SPED AS PRELUDE TO A METAPLASTIC DISEASE: PULMONARY, HEPATIC, GASTROINTESTINAL AND CARDIAC COVID FINDINGS
Or, the induction of “Schizophrenic” cells.
The attack on the Endothelium by the Spike Protein may be a prelude to a more systemic problem – that of Metaplasia. The stressors induced by the Spike Protein may be causing cells (heart, liver, lung, gastrointestinal, endothelial etc.) to TRANSFORM into a DIFFERENT CELL TYPE with obvious catastrophic clinical consequences. I believe SPED is intimately related to the development of the observed Metaplasia. Please note the microvascular involvement discussed in the details associated with each organ.
METAPLASIA
First, let us discuss what Metaplasia is.
Metaplasia is the replacement of one differentiated cell type with another mature differentiated cell type that is not normally present in a specific tissue. Metaplasia may be induced or accelerated by some sort of abnormal stimulus (for example, acid or base, and hence a change in pH; hormones; cigarette smoke; and alcohol) (OR THE SPIKE PROTEIN – my edit). In the context of an abnormal stimulus, the original cells adapt to the environmental stress by changing identity. If the stimulus that caused metaplasia is removed, it is not clear whether the tissues can return to their normal pattern of differentiation. However, if the condition promoting metaplasia persists, metaplasia can progress to dysplasia and occasionally malignancy, as will be discussed later (for example, in the oesophagus. Metaplasia tends to occur in tissues constantly exposed to environmental agents, which are often injurious in nature.
Metaplasia: tissue injury adaptation and a precursor to the dysplasia–cancer sequence
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5998678/
LIVER
We describe the first cases of a unique and profound post–COVID-19 cholangiopathy in patients who recovered from critical COVID-19 and went on to develop chronic cholestasis and liver injury. Histopathologically, these patients have predominant cholangiocyte injury with accompanying microvascular changes. Bile duct paucity, the presence of cytokeratin 7 metaplasia of periportal hepatocytes (characteristic of obstructive cholestasis) in one patient, and evidence of bridging fibrosis all indicate a risk of progression to a secondary biliary cirrhosis.
In all 3 biopsies, portal tract hepatic arteries showed endothelial swelling with luminal narrowing (evidence of SPED – my edit), and there was portal vein endophlebitis. The biopsy from patient 2 exhibited focal features of sinusoidal obstructive syndrome (veno-occlusive disease) with pericentral confluent necrosis. For the biopsies from patients 1 and 2, immunohistochemistry and in situ hybridization for SARS-CoV-2 were negative.
Post–COVID-19 Cholangiopathy: A Novel Entity
https://journals.lww.com/ajg/fulltext/2021/05000/post_covid_19_cholangiopathy__a_novel_entity.33.aspx
The issue here is that these microvascular and metaplastic changes set the stage for long term hepatic morbidity. As the authors of the above paper point out:
Our concern is that this post-COVID cholangiopathy may lead to progressive liver injury with the potential need for liver transplantation.
LUNG
Please note here, also, that SPED is intimately associated with the development of Metaplasia and, ultimately, fibrosis. This may be compared with cirrhosis in the liver.
EndMT occurs when endothelial cells respond to an external insult or an internal pathological condition, transforming themselves into a more aggressive mesenchymal state (Metaplasia), causing irreversible vascular damage or fibrosis. The process of EndMT has been considered as one of the major contributors to several other pathological conditions, such as pulmonary arterial hypertension, arterial fibrosis, atherosclerosis, cardiac fibrosis and malignancy. Endothelial cells undergoing EndMT lose endothelial characteristics, such as a change in morphology, loss of vascular endothelial cadherins (VE-cadherins), CD31 and Tie1/2 with subsequent increase in mesenchymal proteins such as N-cadherin, fibroblast specific protein-1 or S100A4, fibronectin, vimentin, SM22-α, calponin and α-smooth muscle actin. As a part of the process, the basement membrane underlying endothelial cells gets disrupted, facilitating the migration of cells. This occurs through active proteolytic degradation of basement membrane collagen by matrix metalloproteinases mediated by the transitioning cells.
Combet et al., in an interesting case study published in European Respiratory Journal, reported rapid onset of honeycombing fibrosis in a patient with COVID-19, with typical similarity to idiopathic pulmonary fibrosis (IPF); similar questions were raised by Spagnolo et al. regrading post-COVID-19 pulmonary fibrosis. In histopathological micrographs from patients with IPF, we observed high ACE2 expression in the intimal, medial and adventitial layers of the pulmonary arteries. Same areas also had high expression of mesenchymal proteins, such as S100A4 and vimentin, indicative of active EndMT. Furthermore, Movat pentachrome stain showed prominent intimal thickening and luminal narrowing (SPED). It is quite possible that SARS-CoV-2 may lead to such endothelial cell dysfunction.
Endothelial to mesenchymal transition: a precursor to post-COVID-19 interstitial pulmonary fibrosis and vascular obliteration?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7453738/
GASTROINTESTINAL
The significance of this case is that the Spike Protein may not need to invade via the Endothelium to induce Metaplasia. It may induce Metaplasia in ANY exposed tissue.
A 53-year-old man was admitted for respiratory failure due to severe acute respiratory syndrome caused by a severe acute respiratory syndrome coronavirus 2 infection. The patient required prolonged artificial ventilation and extracorporeal membrane oxygenation (ECMO) for respiratory support. Despite successful discontinuation of ECMO, the patient experienced profuse watery diarrhea (5-10 L/day). A colonoscopy revealed an inflamed surface without undulation that uniformly extended throughout the colon. Biopsy specimens revealed complete disappearance of existing crypts and replacement with squamous or transitional epithelium normally observed in the anal transitional zone mucosa, with granulation tissue proliferation in the lamina propria.
Squamous Metaplasia of the Colon Following Severe COVID-19
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9104499/
HEART
The existence of a non-ischemic pattern of myocardial fibrosis with lipomatous metaplasia was also found, suggesting a previous myocarditis, with no signs of pulmonary thromboembolism. The cardiovascular outcome is a real possibility in the clinical experience of the new coronavirus pandemic. The clinical signs should always guide us to put forward such possibilities, thus continuing the alert for myocarditis and Takotsubo syndrome. The patient of this case report presented myocardial injury both at an early stage of the disease and at a later stage.
Cardiac Manifestations Associated With Coronavirus Disease: A Case Report
https://www.scielo.br/j/ijcs/a/s6w9XLTDVtvzGbkdV3HVYnr/?format=pdf&lang=en
This lipomatous metaplasia, as mentioned in one of my recent posts, I believe, may be at the core of the sudden cardiac deaths we are observing. I am suspect of the authors stating: “suggesting a previous myocarditis.” I don’t buy it.
CODA
What I am endeavoring to demonstrate with this post, is that the Spike Protein induces such stress on cells, unlike anything we have ever observed, that they CHANGE WHAT THEY ARE to deal with the stress. One could use a psychiatric comparison: They become Schizophrenic.
And, doesn’t this make sense? After all, couldn’t this response be scaled on a gradient? Some cells change “who” they are in response to the Spike Protein’s stress. Some nobly bow out (become Senescent). And some die.
Living on a break: cellular senescence as a DNA-damage response
https://www.nature.com/articles/nrc2440
SPED AS PRELUDE TO A METAPLASTIC DISEASE: PULMONARY, HEPATIC, GASTROINTESTINAL AND CARDIAC COVID FINDINGS
Practically every article, Walter, screams bioweapon, when taken together.
Have we checked spike protein for latent radioactivity? Just kidding, but what exactly does it not screw up? How could anyone even attempt to claim this is some "therapeutic agent."
"Oh it's OK, we're putting defibrillators in all the grammar schools."
"Another 10,000 defibrillators are being installed in British schools and public places to normalise heart attacks and to make the gullible think that it is normal to have heart attacks at the age of 16 (and to make them believe that the heart attacks are nothing whatsoever to do with the toxic covid-19 jab). Most of the defibrillators will be useless, of course, because no one will know how to use them properly." --Vernon Coleman
Ouch. Is this likely to happen in not - severe covid also, with lasting cellular screw-ups under the surface, unnoticed while people feel like they've recovered?