https://t.me/mspezial/13451

Für den Fall das es wegen dem Typi da unterging: Denkt noch irgendwer, dass ich mit meiner Kritik am Signalfeuerwerkmassaker nach den Schüssen vllt. richtig liegen könnte und nicht nur maßlos übertreibe?

Ist ne megafiese Fangfrage... Habt ihr zugehört?

Bitte, bitte, kommentieren: a), b) oder c)

Hinweis: Endosomaler escape. Geht von Extremszenarien aus.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5668434/

https://s29.q4cdn.com/435878511/files/doc_financials/2022/ar/Moderna-Annual-Report-2022.pdf

sciencedirect.com/science/article/abs/pii/S1568163723001228

Living Nightmare

"Better never try to put anything inside your cell with force: Your PtDins-Circle will the 1st line which is gone to hell while you alterate membrane charge and with that the membrane bound Receptor functions. Next you shoot to hell is p38, RAS downstream to ERK and JNK MAPk and activate among nuclear factors NFkB and E2F. Whilst your PI3K drives crazy. Ever wondered why a lot of the juiced aging rapidly? Guess what PI3K-Akt-Pathway can do to your telomeres. Next funny part: Could also affect epigenetic factors. And the best joke which is absolute evident: You blow off your cytokine expression with more than 8k - 9k alterated geneexpressions including 2fold dropped circadian rhythm, 2 fold dropped PPAR, 2 fold dropped citrat cycle 2 - 3 fold rocket high blown off Nf-KB, TLR, RIG-1 and NOD and so many nice chemocines including CXCL4 (Platelet factor 4). Oh yeah: And maturated dendritic cells (told you Weissman in 2023) are included... And this is the effect of the LNPs (EMPTY).

And hey: Better we don't talk about lysosmal disease cause one could than start to think about what happens with the LNPs not making it to endosomal escape.

"Just say narf."

Sorry. I went off topic, dear Dr. Mikolaj Raszek. I disagree in your prognosis about coming deathwave for different reasons. But you're absolute right that Geert did not understand Immunesystem at all. IgG4 is the consequence of a chronic inflammation cascade triggered by combination of circulating sticky spikes, modRNA and the LNPs already messed up the whole basic Cell setup. With that you already have switched the complete CD4+ subsets (Treg, Tbet, Tfh and Th), CD8+ and with that as consequence of course also the B-Cells. This is evident if you read IL-6, 10, 12, 17, 33, 21, TNF-a (2fold up after LNP-contact). And here we are also in the nerve-system cause the signals will be also interpretated in a "wrong" way. (Maybe not going in, maybe insufficient?) If you now add the fact that each modRNA will hijack also - in randomized transfected Cell types - your miRNA household you become a horrible picture why it was a really bad Idea. And the imprinted immune response is more likely to cause the well known original antigenic sin: "Vaccination impairs de novo immune response to omicron breakthrough infection, a precondition for the original antigenic sin" (Nature 10. April 2024. Funny: Written by Streeck who was one of the German TV clowns promoted the juice)

Btw: If you read doi: 10 . 1101/2021 . 03.07 . 21253098 (sorry for the spaces but otherweise this comment will disappear) you'll figure out that there were already only 17 percent neutralizing ABs while Delta after the shot.

Do you remember, how long it can take, before you see horrible consequences of Tyrosine kinase inhibitors?"

https://www.youtube.com/watch?v=1g9LOsmzLQE

Mein Kommentar unter Dr. Mikolaj Raszeks Video.

SARS-CoV-2 spike S2 subunit inhibits p53 activation of p21(WAF1), TRAIL Death Receptor DR5 and MDM2 proteins in cancer cells

"Our results have implications for the biological effects of spike S2 subunit in human cells whether spike is present due to primary COVID-19 infection or due to mRNA vaccines where its expression is used to promote anti-viral immunity. A perturbed p53 pathway is concerning but also complicated in sorting out since cellular transformation and cancer are a multi-step process that evolves over time. Further detailed studies can more fully characterize the effects of spike, as well as structural determinants within the protein for interaction between the DNA damage sensing and response pathways as well as the p53 tumor suppressing pathway. With respect to the p53 pathway, further studies are needed to unravel how less MDM2 is bound to p53 in the presence of spike and the mechanisms underlying reduced p21(WAF10), TRAIL Death Receptor DR5 as well as MDM2 under conditions where there is less degradation of p53 due to reduced interaction with MDM2."

https://www.biorxiv.org/content/10.1101/2024.04.12.589252v1

🤩UNGLAUBLICHES bei LANZ!!!

Und hätte ich es nicht selbst 👀GESEHEN & GEHÖRT👂🏼, ich hätte NICHT geglaubt, dass es jemals SOO im ÖRR ausgestrahlt wurde!!👏👏

💣BQQMS💣

https://t.me/TiQToQBQQms

Annelise hat es endlich geschafft und dieses Paper publiziert!

Impact of the SARS-CoV-2 Spike Protein on the Innate Immune System: A Review

"Not only can Spike itself be amyloid, but it can also interact with other amyloid fibers; notably the S1 subunit can bind Aβ42. This S1/Aβ42 interaction appears to increase the production of IL-6, one of the most abundant proinflammatory cytokines found in severe forms of COVID-19, via activation of ACE2. In fact, binding with Aβ42 does not impede the S1 subunit from binding with its receptor."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10973921/

Oh man, Fibronectin und Fibronogen sind so furchteinflößend kompliziert prozessierte Proteinkomplexe. Ich erinnere mich an die Fibronectinlektion in Wehner und Gehring - Zoologie. :-S

Und wenn wir schon bei Schwärzungen sind:

Ich könnte gerade loskotzen.