Gigaohm Biological (July 28)
Phoshpholipid
Another excellent presentation with Walter Chestnut discussing his latest findings, also commenting on a Robert Malone video who warns about the LNP delivery mechanism causing problems such as PEG micelles stimulating production of anti-PEG IgM, which led to accelerated clearance of subsequently administered PEGylated liposomes. According to A review on phospholipids and their main applications in drug delivery systems, Phoshpholipid–PE–PEG mixtures could form micelles rather than liposomes if PE–PEG content exceeds certain critical limit. Of course the PEG interests me because it is used along with surfactants for micelle formation in polymerisations. I never thought something like that would be injected into people (lolz). Below is actually a good resource on Lipids (have a look at all the pages very informative):
Heavy metals play a role in neurodegeneration but lipids are important as Anticardiolipin and other antiphospholipid antibodies (are found) in critically ill COVID-19 positive and negative patients Antiphospholipid antibodies (APLAs) are biomarkers of a spectrum of clinical features observed in antiphospholipid syndrome (APS).1 Features of APS include venous and arterial thrombosis involving multiple organs and having various presentations. Positive APLA serology was associated with more severe disease regardless of COVID-19 status. Moreover, Persistent lgG anticardiolipin autoantibodies are associated with post-COVID syndrome. Persistence of various symptoms in patients who have recovered from coronavirus disease 2019 (COVID-1 9) was recently defined as ‘long COVID’ or ‘post-COVID syndrome’ (PCS). They conclude that Immunoglobulin G (lgG) anticardiolipin autoantibodies (aCL) are associated with the severity of COVID-19. In other words an allergic or inflammatory reaction to lipid (in the heart) but also “…persistence of the virus, especially in the nervous system, could be suggested with a post-infectious inflammatory or autoimmune reaction”. Might this have something to do with pumping the body full of phoshpholipids and mRNA spikes? What do I know? (I am just a bucket chemist who used to mix this stuff in buckets not in human bodies).
Unfortunately, many of Walter’s hypothesis are proving to be correct. He is an avid reader of the medical literature and a talented dot-connecter with a big picture overview. His sub-stack is highly recommended. In his latest article he shows how amyloid is a double-edged sword. A large build-up will cause problems, but amyloids also serve protective functions – against autoimmune attacks. So, they are symptomatic rather than causal factors.
Comment: Repeated infection with covids is not good even for the unjabbed and even if they got over it before. A least the omicrons have the PrP silenced. But the HIV and the other nasties and all the humanized nucleic acid etc tacked into the spike yes, will be immune insults that will catch up with us the older we are. Shortened lifetimes, yes. The younger the less shortened. Of course, the jabbed are the ones who will suffer shortest lives.
More study is needed into the mutagenic properties of the spike-protein. Perhaps this explains Nucleic Acid Acid Based Therapeutics against Respiratory Infections?
Comment: The prion promoting sequence in the spike also promotes amyloidosis. They are seeing where there won't be a positive D-dimer test but when they put blood under the scope then you see the amyloid building up. The amyloid is causing the clotting, the heart damage, etc. They look for a test for amyloid in those "rare" pre-jab liver inflammation cases and they find amyloid build up and light chains. The hepatitis victims go on to be found Dx with myloid leukemia (if I have the name correct). The Chinese are making more targeted covid viruses - but it is US research over 25 years that developed those - there is research trail from Baric, Daszak and others and a lot of patents. Baric collaborated with Shi - he trained her! That enrichment is bad news - they did that in the jab for a lot of reasons - it throws off all kinds of cascades along with the defanging IFN-1. IFN-1 has all these cascades which include regulatory ones to down regulate inflammation. But that is all gone because of the jab made to evade being recognized and take IFN-1 out. Enriching with C-G over-glycosylates it possibly more than HIV is so it sails on by more so than the virus construct.
This is very complex and there is so much that we do not know. As someone commented.
Code that codes for multiple things depending happening on how it’s parsed with the folds everybody producing the spikes internally become a mini gain of function study. multiply by a billion consecutive studies running concurrently.
It is not just the structure of the protein but how it folds and polarity as in hydrophilic or hydrophobic nature and charge. Who is to say that the same protein might not fold differently under other circumstances thereby acquiring different properties? Repeat expansions have been proposed to cause disease by both the repeat RNA forming foci that sequester RNA-binding proteins and through toxic dipeptide repeat proteins generated by repeat-associated non-ATG translation discussed in the article G-quadruplex-binding small molecules ameliorate C9orf72 FTD/ALS pathology in vitro and in vivo.
C9orf72 (chromosome 9 open reading frame 72) is a protein which in humans is encoded by the gene C9orf72. The protein is found in many regions of the brain, in the cytoplasm of neurons as well as in presynaptic terminals. The mutations in C9orf72 are significant because it is the first pathogenic mechanism identified to be a genetic link between familial frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). The mutation of C9ORF72 is a hexanucleotide repeat expansion of the six-letter string of nucleotides GGGGCC.
I wonder, I wonder if pumping the body full of mRNA instructions to make spike proteins will deliver the spike proteins that they want? We know already that the mRNA vaccines are not pure but contain fragments. The start codon of a gene is always “ATG” so repeat associated non-ATG translation means that it does not read the correct starting point, or you could say that it reads through the stop condon (runs the red light). It looks like read-through can cause disease. Is that why the above experiment attempted to improve dementia using small peptides that stick to the G-quadruplex?
Walter Chesnut LIVE: Gigaohm Biological High Resistance Low Noise Information Brief (2:50)