protein are produced by the same process
But one is takes longer to degrade and so even though maybe smaller
numbers of
This confirmation come out of the ribosome. They take longer to degrade and so the kinetics of degradation
Play into this and that's what can also make the
onset anywhere from 60 days to
to 40 years as he says
And in theory that kind of makes sense
It sounds like a fuse that could have any length of time depending on the exact parameters of by which it burns
It's also a very convenient story that makes a lot of predictions that should have sort of
Easily testable experiments that can grasp or can get can get at those ideas
So let's listen as he develops this idea where again remember pre on protein in its good form and
Pre on protein in its pre on a genic form are present at all times in all healthy animals
and
That it is only the kinetics of degradation and production that over time
Can result in a preponderance of the scrapie form which can then of course cause this fibro formation, etc
So the whole mechanism isn't quite understood yet, but the ticking time bomb part the one
Molecule part doesn't really make sense anymore because according to this story. It's not just one molecule and now the ticking time bomb starts
You see that's a this is a very different model if you're just gonna flip flop between those two models or
If you're gonna say that Stanley Proustner in 2002 did know what he was talking about and
Just one molecule is enough to cause this disease
hmm interesting
But when the cell gets out of balance it can no longer clear PRP scrapie at the rate that it's formed
I'm talking about very very low levels that we can't detect even buying these animal assays
Then something goes awry and we began to accumulate more and more PRP scrapie and eventually the animal gets sick and goes on to die or the human being
Now I promise you a little chemistry at the end
And if you just look down here at chlorpromisine this is Thorazine
This is one of the first anti-psychotic drugs, and this is the structure of it has these three rings and when Carson Korth added one micromolar
This amount he still saw these protease resistant bands this so the different the three bands are the ones with no sugars one sugar chain and two sugar chains
They're showing a little better here. So what is this?
Is that dr. Drew reason a lot of what I've talked about today
Hilarie seems like cyber is only mode right I mean remember in 20 in 2019. I was fully a believer in vaccines
I didn't know about any of this. I thought it was a godly goop. So so this is fabulous because here's what you got here, right?
Here's what you got here
You got a guy
who basically is one of these many people who now who's an old man who's using testosterone and pushing
pharma products
Here you have a guy that from every other lawyer I can tell they don't take him seriously
They don't think his pedigree is any good. They don't think his arguments that he makes are any good and they're pretty sure
There's something up
Like lawyers not me other lawyers people that I trust and people that I don't trust they're all unanimous that this this can't
be someone to take seriously
And this person is a person whose whose daughter was on Alex Jones at least twice
In the run-up the year before the pandemic
Had a million subscribers on YouTube before I guess jokingly threatened to go to the house of the YouTube CEO and kill her or him
And we're supposed to believe that a retired pharma exec who sold her company to Pfizer by the way and was helping them
I guess testing
People before they tested them so that they if they had cardiac problems that they wouldn't be in the trial and you know
I don't know
maybe better ways to read the QP wave or whatever it's called and and and and the whole point is
Is that it just seems like all the people that are managing to get anywhere with regard to getting their message out
I've always been stepping in front of other people. She has stepped in front of Catherine Watt
She has stepped in front of Craig Particopper
She's been on stage with Robert Malone in Sweden
When the pandemic was still hot and heavy
This guy has been the lawyer of
Andrew Huff
The guy who says that he shot over a hundred and fifty rounds into the woods of of the upper Michigan forest surrounding his house
While he was combating the state police
And now we're supposed to believe that this is this is the these are the people on the white horses that are coming to our rescue
Please we can't possibly take this seriously
This isn't even Fox News level serious
And and to give it airtime or to think that oh we got to get their attention
That's playing right into the game even if even if this man in the middle isn't sophisticated enough to know he's being played
I assure you that
This is a play
And it is a play that that was
Either put in place very early ready to go or already
Ready to go and then some like they were this was always where we were gonna be but I don't think that's the case
But these are always the people these were always the people that were gonna be on the stage that there's no question about it
Brett Weinstein was always gonna be on the stage. I
I
Think Robert Malone was likely always gonna be on the stage. I think
Steve Kirsch maybe was
Very early on
Not gonna be but wanted to be and got on the stage. I think there's a lot of people that
Were kind of reluctant at first didn't think that we would be where we are at this stage
Who are on the stage reluctantly?
Once you sign the page, you can't get off. It's a national security
operation and
So now remember if this is the controlled demolition of America that it makes perfect sense that many of these people would be involved
most of them being privately
rich privately okay with the collapse of America privately okay with the gross over inflation of the dollar and
That's the point here is
That the people who are rising over the last four years the people who get censored and then get on tucker and complain about it are all
independently wealthy
Already intimately connected to the very machine that none of us have ever gotten anything from
None of us have ever sold the company none of us have had multiple consulting companies that worked with the DoD Ditra
none of us have ever sat on on on
DARPA grant committees to evaluate DARPA proposals
none of us have ever gotten the benefit of
taxpayer-funded data
From your university to start a company and then sell it
But all of these people have
All of these people have a book
What we're dealing with here is a controlled operation to make sure that you stay focused on
Something that will not prevent the controlled demolition of America will not prevent us from coming together
But we'll instead keep us fighting about things like where the virus came from or what killed people or whether viruses exist at all
There is no way that it is random
That soaf was on Alex Jones three times in
2019 and now we are listening to her mom for three years as
part of the
alternative
COVID narrative that involves a novel virus that killed millions of people that millions more were saved from
That was definitely gained a function or a toxin that was
sprayed on the world by the United States Department of Defense
Which was a great way to
implode America in a way that
Turns everybody on everybody else. It doesn't realize that the military is a victim of this too
the average
Serving soldier is a victim of this too. They have to follow orders
It's the people above
Lieutenant Colonel now those are the people we need to be holding to account. Those are the people who put the mandate out
Who gave the orders down the chain?
The people at the bottom of the chain cannot be blamed for taking the orders or following them
They are victims of this as well and yet. Who does she want us to blame the Department of Defense?
Without any more specificity than that without any more chain of command to the Department of Human Health and Human Services for the
Department of Homeland Security for DITRA
Nothing's State Department. What's that?
And this guy as I said is not a legal scholar is not some kind of courtroom killer
This is a guy who is a very very very below average lawyer
and
He's probably in way over his head. He's probably not even a bad guy
But people
smarter than me
Do not take him seriously and so the idea that either of these two take him seriously that either
Dr. Drew or Sasha take him seriously it begs
I'm I find it dubious. I find it dubious and and I don't think that
Hey, I just don't
I don't buy him. I don't buy him. I think that we are
You need to be very pessimistic about the number of people. I mean look at how much fun she's having
Americans were murdered ladies and gentlemen and
Children are having needles forced upon them and adults over 50 are having needles coerced into them
As we speak by this system
And it is based on this mythology of a novel virus that is not being questioned here at all
I can guarantee it. I mean they're looking how much fun
it's so much fun to be on dr. Drew's show and
Dr. Drew's weed is so good and
Tom Ren's is doing the right thing. He wants to do the right thing. That's all possible. I guess
But I just don't see it I do not see it if he is used he is used he is not
I'm sorry, but I just I don't see it. I don't see it at all. It's unfortunate, but I just don't see it
And i'm not going to subscribe to
To dr. Drew. I don't think it'll get me in anyway. It's too late
Uh, let's finish this. This is our work. This is our work
We're up even up in here
Rugs and this is the structure of it. It has these three rings
And when karstin corth added one micromolar this amount he still saw these protease resistant bands
This so the different the three bands are the ones with no sugars one sugar chain and two sugar chains
They're showing a little better here. So two sugar chains one and none
Or even up in here
When he added five times as much chloropromacy and he couldn't see any and ten times as much he still couldn't see any as you would expect
And when he had done the first experiments and showed them to me
I said go back and look at some of these other psychoactive drugs like how apparel which doesn't do anything in similar concentrations
And he did that now keep in mind what he's talking about here now. He's talking about chemicals that have anti-psychotic
Properties that are used to treat dementia
Demented people
Which is the joke he made at the beginning of the talk that you can go back and see in the previous episode
Think about that for a minute because now he's testing whether or not these compounds have any effect on the presence of or the degradation of
The prion protein which is a really weird thing to test
And he looked at many of them as you see on this chart
And then I said to him karsten why in the world did you come with me to show me the first experiments?
And what the background of karsten corth was that he
In his late 30s had done a psychiatry residency and decided he wanted to go into molecular biology and began to work with a former postdoctoral fellow of mine
Bruno ersh in Zurich and when Bruno left the university of Zurich to start a biotech company karsten wanted to stay in academic medicine and came here
And I had been telling karsten for about a year and a half that he should solve one of the major problems of psychiatry like schizophrenia or bipolar disorders or autism
And he looked at me and he said to answer my question
Why did you do these experiments?
And he said well you've been telling me to connect my work on prions with psychiatry for two years now
And so I threw in chlorpromazine or thorazine into the culture
Well the karsten's credit he went back and began to look at the literature in detail and all of this really begins with the German dye industry in
Paul Erlich in 1891 who was using methylene blue as a weak anti-malarial substance and then through this pathway eventually these
These more potent anti-malarials were synthesized and chlorpromazine
Which really had marked anti-psychotic effects and chlorpromazine was the first drug to begin to empty out the insane asylums throughout the world
In the 1930s the Germans synthesized
Quinecrin and this turned out to be a potent anti-malarial drug
But it had many more side effects than quinine
But there wasn't enough quinine for use in World War two because it's extracted from the bark of the jacona tree
And there wasn't a chemist in the world who was smart enough to figure out the structure and then how to synthesize it
Until Robert Woodward did this at Harvard in the late 1940s
So quininecrin was given to thousand I should say three million young Americans in World War two
So we know a lot about quininecrin pharmacology
And what karsten corth found was that quininecrin was ten times more potent than chlorpromazine
So each so instead of this being a ten not being a five
That's a one and point five and point one and the structure is very similar
And when karsten corth treated these cultures for six days if he added enough chlorpromazine
He found that there was no return of these protease resistant bands. This is this is the band as I said before that has two sugar chains one and none
And because quininecrin has a 70-year history of the treatment of parasitic diseases the toxicities are well documented
Bruce Miller and Michael Geshwin and I and a number of other people have been involved in this in the School of Pharmacy here
We applied for an IND a new drug
Investigation license from the FDA and we were able to skip what are called phases one and two of these typical clinical trials which amount to
Tens of millions of dollars normally and we began to load patients with one gram followed by 300 milligrams daily
And in a minority of patients what we've seen we believe and it's not just us
It's many neurologists who are in contact with us throughout the world
But we've not seen all these patients because we're hoping that we will get an NIH study funded over the next four or five months
And that this study will provide us the funding we need to really look at all the patients throughout the world who are on quininecrin
But it's our impression in that of a number of other neurologists that in a minority of CJD patients the disease is slowed by quininecrin
And in a few CJD patients with quininecrin who have died later
Steve Diarmidus found that there are lower levels of PRP scraping they seem to be reduced to almost zero
Compared to what is generally found now the problem is that we have so few patients in this group
We've been able to obtain these autopsies that we just don't know at this point the second issue is that
In addition to not knowing
There are some patients where we even have more doubts. These are the patients who get dramatically better on quininecrin and those patients
I think it's good scientists. We're not even sure that they have CJD
So we need a much more controlled study we don't want to fool ourselves
Because you can't know that they have CJD until after they die, right?
So that's a really actually very nice admission
So what I've been telling you tonight is that sporadic and infectious forms of these diseases
It's the wild type or normal form of PRPC that's converted into PRP scraping
So this is an infectious form of the disease that's transmission from an animal to a man or from man-to-man or animal to animal
In the sporadic form of the disease accounts for 90 85 to 90 percent of all cases
We think it's a spontaneous conversion of PRPC into PRP scraping or as I told you before
This is a kinetic race and that there are small amounts of PRP scraping all of us that are normally cleared
So he has two models
One is that it just misfolds and then you're screwed and the other one is is that it's always misfolding and it's a race to get rid of the degradation
And are they gonna test it?
Are they gonna use that to make any predictions either one of those models make any predictions that are testable?
Are you just gonna leave it sit right there? Those are two very very mutually exclusive
Powerful models they make very powerful predictions about how this should or should not work
It's very bizarre
In the inherited forms of these diseases, it's a germline mutation passed from parental offspring
There are a whole series of new ideas that have come out of this the fact that that prions are infectious proteins is totally new
This is unlike all other infectious agents prions cause brain degeneration. They cause sporadic genetic and infectious forms of these diseases
There's no other disease paradigm in which you have both genetic and infectious diseases
And prions are the most well understood among all the neurodegenerative diseases which include of course Alzheimer's disease and Parkinson's disease
So he's saying that they actually understand prion diseases better than the others understand Alzheimer's and Parkinson's. Wow
I mean wow
That's impressive because I don't think I'm convinced not from this talk
I'm not convinced that prions are infectious proteins yet. I'm not convinced that they cause brain degeneration
I think they they can trigger it, but they don't do it
Prions cause sporadic genetic and infectious diseases and humans and animals we think
It's a hypothesis that has definitely not been proven as far as I can tell
Not if you have to inject it into the brain of the animal and they don't do it by ingestion because all of the things that we see
With kuru is ingestion with with the cattle was feeding cattle other cattle even said it
Shh
There are many thousands of times more common than the prion diseases
Now it's the discovery of prions in many other new findings which allows us now
I think to define neurodegenerative diseases in terms of their cause not the effect
So we can I think we all most people would agree now that degenerative diseases of the nervous system are disorders of a parent protein processing
Wow, so I think most people would agree that is that an illusion of consensus to you or is am I what?
Wow, that is spectacular the proteins are being processed abnormally
They give you a little idea of the numbers of cases in the United
So we have 400 cases of prion disease annually in the US
But there are four million people without Alzheimer's disease about a million with Parkinson's disease and about 20,000 with ALS or Lou Gehrig's disease
So these are huge numbers
Good night, Jeff. No, there are many many similarities between these diseases what we see are these abnormal protein deposits
I showed you PRP scraping in the brain and I showed you these PRP amyloid plaques
Well, the brains look very similar if we're not using if we use antibodies, but with these are different proteins now
But the structures look very similar in Alzheimer's disease
There's slightly different in Parkinson's disease and ALS
But what's so interesting about all of these is that?
The mutations in the genes that we find in familial forms of the disease encode the proteins that are found in these protein deposits
Except here. This is less clear with ALS
So the accumulation of misprocessed proteins causes the nervous system malfunction resulting in problems such as dementia
We're back to this word Alan difficulty moving and weakness and
Preventing the accumulation of you know, I'm in theory all down with that because one of the reasons why he says is because
The protein plaques form and then also a lot of times that same protein has some mutation
Which seems to sort with these familial disorders and to the extent to which that's true
That could be useful. But again, remember that's not true with amyloid anymore. They don't think that's the case anymore
They went crazy on it, but then they found out one of these papers wasn't right
And so that just recently happened, right? Maybe we should all look into that a little bit so we understand exactly
How much of this, you know, amyloid disease amyloid beta is is amyl is Alzheimer's disease is true or not a
Lot of these are also just their observations of correlation. Yes, they're there, but are they present? Are they responsible? Are they?
Downstream consequences of whatever's going on here
I don't think we understand these as well as he's in these protein deposits, but I agree
I still agree that it has to do with these proteins perhaps misfolding. That's okay with me, but again
Pre-on proteins are we're supposed to be told that well, you know, you can engineer a spike protein it can have
pre-onogenic sequences and that
This kind of thing can happen now. That's not the same as this. These are very specific proteins that again, we have not
Just because that sequence is different have we demonstrated that those are the so that's all all this work needs to be done
It's less clear with ALS
So the accumulation of misprocessed proteins causes the nervous system malfunction resulting in problems such as dementia
We're back to this word on difficulty moving and weakness and
Preventing the accumulation of these misprocessing protein provide proteins provides I think for the first time a rational approach to treating degenerative diseases
Yes, so and and so we've done lots of things to get rid of the amyloid beta to get rid of these plaques and it doesn't help these people
It oftentimes makes it worse
It's not clear that this is the way to go and the only way to do that is with an immune response of course, which is again
Something we're not prepared to augment nervous system
There's a little summary of CJD
And what went on as I told you I my introduction to this was a patient in 1972 here at UCSF
And that it was 1921 when six patients were described and this disease was thrown into a waste basket a degenerative disorders of a nervous system
But it came out of the waste basket in 1968 when Carlton Gajasek and Joe Gibbs working at the NIH along with a number of collaborators
Transmitted the disease into apes and later into monkeys
Preons and how did they do that they injected it directly in the brain?
I imagine like, you know some preparation unlike all other infectious pathogens viruses, viroids, bacteria, fungi, parasites
All of which multiply by having an RNA or DNA genome direct the synthesis
Interesting that they don't say anything about phage here even though that's one of the most common forms of viruses not one
No mention of bacteriophage here at all. That is a gigantic red flag
No mention of bacteriophage here at all. Why would I care about bacteriophage? Well, let's see. Let's get out of this
And let's go back to the beginning
Let's take a look at this
And current slide just to give you
An example of what's going on here
There's a bacteriophage right there on the third live podcast at the beginning of the pandemic of the Dark Horse podcast
with Brett Bandana and glasses himself
And right there
Conspicuously at the front of the podcast is a coffee cup with a bacteriophage on it
Isn't that weird because it doesn't seem like he really doesn't think that bacteriophages are actually a thing
Phages are maybe he goofs it in with the viruses, but that would be very disingenuous because
Phages are everywhere
Even the no virus people even the no virus people acknowledge that bacteriophages exist isn't that cool
Isn't that funny and he doesn't exogenous at all
Strange the progeny pathogens. It's only prions which contain only a protein
And they co-opt a normal form of that protein to produce more of the misfolded form
PRP scraping
Now all of this like what I'm telling you seem like science fiction to a lot of people
And about seven or eight years ago
I was a meeting in New Mexico and I was hearing everything that I was been saying
But it was being said by somebody else
And I looked at a good friend of mine, Hilary Keprowski, and I said Hilary this is really unbelievable
This guy even thinks he'd found all of this and Hilary said
I'm sorry, what did you just what excuse me what? Holy shit, what?
Did you hear that Mark?
Mark?
Did you hear what he just said?
Holy shit balls
I mean this is red alert time
And Hilary Keprowski and I said Hilary this is really unbelievable
What?
Seriously what?
Here we go
And I was hearing everything that I had been saying
But it was being said by somebody else
And I looked at a good friend of mine, Hilary Keprowski, and I said
Hilary this is really unbelievable
What?
Seriously what?
Here we go
And I was hearing everything that I had been saying
But it was being said by somebody else
Hilary
My good friend Hilary Keprowski
Mark Coolax got some information and stories and connections
Hilary Keprowski
Stanley Plotkin
This goes back right to the
I mean all these people, Gallo, they're all in the same little group of white haired men or whatever
It's absolutely incredible
And all of this
And Hilary said I've got a slide for you, I'll send it to you
So he sent me this slide about the four stages of adopting a new idea
The reaction at first is it's impossible
Second, maybe it's possible but it's weak and uninteresting
Third, it's true and I told you so
And the fourth one you can read
Now there's another way of thinking about this
And Lou Thomas, who was the director at Sloan Kettering in New York for many years
was also
Now he's quoting a director from Sloan Kettering
Are you giving me, is this a joke?
I mean what is happening here is this some kind of Christmas gift
I never thought I would get to open what's going on
There's another way of thinking about this
And Lou Thomas, who was the director at Sloan Kettering in New York for many years
was also a brilliant writer
And in a book called Lives of the Cell in 1974 he wrote an essay about research
And these are a couple paragraphs
Somehow the atmosphere has to be set so that a disquieting sense of being wrong
is the normal attitude of the investigators
It has to be taken for granted that the only way in is by writing the
unencumbered human imagination
With a special rigor required for recognizing that something can be highly improbable
May be almost impossible and at the same time true
Locally, a good way to tell how the work is going is to listen in the corridors
If you hear the word impossible, spoken with an expletive, followed by laughter
You will know somebody's orderly research plan is coming along nicely
Now that's a lot of words
And if you're Winston Churchill you can describe all this in many fewer words
This is 1936 in the House of Parliament
He's talking about Hitler and evaluating the Rhineland
And he says to Stanley Baldwin in the House of Commons
Men occasionally stumble across the truth
But most pick themselves up and hurry off as if nothing had happened
And with that I'll end, thank you
So the question is do prions trigger the immune system?
And the answer is no
And the reason that we think that they don't is that PRPC is present in all of us
And we are tolerant to antibodies and also to immune cells that specifically recognize PRPC
And there are very few regions on PRPC
In fact we've not been able to identify any looking for more than ten years now
That are present on PRPC to which antibodies are formed
That are not present on PRPC
We found others, as I told you about before, where a region is exposed on PRPC
But now becomes buried in PRPC
But that doesn't generate a new antigenic region
Wow, think about how much of a claim that is
That goes against everything that we know about the immune system
That it can't make antibodies specific for prion protein scrappy
It can only make antibodies that recognize both
It can make antibodies that don't recognize prion scrappy
But they don't
That's an incredible claim, that is an abs
And you heard me ask that question earlier in the talk
Like why don't they make antibodies that I think I asked that in the first half
Holy cow
There can be an immune response
And in fact a tremendous step forward in making all of these antibodies
Was created when a collaborative study that we were involved in
With Charles Weissman and Zurich produced knockout mice
In which the prion protein gene of a mouse could be knocked out
These mice are totally resistant to prion disease
And when we immunize these mice
So what does the prion protein do if you can knock the protein out and the mouse is fine?
Because that's not true for very many proteins
Strange, huh?
With the prion protein they form huge numbers of antibodies
In contrast to normal mice which form very few or no antibodies
And if I'm no antibodies, if it's a mouse prion protein
Are you hearing this shit?
He's telling you that when that animal doesn't have that gene
That they produce more antibodies to the prion protein
Which makes them un-susceptible to the prion protein
He's telling you that antibodies play a role in
But they've been unable to generate antibodies to the prion protein
That's specific for the prion protein
They're just generating antibodies to the endogenous epitopes
That are exposed in the endogenous form
Do you see the hand waving is extraordinary?
I do not believe the papers support these as being firm conclusions
But it's extraordinary the kind of exceptional biology
The number of exceptions that we need to make
In order for this to be true
Now is these mice with the prion protein
They form huge numbers of antibodies
In contrast to normal mice which form very few or no antibodies
That is a absolute
It's a mouse model of the disease
That he's saying that if you don't have the prion protein
Then you can make antibodies to the scraping protein
And then you won't get it
And so one of the reasons and the way to understand
That this works is that we could respond to you here
Wait, it's coming, you see
They're going to treat prion disease with antibodies
That's what he's proposing here
And that we should use money and grant proposals
To find the antibodies which we could use to fight prion disease
Antibodies, you know antibodies
The things that they fight all these other diseases with
That they want to produce as the perfect
Inject it in your soldiers and your immune for 30 days
Kind of thing, it's a little cludgy but it works
And if I'm no antibodies if it's a mouse prion protein
If it's a human they might form one
So the immune system
So they could easily use an mRNA to generate the prion antibodies
That they say are found in this mouse
But aren't found in any animals that have the prion protein
Then it would be a cell protein
So, wow!
Quiet in these diseases
Well, alright, so the question is very technical
Is the normal form of the prion protein the kinetic product
Or a kinetically trapped molecule and that
This scraping form is a thermodynamically more stable protein
And the answer is probably yes, but we're not sure
So the normal form of the prion protein is on the surface
And that's where it's converted into PRP scraping
And how much of it remains there we don't know
In some experiments by Stevie Arman where he fractionates these cells
So he grinds them up and looks for the membrane fraction that's found on the surface
He finds as much as 60% of the scraping form
The abnormal form is in the plasma membrane fraction
Others suggest that it's much less than that, so I don't really know
But he's probably right
So the question is what is the mechanism of action of quinocrine?
And how does it work on patients with CJD and new variants CJD?
And the answer is we don't know
Initially I thought what we should do is spend a lot of time
Several years probably to track that down and understand it
Before we would do anything further
But when I realized that the concentrations were close
Probably only off by a factor of 10 to 50
From what an ideal drug would be
We decided to spend a lot of effort starting giving this to people
But we're also now slowly starting to investigate the mechanism of action
I'm sure many other people are doing that too
Alright, so TSE is a term called transmissible spongiform encephalopathy
It's a term I don't particularly like, but maybe that's because other people use it all the time
And the reason I don't like it is that many of these diseases
There's very little spongiform change
But this is a term that really refers to the diseases caused by prions specifically
And the other neurodegenerative diseases are not classified as prion diseases
Or as TSE diseases
They're classified as neurodegenerative diseases
For instance Alzheimer's disease is distinguished
From the prion diseases by the fact that there's a different set of proteins that are involved
And all attempts to really transmit the disease have failed so far
That doesn't mean it won't be transmissible in the proper animal model
But it's not transmissible in a natural setting
See, they're trying to transmit it though
Think about that for a second
And why would they be doing that? Because they're testing this model
Or they're trying to find examples that seem to indicate that this model would work
How do they test it? They probably inject the shit
It's crazy
I don't know how the spongiform change comes about
What we find is that the vacuals
That the more prp scraper there is, the more vaculation there is
So this is correlation between prp scrapers
They want nothing to do with the immune system
If they had anything to do with the immune system
It's immediately a black box that they can't penetrate
So they have to stay away from it
How is the spongiform tissue phenotype formed?
They don't know, of course it's the immune system
Excuse me, prp scraped deposition and the vacuals that are formed
But the mechanism by which the vacuals are formed, I don't understand
Something happens to the signaling mechanisms in the cells
And whether that happens because prp scrapes on the surface
Or whether it's deep in the cell and it mucks up the signaling mechanisms
I don't know, that's a very simplistic answer
Who a very complicated question, but I can't answer it
So the question is, what is the function of prp?
We all have a gene for prp, we all make the protein, prpc
And what is its function and the answer is we don't know its function
And we don't know the function of its brother or sister, papal
We just don't know
No, so the question is, why is it that in Britain
People with new variants CJD are in their teens and early 20s
For the most part, and the answer is we don't have any idea
For a long time I thought that this was really a clue to the fact that
Disease was unconnected to the cows and that there was some other mechanism
But I threw that idea away once we had all this transgenic mouse data
And the answer is I don't have any idea why they're so young
I just don't know
One patient who's 70, another who's 50
But the vast majority of these people are under 40
So the first part of this question is, how did this all start in cows?
And the second question is, how do prions make it through your brain from your gut?
So how did prion disease start?
And I think most people were reasonably well convinced that it began with sheep
Because scrapes and stomach in Britain, it's been there for hundreds of years
And it came from the sheep, but nobody knows the exact statistics
People who are farmers tend to get rid of their animals when they're not doing well
And the easiest way to get rid of them is to get them into the human food chain
Not to burn them up, because they don't get any money for that
So we don't know how many scrapes sheep enter the human food chain every year in Britain
We have scrapes in the United States, too
Then there was a huge inquiry which you can look up on the Internet
If you have nothing better to do, there are 3,500 pages on this question of how to BSE start
And what happened afterwards was an official inquiry that was created by Tony Blair
And they only allowed the inquiry to go up to the day of his election
So they could look at John Majors with severe eyes, but not at Tony Blair
And that's what this does, it goes up to 1996, and it begins in the late 1970s
In terms of questioning what happened
And in that inquiry, you'll see that they think it began with a spontaneous or sporadic case of mad cow disease somewhere in southern England
I don't think there's a lot of evidence for that, but that's what they hypothesized
So prions are resisted to proteases, as I showed you, or enzyme digestion
Which is what happens to proteins when they enter your gut
If we take animals and we do a study, we find that we need about a billion times more prions
When they're ingested, then if you put a needle in the head of the animal and inject them directly into the brain
I thought it was one protein is all you needed, that's weird
But nevertheless, if we give the animals enough, we give them a billion times more, orally, and they all get sick
And so we presume the prions now cross the gut
If we give them a billion times more, he said, that's hilarious
Probably in the small intestine
And that they multiply in lymphoid cells, and then they go through the brain
Through the blood
The other way we think they can make it to the brain is that they travel backwards
Up the nerves of the gut, called the spinaic nerve bed, into the spinal cord
And then up the spinal cord to the brain
Question is, how do you disinfect scalpels and other medical instruments
Because there have been cases where CJD has been transmitted from one patient to another
By this route
And what I was about to say was that it's very difficult to properly disinfect instruments
And we're working on this now very hard
I guess we have some new approaches that seem to be very useful
And I'm very...
Sure, they'll be patentable
I'm very encouraged that soon we'll be able to do this in a much better way
And it's commonly done
Fortunately, the number of examples of that is still small
But as the number of surgical procedures keeps increasing every year, this may become a bigger and bigger problem
Hopefully we can stop it
The question was, how do these poor cannibals in New Guinea keep on perpetuating their society
Because if they keep eating each other and they keep getting sick with Peru, aren't they all going to die out?
And the answer is that in the late 1950s, as this was starting to...
At that point, in fact, Peru was the most common cause of death in women
This was a society that all men would like to have lived in
Because they never had to do anything, women did absolutely everything
And at that point, the most common cause of death in women was Peru
And they died in their 30s
They virtually never made it to age 40
So we had generations of young people who were motherless
And it was in the late 1950s that two things happened
One of the missionaries who began to colonize that area told them that nice people don't eat their relatives
Whether they're dead or alive
And these people were eating their dead relatives to really immortalize them
This was their way of immortalizing them through taking their soul, which they believed was in the brain, not in the heart
And the second thing that happened was that the Australian authorities
Who now began to occupy the Highlands of New Guinea, which up until the late 1940s
Had not seen any Western people
And began to occupy that area and they outlawed cannibalism
So that's how these tribes have now survived
And so what you basically have here is very
Let's say
Outland, outlier examples of where protein misfolding can go wrong
And it's usually an autoimmune reaction to exposure to proteins that would normally not be exposed to your systemic
systemic immune system
And so I don't know exactly how to draw it out on a piece of paper
But it makes sense to me that this phenomenon, however rare it was
Would be something that you would want to understand from the perspective of how ribosomes function
From the perspective of protein folding
And from the perspective of wanting to alter the function of proteins
And knowing how to stay away from this potential danger
So if there's anything that's dual use, it is the research into prions
Because this is the sort of worst case scenario that in the situation where women are eating their dead relatives
And they're eating their brain that occasionally you get this
And more often you get this generated and it could be something to do with this phenomenon
Could also be something to do with an immune reaction to that consumption
An immune reaction that occurs in the gut in the place where tolerance is normally built
And you could have a situation where something happens where that immune response is thrown off kilter
Because self-antigens are present where they shouldn't be present, i.e. in the gut
And so we're throwing out, there's no role for the immune system at all
There's no role at all, and in fact, there's so no role at all
That the picture that we were looking at earlier had no role for the immune system either
This is just something that right, it just starts occurring
And it was happening
No
Damn it
Clicked on the frickin slide, sorry
That there's no immune system here, right?
There's no immune system here, this is just proteins doing their protein thing
Sell the cell spread by nanotunnels
Person to person spread by instruments, what he was talking about here, right there it is
But
There's no, he said earlier in the talk that they don't think that prions activate the immune system
So the immune system does nothing
Think about that
If the immune system
Memorizes damage-associated patterns and the immune system better dang well recognize a protein that could fold other proteins wrong
That can cause protein aggregation, aggregates that are non-degradable
It's interesting, right?
And what did he say was the immune response that was so interesting in those knockout mice? Antibodies
It's absolutely positively immunomythology
I eat meat
The question was do I eat meat?
And I said yes, and then Alan chimed in with do I eat meat in England?
And the answer is not now
There's been a lot of discussion about this, there are no assets
So the question is, is there any screening for blood or blood products?
And right now there's no reliable assay for prions in blood
And so what was done by the FDA was to first, about four years ago, put it into an effect
If you had lived in the UK for six months or more, you could not get blood in the United States
And then last year, this was reduced to three months
And then it was something on the order of three years or four years for the rest of Europe
So this is a cumulative time that you've spent
And you get asked these questions when you get blood
And so basically what has happened is that we've seeded a narrative about this potential
We've seeded a narrative where it could be 60 days or it could be 40 years before
The consequences of you eating contaminated meat
Or the consequences of you being exposed to some farmland or you being exposed to the wrong blood
Could result in symptomatic CJD or something related to it
Alzheimer's disease, this kind of thing
And he's being very imprecise on purpose trying to group them all together
Has they're all related to protein misfolding?
Yet some stories involve induction of the protein
Others involve degradation and production and the rate limiting steps
Somehow outweighing the takeover and eventually the bad protein outweighs the good protein
And then you get the disease state
Now testing those two ideas and how they're contradicting one another or they're mutually exclusive
But okay
One involves an tremendous amount of sort of hand waving with regard to the structure
And function relationship between the sequence of a protein and its tertiary structure
And its function, which we don't know yet
It's an extraordinary biology that we're listening to
So a lot of interest at the level of the FDA and drug companies
To carry out analyses of their methods when they produce a biological such as
Let me give you an example, TPA for heart attacks
Are perceptin for cancer treatment, these are biologics that are produced in cells
And when these kinds of drugs are produced
There's a lot of interest in analyzing whether there's any possibility that prions could be carried along with them
So this is going on now
Some thought about prions and schizophrenia
I think that we're going to see many, many more diseases that are due to these changes in protein shape
Of course!
Every disease from which we have no understanding is right for such a possibility
Of course!
I think one can't speculate with any certainty
But I love to speculate
Okay, so could I talk more about how understanding prions would be used
Can benefit an understanding of Alzheimer's disease?
So if one understands any of these degenerative diseases in great detail
The implications for understanding the others are immense
They're immense in terms of new ways of thinking about the control of protein shape
And the control of protein processing going from a normal form to an abnormal form
Do you understand?
We're talking about protein processing and protein folding
We're not talking about anything else
And so this is an excuse to understand aberrant forms of it
It's an excuse to induce aberrant forms of it
And explore the possibility of harnessing that in a biological weapon scenario
Avoiding it in a gene therapy scenario
Avoiding it in a transfection or transformation scenario going forward
That's what this is on its surface and at its heart
It's all the same operation to get you to accept a gene therapy
And the consequences of it
And to think that there is a reflected natural threat that has an analog
So every single thing that they thought that was going to happen
As a result of transforming and transfecting humans in a medical way
Using CRISPR or whatever all this shit is
They've got to convince you that there is a natural way for these disasters to occur
A natural way for this disease cascade to exist
So that when it finally came
And maybe we're here right now in 2024-2025-2026
They know it's coming
They had to tie it to the virus to the spike
So that they could absolve transfection as a methodology
Even though they were seeding it this far back probably because they knew
Or let's say it's very possible that they knew
And that's why this guy is so confident that this
Wide net that he's casting that we can understand one mechanism
We understand all the mechanisms and protein folding and folding and folding
Remember the lady Susan Lindquist from MIT that we've been listening to
Over the last few weeks as well
That lady was working in the same department as Venki
Rosham-Shami
Whatever the guy that Mark has done a couple programs on that has done
Got the Nobel Prize for the ribosome
These are all in the same small group of people trying to figure out how the machinery of a cell works
How the machinery on DNA works
How DNA to RNA to protein can be understood and harnessed and hijacked
And so they talk a mean game about how much we understand
But we don't understand this stuff like this
And I'm learning a lot from this
Accumulating an abnormal form, causing as we had questions before
About how do these changes in protein shape
And then manifest themselves in neurologic signs and symptoms
Decrease thinking, decrease memory, inability to walk
What is the process by which this goes on? We have no idea
And so what we're seeing is
We have no idea, he couldn't at least say we think it's the immune system
Seriously? It's kind of sad
Why is it sad? Because once you invoke the immune system
Your protein
Your protein is no longer the center
It's no longer a target
It's no longer a toy
It's no longer a thing that you have
That you have intellectual property rights over
Instead, now you're going into the immune system
Where antibodies dominate
Where we can't study T cells
T cells are so hard to study that Christian Anderson decided to drop out of that
PhD and go into infectious diseases instead
He told that story on Twiv in 2021
It's hilarious these people
As more and more information
Anything to stay away from the sacred biology
That irreducible complexity, stay far away from it
And go somewhere where it's only smoke and mirrors
Like infectious diseases
It comes from all these neurodegenerative diseases
About them and the mechanisms
We're going to see more and more cross fertilization
The prion diseases have the advantages that we know much more about prions
Than we do about the process of Alzheimer's disease
We have much better animal models
These transgenic or genetically...
I am really upset with the disease, the use of the word disease
Because it's super annoying
We shouldn't have infectious disease
And then genetic disease
It should be genetic disorder
Protein folding disorder
Malaria disease
Something like that
I don't like this, but that's the way we do it
And it's frustrating, but it's biologically confusing
And biologically imprecise
Near mice reproduce every aspect of a prion disease
Of humans, of a cow, depending on what gene we express in the mouse
And so we have tools with prion diseases that we don't have with any of the other diseases
And I think if we're successful in the therapy and prion disease
This will generate an enormous interest in the drug companies
As well as the governments as well as foundations throughout the world
But enormous amounts more money into solving a problem like Alzheimer's disease
Anybody's, anybody's for amyloid beta
I mean, it's hilarious how naive he sounds here
Because we have, of course, the benefit of 22 years of research
But it's very, very funny
How naive he sounds here
I'm so excited about these antibodies as therapeutics
And also as bench tools
And even structural dissection tools
It's hilarious how naive he is to what he's using as tools
Anybody's for a long time have played various roles like this
That lots and lots of academic biologists are unaware of the huge, huge grey area
That they've been playing with unless they've been using the proper controls
Which is a growing and growing problem because of the change in demography of our populations
When you're 85 years old, you have a one and three chance of having Alzheimer's disease
And as we have more and more people who become octogenarians
The number of people without Alzheimer's diseases that keep going up
Other questions?
So the question is, in late onset muscular dystrophies
Where they have these mutations that expand the size of the protein
Or sometimes don't expand the size of the protein but expand the gene
Are there similarities? And the answer is yes
One of the diseases I put up, but I didn't talk about was Huntington's disease
And then I put up some of the spinal cerebellar ataxios
And these diseases have these same kinds of expanded repeats
And the answer is, I think we're talking about many similar phenomena
Now in these cases, these are all inherited diseases
So it's only the genetic form of disease
But we have no understanding of why it is that these diseases have such a late onset
What is clear is that the bigger the repeat, the earlier the onset
But then all of that has to be qualified by many other factors
That shift these curves up and down with respect to the repeats
In the prion diseases, we have absolutely no understanding why it is that
A single mutation, meaning one amino acid has changed
Some members of the family, the same family, are 40 years old when they get the disease
And others are 80 or 90 years old
It's more likely to be exposure to a toxin or some other trigger than
Rather than a disease process that's like a ticking clock or a degradation against production rate
So again, the model makes predictions but he doesn't bother to test him
He doesn't even bother to list the options that he sees
It's really disingenuous
The question is about these areas where PRPC is converted into PRPC scraping
On the surface of the cell, these cholesterol-rich micro-domains
One of the reasons we know they're cholesterol-rich is that with low estatin and other drugs
We can completely abolish the formation of PRPC scraping
Now we can't give that drug in high enough concentrations to humans
Because we would dissolve the human
The cells are not very happy in these very high concentrations of low estatin
These are very important regions, these cholesterol-rich micro-domains are rafts
That people have been studying only for the last few years
They seem to coalesce and form caves or cabbioli
And we really don't understand their function
But there are more and more studies in this area
And I think as time goes on we'll understand much more about them
So the way the protein is multiplying is that we're seeing new PRPC being made all the time
And then it's being degraded
But about 5% of it in a scraping-infected cell is being bled off into the formation of new PRPC scraping
And the old PRPC scraping, the existing PRPC scraping, drives the formation of new PRPC scraping
See, he's saying it like he knows
He's saying it like they have all these high fidelity images of it happening in a time-lapse photograph
With stains that show everything and can double-dip control
And it's just ridiculous, it's still just that cartoon
It's still just a series of assumptions that haven't been confirmed by much other than that they can
Sometimes see a fraction that's degradable and sometimes not
Ting is multiplying
So again, that's the same answer that I gave of question is what's the relationship of scraping to Parkinson's disease?
So the same answer that I gave about the relationship of pre-owned research
To Alzheimer's disease is the answer to what is the relationship to Parkinson's disease
As we learn more about all of the processes that occur in
So that kind of already helps you understand why it's a little ridiculous
That people with regard to the spike protein will flip-flop between it being amyloidogenic
And it being pre-anagenic
Because as he's telling you right now, they're different proteins
They're likely different mechanisms, they're likely different causes
We just think that one might help us think about the other one
There's no reason to believe if the protein is completely different
That the mechanism is that all related and yet somehow or another
These amateur hour worst case scenario
Whitting or unwitting narrative pushers from 2020
Have been interchangeably using the word pre-anagenic and amyloidogenic
As though they're kind of just synonyms
When here's the Nobel Prize winner telling you they are definitely not
In scrapie, in the pre-owned diseases, those will translate into learning much more about Parkinson's disease
In Parkinson's disease, there is a protein called alpha-synuclein
Which is normally made in all of us
And when the disease occurs, or even long before the disease occurs
Alpha-synuclein is being mishandled, improperly handled
It starts accumulating not outside the cell as big plaques
But inside the cell as what are called lewy bodies
And specifically in the cells of the substantia nigra
Which are the cells that die out in Parkinson's disease
So there is a PRP in birds, it's very much different than mammalian PRP
And whether birds have pre-owned diseases, I don't know
So the question is, are there cases of CJD where it's come from a vaccine
Or it's come from a blood transfusion
There are several cases where there have been blood transfusions
But one can't be sure that it either came from the blood transfusion
Or it was simply a sporadic case of CJD
And the same thing's true of a couple of vaccine cases
But the problem is everybody's vaccinated
And so we can't really make any relationship there
So the question is, since ALS is a relatively rare disease
Is there much research being done here at UCSF?
And the answer is that
There's a small amount of research being done here
But it's significant
And we have a clinical center and in that clinical center
We're trying to get much more information
And our hope is to expand ALS research in the near future
You stand on behalf of many men, thank you so much
Thanks guys
I hope you found that useful
I hope you find it definitely a little bit useful
Please stop transfection in humans
They are trying to eliminate the control group
Especially in the old people, don't let those over 50 in your life
Take any vaccine advice from their doctor
Intramuscular injection of any combination of substances with the intent of augmenting the healthy immune system
Of your friends, your relatives, your neighbors
It's dumb
Transfection in healthy humans is criminally negligent in RNA camp pandemic
Mark got a new Lego train
But it's wheels don't turn
It's kind of annoying
I don't see if there's any dinner left over for me
Thank you very much for joining me
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Actually, as I left this play
I'm going to cut over to the desk
And I got a card from New Mexico today
Thanks very much Christy, it made it
And thanks for the grocery money
You know, like every little bit counts
And this is not a little bit, so thanks a lot
Christy, thanks a lot
See you guys again tomorrow