1) LESSONS FROM THE PAST INTENTIONALLY SUPPRESSED: PRE SARS-CoV-2 KNOWLEDGE OF ACE2, ITS FUNCTIONS AND THE SARS-CoV SPIKE PROTEIN
To begin with, please read the following paragraph:
To further clarify whether the intraperitoneally injected Spike-Fc protein directly affected lung
2) pathology in mice, we examined the localization of the injected Spike-Fc protein in lung. Spike-Fc was detected in lung homogenates by western blot using human Fc–specific antibody, whereas injected control-Fc was not detected. In addition, using immunohistochemistry, we found
3) that Spike-Fc protein localized to bronchial epithelial cells, inflammatory exudates and alveolar pneumocytes. Notably, Spike-Fc primarily localized to severe lesions. This localization of Spike-Fc protein is similar to Spike antigen staining in SARS-CoV–infected mice.
4) Spike-Fc treatment resulted in downregulation of ACE2 protein expression in lungs of acid-treated wild-type mice in vivo, consistent with ACE2 protein downregulation in SARS-CoV–infected mice and Spike-Fc protein–treated cells in vitro. These results show that the SARS-CoV
5) Spike protein can directly affect the development of severe acute lung failure through ACE2.
This is not new. This was written in 2005. It was known then that the Spike Protein of SARS-CoV downregulated ACE2 and enhanced the severity of acute lung injury. The Spike Protein of
6) SARS-CoV-2 interacts FAR MORE STRONGLY with ACE2 than does the Spike Protein of SARS-CoV.
To be clear, the Spike Protein of SARS-CoV worsened ANY acute lung injury: Treatment with Spike(S318-510)-Fc again worsened acid-induced acute lung injury in wild-type mice. Notably, in
7) vivo Spike-Fc protein administration did not affect the severity of lung failure in Ace2 knockout mice, indicating that the effect of Spike protein on acute lung injury is ACE2 specific.
Now, what have we learned since 2005 about ACE2? The answer is: quite a lot.
8) PROGRESSIVE CARDIAC DYSFUNCTION
The progressive cardiac dysfunction observed in the first ACE2 mouse knockout model resembled that of tissue subjected to long-term hypoxia of the type that occurs after coronary artery disease or bypass surgery in humans.
Perhaps more can be
9) learned by observing what ACE2 CAN do:
Viral delivery of ACE2 after induction of myocardial infarction is protective, reducing the adverse cardiac remodelling and fibrosis. Similar antifibrotic effects have been seen with an ACE2 activator along with attenuation of
10) Ang-II-induced thrombus in hypertensive rats and a modest reduction in the blood pressure of spontaneously hypertensive rats. Over the past 18 months a number of studies have been carried out examining the effect of recombinant human ACE2 on a range of disease conditions.
11) To date, administration of ACE2 to mouse models of Ang-II-induced diseases has been shown to reverse the pathological effects of Ang II in diabetic nephropathy, heart disease, renal oxidative stress as well as reversal of Ang-II-induced hypertension.
Do the math if we invert
12) the observations of the above paragraph.
DIABETES
ACE2 hydrolyzes the octapeptide angiotensin (Ang)-II to heptapeptide Ang-(1-7), which has an important protective effect on blood sugar. ACE2 knockout mice respond to glucose with impaired glucose tolerance and impaired
13) insulin secretion.
SYMPATHETIC NERVOUS SYSTEM (SUDDEN CARDIAC DEATH, NEURODEGENERATION)
Brain ANG II plays an important role in modulating sympathetic function and homeostasis. The generation and degradation of ANG II are carried out, to a large extent, through the
14) angiotensin-converting enzyme (ACE) and ACE2, respectively. In disease states, such as hypertension and chronic heart failure, central expression of ACE is upregulated and ACE2 is decreased in central sympathoregulatory neurons. In this study, researcher determined the
15) expression of ACE and ACE2 in response to ANG II in a neuronal cell culture and the subsequent signaling mechanism(s) involved.
There are additional implications for ACE2 in the prevention of cancer metastasis and further beneficial biological function.
I am horrified by the
16) medical establishment. Either I am one of the greatest medical geniuses the world has ever seen, or people with desperately needed knowledge are maliciously hiding the truth and/or are actively lying. Which is it? As much as anyone would like to be the GOAT of anything, human
17) nature may be the Occam’s Razor which quickly and efficiently answers this question.
hindawi.com/journals/ijhy/…
ubigene.us/about/article/…
nature.com/articles/nm1267

• • •

Missing some Tweet in this thread? You can try to force a refresh
 

Keep Current with Walter M Chesnut

Walter M Chesnut Profile picture

Stay in touch and get notified when new unrolls are available from this author!

Read all threads

This Thread may be Removed Anytime!

PDF

Twitter may remove this content at anytime! Save it as PDF for later use!

Try unrolling a thread yourself!

how to unroll video
  1. Follow @ThreadReaderApp to mention us!

  2. From a Twitter thread mention us with a keyword "unroll"
@threadreaderapp unroll

Practice here first or read more on our help page!

More from @Parsifaler

17 Nov
1) COVID-19, ACE2 DEPLETION AND RAMPANT ANG II OVEREXPRESSION: A DISEASE OF LOCAL AND SYSTEMIC RAS
The great puzzle of COVID-19 may finally be solved. The immense number of systems involved, and the vast number of symptoms presented can be explained by the implication of Systemic
2) and Local Renin-Angiotensin Aldosterone (RAS) systems.
The RAS systems (both local (non-Renin dependent) and systemic (Renin-dependent) are primarily responsible for fluid homeostasis, most notably blood pressure regulation. However, the RAS system has evolved over time to
3) be responsible for far, far more than just fluid homeostasis. Everything we are seeing in COVID-19, both acute and in its sequelae, can be explained by the overexpression of a single peptide: Angiotensin II. This peptide, necessary to maintain a healthy blood pressure, is kept
Read 20 tweets
16 Nov
1) THE LOSS OF ACE2 RESULTS IN THE ULTRA-RAPID DEVELOPMENT AND PROGRESSION OF ACUTE AND CHRONIC AGE-RELATED DISEASES
If one were to be an enemy of humanity and wished to end the lives of as many people as possible and in the stealthiest way possible and could choose only one
2) protein to remove from the body to accomplish this task – that protein would certainly be ACE2.
The loss of ACE2 causes a massive upregulation of Angiotensin II. This hormone is involved in all the pathologies of aging. Microvascular disease, cancer, neurodegeneration, heart
3) disease, sudden death and immune dysfunction.
GROUND GLASS OPACITIES/LUNG INJURY
As an immediate concern, it is thought that the upregulation of ANG II is responsible for the ventilation-perfusion mismatch seen in COVID-19: We hypothesize that hypoperfusion of apparently
Read 19 tweets
15 Nov
1) IS COVID-19 A DISEASE OF INDUCED DNA AND MASSIVE FREE RADICAL DAMAGE WHEREIN CLINICAL SYMPTOMS ARE ACTUALLY A “POST-VIRAL SYNDROME?” THERE IS NO “ASYMPTOMATIC SPREAD” AS THE MAIN PHASE OF “SYMPTOMATIC COVID-19” OCCURS WITHIN THE TRANSCRIPTOME.
Before COVID-19, the medical
2) community spoke of anosmia, in relation to viruses, as post viral olfactory loss.
If we look at lung radiation damage (not in the context of actual radiation, but in context of the massive amounts of free radicals, which it generates) we see a direct parallel to the lung
3) findings of COVID-19. Ionizing radiation produces reactive oxygen species that induce lesions, and not only is tumor tissue damaged, but overwhelming inflammatory lung damage can occur in the alveolar epithelium and capillary endothelium. Is this not COVID-19?
Read 8 tweets
11 Nov
peptides besides angiotensin I and thereby affects diverse physiological functions, including renal development and male reproduction. In addition, ACE has a role in both innate and adaptive responses by modulating macrophage and neutrophil function — effects that are magnified
when these cells overexpress ACE. Macrophages that overexpress ACE are more effective against tumours and infections. Neutrophils that overexpress ACE have an increased production of superoxide, which increases their ability to kill bacteria. These effects are due to increased
ACE activity but are independent of angiotensin II. ACE also affects the display of major histocompatibility complex (MHC) class I and MHC class II peptides, potentially by enzymatically trimming these peptides. Understanding how ACE expression and activity affect myeloid cells
Read 4 tweets
11 Nov
1) MY MOST IMPORTANT WORK TO DATE:
THE SPIKE PROTEIN ITSELF INDUCES RAAS HYPERACTIVATION VIA “CHRONIC ANG II INFUSION”
EVERYTHING IS A DECOY. WE HAVE BEEN FOCUSED ON THE PRESENCE OF THE SPIKE PROTEIN (THE INSTIGATOR). YET, IT IS THE ABSENCE OF ACE2 THAT IS ALL OF COVID-19 AND ImageImageImage
2) ITS SEQUELAE.
COVID-19 IS A DISEASE OF OVEREXPRESSED ANG II: ACE2 DEGRADING/DOWNREGULATION BY THE SPIKE PROTEIN RESULTS IN PRIMARY ARTERIAL HYPERTENSION, MICROVASCULAR DISEASE AND DNA DAMAGE
THE SPIKE PROTEIN CAUSES HUMANS TO “SELF-INJECT” THEMSELVES WITH ANG II. JUST AS IS
3) DONE IN LAB MICE EXPERIMENTS
Let us begin by looking at one of those very lab mice experiments using ANG II. In C57BL/6-mice equipped with osmotic mini pumps, delivering AngII in four different concentrations between 60 ng/kg per min and 1 μg/kg per min during 28 days,
Read 20 tweets
9 Nov
Apologies for sounding the alarm again today, but given my research of the past 24 hours, it is far, far worse than I thought it was yesterday.
1) BEYOND PULMONARY ARTERIAL HYPERTENSION: THE SPIKE PROTEIN INDUCES SYSTEMIC MICROVASCULAR DISEASE, SIMILARLY AFFECTING ALL ORGANS
2) THIS IS COVID-19 OF THE S PROTEIN (WITHOUT THE IMMEDIATELY PATHOLOGICAL AND DELETERIOUS EFFECTS OF THE E PROTEIN (ARDS INDUCING))
PLEASE SEE MY PREVIOUS POST FOR LUNG INVOLVEMENT
I believe the small vessel damage and endothelial tissue remodeling, which are hallmarks of
3) Pulmonary Arterial Hypertension, are also occurring in all major organs.
HEART
To understand what I believe is happening, let us first look at Small Vessel Disease. Small vessel disease is a condition in which the walls of the small arteries in the heart aren't working
Read 17 tweets

Did Thread Reader help you today?

Support us! We are indie developers!


This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3/month or $30/year) and get exclusive features!

Become Premium

Too expensive? Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal

Thank you for your support!

Follow Us on Twitter!

:(