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Finally, a comparison between the BNT162b2 vaccine-induced gene expression signatures at day 7 post-prime (d7PP) and post-boost (d7PB) doses and that of other vaccine types (e.g., inactivated or live-attenuated vaccines) exhibited weak correlation both between d7PP and d7PB as well as with other vaccines .
These findings suggest the evolution of novel genomic responses after the second dose and, more importantly, the unique biology of mRNA vaccines versus other more conventional platforms.
Of particular interest is also the report of a cytokine release syndrome (CRS) – an extremely rare immune-related AE of immune checkpoint inhibitors – post-BTN162b2 vaccination in a patient with colorectal cancer on longstanding anti-programmed death 1 (PD-1) monotherapy; the anti-PD1 blockade-mediated CRS was evidenced by increased inflammatory markers, thrombocytopenia, elevated cytokine levels, and steroid responsiveness .
These proinflammatory effects could be particularly pronounced in the elderly, since recent data revealed that senescent cells become hyperinflammatory in response to the S1 subunit, followed by increased expression of viral entry proteins and reduced antiviral gene expression in nonsenescent cells through a paracrine mechanism
originally posted by: JBHemi
Makes me wonder if this big conspiracy of trying to control the population is not true and that humans are very good at making it happen naturally - just look at the world right now, we're almost at another world war, that's a better population control tool than anything else.
I also wonder, with how healthy my wife and I are, that maybe this vaccine only targets certain types of people with genetic markers?! Because I do not know anyone who has died or become sick from the vaccine. Everyone I know is vaccinated.
a reply to: Sander1976
originally posted by: thethinkingman
a reply to: anonentity
I think the tactic with all of this stuff is to ignore it for aslong as possible to rile people up, so THOSE people look crazed because ...some of them are gonna over react after being ignored over and over. If people just were saying up was down and day time was night time.... its maddening.
Its like if you witnessed an insane crime and everyone just turned away everytime you tried to tell anyone about it, it would drive you completely nuts. It then can make these people just anticipate there will be no reasoning due to their memories experiencing being ignored multiple times previously.
Thats all these people are doing, its psychological. Then they come along later and say everything you were saying, like they're the nobel ones. They're watching the internet, they analyse the data. They see what people are saying so they can figure out all the best ways to manipulate and how to answer questions...
They see all the best points that people react too, the popular things....they can do whatever they want. Find the major voices of dissent, crush them....see what people are responding too, see what they like and dont like....they use all this so they can script what they're going to say or do.... a liar is better to be prepared for how they will be questioned....this is why liars NEVER have debates live. This is why none of these people will talk with anyone with opposing points of view.
Its crazy man. They want you to live a lie so they can seem right, so they can seem great and successful, it makes you wanna puke.
The sad thing is, someone with an innocent mind isnt going to think these people are such liars because the innocent minded person is so unlike that, is so non manipulating, it would be difficult and also horrible for them to imagine or to realise this is what is actually happening and its that simple.
originally posted by: whiteblack
a reply to: AaarghZombies
Look at how many star you got for this "how horrifying" post. Only one agree with you and 8 agrees with me. You have done nothing, useless posts. I have deeply concerned with these covid vaccines side effects, for ALL ages. I saw with my own eyes. I speak out for that, not shutting my mouth.
🔥
The potential interaction at a whole-organism level of the native-like S protein and/or subunits/peptide fragments with soluble or cell-membrane-attached ACE2 can promote ACE2 internalization and degradation .
In support of this, soluble ACE2 induces receptor-mediated endocytosis of SARS-CoV-2 via interaction with proteins related to the RAS. Prolonged loss or reduced ACE2 activity may result in extensive destabilization of the RAS which may then trigger vasoconstriction, enhanced inflammation, and/or thrombosis due to unopposed ACE and angiotensin-2 (ANG II)-mediated effects.
Indeed, decreased ACE2 expression and/or activity contributes, among other things, to the development of ANG II-mediated hypertension in mice, indicating vasculature dysfunction [67]. The baseline expression levels of ACE2 in endothelial cells, or its induced expression levels upon stimulation from other tissue-resident cells, along with the potential of endothelial cells to shed ACE2 to the circulation, or their sensitivity to SARS-CoV-2 infection is debatable .
Nonetheless, even relatively low ACE2 expression levels in endothelial cells (e.g., compared to levels in epithelial cells) , along with the high expression levels of ACE2 in other cell types of the vasculature (e.g., heart fibroblasts/pericytes) indicate that the vasculature can be sensitive to free-floating S protein or its subunits/peptide fragments .
These effect(s), especially in capillary beds, and the prolonged antigen presence in the circulation, along with the systemic excessive immune response to the antigen, can then trigger sustained inflammation (discussed later) which can injure the endothelium, disrupting its antithrombogenic properties in multiple vascular beds.
Reportedly, intravenous (i.v.) injection of the S1 subunit in mice results in its localization in endothelia of mice brain microvessels showing colocalization with ACE2, caspase-3, IL-6, tumor necrosis factor a (TNF-a), and C5b-9; it was thus suggested that endothelial damage is a central part of SARS-CoV-2 pathology which may be induced by the S protein alone .
Also, the S1 subunit (or recombinant S1 RBD) impaired endothelial function via downregulation of ACE2 and induced degradation of junctional proteins that maintain endothelial barrier integrity in a mouse model of brain microvascular endothelial cells or cerebral arteries; this latter effect was more enhanced in endothelial cells from diabetic versus normal mice . Similarly, the S1 subunit decreased microvascular transendothelial resistance and barrier function in cultured human pulmonary cells .
Further, S protein disrupted human cardiac pericytes function and triggered increased production of proapoptotic factors in pericytes, causing endothelial cells death . In support of this, administration of the S protein promoted dysfunction of human endothelial cells as evidenced by, for example, increased expression of the von Willebrand factor .
Other reports indicate that S1 can directly induce coagulation by competitive binding to both soluble and cellular heparan sulfate/heparin (an anticoagulant), while cell-free hemoglobin, as a hypoxia counterbalance, cannot attenuate disruption of endothelial barrier function, oxidative stress, or inflammatory responses in human pulmonary arterial endothelial cells exposed to S1 .
Consistently, S protein binds fibrinogen (a blood coagulation factor), and S protein virions have been found to enhance fibrin-mediated microglia activation (data not yet peer-reviewed) and induce fibrinogen-dependent lung pathology in mice, while S1 binding to platelets' ACE2 triggers their aggregation.
Interestingly, both the ChAdOx1 (AstraZeneca) and BNT162b2 vaccines can elicit antiplatelet factor 4 (anti-PF4) antibody production even in recipients without clinical manifestation of thrombosis .
Intriguingly, the S protein increases human cell syncytium formation, triggering pyroptosis of syncytia formed by fusion of S and ACE2-expressing cells .
Also, in cells or mouse experimental models, it was shown that S removes lipids from model membranes and interferes with the capacity of high-density lipoprotein to exchange lipids , inhibits DNA damage repair processes , and induces Snail-mediated epithelial–mesenchymal transition marker changes and lung metastasis in a breast cancer mouse model
originally posted by: AaarghZombies
a reply to: Grenade
And yet you are completely unable to counter a single thing that I've said. So I'm still on top.
Sources in my signature show the vax is safe and effective, and you have... Nadda?
originally posted by: AaarghZombies
a reply to: Grenade
And yet you are completely unable to counter a single thing that I've said. So I'm still on top.
this demonstrates that I'm right. When anti vaxxers get this angry it's usually because they've met an argument that they know makes sense but can't admit to it.
originally posted by: AaarghZombies
a reply to: Grenade
And yet you are completely unable to counter a single thing that I've said. So I'm still on top.
Sources in my signature show the vax is safe and effective, and you have... Nadda?
originally posted by: AaarghZombies
originally posted by: whiteblack
a reply to: AaarghZombies
Look at how many star you got for this "how horrifying" post. Only one agree with you and 8 agrees with me. You have done nothing, useless posts. I have deeply concerned with these covid vaccines side effects, for ALL ages. I saw with my own eyes. I speak out for that, not shutting my mouth.
🔥
Given the echo chamber nature of this site, this demonstrates that I'm right. When anti vaxxers get this angry it's usually because they've met an argument that they know makes sense but can't admit to it.
If you'd read the OP's link yo would know that it concludes that the vax is safe for nursing mothers, and that the amount of vax that crosses over is so small as to be no concern.
The OP's own source debunks you.
Side effects are mostly just mild flu like symptoms. Same as with most vax.
Big whoop.