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They post, we refute with facts.  They don't/can't refute facts.  They throw out more conspiracies, we refute with facts.  They don't/can't refute facts.  Toss out some off the wall doctor on youtube.  We post several facts concerning said doctor in video.  They call us snowflakes.  And so on and so on and so on.  You can see the pattern through out this entire thread and the last one.  

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2 hours ago, Arielle Popstar said:

In past these were considered discussions of current events but with the advent of sjw's and snowflakes, opposing views have become fake news and misinformation. Lively debates are now relics of the past it seems.

I don't think I am a snowflake posting fake news.  I'm not even sure what this snowflake name means.  

But, I don't think A) you understand that Covid is a very vicious virus as well as a rapid evolver and that B) Ivermectin is not some kind of miracle drug.  

Perhaps a cocktail will be found eventually but it takes time, perhaps years, but until then the virus has mutated into a more severe and more deadly virus.  The more that are vaccinated the better but I don't believe in forcing anyone either.  But, don't just act like a Trump clone being an SJW against the wicked corruption in Washington and the media who are making all this up.  See point A and B above.  My friend's daughter is a nurse.  My friend was suicidal from all her daughter has had to go through.  This is not some game.

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C'mon, it is all very simple.

1. Never believe mainstream medicine and doctors who spend a lifetime studying and researching, ever. Life can't be that simple. They studied to misinform people and implant secret WiFi transmitters.

3. Always blame Bill Gates and the Clintons somehow.  They did meet each other you know. And of course her e-mails.

4. Never have a point 2 in your argumentation.

More seriously:

I don't give s*** any longer what others think about the whole covid-19 situation.
I stick to the basic rules (1.5 meters distance, wash my hands often, stay away from crowded places, wear a mask in public spaces, get vaccinated and stick to the rules anyhow, but less frightened to go out.)

I don't feel the urge any longer to try and explain stuff. If experts can't convince certain people, I certainly can't.
There is unfortunately no medicine against stupidity and stubbornness.

Edited by Sid Nagy
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2 hours ago, Nalates Urriah said:

If this were a perfect world, yes. But there is way more going on than just legitimate evaluation for drugs.

Consider the Johnson & Johnson CoVid vaccine. Six people out of about 7 million had a bad reaction and died. Tylenol kills 150 per year. Yet J&J was considered dangerous!?! J&J was being given to prevent a "likely possibility" of death. Tylenol is given for minor aches and pains, among other things. Something seems out of wack.

Have you looked to see how many members at the top of the FDA and the boards making recommendations to the FDA have ties to big pharma?

Have you looked at Cytodyn's Leronlimab and the challenges they are having getting FDA approval for a treatment that for all practical purposes cures most viral infections? They started developing it for HIV. They have had awesome results with CoVid and few if any side-effects. But they can't get a EUA from the FDA for use with CoVid as a treatment. They are being forced into more and more studies. The Philippines is using it and UK is using it in trails. What's with the FDA?

There is no hard proof the FDA is misusing their position. But it wouldn't be the first time people running a government agency miss used a position of authority. And the appearance of miss use is striking. If there is an effective treatment with no or few side-effects, why take an experimental vaccine that may induce ADE? People wouldn't and that would have a multi-billion dollar impact on big pharma.

So, my actual answer is, not necessarily.

Yes, but I think I mentioned that my niece and her fiancé both work in British NHS hospitals, so they're subject to UK regulation, and our regulators move pretty quickly when they have to.

Experimental treatments for Covid are being tested all the time and, if and when they prove safe and effective, they go into general use.    It's happening all the time

https://www.bbc.co.uk/news/health-52354520

The idea that caring professionals like my niece and her fiancé are standing by helplessly watching patients die because they're not allowed to administer particular drugs they believe would help the patient is insulting nonsense, to my mind.

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5 hours ago, Nalates Urriah said:

Consider the Johnson & Johnson CoVid vaccine. Six people out of about 7 million had a bad reaction and died. Tylenol kills 150 per year. Yet J&J was considered dangerous!?! J&J was being given to prevent a "likely possibility" of death. Tylenol is given for minor aches and pains, among other things. Something seems out of wack.

I'm not sure what point you're trying to make. J&J makes both the scrutinized vaccine and Tylenol.

Like it or not, public policy can both reflect and affect public perception, even intentionally. The public is understandably wary of the new (J&J vaccine) and comfortable with the old (J&J Tylenol), regardless of the actual risks.  
@Lyssa Greymoonposted a parody that explains how things might get or seem out of whack.

5 hours ago, Nalates Urriah said:

Have you looked at Cytodyn's Leronlimab and the challenges they are having getting FDA approval for a treatment that for all practical purposes cures most viral infections?

That's a remarkable claim, Nalates. Cytodyn has only promoted Leronlimab as a treatment.

The following is a synopsis of my quick look into Leronlimab. I'm not an immunologist, so take my take on this with some salt.

Leronlimab is potentially anti-viral for the CCR5-tropic strain of HIV (90% of current cases), where it blocks the CCR5 receptor on the human cell wall, thwarting step two in the HIV entry pathway. It doesn't work for the other 10%. There go your "cure" and "most viral infections" claims, and I haven't even stepped outside of HIV. If it were approved as an HIV treatment, one would take it, perhaps twice a month, for life.

Covid-19 does not use the CCR5 pathway to infect, so Leronlimab cannot function as a true anti-viral there. Instead, it modulates the cytokine immune response (which does use CCR5), tamping down cytokine storms we've read about since Covid-19 first knocked on our door. This is only useful in late stage infection, and only in those who actually endure a cytokine storm. Inexpensive steroids have been used to perform this same function.

I imagine there are thousands of viruses (measles, polio, influenza, rhino, etc) that don't use the CCR5 enabled pathway. To suggest Leronlimab has any potential to cure those viruses is nonsense.

In fact, research into the function of CCR5 in immune function suggests that drugs like Leronlimab might cause harm in certain circumstances.

From this article... https://academic.oup.com/jid/article/197/2/183/809887

"Although there is reason to be optimistic about the development of CCR5 antagonists for the treatment of HIV-1 infection, it is also reasonable to hypothesize that antagonism of CCR5 will be advantageous in certain circumstances but disadvantageous in others."

The highlighted part of that quote refers to the paragraph above it in the article where there's a short explanation of encephalitis research suggesting a potential that CCR5 antagonists might actually help transmission of HIV inside the central nervous system.

Leronlimab is but one of many drugs jockeying for attention from the medical community. Here's a short list of competitors...

https://pharmaceutical-journal.com/article/feature/everything-you-need-to-know-about-the-covid-19-therapy-trials

Cytodyn released the results of its most recent clinical trial last month, cratering the company's stock price. Their chief scientific officer stepped down shortly after, without explanation...

https://www.fiercebiotech.com/biotech/cytodyn-s-chief-scientific-officer-rahman-quietly-exits-amid-leronlimab-limbo

While it might be possible to treat the symptoms of an infectious viral disease to the point it's just a minor nuisance,  such treatment does nothing to stop the proliferation and mutation of the virus. That puts us perpetually in peril of dealing with a mutation that can't be treated. That's why vaccination is the go-to "cure" for communicable disease. If we can teach our own immune systems to recognize and destroy the pathogen, we've cut off proliferation at the knees and increased the possibility of extinction.

Those who refuse vaccination for other than medically sensible reasons are, to my mind, condemning humankind to suffer their ignorance, indefinitely.

Let me repeat your claim, Nalates... Leronlimab is "a treatment that for all practical purposes cures most viral infections?

Do you still stand by that claim?

This was an interesting dive. My reticular activating system is now primed for CCR5. I look forward to accidentally learning more about it.

...goes off to plant more marigolds.

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2 hours ago, Madelaine McMasters said:

I'm not sure what point you're trying to make. J&J makes both the scrutinized vaccine and Tylenol.

Like it or not, public policy can both reflect and affect public perception, even intentionally. The public is understandably wary of the new (J&J vaccine) and comfortable with the old (J&J Tylenol), regardless of the actual risks.  
@Lyssa Greymoonposted a parody that explains how things might get or seem out of whack.

That's a remarkable claim, Nalates. Cytodyn has only promoted Leronlimab as a treatment.

The following is a synopsis of my quick look into Leronlimab. I'm not an immunologist, so take my take on this with some salt.

Leronlimab is potentially anti-viral for the CCR5-tropic strain of HIV (90% of current cases), where it blocks the CCR5 receptor on the human cell wall, thwarting step two in the HIV entry pathway. It doesn't work for the other 10%. There go your "cure" and "most viral infections" claims, and I haven't even stepped outside of HIV. If it were approved as an HIV treatment, one would take it, perhaps twice a month, for life.

Covid-19 does not use the CCR5 pathway to infect, so Leronlimab cannot function as a true anti-viral there. Instead, it modulates the cytokine immune response (which does use CCR5), tamping down cytokine storms we've read about since Covid-19 first knocked on our door. This is only useful in late stage infection, and only in those who actually endure a cytokine storm. Inexpensive steroids have been used to perform this same function.

I imagine there are thousands of viruses (measles, polio, influenza, rhino, etc) that don't use the CCR5 enabled pathway. To suggest Leronlimab has any potential to cure those viruses is nonsense.

In fact, research into the function of CCR5 in immune function suggests that drugs like Leronlimab might cause harm in certain circumstances.

From this article... https://academic.oup.com/jid/article/197/2/183/809887

"Although there is reason to be optimistic about the development of CCR5 antagonists for the treatment of HIV-1 infection, it is also reasonable to hypothesize that antagonism of CCR5 will be advantageous in certain circumstances but disadvantageous in others."

The highlighted part of that quote refers to the paragraph above it in the article where there's a short explanation of encephalitis research suggesting a potential that CCR5 antagonists might actually help transmission of HIV inside the central nervous system.

Leronlimab is but one of many drugs jockeying for attention from the medical community. Here's a short list of competitors...

https://pharmaceutical-journal.com/article/feature/everything-you-need-to-know-about-the-covid-19-therapy-trials

Cytodyn released the results of its most recent clinical trial last month, cratering the company's stock price. Their chief scientific officer stepped down shortly after, without explanation...

https://www.fiercebiotech.com/biotech/cytodyn-s-chief-scientific-officer-rahman-quietly-exits-amid-leronlimab-limbo

While it might be possible to treat the symptoms of an infectious viral disease to the point it's just a minor nuisance,  such treatment does nothing to stop the proliferation and mutation of the virus. That puts us perpetually in peril of dealing with a mutation that can't be treated. That's why vaccination is the go-to "cure" for communicable disease. If we can teach our own immune systems to recognize and destroy the pathogen, we've cut off proliferation at the knees and increased the possibility of extinction.

Those who refuse vaccination for other than medically sensible reasons are, to my mind, condemning humankind to suffer their ignorance, indefinitely.

Let me repeat your claim, Nalates... Leronlimab is "a treatment that for all practical purposes cures most viral infections?

Do you still stand by that claim?

This was an interesting dive. My reticular activating system is now primed for CCR5. I look forward to accidentally learning more about it.

...goes off to plant more marigolds.

Priceless.

I knew there was a reason I kept you around.

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The therapeutics debate is ongoing in India - meanwhile they are going ahead and prescribing Ivermectin, Remdesivir and various other things. If they didn't people would probably purchase it anyway on the black market and self-medicate with who knows what. 

I think the best lesson we can learn from India at this point is, keep masking, strict hygiene, social distancing, get vaccinated if we possibly can, and do our utmost not to swamp the healthcare system. It's terrifying to think of this sweeping through Southeast Asia. Several countries are already finding the more infectious strain.  Next couple of weeks are going to be tense. 🙏

Edited by Akane Nacht
i kenot spell
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2 hours ago, Coffee Pancake said:

JFC. There so needs to be a "We're not worthy" response button.

I wrestled with this, Coffee. I think you were showing appreciation for my response to Nalates. I hovered over the "Thank You" icon for quite some time, thinking it might be a little presumptuous to presume that's what you were actually doing. Scylla helped me over the edge.

The fact is we're all worthy of taking time to bat away ignorance and misinformation.

I hope that's what I'm doing.

It's hard to tell.

Edited by Madelaine McMasters
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1 hour ago, Akane Nacht said:

The therapeutics debate is ongoing in India - meanwhile they are going ahead and prescribing Ivermectin, Remdesivir and various other things. If they didn't people would probably purchase it anyway on the black market and self-medicate with who knows what. 

The same would probably be happening more here also in the US, if the US were having the COVID outbreak levels and treatment availability as India. 

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1 minute ago, Love Zhaoying said:

With 2 shots, did I get 2 implants, or does the second shot activate the chip?

Two.

Most people think the implants are for monitoring. They're actually for control. With one implant, they can only move you about by applying force, and that looks eerily unnatural. With two implants, they can apply torque, pointing you in the desired direction, attracting less attention.

Two implants also provides redundancy.

And finally, the real reason for two...

They can mate and reproduce.

It's all over, Love.

 

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5 hours ago, Madelaine McMasters said:

Leronlimab is "a treatment that for all practical purposes cures most viral infections?

Death, for all practical purposes.."cures" disease in 100% of patients who died - they are never bothered again by the disease or its symptoms. Found the parody!

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53 minutes ago, Madelaine McMasters said:

The fact is we're all worthy of taking time to bat away ignorance and misinformation.

I hope that's what I'm doing.

It's hard to tell.

Yeah, this. The part most amazing about your responses is their dispassionate rationality even after all this time. Personally, I can't do it anymore. I can't count the times I've hovered over the Submit button before deleting a response that "explains" in florid detail how I marvel at their cognitive condition. (Why are they so proud to be so gullible? How can they cite the authority of these quack "doctors" then dismiss the vast majority of medical science? What makes them so very sure of so many things that are at best tragically wrong? Where do they gather all this disinformation, and why? How many more of them are out there, naively acting in earnest, not merely adding entropy for the grins and giggles of Mother Motherland?) You can see where this would take the discussion, which you so patiently avoid, still.

So instead I've taken to bringing up topics into which their "sources" may not yet have delved. Here, for example, an historical tidbid from an Economist summary of the emerging science of Long COVID:

Quote

In the 1890s one of the biggest pandemics in history, known at the time as “Russian flu”, swept the world. It left 1m people dead. Russian flu is now thought to have been misnamed. It was probably not influenza, but rather a coronavirus ancestral to one that now just causes symptoms described by sufferers as “a cold”. When it was new, however, few people had immunity to it, so it was often lethal. And not only that. For, as the pandemic receded, it left in its wake a wave of nervous disorders.

 

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Our cases reduced rapidly in 2-3 day. Is it a magic or is it a miracle? :P or lock downs? nope.. It is tourism season.

We are still under lock down but tourist on the street :) I will pretend as tourist and try my luck.

E0ewtWdXEAQIIc9?format=jpg&name=large

Edited by RunawayBunny
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10 hours ago, Madelaine McMasters said:

The following is a synopsis of my quick look into Leronlimab. I'm not an immunologist, so take my take on this with some salt.

Leronlimab is potentially anti-viral for the CCR5-tropic strain of HIV (90% of current cases), where it blocks the CCR5 receptor on the human cell wall, thwarting step two in the HIV entry pathway. It doesn't work for the other 10%. There go your "cure" and "most viral infections" claims, and I haven't even stepped outside of HIV. If it were approved as an HIV treatment, one would take it, perhaps twice a month, for life.

Covid-19 does not use the CCR5 pathway to infect, so Leronlimab cannot function as a true anti-viral there. Instead, it modulates the cytokine immune response (which does use CCR5), tamping down cytokine storms we've read about since Covid-19 first knocked on our door. This is only useful in late stage infection, and only in those who actually endure a cytokine storm. Inexpensive steroids have been used to perform this same function.

I imagine there are thousands of viruses (measles, polio, influenza, rhino, etc) that don't use the CCR5 enabled pathway. To suggest Leronlimab has any potential to cure those viruses is nonsense.

In fact, research into the function of CCR5 in immune function suggests that drugs like Leronlimab might cause harm in certain circumstances.

From this article... https://academic.oup.com/jid/article/197/2/183/809887

"Although there is reason to be optimistic about the development of CCR5 antagonists for the treatment of HIV-1 infection, it is also reasonable to hypothesize that antagonism of CCR5 will be advantageous in certain circumstances but disadvantageous in others."

 

The idea of treating C19 cytokine storms with antivirals or rheumatoid arthritis drugs came up last year while trying to figure out why some patients had awful outcomes after contracting COVID19 while others sailed through with a minor cold.

The gravely ill ones presented a cytokine storm syndrome. The problem was to try and determine what kind of storm, as inflammatory responses produce certain signatures (the interleukins IL-s and CCRs). So as you correctly pointed out, the correct storm needs to be defined before the appropriate treatment is given.

At the start of the pandemic it was noted that very ill patients presented elevated concentrations of IL-6. Leronlimab disrupts signaling to CCR5 receptors so in a way, it tells the immune system to stop recruiting T and macrophages (the inflamatory cells). In trials (out of desperation) ICU patients were given Leronlimab and that stopped the inflamatory process.

The problem though is that in randomised studies it did not work as well. What worked better was giving patients IL-1 receptor antagonists. Tocilizumab also binds the IL-6 receptors and was also used in trials. I believe there are still trials in this area.

I am not an immunologist, just a vet but immune systems are like biological machines and each one of us is tuned slightly different so responses to aggressors can be dramatically different in people that otherwise on the surface look perfectly similar. 🙂

 

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5 hours ago, Krystina Ferraris said:

The idea of treating C19 cytokine storms with antivirals or rheumatoid arthritis drugs came up last year while trying to figure out why some patients had awful outcomes after contracting COVID19 while others sailed through with a minor cold.

The gravely ill ones presented a cytokine storm syndrome. The problem was to try and determine what kind of storm, as inflammatory responses produce certain signatures (the interleukins IL-s and CCRs). So as you correctly pointed out, the correct storm needs to be defined before the appropriate treatment is given.

At the start of the pandemic it was noted that very ill patients presented elevated concentrations of IL-6. Leronlimab disrupts signaling to CCR5 receptors so in a way, it tells the immune system to stop recruiting T and macrophages (the inflamatory cells). In trials (out of desperation) ICU patients were given Leronlimab and that stopped the inflamatory process.

The problem though is that in randomised studies it did not work as well. What worked better was giving patients IL-1 receptor antagonists. Tocilizumab also binds the IL-6 receptors and was also used in trials. I believe there are still trials in this area.

I am not an immunologist, just a vet but immune systems are like biological machines and each one of us is tuned slightly different so responses to aggressors can be dramatically different in people that otherwise on the surface look perfectly similar. 🙂

Thanks for jumping in and adding more background, Krystina. I'm neither immunologist nor vet, but I am endlessly curious and the immune system fascinates me, particularly since mine doesn't work quite right.

Now it's time for some bad analogies.

Yesterday, I learned that CCR5 isn't just something a virus can use to get into a cell, but it's also something a cell can use to call for help. This really complicates things. If most HIV infections are using CCR5 to kill, it might be worth blocking access. But if 10% are using CXCR4, you don't really want to compromise the body's ability to call for help via CCR5. If your volunteer fire department is full of nutcases, tone down the urgency of your call.

I think a lot of us are familiar with the analogy of a virus having a key to a door on the cellular factory, but now I realize it ain't that simple (is anything?). There are circumstances in which nailing the the front door shut so the key won't work also disconnects your phone, and some intruders have a key to the back door.

Even more interesting is the possibility that doors operate differently depending on where the factory is located. In most of the body, blocking a doorway prevents access, but in the central nervous system, blocking a doorway might allow it. That was hinted at by the encephalitis research I cited, raising concern that Leronlimab might actually exacerbate NeuroAIDS.

It really comes as no surprise to me that virtually any knob or switch you find in the human machine is potentially connected to multiple things in the weirdest way imaginable.

So much to wonder about, I love it.

Edited by Madelaine McMasters
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19 hours ago, Sid Nagy said:

4. Never have a point 2 in your argumentation.

This has actually been shown to be very good advice. Every point in an argument is an attack surface. Though data driven people like me love to dig up facts, that is often counterproductive. If I present only one point, I can make only one error. If I present fifty, I'm toast. Any error in the fifty taints them all. If all points are correct, every point is still only 1/50th of the argument.

Put all your wood behind one arrow.

Edited by Madelaine McMasters
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