Wuhan Coronavirus / COVID-19 Thread 2: Booster Shot - Resume all Corona sperging here.

I know this is literally Alex Jones, but still, they have some interesting guests on, now and then:


The Spike protein, both in vaccination and from COVID-19 infection, is making giant amyloid fibrin clots. Embalmers are basically pulling fibrous protein rubber bands out of people who had the vaccine, because of the Spike protein aggregating amyloid in their blood vessels.

Researchers are actually stating that amyloidosis is the true cause for "Long COVID", and are straight up admitting that SARS-CoV-2 Spike triggers the formation of "aberrant amyloid fibrin microclots":

A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications

Post-acute sequelae of COVID (PASC), usually referred to as ‘Long COVID’ (a phenotype of COVID-19), is a relatively frequent consequence of SARS-CoV-2 infection, in which symptoms such as breathlessness, fatigue, ‘brain fog’, tissue damage, inflammation, and coagulopathies (dysfunctions of the...
portlandpress.com portlandpress.com

At present there is no established treatment for long COVID (e.g. [13,14], so from a systems point of view it is important to understand which symptoms are ‘primary’, and which are simply secondary effects of the primary symptoms themselves. This would allow treatment strategies to focus on the primary symptoms and their causes. We here make the case (with evidence) that much of the aetiology of long COVID can be attributed to the formation of aberrant amyloid fibrin microclots, triggered in particular by the SARS-Cov-2 spike protein, and that by inhibiting the transport of erythrocytes to capillaries, and hence O2 transfer, it is these amyloid microclots that are mainly responsible for the various long COVID symptoms observed. The microclots may also present novel antigens that lead to the production of autoantibodies, that can exacerbate symptoms further. This understanding of the role of such microclots may be expected to lead to an effective strategy for treating long COVID (and probably for other, related conditions such as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)).
Click to expand...


The study authors note that the S-protein on its own would not likely break down into amyloids. They theorized that the S-protein would need to react with something for amyloids to form, such as an enzyme that would break down the S-protein into smaller components.

When they combined the S-protein in vitro with neutrophil elastase—a proteolytic enzyme (protease) that is produced in the human body by a type of white blood cell released early in SARS-CoV-2 infection called neutrophils—the researchers found that the S-protein broke up into sections that could lead to amyloid production.

They also found that combining the S-protein with protease neutrophil elastase formed amyloid-like fibrils.
Click to expand...


Amyloidosis from several culprit proteins manifests as systemic and localized disorders with many phenotypes overlapping with reported COVID-19 symptoms. It has been proposed that severe inflammatory disease including ARDS in combination with SARS-CoV-2 protein aggregation might induce systemic AA amyloidosis. (5) Neurotropic colonization and cross-seeding of S-protein amyloid fibrils to induce aggregation of endogenous proteins has been discussed in the context of neurodegeneration. (6) Notably, blood clotting associated with extracellular amyloidotic fibrillar aggregates in the bloodstream has been reported in COVID-19 patients. (7) Hypercoagulation/impaired fibrinolysis was demonstrated in blood plasma from healthy donors experimentally spiked with S-protein. (7)

Amyloidosis is associated with cerebral amyloid angiopathy, blood coagulation disruption, fibrinolytic disturbance, (8,9) FXII Kallikrein/Kinin activation, and thromboinflammation, (10) suggesting potential links between S-protein amyloidogenesis and COVID-19 phenotypes. We therefore hypothesized a potential molecular link between S-protein and amyloid formation. Inspired by previous hypotheses about human and viral protein amyloids and interactions between them, (11−13) in particular SARS-CoV spike proteins, (6,14,15) we asked the question: Is SARS-CoV-2 S-protein amyloidogenic?
Click to expand...

This is why people with severe COVID-19 have very low platelet counts and high D-dimer readings. It's basically consumption of platelets by coagulopathy, due to the Spike being broken down into chunks that act like prions and aggregate amyloid. These abnormal clots actually resist fibrinolysis. Early on in the pandemic, they gave COVID-19 sufferers tons of heparin and tissue plasminogen activator:


A hallmark of severe COVID‐19 is coagulopathy, with 71.4% of patients who die of COVID‐19 meeting International Society on Thrombosis and Haemostasis criteria for disseminated intravascular coagulation (DIC), whereas only 0.6% of patients who survive meet these criteria. 1 Additionally, it has become clear that this is not a bleeding diathesis but rather a predominantly prothrombotic DIC with high venous thromboembolism rates, elevated D‐dimer levels, high fibrinogen levels in concert with low antithrombin levels, and pulmonary congestion with microvascular thrombosis and occlusion on pathology in addition to mounting experience with high rates of central line thrombosis and vascular occlusive events (eg, ischemic limbs, strokes) observed by those who care for critically ill COVID‐19 patients. 1 , 2 , 3 , 4 , 5 , 6 , 7 There is evidence in both animals and humans that fibrinolytic therapy in acute lung injury and acute respiratory distress syndrome (ARDS) improves survival, which also points to fibrin deposition in the pulmonary microvasculature as a contributory cause of ARDS. This would be expected to be seen in patients with ARDS and concomitant diagnoses of DIC on their laboratory values such as what is observed in more than 70% of those who die of COVID‐19. 8 , 9 , 10 The following are three case reports of using tissue plasminogen activator (tPA) in critically ill, mechanically ventilated COVID‐19 positive patients with ARDS where extracorporeal membrane oxygenation capabilities, staffing, and resources are extremely limited as a result of the current COVID‐19 pandemic.
Click to expand...

Even people who had "mild" cases of COVID-19 may be more susceptible to DVT, PE, TIAs, strokes, heart attacks, basically anything that can be caused by a clot. If you had COVID-19 recently, even a mild case, you should take aspirin or nattokinase for at least six months afterward (along with the other supplements I mentioned), if you are healthy enough to tolerate it and don't have a bleeding disorder that would be a contraindication for blood thinners.

If you took the vaccine, and you have Spike protein being produced by your cells constantly and aggregating amyloid in your blood vessels, I don't even know what to say. Maybe do the same regimen for after-COVID care and hope for the best?

If you haven't taken the vaccine and are on the fence, do not take it. Period. The Spike protein is unequivocally a deadly toxin and has no business being produced in the body using human cells as bioreactors.

This shit has gone too far. It's time for pushback. Big time.
 
  • Informative
  • Like
  • Agree
Reactions: Saltynotsosweet, GloJojo, The handsome tard and 19 others
@Drain Todger
Sorry quote's not working, but you said:

Even people who had "mild" cases of COVID-19 may be more susceptible to DVT, PE, TIAs, strokes, heart attacks, basically anything that can be caused by a clot. If you had COVID-19 recently, even a mild case, you should take aspirin or nattokinase for at least six months afterward (along with the other supplements I mentioned), if you are healthy enough to tolerate it and don't have a bleeding disorder that would be a contraindication for blood thinners.

I currently have covid, and just placed an order for the nattokinase. It should arrive in a few days, but is there any counter indicator for adding it to the vitamin regiment when it arrives or should I wait until covid has fully cleared my system? I'm probably still in the viral phase right now, but my temperature's almost back to normal, but the cough persists. It's been about 3 days.
 
  • Like
Reactions: Ted_Logan, Forsaken Wanderer and Justa Grata Honoria
ducktales4gameboy said:
Were those specifically advertised for kids? That's kinda weird.

Gummy melatonin has been around for decades targeting the adult market though as well as chewable strawberry flavored tablet form which screams lawsuit waiting to happen. Worth noting that if you're in the US and have a grocery outlet nearby you can probably get 300x10mg of these for 6 bucks and they're trivially easy to split with a pill cutter.

If you really want a moment of cosmic horror related to drug marketing check out the supplement aisle at a Walmart and just count how many things come in gummy form that don't have any reason to. The concept of pitching meds to people by appealing to their sweet tooth on a childish level just distresses me.
Click to expand...
Have you seen American prescription drug ads? Fucking animated bladders n shit. Juvenile as hell but apparently it works.
 
  • Like
Reactions: Forsaken Wanderer
JustSomeDong said:
They sell melatonin gummies now, for kids!
Click to expand...
The gummies are more about getting autistic kids to actually take them. It's hard enough getting 'normal' kids to swallow shit, try that with a kid who has all sort of sensory issues, I have a friend in their 30s that still has trouble swallowing a single tablet of anything.

Like with NAC I think the most they'll do is restrict sales in places, it's something that will help fight against the effects, so it inhibits their depopulation agenda.
 
  • Like
  • Informative
Reactions: The handsome tard, Forsaken Wanderer, Dark Horse and 2 others
ToroidalBoat said:
A newspaper headline at the store spoke of "COVID generation" and says there's developmental issues in kids during the scamdemic.

"Zoom meetings" over IRL, muzzling up, and endless lockdowns have a negative psychological impact? Who could've seen that coming?

:thinking:
Click to expand...
Yeah, and I’m sure this won’t have terrible long term effects on society, especially since many of their parents have been driven some kind of fucking insane to some degree by this.

Buuuut sure, according to retards this is all fine and it’s all over

Honestly I hate both varieties of retard: the ones who think all of this was good and necessary and would do it again and the ones who wanna say it’s all over and forget it ever happened and deny the increasing number of obvious and terrible effects.
 
  • Feels
  • Like
  • Agree
Reactions: Exterminatus, peetz cum sock, The handsome tard and 10 others
Getting tard comed said:
Now, idk if real or true or fake and gay, but considering that long rope of clot Drain posted a while ago, when I saw this I thought of that.
Click to expand...
The doctor, Jane Ruby? that put all of it together, pulled all the contacts together has been looking at clotting for quite some time, pretty sure going back to early last year.
ToroidalBoat said:
A newspaper headline at the store spoke of "COVID generation" and says there's developmental issues in kids during the scamdemic.
Click to expand...
There have already been studies done showing a drop in IQ of 20points, meaning the average IQ is now dumb black person level in white kids.
Meriasek said:
After he recently said that this winter will be tough because all the isolation and shit resulted in our immune systems being shot so that this winter we'll get the double whammy of Coof and Flu, and finally admitting that post-vaccine syndrome is apparently a thing that shouldn't be underestimated.
Click to expand...
So all lockdown fault, nothing to do with the not-vax of course, nah that's safe and effective, even when they tell us what is actually wrong.

I saw a comment recently that had a very valid point, saying that even with all the scrubbing from VAERS that has been done, the fact that they have raised the myocarditis level from rare, means that it's a lot more serious most people even feared it would be.


On the topic of getting the coof, a few months ago my housemate came down with the flu, thought they'd test themselves, and what do you know, rat test said positive. I came down with something a week later, didn't bother testing.
I don't know if it's because I've had us on almost the whole lot of DT's supplement list for quite some time, plus we had been pretending we were sheep for a few months prior as per borsabil's instructions, and upped the frequency when the test showed positive (for me personally I only needed to add the NAC, everything else I've been taking for years, housemate needed to add one or two others), neither of us got a fever, or lost smell or taste. For both of us, it was just a normal run of the mill flu, like we've had every year. Coughing was annoying as fuck, like normal, I learnt to control coughing when I was a kid so just kept up the lozenges and throat sprays with a few 'cold & flu' hot drinks, barely any to no congestion (we both have allergies/sinus issues to start off with anyway).
The only thing that changed was that I made them stop walking (they normally walk an hour a day) just in case it actually was the coof, and only due to delta still hanging around. In saying that after two weeks they went back to their normal routine, which includes a 12km walk every weekend.
 
  • Like
  • Feels
Reactions: GloJojo, Forsaken Wanderer, Coral Apples and 1 other person
Looks like the U.S. Health Secretary didn't used HCQ or Ivermectin under the table, because corona-chan visited him.

Washington — Health and Human Services (HHS) Secretary Xavier Becerra has tested positive for COVID, less than 30 days since he previously contracted the virus, according to a news release from the department.
Becerra tested positive on an antigen test Monday and is experiencing mild symptoms. He also tested positive for COVID-19 on May 18 while in Europe and experienced mild symptoms then, HHS said at the time.

“This morning in Sacramento, U.S. Health and Human Services Secretary Xavier Becerra tested positive for COVID-19 after taking an antigen test,” an HHS spokesperson said in a statement Monday. “He is fully vaccinated and boosted, and is experiencing mild symptoms. He will continue to perform his duties, working in isolation.
Click to expand...

Looks like the boosts and vaccine doses he got was a piece of crap.
 
  • Informative
  • Like
Reactions: Forsaken Wanderer, SCSI, Big Brown Schlub and 1 other person
Meriasek said:
How could the vaccine cause permanent or constant spike protein production?
Click to expand...
Normally, mRNA is broken back down and recycled when it's done being used to synthesize proteins.

These Franken-mRNA strands are pseudouridylated, with all the Uracil (U) replaced with Pseudouridylyl (Ψ), such that the mRNA sequence reads with every U substituted with Ψ.


bnt162b2.png

This is based on the work of Katalin Karikó, who years ago determined that pseudouridylated mRNA escapes immune detection by bypassing toll-like receptors. Her work is lauded for "making mRNA vaccines possible". However, I've gone over her work and found a fatal flaw. I don't think she checked to see if pseudouridylated mRNA is merely ignored by TLRs, or if it actually inhibits TLR pathways. A TLR inhibitor is a very bad thing in certain contexts, because TLRs act like little molecular smoke alarms and help detect DAMPs indicative of infection or cancer. I've seen some preprints that suggest a reduction in TLR 7/8 activity after someone received a COVID-19 mRNA vaccine. Whoops!

Pseudouridylated mRNA is also very resistant to nucleases. The process of replacing uracil with pseudouridylyl produces a molecule that is very stable and resistant to biodegradation. It is not readily broken down and recycled. It persists in the body for a very, very long time, almost like microplastics. In fact, they found that mRNA vaccines had a much longer shelf life than they expected, even without specialized cryogenic refrigeration, and this is probably one reason why.

This persistence of pseudouridylated mRNA makes it more likely for it to be taken up by LINE-1 retrotransposons (that is, endogenous reverse transcriptase activity), converted into DNA, and integrated into the genome. If the region it's integrated into is not silent and expresses a protein, then that somatic cell may express Spike for as long as it lives. That is, until the immune system comes and kills it, which, given that it's expressing Spike on its surface, is practically guaranteed to happen. Immune cells don't know the difference between a cell with viral proteins on its surface or a virus with viral proteins on its surface. They're like blind guys feeling around with a cane. If macrophages and neutrophils feel something wrong, some foreign object that's not supposed to be there, then they automatically swallow and digest whatever it is.


Anyway, Spike is definitely toxic, either from vaccination, or infection. Any exposure to this protein is bad.


SARS-CoV-2 infects cells via its spike protein binding to its surface receptor on target cells and results in acute symptoms involving especially the lungs known as COVID-19. However, increasing evidence indicates that many patients develop a chronic condition characterized by fatigue and neuropsychiatric symptoms, termed long-COVID. Most of the vaccines produced so far for COVID-19 direct mammalian cells via either mRNA or an adenovirus vector to express the spike protein, or administer recombinant spike protein, which is recognized by the immune system leading to the production of neutralizing antibodies. Recent publications provide new findings that may help decipher the pathogenesis of long-COVID. One paper reported perivascular inflammation in brains of deceased patients with COVID-19, while others showed that the spike protein could damage the endothelium in an animal model, that it could disrupt an in vitro model of the blood-brain barrier (BBB), and that it can cross the BBB resulting in perivascular inflammation. Moreover, the spike protein appears to share antigenic epitopes with human molecular chaperons resulting in autoimmunity and can activate toll-like receptors (TLRs), leading to release of inflammatory cytokines. Moreover, some antibodies produced against the spike protein may not be neutralizing, but may change its conformation rendering it more likely to bind to its receptor. As a result, one wonders whether the spike protein entering the brain or being expressed by brain cells could activate microglia, alone or together with inflammatory cytokines, since protective antibodies could not cross the BBB, leading to neuro-inflammation and contributing to long-COVID. Hence, there is urgent need to better understand the neurotoxic effects of the spike protein and to consider possible interventions to mitigate spike protein-related detrimental effects to the brain, possibly via use of small natural molecules, especially the flavonoids luteolin and quercetin.
Click to expand...

Escaped Abortion said:
@Drain Todger
Sorry quote's not working, but you said:

Even people who had "mild" cases of COVID-19 may be more susceptible to DVT, PE, TIAs, strokes, heart attacks, basically anything that can be caused by a clot. If you had COVID-19 recently, even a mild case, you should take aspirin or nattokinase for at least six months afterward (along with the other supplements I mentioned), if you are healthy enough to tolerate it and don't have a bleeding disorder that would be a contraindication for blood thinners.

I currently have covid, and just placed an order for the nattokinase. It should arrive in a few days, but is there any counter indicator for adding it to the vitamin regiment when it arrives or should I wait until covid has fully cleared my system? I'm probably still in the viral phase right now, but my temperature's almost back to normal, but the cough persists. It's been about 3 days.
Click to expand...
So long as you don't have any bleeding problems, it shouldn't hurt. Taking one nattokinase pill is very much like taking one aspirin, in terms of the anticoagulant effect. Don't combine them, though. That's too much thinning.


Nattokinase encourages fibrinolysis and breaks down amyloid fibrils. It would probably be helpful both during and after infection.


More than 20 unrelated proteins can form amyloid fibrils in vivo which are related to various diseases, such as Alzheimer's disease, prion disease, and systematic amyloidosis. Amyloid fibrils are an ordered protein aggregate with a lamellar cross-beta structure. Enhancing amyloid clearance is one of the targets of the therapy of these amyloid-related diseases. Although there is debate on whether the toxicity is due to amyloids or their precursors, research on the degradation of amyloids may help prevent or alleviate these diseases. In this study, we explored the amyloid-degrading ability of nattokinase, a fibrinolytic subtilisin-like serine protease, and determined the optimal conditions for amyloid hydrolysis. This ability is shared by proteinase K and subtilisin Carlsberg, but not by trypsin or plasmin.
Click to expand...

There are so many natural, plant and bacterial fermentation-derived substances that could be useful for treating COVID-19. Take the overactive neutrophils in COVID-19, for instance. Apocynin could treat that by inhibiting myeloperoxidase activity without harming neutrophil phagocytosis. In fact, anti-inflammatory plant polyphenols may be very useful against this disease, and at preventing negative effects from the vaccine, so long as they're reasonably bioavailable.


The S protein is a large membrane glycoprotein that belongs to a group of class I viral fusion glycoproteins that also includes HIV glycoprotein 160 (Env), influenza haemagglutinin (HA) and Ebola virus glycoprotein [9]. The peripheral amino (S1) subunit can independently bind cellular receptors while the carboxy (S2) terminus is embedded into the viral envelope and is required to mediate fusion of viral and cellular membranes [10]. In coronaviruses, the S protein is the sole viral membrane protein responsible for cell entry. It defines viral tropism by its receptor specificity and membrane fusion activity during virus entry into cells [11]. Drugs targeting SARS-CoV-2 spike protein impede spike-mediated membrane fusion and prevent virus entry into the host cells. These therapeutic agents include vaccines, antibodies, small interfering RNAs, peptides, and non-peptidic small molecules such as polyphenols [9].

Luteolin and quercetin inhibited SARS-CoV infection by preventing virus entry into Vero E6 cells with EC50 values of 10 μM and 83 μM, respectively [12•]. In the same study, luteolin was found to bind with high affinity to SARS-CoV S protein, suggesting an antiviral mechanism of action involving interference with the function of the S protein. A literature-based discovery approach [13] revealed that emodin, an anthraquinone-type polyphenol found in rhubarb roots (Rheum officinale) interfered with the S protein-ACE2 interaction in a cell-free competition assay with an IC50 of 200 μM [14]. The same study also revealed that emodin reduced the infection of Vero E6 cells expressing ACE2 by an S protein-pseudo typed retrovirus. Although the mechanism of action is still unclear, these results suggest competition at the S protein receptor binding domain (RBD). Following the findings of a host-virus interactome network analysis of various viruses including SARS-CoV [15••], emodin has emerged as one of 16 most repurposable agents for COVID-19 with least expected adverse effects and highest target specificity [16].

Molecular docking and dynamic simulation studies predict polyphenols from plants such as Citrus and Curcuma species to have a potential inhibitory effect on SARS-CoV-2 infection by interacting with the S protein RBD. A study has shown stronger interactions of polyphenols from Curcuma spp. (curcumin and derivatives) and Citrus spp. (tangeretin, hesperetin, hesperidin) to the S protein (PDB: 6LXT) than nafamostat [8], the reference antiviral [17]. Hesperidin was predicted to target the binding interface between S protein and ACE2 by positioning on the middle shallow pit of the surface of the S protein RBD [18•]. Naringenin, found in a variety of herbs and fruits, had a stronger binding energy with the spike glycoprotein (PDB: 6VSB) than remdesivir [19], an antiviral temporarily approved by the FDA in the treatment of COVID-19 [20]. Epigallocatechin gallate, abundant in tea, as well as herbacetin from Rhodiola spp. (golden root) and other flavonoids also interacted strongly with S protein RBD (PDB: 6VXX) in silico [21].
Click to expand...

Molecular docking studies suggest that curcumin may have a direct inhibitory effect on the receptor binding domain of SARS-CoV-2 Spike itself.

My regimen for SARS-CoV-2 is as follows:
  • Vitamin D, to pump excess calcium out of cells and reduce metabolic and oxidative stress resulting from excess intracellular Ca2+ influx.
  • Vitamin K, to move any excess calcium to your bones.
  • Selenium, Glycine, and NAC, to enhance glutathione and selenoprotein production and improve antioxidant pathway function.
  • Pepcid and Benadryl, both for their antihistamine effect (COVID-19 may involve mastocytosis) and their antioxidant effects (famotidine inhibits the Fenton reaction).
  • Resveratrol, Quercetin, Curcumin, Melatonin, Lactoferrin, and Nattokinase for their antioxidant, antiviral, anti-inflammatory, anti-amyloid, anticoagulant, and Nrf2-activating effects.
  • Kutki powder for the apocynin and its potent antioxidant activity.
All this stuff can be fairly easily obtained without a prescription. Only a maintenance dose of 5000 IU of Vitamin D a day is really vital. The rest, for a daily pre-COVID regimen, is kind of optional, but the Quercetin may be preventive. The general idea is to avoid taking excess NAC or selenium all the time, which could potentially be a little toxic. Instead, one should strive to obtain sufficient Vitamin D, K, selenium, and cysteine from their diet to maintain proper calcium handling and endogenous antioxidant levels without having to resort to using supplements.

Fish for Vitamin D, leafy greens for dietary nitrate, sunflower seeds and Brazil nuts for cysteine and selenium, et cetera. Way healthier than popping fistfuls of supplements. Higher bioavailability, too.

When symptoms of COVID-19 appear, you start taking all of it, at least once a day. This protocol really helps with the muscle aches and stuff. I certainly don't recommend taking Pepcid and Benadryl all the time. Benadryl is some nasty stuff.


However, it may be helpful for COVID.


That combo will help knock it down pretty quick and speed recovery. After the infection is cleared, continue taking at least the Curcumin, Melatonin, and Nattokinase for their anti-amyloid effects, which may prevent the post-acute sequelae of COVID-19 (a.k.a. "Long COVID"), but definitely stop taking the Pepcid and Benadryl.

I think diet quality really plays a serious role in how severe COVID-19 is. People with severe COVID-19 have very, very poor Vitamin D levels and glutathione stores, so the oxidative stress just walks all over them. Doctors are very surprised at how low the glutathione levels of COVID-19 sufferers are, even young people who should have fairly high endogenous antioxidant levels are deficient.

www.bcm.edu

COVID-19 patients have increased oxidative stress, oxidant damage, and glutathione deficiency

Researchers at Baylor College of Medicine have investigated the effect of infection with COVID-19 on the levels of oxidative stress, oxidant damage and...
www.bcm.edu www.bcm.edu

“Increased oxidative stress and reduced glutathione levels are associated with a number of conditions including ageing, diabetes, HIV infection, neurodegenerative disorders, cardiovascular disorders, neurometabolic diseases, obesity and others,” said corresponding author Dr. Rajagopal Sekhar, associate professor of medicine in the section of endocrinology, diabetes and metabolism at Baylor. “We suspected that COVID-19 also might be affecting oxidative stress and glutathione, and in this study we confirmed this in adults hospitalized with COVID-19. We found that these defects occur in all adult age groups, including young people, and worsen with increasing age.”
Click to expand...

That's diet. I mean, it's literally diet. It all comes down to how many of the substrates or their precursors people ingest. If you aren't getting sufficient micronutrients and amino acids, your enzymes won't have enough of the necessary substrates to detoxify ROS. Enzymes don't perform chemical reactions for free. They need catalytic substrates to use as "ammo".

This is how glutathione synthesis works:


And this is how the enzymes that use glutathione work:


No cysteine, glutamic acid, and glycine to make glutathione? No selenium to make selenoproteins? Oops, antioxidant enzymes stop working. ROS and chronic oxidative stress take over.

What the hell are people eating all day? Snack crackers?
 
  • Informative
  • Like
Reactions: Saltynotsosweet, Ted_Logan, The handsome tard and 15 others
annoyingfuck said:
The doctor, Jane Ruby? that put all of it together, pulled all the contacts together has been looking at clotting for quite some time, pretty sure going back to early last year.

There have already been studies done showing a drop in IQ of 20points, meaning the average IQ is now dumb black person level in white kids.

So all lockdown fault, nothing to do with the not-vax of course, nah that's safe and effective, even when they tell us what is actually wrong.

I saw a comment recently that had a very valid point, saying that even with all the scrubbing from VAERS that has been done, the fact that they have raised the myocarditis level from rare, means that it's a lot more serious most people even feared it would be.


On the topic of getting the coof, a few months ago my housemate came down with the flu, thought they'd test themselves, and what do you know, rat test said positive. I came down with something a week later, didn't bother testing.
I don't know if it's because I've had us on almost the whole lot of DT's supplement list for quite some time, plus we had been pretending we were sheep for a few months prior as per borsabil's instructions, and upped the frequency when the test showed positive (for me personally I only needed to add the NAC, everything else I've been taking for years, housemate needed to add one or two others), neither of us got a fever, or lost smell or taste. For both of us, it was just a normal run of the mill flu, like we've had every year. Coughing was annoying as fuck, like normal, I learnt to control coughing when I was a kid so just kept up the lozenges and throat sprays with a few 'cold & flu' hot drinks, barely any to no congestion (we both have allergies/sinus issues to start off with anyway).
The only thing that changed was that I made them stop walking (they normally walk an hour a day) just in case it actually was the coof, and only due to delta still hanging around. In saying that after two weeks they went back to their normal routine, which includes a 12km walk every weekend.
Click to expand...
Worse, they didn't only admit that myocarditis does happen, they also admitted that Long Covid symptoms and "post vaccine" syndrome have the same symptoms. But nobody cares.
 
  • Informative
  • Feels
  • Like
Reactions: Exterminatus, GloJojo, The handsome tard and 11 others
Meriasek said:
Worse, they didn't only admit that myocarditis does happen, they also admitted that Long Covid symptoms and "post vaccine" syndrome have the same symptoms. But nobody cares.
Click to expand...

"Long COVID" is not actually anything new to medical science. It was well understood back in the 2000s that SARS had long-term sequelae. It was probably SARS-CoV Spike that was the causative agent of that, too.

www.ncbi.nlm.nih.gov

SARS: prognosis, outcome and sequelae

Severe acute respiratory syndrome (SARS) is associated with considerable morbidity and mortality in the acute phase. Worldwide case fatality rate is 11% (range 7 to 27%) for the most severely affected regions. Several adverse prognostic factors have been ...
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov

Severe acute respiratory syndrome (SARS) is associated with considerable morbidity and mortality in the acute phase. Worldwide case fatality rate is 11% (range 7 to 27%) for the most severely affected regions. Several adverse prognostic factors have been identified, including advanced age, presence of comorbidity, higher lactose dehydrogenase levels and initial neutrophil count, but the impact of viral and other host factors on outcome is unknown. Published data on sequelae of SARS are limited. Clinical follow‐up of patients who recovered from SARS has demonstrated radiological, functional and psychological abnormalities of varying degrees. In the early rehabilitation phase, many complained of limitations in physical function from general weakness and/or shortness of breath. In a small series of subjects who underwent CT scan of the chest, over half showed some patchy changes consistent with pulmonary fibrosis. Lung function testing at 6–8 weeks after hospital discharge showed mild or moderate restrictive pattern consistent with muscle weakness in 6–20% of subjects. Mild decrease in carbon monoxide diffusing capacity was detected in a minority of subjects. Preliminary evidence suggests that these lung function abnormalities will improve over time. Psychobehavioural problems of anxiety and/or depression were not uncommon in the early recovery phase, and improved over time in the majority of patients. Avascular necrosis of the hip has been reported as another complication. The long‐term sequelae of SARS are still largely unknown. It is important to follow up these patients to detect and appropriately manage any persistent or emerging long‐term sequelae in the physical, psychological and social domains.
Click to expand...


There is a lot of evidence that when a severe infection sweeps through the population, ME/CFS will often follow. The Institute of Medicine’s (NAM) 2015 report concluded that ME/CFS may be triggered by a number of acute viral infections, including herpesviruses such as EBV or HHV-6, enteroviruses, and echoviruses. A study on Epstein-Barr virus, Q Fever, and Ross River virus showed that ~12% of subjects across the board met ME/CFS criteria at 6 months after clearing the infection; and another study of people with mononucleosis (Epstein-Barr virus) produced identical numbers. 20% of patients with West Nile Virus (n=140) met the criteria for CFS six months after tests first returned negative for West Nile. There are also a handful of highly-publicized outbreaks leading to ME/CFS: some of the biggest ones include the Epstein-Barr Viral outbreaks in New York; the Lake Tahoe outbreak in Nevada; and the Royal Free Outbreak in London.

SARS-CoV-2 would not be the first coronavirus to result in documented ME/CFS. Studies have shown that long-lasting disabling symptoms commonly occur in people who contracted two other coronaviruses that cause SARS and Middle East Respiratory Syndrome (MERS). In one study, 27% of SARS survivors were found to meet CFS criteria several years after developing SARS.
Click to expand...

SARS survivors reported persistent loss in lung capacity, neurological/mental issues, ME/CFS, et cetera. In other words, before there was such a thing as "Long COVID", scientists already knew about "Long SARS" well over a decade ago, and anticipated that COVID-19 may have persistent sequelae as well.

Spike and its toxicity and amyloidogenic effects may be causing both post-COVID sequelae and post-vaccine symptoms. If that is the case, and the vaccine is triggering systemic (or vascular, or cerebrovascular) amyloidosis, then it needs to be taken off the shelf immediately.
 
  • Informative
  • Like
Reactions: Exterminatus, GloJojo, Discourteous Discourse and 11 others
The daughter of one US Rep. passed away and some wonder if the vaxx was behind this?

Democratic U.S. Rep. Sean Casten's 17-year-old daughter, Gwen, died Monday morning at the family's Downers Grove home, his office and police announced.
Downers Grove police went to the Casten home about 6:50 a.m. Monday after receiving a call about an unresponsive teen, the department said in a news release. Gwen was dead, first responders determined, and the DuPage County coroner's office was called. Her death is under investigation.
Click to expand...
 
  • Feels
  • Informative
  • Like
Reactions: Discourteous Discourse, Cpl. Long Dong Silver, Forsaken Wanderer and 9 others
  • Feels
  • Like
  • Optimistic
Reactions: Exterminatus, GloJojo, Dude Snakes and 16 others
@Drain Todger
This persistence of pseudouridylated mRNA makes it more likely for it to be taken up by LINE-1 retrotransposons (that is, endogenous reverse transcriptase activity), converted into DNA, and integrated into the genome. If the region it's integrated into is not silent and expresses a protein, then that somatic cell may express Spike for as long as it lives. That is, until the immune system comes and kills it, which, given that it's expressing Spike on its surface, is practically guaranteed to happen. Immune cells don't know the difference between a cell with viral proteins on its surface or a virus with viral proteins on its surface. They're like blind guys feeling around with a cane. If macrophages and neutrophils feel something wrong, some foreign object that's not supposed to be there, then they automatically swallow and digest whatever it is.
Click to expand...
So it's not permanent if you have an immune system, innit? It'll just take longer than planned until the spike expression is stopped, and since it's not a replicating virus it should still be over a bit faster than an infection, I guess?
But then there's the question of the effect of the distribution of the spike-producing cells in the body. With an infection it'll likely be mostly concentrated around the respiratory tract, but with the vaccine the mRNA gets potentially distributed a bit more, and spike-producing cells are in places where it'd do more damage, I guess?
 
  • Like
  • Agree
Reactions: Forsaken Wanderer, Brain Problems, SCSI and 3 others
Meriasek said:
@Drain Todger

So it's not permanent if you have an immune system, innit? It'll just take longer than planned until the spike expression is stopped, and since it's not a replicating virus it should still be over a bit faster than an infection, I guess?
But then there's the question of the effect of the distribution of the spike-producing cells in the body. With an infection it'll likely be mostly concentrated around the respiratory tract, but with the vaccine the mRNA gets potentially distributed a bit more, and spike-producing cells are in places where it'd do more damage, I guess?
Click to expand...
That's the main misconception about SARS-CoV-2. The primary site of infection is not the respiratory tract. It enters via the respiratory tract and likely infects pulmonary pneumocytes, but then quickly and opportunistically migrates to the endothelial cells of pulmonary capillaries and larger blood vessels, infecting them.



COVID-19 is an airborne blood vessel disease. It primarily has tropism for cells expressing ACE2, and because of the close relationship between the RAAS and the circulatory system, that means vascular ECs and pericytes are the most affected cells.

The mRNA vaccines, consisting of pseudouridylated mRNA stuffed in a PEGylated lipid shell, can basically transfect any cells they come in contact with, forcing them to produce Spike.

If that's heart muscle cells, and it lures in immune cells to attack them, whoops!


In conclusion, it is essential to underline that every human cell that intakes the LNPs and translates the viral protein (in case of the mRNA vaccines), or that gets infected by the adenovirus and expresses and translates the viral protein (in case of the adenovirus-based vaccines), is inevitably recognized as a threat by the immune system and killed (Figure 1). There are no exceptions to this mechanism. The severity of the resulting damage and the consequences for health depend on the quantity of the cells involved, on the type of tissue and on the strength of the following autoimmune reaction. For instance, if the mRNA contained in the LNPs would get internalized by cardiac myocytes, and such cells would produce the spike protein, the resulting inflammation would likely lead to the necrosis of the myocardium, with an extent proportional to the number of involved cells. Therefore, it is fundamental to perform pharmacokinetic evaluations in humans, in order to determine the exact biodistribution of the vaccines against COVID-19, and thus to identify the possible tissues at threat.
Click to expand...


Low power scanning of heart sections showed blue stained thickened visceral pericardium over the right atrium and ventricle at 1 dpi of IV vaccine, which became more prominent at 2 dpi (Figure 2A). At higher magnification, calcific deposits were seen in these thickened pericardial tissues (Figure 2D). Multifocal pericardial and myocardial inflammatory cell infiltrates and interstitial oedema were also observed (Figure 2C). Frequent foci of cardiomyocytes had degenerative changes as evident by the loss of the normal pattern of cross-striation and occasionally sarcoplasmic vacuolation, and necrotic changes as distinguished by the attainment of a homogenous appearance, sarcoplasmic fragmentation, or pyknosis (Figure 2E). These changes were significantly more frequent in the IV vaccine group at 2 dpi (Table 1) and more often in the right atrium and right ventricles of the affected animals and especially prominent on their pericardial side. Immunohistochemical staining with anti-CD45 (biomarker for immune cells of lymphoid or myeloid origin) indicated that these were leukocytes, of which many were macrophages or histiocytes positive for CD68. CD3-positive T cells were seen less often (Figure 2G).The numbers of leukocytes were more than 14 per square millimeter in the affected myocardial foci. These findings suggested that mice given IV mRNA COVID-19 vaccine can develop acute myopericarditis. Similar histopathological changes and severity were found in male mice (Supplementary Figures 2B, 2C).
Click to expand...

The virus is, essentially, gated behind its tropism for specific cells expressing specific proteins that it can latch onto. Gene therapy drugs with lipid nanoparticles for delivery, on the other hand, can transfect anything. Anything at all.
 
  • Informative
  • Like
Reactions: Forsaken Wanderer, Ted_Logan, Ira the Weatherman and 6 others
You must log in or register to reply here.
Back