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I would like to get funding to conduct limited in vitro and ideally clinical trials for therapeutic antivirals as options are fast diminishing, but you need to set the frame of reference correctly or you will get nowhere.

This study shows some of the TLR range characteristics, I understand that possibly 2, 7 & 8 are being inhibited ie further variant infections & influenza especially:

Properties of toll-like receptors

TLRs Localization Ligands

TLR1/2 [33–35] Cell surface Triacylated lipopeptides

TLR2/6 [36–41] Cell surface Diacylated lipopeptides (Mycoplasma), Lipoteichoic acid (Streptococcus), Zymosan (Saccharomyces cerevisiae)

TLR2 [38, 42–48] Cell surface Peptidoglycan (Gram-positive bacteria), Lipoarabinomannan (Mycobacteria), Hemagglutinin (measles virus), phosphatidylinositol mannoside 6 (Mycobacteria), Glycosylphosphatidylinositol (Trypanosoma)

TLR3 [49–52] Endosome ssRNA virus (West Nile virus), dsRNA virus (Respiratory syncytial virus, murine cytomegalovirus)

TLR4 [43, 53–59] Cell surface Lipopolysaccharide (Gram-negative bacteria), Mannan-binding lectin (Candida albicans), glycoinositol- phospholipids (Trypanosoma cruzi), Envelope proteins (respiratory syncytial virus, mouse mammary tumor)

TLR5 [60, 61] Cell surface Flagellin (flagellated bacteria)

TLR7 [62, 63] Endosome ssRNA viruses (vesicular stomatitis virus, influenza virus)

TLR8 [64–66] Endosome ssRNA from RNA viruses

TLR9 [67–71] Endosome dsRNA viruses (herpes simplex virus, murine cytomegalovirus), CpG motifs from bacteria and viruses, Hemozoin (Plasmodium)

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7726878/

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The problem is not being inhibited by the infection, your body will deal with the viral infection via multiple mechanisms. My argument (and the evidence from Pfizer itself, and their patents) was that the vaccine turns off the TLR in millions of cells, all at once.

Messing with molecules that important will have dire consequences, and some researchers argue that it literally reprograms your immune system (makes you more susceptible to certain type of infections).

4, 7, 8 are really important, 2 is also one that cascade into a mess if messed with.

Wish I had funding to run certain research too, but alas we find ourselves relying on meta-analysis to try and help people.

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Great read. I still need to read the past posts 3 times. Not looking good is my position. And purely from an economic standpoint how on earth do the vaccine companies try & sell these new vaccines when the last ones went from doses 2 to 4 & still didn’t work like sold? In any other situation you’d want a refund, not another billion dollar bill, for the newest shitty product that comes with no guarantees or definite amount. If we yet again get mandated into these vaccines surely their will be an uproar?

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No problem, just tell them from the beginning that 3-4 doses will be required ("as was planned from the beginning for the first shots"). Oh, and of course for any other shot against future (already historical) new types. People will accept anything at this point.

As Klaus says: They eat the vax and be happy.

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yeah well ... didnt the FDA panel member stated clearly we have to try to see if it works or not on children ...

now CDC director said US will vaxx 20 million kids under 5 years old ... in the hopes that works.

if it doesnt well bad luck what we gonna do ... i wonder if they really take these jabs themselves in the hopes that works ...

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“with adjusted odds ratios of myocarditis of 8.1”

I believe any OR above 1 means you’re more likely to get the event A (myocarditis) with event B (vaccine), which isn’t a surprise to any of your subscribers; but I’m not sure how to interpret the magnitude. Can you explain? I thought most studies were ball-parking the risk at 1 in 3-5k range for young men.

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Every clinical practice should have this circulated amongst staff:

Vax induced myocarditis in young children.

It's easy to misdiagnose until a lot of damage may have occurred.

Key takes:

The Diagnostic and Clinical Approach to Pediatric Myocarditis: A Review of the Current Literature (2019)

..Children were often given an initial diagnosis of asthma or pneumonia.

...In contrast to adults with myocarditis, chest pain is seldom reported in younger children though it may be a more common feature in adolescents.

...The presence of myocardial fibrosis detected by cardiac magnetic resonance late enhancement is more common in males and younger patients, and the pattern of myocardial injury sustained in young patients tends to be more regional and more severe, with a higher incidence of irreversible myocardial scarring [28]. This pattern of myocardial injury may explain why younger patients are at risk of adverse cardiac outcomes — the presence of gadolinium late enhancement 4 weeks after the acute presentation is also correlated with reduced left ventricular ejection fraction and clinical symptomatology at 30-month follow-up

...However, a large, multi-centre study including all age groups showed that there was significant mortality in neonates and infants (33-45% survival, 23-32% improvement) with better outcomes in children between 1 and 18 years of age (78-80% survival, 46-67% improvement) [18].

Overall, 1-8% of patients with acute myocarditis eventually go on to transplant [25]. Owing to the potential for recovery, even with severe disease at presentation, patients are not typically listed for cardiac transplant unless a recovery is considered extremely unlikely despite reasonable management and a period of observation.

Full article:

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC6352488/

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Please keep it coming

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Thanks for your work. Enjoyed this !

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Wow, you were forecasting increased SADS back in April 2020.

I look forward to your next posts on this matter. 🙏💕

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Look into the new MonkeyPox one, I forecasted the rise of old diseases this year too hehe...

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Yup. You're just a regular Nostradamus. 😊

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