Outstanding work, again Walter. WOW. Passing this onto my primary care doctors and a friend whose daughter is a doctor and also treating post-jab and long hauls.
Strikingly, hydroxychloroquine, which improves the prevention and treatment of Q fever endocarditis,[29,30] directly reduces the binding of antiphospholipid antibodies to phospholipid bilayers,[31] prevents thrombogenic properties of antiphospholipid antibodies,[32–35] and lowers the odds of having persistently positive antiphospholipid antibodies or lupus anticoagulant.[36,37] Consequently, adding hydroxychloroquine to doxycycline in acute Q fever patients with elevated IgG aCL levels could be useful in preventing antiphospholipid-associated complications, including thrombosis, and should be tested in future studies
Something I posted Nov. 20, 2020, yea, I had a feeling about this....and like you, no one listened....
MO-MInts
November 20, 2020 ·
Sorry this goes along with the nature article on "Thrombocytopathy and endotheliopathy: crucial contributors to COVID-19 thromboinflammation"
"Interestingly, several single-cell analyses of human lungs have not reliably demonstrated detectable levels of ACE2 expression in lung endothelial cells170,171, which requires future investigation"
No ACE2 for the SCV2 to bind-enter, this means something else, right? Maybe nicotinic receptors in the lungs? In the Mks- Phagotized!! ( actually called emperipolesis, I will provide a link to this)
Cunin P, Bouslama R, Machlus KR, et al. Megakaryocyte emperipolesis mediates membrane transfer from intracytoplasmic neutrophils to platelets. Elife. 2019;8:e44031. Published 2019 May 1. doi:10.7554/eLife.44031
There are a lot of these questions throughout the print, which hints to some of of my theoretical opinions.
They state,
"Alveolar capillary microthrombi were nine times more prevalent in patients with COVID-19 than in patients with influenza in a small series of patient autopsy evaluations43. These occluding microthrombi have been found not only in the lungs, but also in the heart, kidneys and liver in patients with COVID-19 (ref.44), supporting the presence of widespread thrombotic microangiopathy in these patients".
And ,
"An increased frequency of peripheral artery thrombosis manifesting as acute limb ischaemia with high rates of revascularization failure has been reported in patients with COVID-19 compared with patients presenting with acute limb ischaemia during a similar period in 2019 (ref.51)".
This is outside the lungs, which means what??? Its not localized clotting, its systemic!! VIremia, not what they call it!! Snake bite? Maybe!! LOL!! hmmmm..
As well as they state,
"The combined presence of venous thrombosis, arterial thrombosis and small-vessel thrombosis is rare in a single disease entity and can point towards a unique mechanism of disease. Interestingly, a similar constellation of vascular complications is found in antiphospholipid syndrome55. Indeed, data are now emerging indicating that some patients with COVID-19 can develop antiphospholipid syndrome56".
Ill let you chew on the antiphospholipid syndrome for a while, Ill come back to this like a snake bite, hurt me!!
Hmm, this, " Post-mortem analysis of lung samples has shown that both intussusceptive (non-sprouting) and sprouting angiogenesis are more frequent in patients with COVID-19 than in patients with influenza4".
What? This will come up later...justsssss sssooo you know!!!
I keep on going back to the Pradhan paper on gp120. Is it possible that these spike elements act as superantigens, that increase inflammation whilst inducing Lymphopenia? A deadly combo in people with comorbidities or immune senescence!
Does anyone know of treatments and testing for this. I'm concerned about my father. Twice injected. 74 years old. Having severe trouble with his legs (knee replacement) and Balance. He's depressed and sounds very tired all the time.
its not antiphospholipids, so much as antiEVILphospholipids, but just hasnt learnt yet how to distinguish the 4PROFIT - EVIL ones from the ones we were born with FOR LIVING
CAPS by any other name is SADS. The tests are not getting done to prove it in every case.
Outstanding work, again Walter. WOW. Passing this onto my primary care doctors and a friend whose daughter is a doctor and also treating post-jab and long hauls.
Wow! I'm hoping Jessica Rabbit takes a look at this.
Strikingly, hydroxychloroquine, which improves the prevention and treatment of Q fever endocarditis,[29,30] directly reduces the binding of antiphospholipid antibodies to phospholipid bilayers,[31] prevents thrombogenic properties of antiphospholipid antibodies,[32–35] and lowers the odds of having persistently positive antiphospholipid antibodies or lupus anticoagulant.[36,37] Consequently, adding hydroxychloroquine to doxycycline in acute Q fever patients with elevated IgG aCL levels could be useful in preventing antiphospholipid-associated complications, including thrombosis, and should be tested in future studies
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5521934/
And, every single one of these are associated with low Vit D!
Covid Conveniently get rid of the unwanted doesn’t it
Something I posted Nov. 20, 2020, yea, I had a feeling about this....and like you, no one listened....
MO-MInts
November 20, 2020 ·
Sorry this goes along with the nature article on "Thrombocytopathy and endotheliopathy: crucial contributors to COVID-19 thromboinflammation"
"Interestingly, several single-cell analyses of human lungs have not reliably demonstrated detectable levels of ACE2 expression in lung endothelial cells170,171, which requires future investigation"
No ACE2 for the SCV2 to bind-enter, this means something else, right? Maybe nicotinic receptors in the lungs? In the Mks- Phagotized!! ( actually called emperipolesis, I will provide a link to this)
Cunin P, Bouslama R, Machlus KR, et al. Megakaryocyte emperipolesis mediates membrane transfer from intracytoplasmic neutrophils to platelets. Elife. 2019;8:e44031. Published 2019 May 1. doi:10.7554/eLife.44031
There are a lot of these questions throughout the print, which hints to some of of my theoretical opinions.
They state,
"Alveolar capillary microthrombi were nine times more prevalent in patients with COVID-19 than in patients with influenza in a small series of patient autopsy evaluations43. These occluding microthrombi have been found not only in the lungs, but also in the heart, kidneys and liver in patients with COVID-19 (ref.44), supporting the presence of widespread thrombotic microangiopathy in these patients".
And ,
"An increased frequency of peripheral artery thrombosis manifesting as acute limb ischaemia with high rates of revascularization failure has been reported in patients with COVID-19 compared with patients presenting with acute limb ischaemia during a similar period in 2019 (ref.51)".
This is outside the lungs, which means what??? Its not localized clotting, its systemic!! VIremia, not what they call it!! Snake bite? Maybe!! LOL!! hmmmm..
As well as they state,
"The combined presence of venous thrombosis, arterial thrombosis and small-vessel thrombosis is rare in a single disease entity and can point towards a unique mechanism of disease. Interestingly, a similar constellation of vascular complications is found in antiphospholipid syndrome55. Indeed, data are now emerging indicating that some patients with COVID-19 can develop antiphospholipid syndrome56".
Ill let you chew on the antiphospholipid syndrome for a while, Ill come back to this like a snake bite, hurt me!!
Hmm, this, " Post-mortem analysis of lung samples has shown that both intussusceptive (non-sprouting) and sprouting angiogenesis are more frequent in patients with COVID-19 than in patients with influenza4".
What? This will come up later...justsssss sssooo you know!!!
Peace
NCBI.NLM.NIH.GOV
www.ncbi.nlm.nih.gov
Peace!!
M. tuberculosis and Antiphospholipid Syndrome
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6830129/
https://www.indianpediatrics.net/jan2021/jan-82-83.htm
M. tuberculosis and M. avium genome comparison
http://eknygos.lsmuni.lt/springer/538/151-174.pdf
I keep on going back to the Pradhan paper on gp120. Is it possible that these spike elements act as superantigens, that increase inflammation whilst inducing Lymphopenia? A deadly combo in people with comorbidities or immune senescence!
Does anyone know of treatments and testing for this. I'm concerned about my father. Twice injected. 74 years old. Having severe trouble with his legs (knee replacement) and Balance. He's depressed and sounds very tired all the time.
its not antiphospholipids, so much as antiEVILphospholipids, but just hasnt learnt yet how to distinguish the 4PROFIT - EVIL ones from the ones we were born with FOR LIVING
No one has defined "rare".
"serious concerns that repeated exposure to the virus and its proteins"
And it's proteins - meaning the clot shots?