Monday, 2 November 2020

Malevolent Designer News - Covid-19 Designed to Cause Brain Damage


SARS-CoV-2 subunit S1 alters barrier status in a 3D tissue engineered microfluidic model of the human BBB. Confocal microscopy and volumetric rendering were used to visualize the tissue engineered vessel. (A) Shows a longitudinal view of an endothelialized void after perfusion that formed a predictive vessel geometry analogous to those found within the brain. (B) provides a cross sectional perspective indicating a single layer of endothelial cells. In (C) a representative merged image of the engineered vessel constructs fixed and immunestained for the tight junction protein, ZO-1, along with phalloidin to label actin and the nuclear stain, DAPI. (D) shows the typical ZO-1 membranous pattern expected in mature barrier forming brain endothelial cells. (E) after perfusion for 2 h of SARS-CoV-2 subunit S1 (10 nM), constructs were also fixed and immunolabeled for ZO-1. The arrows point to areas in which the ZO-1 cellular pattern is discontinuous, punctate or absent signifying areas of barrier breach. Scalebar = 20 μm. (F) Fluorescence intensity after ten minutes of perfusion with 4 kDa FITC-dextran, indicating the impaired barrier function in vessels perfused after 2 h of the S1 spike protein versus untreated controls. (G) Quantitative measurements for permeability coefficients of vessels exposed to the SARS-CoV-2 subunit S1 compared to untreated controls. Data was analyzed using Kruskal-Willis test, n = 3, *p < 0.05.
SARS-CoV-2 Spike Proteins Disrupt the Blood-Brain Barrier, Potentially Raising Risk of Neurological Damage in COVID-19 Patients | Temple Health

The findings of a researchers from The Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA should have devotees of the malevolent designer thrilling at its sheer brilliance.

This is the intelligent [sic] designer whom they believe created the SARS-CoV-2 virus to cause the coronavirus pandemic, and this research shows how it was designed to cause neurological damage to its human victims.

While there is no direct evidence yet that the virus invades brain cells, the team at the Lewis Katz School of Medicine have shown that the spike proteins on its coat that SARS-CoV-2 uses to gain entry into a cell promote an inflamatory response in the endothelial cells that form the blood-brain barrier, potentially causing it to become leaky.

SARS-CoV-2 gains entry to a cell by binding to the angiotensin converting enzyme 2 (ACE2) on the cell surface and the researchers has show that ACE2 is present on the surface of endothelial cells lining the inner surface of blood vessels. The Temple Health press release explains further:
It has been unclear, however, whether ACE2 is also present in the brain vasculature or whether its expression changes in health conditions that worsen COVID-19, such as high blood pressure (hypertension). To find out, the team began by examining postmortem human brain tissue for vascular ACE2 expression, using tissues from individuals without underlying health conditions and from individuals in whom hypertension and dementia had been established. Analyses showed that ACE2 is in fact expressed throughout blood vessels in the frontal cortex of the brain and is significantly increased in the brain vasculature of persons with a history of hypertension or dementia. The researchers then investigated the effects of the SARS-CoV-2 spike protein on brain endothelial cells in cell culture models. Introduction of the spike protein, particularly a portion designated subunit 1, produced substantial changes in endothelial barrier function that led to declines in barrier integrity. The researchers also uncovered evidence that subunit 2 of the SARS-CoV-2 spike protein can directly impact blood-brain barrier function. “This is of importance because unlike subunit 1, subunit 2 of the spike protein doesn’t bind to ACE2, meaning that a breach to the blood-brain barrier could occur in a manner that is independent of ACE2,” explained postdoctoral fellow and first author on the new report Tetyana P. Buzhdygan, PhD.
The team's results were published recently, open access, ahead of print in the journal Neurobiology Diseases:

Highlights

  • SARS-CoV-2 is known to bind to ACE2. ACE2 is upregulated in the human brain vasculature of hypertensive and dementia cases.
  • The SARS-CoV-2 spike protein does not acutely affect the viability of brain endothelial cells.
  • Blood-brain barrier function is negatively affected by SARS-CoV-2 spike protein subunits.
  • Brain endothelial cells show a distinct pro-inflammatory response when exposed to various SARS-CoV-2 spike protein subunits.
  • Mechanistically, barrier disruption may be explained by induction of members of the MMP family of proteins.

Abstract


As researchers across the globe have focused their attention on understanding SARS-CoV-2, the picture that is emerging is that of a virus that has serious effects on the vasculature in multiple organ systems including the cerebral vasculature. Observed effects on the central nervous system include neurological symptoms (headache, nausea, dizziness), fatal microclot formation and in rare cases encephalitis. However, our understanding of how the virus causes these mild to severe neurological symptoms and how the cerebral vasculature is impacted remains unclear. Thus, the results presented in this report explored whether deleterious outcomes from the SARS-CoV-2 viral spike protein on primary human brain microvascular endothelial cells (hBMVECs) could be observed. The spike protein, which plays a key role in receptor recognition, is formed by the S1 subunit containing a receptor binding domain (RBD) and the S2 subunit. First, using postmortem brain tissue, we show that the angiotensin converting enzyme 2 or ACE2 (a known binding target for the SARS-CoV-2 spike protein), is ubiquitously expressed throughout various vessel calibers in the frontal cortex. Moreover, ACE2 expression was upregulated in cases of hypertension and dementia. ACE2 was also detectable in primary hBMVECs maintained under cell culture conditions. Analysis of cell viability revealed that neither the S1, S2 or a truncated form of the S1 containing only the RBD had minimal effects on hBMVEC viability within a 48 h exposure window. Introduction of spike proteins to invitro models of the blood-brain barrier (BBB) showed significant changes to barrier properties. Key to our findings is the demonstration that S1 promotes loss of barrier integrity in an advanced 3D microfluidic model of the human BBB, a platform that more closely resembles the physiological conditions at this CNS interface. Evidence provided suggests that the SARS-CoV-2 spike proteins trigger a pro-inflammatory response on brain endothelial cells that may contribute to an altered state of BBB function. Together, these results are the first to show the direct impact that the SARS-CoV-2 spike protein could have on brain endothelial cells; thereby offering a plausible explanation for the neurological consequences seen in COVID-19 patients.


So, from an intelligent [sic] design creationist's point of view, this intelligent [sic] designer has designed a virus that not only causes acute respiratory problems for us, but also damages our brain in the process of killing us or making us very sick, possible for a long time.

And yet they insist this designer is the same all-loving god they claim to worship and adore and look to for moral guidance. Like worshiping a genocidal, sadistic misanthropist. No wonder creationists are prone to idolising thoroughly unpleasant people like Donald Trump and other nasty little depots with acute personality disorders.







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