This will be the second short e-mail as I previously wrote about it, but since I am not very fond of those, I will “stitch” other information here, also important, not directly related to health or science. First things first.
Also from a moral standpoint, I must say something. I find the horrendous Canadian government’s behavior concerning the vaccination injury, to say the least (you could actively label it satanic without exaggeration). In case you missed it, Canada now offers just one option for you, if you suffered severe enough damage from the vaccine. MAID, medically assisted suicide.
As a refresher, a reminder, this same group found a similar pattern in Long Covid cases, in which a significant number of the patients had persistent Spike Protein in some of their immune cells, the source being solely the viral infection. Here, the source is solely vaccination, referred to in some circles as “Long Vaccine”.
I extremely shortly covered it below.
Persistence of S1 Spike Protein in CD16+ Monocytes up to 245 Days in SARS-CoV-2 Negative Post COVID-19 Vaccination Individuals with Post-Acute Sequalae of COVID-19 (PASC)-Like Symptoms
This study is incredibly important and pretty similar to their older paper, with a few yet significant differences. The variance between symptoms and vaccine manufacturer existed, but the predominant symptoms between the vaccines were the same, those being fatigue (28/50), neuropathy (27/50), brain fog (23/50), and headache (23/50). Shortness of breath and loss of taste and smell were infrequent, meaning these are characteristic of the viral infection.
Post-vaccination patients had statistically significant elevation in CCL5 (p=0.006), sCD40L (P<0.001), IL-8 (P<0.001), and IL-6 (P=0.04) (Figure. 3). Vaccinated individuals without PASC-like symptoms had elevated IL-2 (P=0.007) and reduced CCL4 (P=0.001) compared to the group of vaccinated individuals with PASC-like symptoms. Elevated IL-8 was a key difference in post-vaccine patients compared to the elevated cytokines in PASC.
Long-time readers, or more attentive readers will recognize a few of these. IL-6 is a well-known and powerful protein that can modulate your entire immune response, often correlated with strong inflammation. But what one may remember is sCD40L. sCD40L is the “soluble” (meaning moving freely in the blood) form of a potent protein that plays different roles, but it is directly connected with both immunosuppression and coagulation cascade.
CCL-5 is also related to coagulation, enabling cells to “glue” themselves into inflamed endothelium and acting as a signal for more inflammatory cells to come to the rescue. Similar to their older paper, this implies that the persistence of S1 in CD16+ Monoctes is most likely one major contributor to “Long Vaccine” and its pathology, similar to how in some Long Covid patients, S1 in their cells does the same. So, are they just publishing the same findings ? No.
The distinction here is that similar to another researcher (that I can’t find anymore, maybe she left social media, or was banned since I saw her tweets at some point in 2022), is that only vaccinated patients have Mutant S1 and S2 proteins in said monocytes.
It is going to take time for researchers to analyze the significance of these persistent peptide sequences inside cells, clearly at least some of these will elicit signals so there is persistent, long-term, low-grade (chronic) inflammation in some of the “Long Vaccine” patients. I have spent a considerable amount of time recently on one “new” (to me, but I found a few researchers referring to this mechanism in 2020 already) and it will play a role here.
Antigen persistence is not solely or unique to SARS-CoV-2, Influenza and a few other pathogens also induce antigen persistence and long-term inflammation, but elucidating the mechanism is the question. Often the antigens will persist in the Lymphatic tissues, but in the case of SARS-CoV-2, it can persist almost anywhere, which led me to write this on Twitter.
The following are both older articles that I missed but are poignant for our moment.
Near Misses at UNC Chapel Hill’s High-Security Lab Illustrate Risk of Accidents With Coronaviruses
Reports indicate UNC researchers were potentially exposed to lab-created coronaviruses in several incidents since 2015. These incidents highlight the risks even in the most secure and respected research facilities.
As she carried the mouse, it climbed up its tail and bit her hard, breaking through the gloves and plunging its teeth — and potentially the virus — into her ring finger.
Records show that during the five years before the pandemic began, at least six UNC researchers were required to undergo medical monitoring following four incidents where they were potentially exposed to what the NIH now confirms were types of lab-created SARS coronaviruses.
In retrospect, in 2015 the UNC, potentially being the source of SARS-CoV-2 progenitor (and in my opinion, it is the source of SARS and MERS, and I have some receipts to this proposition), experienced accidents that could lead to potential leaks. The author of the article above (Alison Young) now has a book chronicling all the near misses in laboratories and they are far more common than expected. But a lingering question in my mind is what happened between 1990 and 2001 ?
Did labs suddenly develop strict, state-of-the-art security measures, until all hell breaks lose and we start experiencing multiple significant leaks within years of each other (with our favorite pathogen leaking multiple times within years.
Eight mice, some of which may have possibly been infected with SARS or the H1N1 influenza virus, escaped primary containment at a laboratory at the UNC in 2014 (plus many other incidents). It is either by sheer luck, human stupidity, or divine intervention we didn’t have a worse pandemic on our hands with dead neighboring in the hundreds of millions.
And remember the avian flu problem. Well, you can grab your notebook, and mark this one as another rather intriguing coincidence.
Lab-created bird flu virus accident shows lax oversight of risky 'gain of function' research
The story of how the H5N1 viruses came to be created – and the response to a 2019 safety breach – raises uncomfortable questions about the tremendous trust the world is placing in research labs.
The experiment underway involved one of two infamous lab-made bird flu viruses that had alarmed scientists around the world when their creation became widely known nearly a decade earlier. In each case, scientists had taken an avian influenza virus that was mostly dangerous to birds and manipulated it in ways that potentially increased its threat to humans.
In nature, the H5N1 virus has rarely infected humans. But when people have been sickened, usually through close contact with infected birds, more than half died. So it is fortunate that the H5N1 virus isn’t capable of spreading easily from person to person. If the virus were ever to evolve in ways that gave it that ability, it could cause a devastating pandemic.
UW officials waited two months – until Feb. 10, 2020 – to file a report that should have been made immediately to the NIH Office of Science Policy, which oversees U.S. research with genetically manipulated organisms like the engineered H5N1 influenza virus involved in the experiment.
The experiment they were performing involved a virus whose name describes the components of its engineering: VN1203HA(N158D/N224K/ Q226L/T318I)/CA04. It was the virus described in Kawaoka’s controversial H5N1 gain-of-function experiments that had been published nearly eight years earlier, the NIH would later confirm in written responses to my questions.
Records show the university’s internal biosafety committee, which had approved the Kawaoka lab’s research, wasn’t “apprised” of the Dec. 9, 2019, incident until Feb. 5, 2020.
The university was less slow in reporting the incident to the federal funding officials at NIH’s National Institute of Allergy and Infectious Diseases, which provided the grant for the controversial experiments. But UW still waited 10 days – until Dec. 19, 2019 – to report the incident to NIAID program staff, according to information provided to me in writing by NIH officials.
So shortly before the SARS-CoV-2 pandemic, a reference laboratory suffered an accident with a Gain of Function Influenza virus, which by the very definition of the term, is a Potential Pandemic Pathogen, and all parties involved didn’t think much of it, which is usual from bureaucrats that only thing about saving face and their own skin.
And months later the world experienced an unprecedented pandemic of H5N1 that abnormally has persisted for 3 years and counting. Grab your notebook and mark it down as a very peculiar coincidence… also as a little flak of trivia, I remember a rather insightful researcher spilling the beans in 2021 (later banned) on how he firmly believed most influenza pandemics since 2000 were laboratory leaks from vaccine research, and he had the receipts too.
We lost so much incredibly important information and data because of the polarization between sides…depresses me sometimes. The only “defense” is content in languages automation has an extremely hard time with (Chinese, Japanese).
To close this shorter article, and I expect to write some sort of essay on the following, connecting with certain works of fiction and age-old propositions, this recent article from Nature had me smiling.
Memories are made by breaking DNA — and fixing it
Nerve cells form long-term memories with the help of an inflammatory response, study in mice finds.
When a long-term memory forms, some brain cells experience a rush of electrical activity so strong that it snaps their DNA. Then, an inflammatory response kicks in, repairing this damage and helping to cement the memory, a study in mice shows.
The findings, published on 27 March in Nature1, are “extremely exciting”, says Li-Huei Tsai, a neurobiologist at the Massachusetts Institute of Technology in Cambridge who was not involved in the work. They contribute to the picture that forming memories is a “risky business”, she says. Normally, breaks in both strands of the double helix DNA molecule are associated with diseases including cancer. But in this case, the DNA damage-and-repair cycle offers one explanation for how memories might form and last.
It also suggests a tantalizing possibility: this cycle might be faulty in people with neurodegenerative diseases such as Alzheimer’s, causing a build-up of errors in a neuron’s DNA, says study co-author Jelena Radulovic, a neuroscientist at the Albert Einstein College of Medicine in New York City.
The team pinpointed the cause of the inflammation: a protein called TLR9, which triggers an immune response to DNA fragments floating around the insides of cells. This inflammatory response is similar to one that immune cells use when they defend against genetic material from invading pathogens, Radulovic says. However, in this case, the nerve cells were responding not to invaders, but to their own DNA, the researchers found.
TLR9 was most active in a subset of hippocampal neurons in which DNA breaks resisted repair. In these cells, DNA repair machinery accumulated in an organelle called the centrosome, which is often associated with cell division and differentiation. However, mature neurons don’t divide, Radulovic says, so it is surprising to see centrosomes participating in DNA repair. She wonders whether memories form through a mechanism that is similar to how immune cells become attuned to foreign substances that they encounter. In other words, during damage-and-repair cycles, neurons might encode information about the memory-formation event that triggered the DNA breaks, she says.
When the researchers deleted the gene encoding the TLR9 protein from mice, the animals had trouble recalling long-term memories about their training: they froze much less often when placed into the environment where they had previously been shocked than did mice that had the gene intact. These findings suggest that “we are using our own DNA as a signalling system” to “retain information over a long time”, Radulovic says.
Not only is a remarkable finding on how memory formation occurs in certain regions of the brain, and which mechanisms. Memory formation on some level is a literal inflammatory process using a very important Toll-Like Receptor (9) and breaking DNA itself. Given how DNA is one of if not the most information/data-dense mediums in nature.
It is quite interesting to pair this information with its 2020 article “Brain Cell DNA Refolds Itself to Aid Memory Recall”.
Peering into the nuclei of these engram cells, the researchers spotted fine-grained changes in the architecture of the chromatin — the complex of DNA and regulatory proteins that makes up chromosomes — as the memory took shape. Parts of the chromatin reorganized in such a way that memory-associated genes could more easily spring into action to strengthen and preserve a memory. “Basically, the entire memory formation process is a priming event,” said Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory and the senior author on the study.
If you are willing to be a little more open-minded, one could propose that at some level “genetic memory” is real. And as I proposed multiple times since 2019, memes could be the genes of the conscious/soul. But this is something to talk in another context.
To end this article, can you guess which receptor the mRNA vaccines and multiple Covid infections can do long-term ?
Mess with your TLR9 expression for a while. Heard of any memory problems lately ?Hum…coincidences…
If you choose or support my work at any point, thank you !
I will now focus on the simplified "Stack" my suggestion for recover of many things, easy to read. It may take a few days because I need to write without my worst bias (which is If I know something, probably everyone else knows it too...lol).
In case you don't follow me on Twitter (I am now active again). My grandmother (100 years old) almost died after some stealthy infection, she is recovering now, but it was very very close but in case I spend more than 5 days without any signs of life, that is the reason, she passed and I am helping my mom around for a few days. I will let people know if it ever comes to that.
I wish everyone a great weekend.
Professor - My best for your Meemaw.
LIM FAO or LMFAO? All is revealed at 3:04 of this MI5 classified video Mr. Mulder. https://youtu.be/3KO8OPejaXY?t=184