A friends wife is suffering from low iron. She's passed out and had 1blood infusion in rhe past month. She isnt making red blood cells like she used to.
2x vaxxed, they can't find root cause. This sounds like the reason.
So where is the unused iron going, if it's not being made into blood cells after spike protein exposure? Is it relevant that the solid substances removed from the veins of people who died unexpectedly after their Covid shots, and sent to Mike Adam's lab for mass spec analysis, are full of metals including tin and iron, but not full of blood proteins at all?
I was most concerned over the biodistribution to the bone marrow due to the fact it could potentially affect all new progenitor cells (hemopoietic) being made by bone marrow. Other places of biodistribution are bad too, regarding potential fertility and organ damage, but if one survives in spite of those issues having the bone marrow affected concerned me that it could result in a never ending assault on cellular renewal affecting the blood, vascular & circulatory systems and many of the biochemical cell signaling cascades!
More TLR4 news. There are methods to add to vaxx recovery protocols to modify and interfere with adverse action there. Hope you can get the attention of medical doctors reading this who can explore further.
NATURE "In addition to these two receptors, SARS-CoV-2/COVID-19 may also interact with the extracellular matrix metalloproteinase inducer basigin, known as cluster of differentiation 147 (CD147) as well as recently proposed with C-type lectin receptor and Tweety family member 2"
Is there a way to explain what "Tweety family member" means in more of a dinner with the neighbors type description than uber Chestnut science?
It's more curiosity about terminology. In the 1990's bone marrow transplants evolved to stem cell transplants, then T-cell transplants which were called "A Buffy Coat" by HUTCH team.
It hasn't crossed my mind since until the "Tweety family" showed up and made me wonder if it's connected. Buffy & Tweety sounds like a good pair to me.
Thanks for doing what you do & God bless all the good hearted brainiacs! <3
It seems to me that humanity has become the lab rat for mRNA injectables. This is the sense I am getting from all responses above. I also believe that mRNA that was first injected was no longer the same in the booster. Why? I am not any kind of a health practitioner. Just scratching my head and posting out loud. Because the symptoms and reactions change with each booster. Also as the age groups become younger we see different reactions to the jab. This is an experiment by pharma paid for us with our taxes, health and ultimately our lives.
What is the true objective? What are pharma learning by tweaking the mRNA injectables? Still scratching my head???
high M-CSF serum levels significantly correlated with high 25-hydroxyvitamin D3 serum levels suggesting that 25-hydroxyvitamin D3 might modulate M-CSF release
C-Fos is involved in cell proliferation, differentiation and survival and its dysregulation is an important factor for cancer development as well as inflammation and autoimmunity.
GSK-3B is a serine-threonine protein kinase involved in several signaling pathways also regulating cell proliferation, differentiation, and apoptosis and is implicated in diabetes, Alzheimer's Disease, Parkinson's Disease, schizophrenia, and some types of cancer.
It is also one of five genes that seem to facilitate infection with SARS-CoV2!
“MITF also modulates the expression of coinhibitory receptors, i.e., PD-L1 and HVEM, and the production of an inflammatory secretome, which directly affects the infiltration and/or activation of the immune cells”
“We also demonstrated that another unusual pathway, the calcium-independent PI3K/PKCE/JNK/CREB pathway, functioned in cooperation with the calcium-dependent pathway to induce COX-2 expression upon stimulation by spike protein.”
Just thinking out loud here. Would Cox-2 inhibitors be useful or harmful?
A friends wife is suffering from low iron. She's passed out and had 1blood infusion in rhe past month. She isnt making red blood cells like she used to.
2x vaxxed, they can't find root cause. This sounds like the reason.
As a J&J vax injured person, this is pretty interesting. I’ve had two blood tests and both show abnormally low iron
So where is the unused iron going, if it's not being made into blood cells after spike protein exposure? Is it relevant that the solid substances removed from the veins of people who died unexpectedly after their Covid shots, and sent to Mike Adam's lab for mass spec analysis, are full of metals including tin and iron, but not full of blood proteins at all?
I was most concerned over the biodistribution to the bone marrow due to the fact it could potentially affect all new progenitor cells (hemopoietic) being made by bone marrow. Other places of biodistribution are bad too, regarding potential fertility and organ damage, but if one survives in spite of those issues having the bone marrow affected concerned me that it could result in a never ending assault on cellular renewal affecting the blood, vascular & circulatory systems and many of the biochemical cell signaling cascades!
More TLR4 news. There are methods to add to vaxx recovery protocols to modify and interfere with adverse action there. Hope you can get the attention of medical doctors reading this who can explore further.
NATURE "In addition to these two receptors, SARS-CoV-2/COVID-19 may also interact with the extracellular matrix metalloproteinase inducer basigin, known as cluster of differentiation 147 (CD147) as well as recently proposed with C-type lectin receptor and Tweety family member 2"
https://web.archive.org/web/20220117202805/https://www.nature.com/articles/s41375-021-01332-z
Is there a way to explain what "Tweety family member" means in more of a dinner with the neighbors type description than uber Chestnut science?
It's more curiosity about terminology. In the 1990's bone marrow transplants evolved to stem cell transplants, then T-cell transplants which were called "A Buffy Coat" by HUTCH team.
It hasn't crossed my mind since until the "Tweety family" showed up and made me wonder if it's connected. Buffy & Tweety sounds like a good pair to me.
Thanks for doing what you do & God bless all the good hearted brainiacs! <3
Thank you Walter, I have shared this.
I know of someone in his sixties that had to take iron post vaccination because he felt fatigued, questioned if it was usual for a male?
It seems to me that humanity has become the lab rat for mRNA injectables. This is the sense I am getting from all responses above. I also believe that mRNA that was first injected was no longer the same in the booster. Why? I am not any kind of a health practitioner. Just scratching my head and posting out loud. Because the symptoms and reactions change with each booster. Also as the age groups become younger we see different reactions to the jab. This is an experiment by pharma paid for us with our taxes, health and ultimately our lives.
What is the true objective? What are pharma learning by tweaking the mRNA injectables? Still scratching my head???
Yes, and M-CSF is activated by UVB and Vit D
“UVB‐induced GM‐CSF production is suppressed by dexamethasone in HaCaT Cells”
https://www.researchgate.net/publication/227684171_UVB-induced_GM-CSF_production_is_suppressed_by_dexamethasone_in_HaCaT_Cells
https://www.researchgate.net/publication/262228981_Erratum_Vitamin_D_endocrine_system_and_osteoclasts
high M-CSF serum levels significantly correlated with high 25-hydroxyvitamin D3 serum levels suggesting that 25-hydroxyvitamin D3 might modulate M-CSF release
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144809/
And so is HIF-1
“UVB radiation induces expression of HIF-1alpha and VEGF through the EGFR/PI3K/DEC1 pathway”
https://pubmed.ncbi.nlm.nih.gov/16964427/
“Calcitriol Suppresses HIF-1 and HIF-2 Transcriptional Activity by Reducing HIF-1/2α Protein Levels via a VDR-Independent Mechanism”
https://pubmed.ncbi.nlm.nih.gov/33182300/
Light controls life!
Autoimmunity is related to Th1/Th2 and Th17/Treg balance - which is related to the balance between UVB and Ozone!
UVB inhibits Thl responses and stimulates Th2 responses
https://repub.eur.nl/pub/20439/001025_Boonstra,%20Pieter%20Andre.pdf
Whereas, ozone can have the opposite effect:
“Th1 cells activation might be predominant over Th2 activation upon ozone exposure in asthmatic children”
https://pubmed.ncbi.nlm.nih.gov/24641287/
https://www.nature.com/articles/pr2009119/
UVB also reduces Th17
https://pubmed.ncbi.nlm.nih.gov/24617827/
And increases Tregs
leading to a restoration of the balance between Th17 and Tregs with a shift towards the Tregs side.
https://onlinelibrary.wiley.com/doi/10.1111/exd.12369
UVB also activates PI3K and CREB
https://pubmed.ncbi.nlm.nih.gov/11965545/
Which in turn activates c-Fos
https://www.sciencedirect.com/science/article/abs/pii/S0378111902007230
c-Fos is increased in SARS-CoV2
https://pubmed.ncbi.nlm.nih.gov/33284859/
C-Fos is involved in cell proliferation, differentiation and survival and its dysregulation is an important factor for cancer development as well as inflammation and autoimmunity.
https://pubmed.ncbi.nlm.nih.gov/32042069/
The PI3K pathway also regulates GSK-3Beta
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694284/
GSK-3B is a serine-threonine protein kinase involved in several signaling pathways also regulating cell proliferation, differentiation, and apoptosis and is implicated in diabetes, Alzheimer's Disease, Parkinson's Disease, schizophrenia, and some types of cancer.
It is also one of five genes that seem to facilitate infection with SARS-CoV2!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9014212/
UVB inhibits GSK-3B which plays a role in the increase of COX2
https://pubmed.ncbi.nlm.nih.gov/11389054/
Whereas chronic Ozone exposure increases GSK-3B
https://www.sciencedirect.com/science/article/abs/pii/S0161589018300336
“Chronic O3 exposure induced increases of collagen deposition, MMP8, MMP9, HIF-1α, VEGF, α-SMA, and GSK-3β”
Th17 Polarization also depends on GSK3β and GSK3β Inhibition Enhances Treg Function.
https://www.frontiersin.org/articles/10.3389/fonc.2020.01221/full
GSK-3B also controls PD-1 PDL1 levels
https://pubmed.ncbi.nlm.nih.gov/31604533/
PD-1 regulates the balance between T cell activation, tolerance, and immunopathology!
https://pubmed.ncbi.nlm.nih.gov/18173375/
UVB increases PD-L1
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6548650/
And PD-1/PD-L1 plays a role in the maintenance of UVB-induced tolerance.
https://pubmed.ncbi.nlm.nih.gov/27556047/
GSK-3B is also important for the activation of MITF
“activation of GSK3beta by cAMP facilitates MITF binding to the tyrosinase promoter”
https://pubmed.ncbi.nlm.nih.gov/12093801/
Moreover, the PI3K pathway drives the maturation of mast cells via MITF
https://pubmed.ncbi.nlm.nih.gov/21791431/
And MITF can regulate chemokine expression, immune cell attraction and infiltration.
https://europepmc.org/article/PMC/6290759
“MITF also modulates the expression of coinhibitory receptors, i.e., PD-L1 and HVEM, and the production of an inflammatory secretome, which directly affects the infiltration and/or activation of the immune cells”
https://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-020-01290-7
MITF is activated by UVB
https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1755-148X.2010.00775.x
MITF is partially located in the mitochondria and regulates PDH.
Overexpression of MITF reduces PDH activity, indicating that MITF is a negative regulator of PDH
https://www.jacionline.org/article/S0091-6749(16)31344-6/fulltext
And, PDH is reduced in SARS-CoV2
https://www.nature.com/articles/s41467-021-22166-4
With a corresponding increase in MITF!
“Bost et al.’s study of SARS-CoV-2 host-viral infection maps identified MITF as one of the up-regulated genes”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8145325/
So, why is MITF increased in Covid?
“We also demonstrated that another unusual pathway, the calcium-independent PI3K/PKCE/JNK/CREB pathway, functioned in cooperation with the calcium-dependent pathway to induce COX-2 expression upon stimulation by spike protein.”
Just thinking out loud here. Would Cox-2 inhibitors be useful or harmful?