Once again, old science (image to the left) predicts new findings (image to the right). One thing remains common: negligence

Accumulation of nanocarriers in the ovary: A neglected toxicity risk? sciencedirect.com/science/articl…
Reviewed here:
Potential adverse effects of nanoparticles on the reproductive system
The literature is full of papers that describe lipid nanoparticles as specific delivery machines of (e.g. anti-cancer) drugs to the ovaries.
I’ve been hearing two types of anecdotes from my teenage daughters as well as online:
1) Vaginal hemorrhage not in sync with menstruation cycle.
2) Painful and growing (!) breasts. (Some may rejoice, but what’s the price to pay?)
Are these indeed widespread?

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More from @gerdosi

11 May
1/ I have a thread about natural immunity to SARS-CoV-2, but I was asked to do a comparison with vaccine induced immunization. Interestingly, deep analysis of the two is largely missing. A recent study will do the job,
2/ but we need to focus on results, not conclusions, because even though the study was designed to compare the two types of immunization, plus added the effect of a booster jab on top of infection, the interpretation is a bit twisted to mostly compare the 2 jab scenarios.
3/ Quote:
"Three individuals who previously showed a response, despite lack of laboratory evidence for infection (therefore presumably a cross-reactive response to an endemic human coronavirus) showed an unchanged or decreased [T cell] response to spike after vaccination."
Read 29 tweets
28 Apr
There’s a curious correlation between countries/regions of high prior SARS2 exposure and a resurgence upon the start of mass V immunization programs. I’ve been thinking a lot about this lately, and the only explanation that could fit observations is… 1/
reactivation of dormant viruses in the population. (Seasonal) respiratory viral dormancy has been debated a lot for decades, but there’s still no consensus on where exactly these virions could lay dormant in the body, nor on the trigger(s) & mechanism(s) responsible for… 2/
reactivation. In light of recent research, my (educated?) guess is that the small intestine, and associated immune structures, is more likely place for this to occur than the respiratory tract. Admittedly, this is speculative, but neither implausible nor could I come up with… 3/
Read 16 tweets
20 Jan
The autoimmunity problem raised by below article requires rethinking of pathophysiology and treatment of severe COVID-19. The level of mimicry between spike and human peptides is very high (see attached figure from a researcher featured in the article).
nature.com/articles/d4158… Image
Unfortunately, this seems more than theoretical matches.
“SARS-CoV-2 antibodies had reactions with 28 out of 55 tissue antigens, representing a diversity of tissue groups that included barrier proteins, gastrointestinal, thyroid and neural tissues” & more.
An excellent bird’s view of the same topic.
Read 12 tweets
28 Dec 20
New mRNA vaccine technologies may offer 94-95 % efficacy. What an achievement of 21st century science!
On the other hand, good old natural immunity provides 100 % protection from symptomatic COVID-19, as shown in the study of 12.5k healthcare workers below.
Another large study finds precisely the same thing: 100 % natural immune protection from symptomatic COVID-19 within 6 months of first infection. journalofinfection.com/article/S0163-…
What could provide lasting protection? Repeated exposure.
Tissue resident memory T cell presence “required airway vaccination and antigen persistence in the lung, as non-respiratory routes of vaccination failed to support long-term lung TRM maintenance.”
Read 10 tweets
13 Dec 20
What a coincidence
“The binding epitope on S harbors a sequence motif unique to SARS-CoV-2 (not present in other SARS-related coronaviruses), which is highly similar in both sequence and structure to the bacterial superantigen staphylococcal enterotoxin B”
pnas.org/content/117/41… Image
Now, this story keeps unfolding.
“the trimeric spike protein of SARS-CoV-2 could bind to TLR4 directly and robustly activate downstream signaling in monocytes and neutrophils.” Via MyD88 and NFκB
See how MyD88 activation is THE problematic pathway, especially when amplified by elevated LPS exposure. I.e. by metabolic diseases.
How the two pathways join at this signaling node
Read 21 tweets
27 Oct 20
1/ Thread on immunity in the respiratory system: how it does and doesn't work (i.e. myths), simplified as much as I could. I’ll use the apropos of a new press release by Imperial College. To avoid mainstream media fantasies, let's use the original piece. imperial.ac.uk/news/207333/co…
2/ The main pillars of mucosal immunity in the respiratory system are:
– Innate immunity. This ancient part includes the physical barrier: mucus production and continuous flow upwards, driven by ciliary epithelial cells. There are also phagocytes ("eating cells") and…
3/ …other cellular components that produce signaling molecules, set traps, etc.

– Adaptive immunity
---> B & plasma cells that release antibodies into the airways through the single cell layer called the epithelium.
Read 21 tweets

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