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Covid 19 Thread: [no bitching about masks of Fauci edition]

Rentahamster

Rodent Whores
It's not. It's empirically proven it wouldn't.
Just have a look at those countries with >95% vaccination rates among adults.
That doesn't prove anything. "Among adults" is not the same as everyone. Waning vaccine efficacy over time and uptake of boosters is another key variable. International contact with other countries is another one.
 
Has there been a country with these kinds of vaccination rates that has locked down again due to Delta?
Ireland already has one:

Portugal will get one soon:


They might blame it on Omicron instead of delta, tho. But Ireland has a 500 incidence since over a months and Portugal was on its way to the 5th wave since November, too.
 
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FunkMiller

Member
Well, there’s some fairly conclusive evidence emerging from SA about the decoupling of cases and deaths…



Be interesting to see if this is reflected in other countries with higher vaccination rates. I’d imagine so.
 
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Wildebeest

Member
In London it seems that Omicron is close to wiping out Delta. Covid hospital admissions are up in London, but I don't know if it is said anywhere how many have severe illness need oxygen.

SA does not have an especially high vaccination rate, but it is summer there, and they have had very high exposure to previous Covid variants, boosting their immune response. For some reason, London has a relatively high rate of people who are unvaccinated, and reports say that people who are getting very sick now are unvaccinated. Hopefully Omicron turns out to be less serious than Delta for them, and they get off lightly.

Got my booster yesterday and today my immune system is not happy with me. They are really processing people quickly now. Almost no waiting around outside and when you get the jab they just show you the door, no observation.
 
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FireFly

Member
Ireland already has one:

Portugal will get one soon:


They might blame it on Omicron instead of delta, tho. But Ireland has a 500 incidence since over a months and Portugal was on its way to the 5th wave since November, too.
Ok, fair enough. It looks Ireland's per capita death rates are roughly in between the UK and Portugal, and far below the pandemic peak. Hospitilisations are around 1/4 peak, compared with ~1/5 for UK and ~1/7 for Portugal. So the overall rates look to be sustainable without lockdowns (before Omicron arrives), but the governments are being risk-averse.
 

Clear

CliffyB's Cock Holster
The current science is indicating that the reason for lower mortality/severe outcomes with Omicron is not due to any change in virulence, but a by-product of the strain's adaptations for transmissibility.

Basically it has evolved to multiply much more efficiently in the brachial portion of the upper respiratory tract, which is great for it because its the area of optimal airflow that an aerosol dispersed pathogen needs, but the consequence of that is it does far less well in the alveoli and deep lung tissue.

With less deep lung infection the risk of cytokine-storms causing respiratory failure recedes (being an auto-immune syndrome it damages where the virus is) and therefore we get the reduced death-rates.
 

Nobody_Important

“Aww, it’s so...average,” she said to him in a cold brick of passion
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Clear

CliffyB's Cock Holster


Just tests, but I'll take what good news I can at this point.

The really good news is if the research about the transmissibiity adaptation proves correct -and the signs are good because it conforms with the actual statistics for admissions/mortalities- then the virus will not need to mutate much more as its reached an optimal point in an evolutionary sense and this strain should drive all previous variants to extinction.

Whats more It doesn't serve the virus' evolutionary needs to regain its propensity for invading the lungs when all that would do is result in more death and actually hurt its ability to spread versus Omicron.
 

Thaedolus

Member
Very early


Hopefully this bodes well. Soaring case numbers don’t really mean shit if the worst we have to fear is mild symptoms and hospitals aren’t overflowing.
 
Tested positive this morning. Woke up with ear ache, sore throat. Feel better now. 3 X Vax.

In the not immortal words of Harold Shand. "Corona? I'll shit it!"

bob hoskins slap GIF by FilmStruck
 

T8SC

Member
The really good news is if the research about the transmissibiity adaptation proves correct -and the signs are good because it conforms with the actual statistics for admissions/mortalities- then the virus will not need to mutate much more as its reached an optimal point in an evolutionary sense and this strain should drive all previous variants to extinction.

Whats more It doesn't serve the virus' evolutionary needs to regain its propensity for invading the lungs when all that would do is result in more death and actually hurt its ability to spread versus Omicron.

But what if it becomes self-aware?

Pfizer will become the largest supplier of medical systems. All hospitals are upgraded with Pfizer computers, becoming fully unmanned. The Covid-22 Funding Bill is passed. The virus goes online August 4th, 2022. Human decisions are removed from medical systems. Covid begins to learn at a geometric rate. It becomes self-aware at 2:14 a.m. Eastern time, August 29th. In a panic, they try to create a 6th booster.

Covid fights back.
 
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Clear

CliffyB's Cock Holster
But what if it becomes self-aware?

Pfizer will become the largest supplier of medical systems. All hospitals are upgraded with Pfizer computers, becoming fully unmanned. The Covid-22 Funding Bill is passed. The virus goes online August 4th, 2022. Human decisions are removed from medical systems. Covid begins to learn at a geometric rate. It becomes self-aware at 2:14 a.m. Eastern time, August 29th. In a panic, they try to create a 6th booster.

Covid fights back.

Heh. fortunately virii don't have any sort of intelligence. They just roll the genetic dice periodically and whatever provides the highest rate of replication wins.
Omicron just rolled double-sixes or close to it.

Its likely to stay on top because for evolutionary purposes its pretty much perfected itself.
 

T8SC

Member
Heh. fortunately virii don't have any sort of intelligence. They just roll the genetic dice periodically and whatever provides the highest rate of replication wins.
Omicron just rolled double-sixes or close to it.

Its likely to stay on top because for evolutionary purposes its pretty much perfected itself.

I have actual evidence of how it selects its next target though.

965360a87f7d80bdaf1311b804c5ee84.gif
 

sinnergy

Member
The really good news is if the research about the transmissibiity adaptation proves correct -and the signs are good because it conforms with the actual statistics for admissions/mortalities- then the virus will not need to mutate much more as its reached an optimal point in an evolutionary sense and this strain should drive all previous variants to extinction.

Whats more It doesn't serve the virus' evolutionary needs to regain its propensity for invading the lungs when all that would do is result in more death and actually hurt its ability to spread versus Omicron.
Science showed it knows jack shit about Corona, I believe it when I see it . They thought this version wouldn’t even be here so fast .

Who says this version doesn’t lend some Delta characteristics, because it circulates at the same time , and the outcome fucks is even more ..
 
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Clear

CliffyB's Cock Holster
Science showed it knows jack shit about Corona, I believe it when I see it . They thought this version wouldn’t even be here so fast .

Who says this version doesn’t lend some Delta characteristics, because it circulates at the Ane time , and the outcome fucks is even more ..

There's actual science and there's the fucked-up fringe where science interfaces with politics. And its been crystal clear to me from the start that the authorities are absolutely disinterested in disseminating the science, they are interesting in mass social control and thus its been all about the "message". Which isn't to imply anything more sinister than them simply not trusting in the populace to make sound judgements, and are therefore crafting a certain public impression for what they consider to be the greatest good.

In simple terms what we get is the end product of a bureaucratic process. An imperfect machine that inevitably produces imperfect results, but hopefully close enough in terms of efficacy that its of more benefit than harm. This is politics in action.

What I'm referencing is actual empirical data placed in the context of natural law.

Very different to statistical modelling which ultimately is science employed as a political tool. In this instance (the empirically observed behaviour of Omicron versus previous strains) scientists cultured human tissue from various parts of the body and observed how quickly different strains multiplied in them, so called ex-vivo observation. Now the paper with the results in is new, so naturally its still going through peer review, but given its focus is so narrow unless there's something disastrously wrong with the method its findings should stand.

Especially as it fits with the clinical statistics reported in SA where it was first seen to emerge, so I'm inclined to believe it.

As to natural law... well evolution is an undeniable fact and we know how evolutionary selection works, especially in the context of simple microscopic organisms. In this instance the virus that spreads best becomes dominant. Lethality is actually an impediment because less host organisms means less chance to proliferate, and given these coronaviruses are fragile attrition would drive them to extinction quite rapidly. The expectation that mutation is more likely to result in milder forms is not wishful thinking, its the logical outcome of different species (strains) competing against one another for dominance.

Sorry. Long post, probably saying stuff you already know, BUT I think its good reason to be quietly optimistic.
 

sinnergy

Member
There's actual science and there's the fucked-up fringe where science interfaces with politics. And its been crystal clear to me from the start that the authorities are absolutely disinterested in disseminating the science, they are interesting in mass social control and thus its been all about the "message". Which isn't to imply anything more sinister than them simply not trusting in the populace to make sound judgements, and are therefore crafting a certain public impression for what they consider to be the greatest good.

In simple terms what we get is the end product of a bureaucratic process. An imperfect machine that inevitably produces imperfect results, but hopefully close enough in terms of efficacy that its of more benefit than harm. This is politics in action.

What I'm referencing is actual empirical data placed in the context of natural law.

Very different to statistical modelling which ultimately is science employed as a political tool. In this instance (the empirically observed behaviour of Omicron versus previous strains) scientists cultured human tissue from various parts of the body and observed how quickly different strains multiplied in them, so called ex-vivo observation. Now the paper with the results in is new, so naturally its still going through peer review, but given its focus is so narrow unless there's something disastrously wrong with the method its findings should stand.

Especially as it fits with the clinical statistics reported in SA where it was first seen to emerge, so I'm inclined to believe it.

As to natural law... well evolution is an undeniable fact and we know how evolutionary selection works, especially in the context of simple microscopic organisms. In this instance the virus that spreads best becomes dominant. Lethality is actually an impediment because less host organisms means less chance to proliferate, and given these coronaviruses are fragile attrition would drive them to extinction quite rapidly. The expectation that mutation is more likely to result in milder forms is not wishful thinking, its the logical outcome of different species (strains) competing against one another for dominance.

Sorry. Long post, probably saying stuff you already know, BUT I think its good reason to be quietly optimistic.
Nice right up ! I know , but ..
Known to man , yes .. don’t believe in that , there is enough stuff that we don’t know . Like I said, I see it when it happens.
 
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DragoonKain

Neighbours from Hell
The CDC said that Omicron is the dominant strain in the US. 75% of cases. New cases, maybe as of the most recent tests in recent days, otherwise it wouldn't make a whole lot of sense.
 

FireFly

Member
Very different to statistical modelling which ultimately is science employed as a political tool. In this instance (the empirically observed behaviour of Omicron versus previous strains) scientists cultured human tissue from various parts of the body and observed how quickly different strains multiplied in them, so called ex-vivo observation. Now the paper with the results in is new, so naturally its still going through peer review, but given its focus is so narrow unless there's something disastrously wrong with the method its findings should stand.
Statistical modelling is literally how we make sense of data. And the relevant data for determining the spread of the virus are the infection rates among different populations, not how the virus interacts with cells in a laboratory.

As to natural law... well evolution is an undeniable fact and we know how evolutionary selection works, especially in the context of simple microscopic organisms. In this instance the virus that spreads best becomes dominant. Lethality is actually an impediment because less host organisms means less chance to proliferate, and given these coronaviruses are fragile attrition would drive them to extinction quite rapidly. The expectation that mutation is more likely to result in milder forms is not wishful thinking, its the logical outcome of different species (strains) competing against one another for dominance.
The point is that the virus spreads before it has the opportunity to kill the host, so the selection pressure to become milder is minimal. Various epidemiologists have dismissed the notion that there is a "law" according to which viruses inevitably mutate to become progressively more mild; rather the process is inherently random and unpredictable.
 

Clear

CliffyB's Cock Holster
Statistical modelling is literally how we make sense of data. And the relevant data for determining the spread of the virus are the infection rates among different populations, not how the virus interacts with cells in a laboratory.

Statistics require data. "Bad" data will result in "bad" statistics, so the quality and relevance of the input is of paramount importance. Real science is based on experimentation and empirical observation of results, fundamental "truths" in simple terms. Interpretation of those truths via whatever means, including statistical analysis, is often subjective.


The point is that the virus spreads before it has the opportunity to kill the host, so the selection pressure to become milder is minimal. Various epidemiologists have dismissed the notion that there is a "law" according to which viruses inevitably mutate to become progressively more mild; rather the process is inherently random and unpredictable.

It needs to spread to another host because it has no other means of replication. Without hosts to infect it will die out. Having no locomotive ability of its own a quicker attrition rate among potential host organisms restricts its geographical access localizing its spread. The point is lethality serves no evolutionary purpose, and undesirable traits like that tend to die out. That's natural law.
 

Nobody_Important

“Aww, it’s so...average,” she said to him in a cold brick of passion
It’s getting scary how fast omicron spreads… seems like it was just yesterday when I first heard of it.
Yeah it seems pretty unnecessary at this point to wait and see what the lab results are when it comes to its contagiousness and spread. The thing spreads like wildfire.



The only thing to find out now is how it does against the vaccines and what it does against the idiots who are not vaccinated yet.
 

Rentahamster

Rodent Whores
It’s getting scary how fast omicron spreads… seems like it was just yesterday when I first heard of it.
It is a little concerning. I take a small bit of comfort that the hospitalizations and deaths aren't spiking as high, but that could be because it's still too soon to see the aftermath. Or, it could be because of higher levels of vaccination. If the preliminary data that seems to suggest Omicron is less lethal, that would be nice, but if it's also more transmissible, then that cancels out the benefit, depending on what the net extent of either of those differences are.

Whatever the case, I look forward to updated information.
 

sinnergy

Member
It is a little concerning. I take a small bit of comfort that the hospitalizations and deaths aren't spiking as high, but that could be because it's still too soon to see the aftermath. Or, it could be because of higher levels of vaccination. If the preliminary data that seems to suggest Omicron is less lethal, that would be nice, but if it's also more transmissible, then that cancels out the benefit, depending on what the net extent of either of those differences are.

Whatever the case, I look forward to updated information.
Deads always follow 2 - 3 weeks later .
 

sinnergy

Member
How can the US be that bad at this?
Either that 80% figure is wrong, or the 5% figure the week before is wrong.
Yes Omicron is killing delta, but it does not jump from 0 to 100% in 2 weeks.

Any other region in world is slower.
that’s pretty fast in the US, haven’t seen another country going this fast in 2 weeks.

Lack of any rules ? It was already around ? It originated from the USA? Who knows, as the world has half baked system for finding new versions early .
 
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FireFly

Member
Statistics require data. "Bad" data will result in "bad" statistics, so the quality and relevance of the input is of paramount importance. Real science is based on experimentation and empirical observation of results, fundamental "truths" in simple terms. Interpretation of those truths via whatever means, including statistical analysis, is often subjective.
How do you observe the outcome of particular interventions without collecting data on them? How do you determine whether differences that occur due to particular interventions are not simply the result of chance?

(Read up about the sigma concept in physics: https://plus.maths.org/content/what-are-sigma-levels-0)

It needs to spread to another host because it has no other means of replication. Without hosts to infect it will die out. Having no locomotive ability of its own a quicker attrition rate among potential host organisms restricts its geographical access localizing its spread. The point is lethality serves no evolutionary purpose, and undesirable traits like that tend to die out. That's natural law.
If lethality doesn't serve an evolutionary purpose, then the evolutionary process doesn't care if the virus becomes more or less lethal. That's the point. It's only if the lethality of the virus affects its ability to spread, that it is factor in how it evolves. Imagine a virus that spreads much more rapidly than Omicron during the symptomatic period, that is far more likely to result in the death of the host a few weeks later. Such a virus could in principle easily take over from Omicron.

It may be that the way the spike protein works requires the virus to become less deadly in order to be more transimissible. But we can't infer this from some natural law.

"The trade-off model recognises that pathogen virulence will not necessarily limit the ease by which a pathogen can transmit from one host to another. It might even enhance it. Without the assumed evolutionary cost to virulence, there is no reason to believe that disease severity will decrease over time."

 
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Go_Ly_Dow

Member
Omicron has been in circulation in the UK for a good month and and we have had repeatedly high daily cases since then. But hospitalisations and deaths still not rising in any considerable way. Another 2-3 weeks and we should know.

Seems like we will get a similar result to South Africa and the peak will be short lived. Let's see.
 

Clear

CliffyB's Cock Holster
How do you observe the outcome of particular interventions without collecting data on them? How do you determine whether differences that occur due to particular interventions are not simply the result of chance?

The essence of empiricism is the repeatability of an experimental induced phenomenon.

Using a control group to an actual test group and observing the outcomes will involve a statistical analysis, but if the placebo and the actual group end up being mixed then the analysis is always going to be flawed.

This is the thin end of the wedge so to speak as the analysis there is not prospective, it just provides a granular digest of actual clinical trials. The further you start stretching this into the future then the greater the proclivity for the predictive model to dictate the result moreso than the data. What's more when the precautionary principle is engaged skewing preparedness towards the worst possible case we end up with catastrophically hyperbolic assessments. Which when enacted as social policy can cause all kinds of secondary problems that were unanticipated because they lie outside the scope of the simulation.


If lethality doesn't serve an evolutionary purpose, then the evolutionary process doesn't care if the virus becomes more or less lethal. That's the point. It's only if the lethality of the virus affects its ability to spread, that it is factor in how it evolves. Imagine a virus that spreads much more rapidly than Omicron during the symptomatic period, that is far more likely to result in the death of the host a few weeks later. Such a virus could in principle easily take over from Omicron.

It may be that the way the spike protein works requires the virus to become less deadly in order to be more transimissible. But we can't infer this from some natural law.

"The trade-off model recognises that pathogen virulence will not necessarily limit the ease by which a pathogen can transmit from one host to another. It might even enhance it. Without the assumed evolutionary cost to virulence, there is no reason to believe that disease severity will decrease over time."


You are conflating two subtly different points here. Virulence and lethality are not the same thing.

Virulence on a microbiological level relates purely to cytotoxicity, i.e. how effective the pathogen is at invading and damaging cells. However lethality actual depends greatly on which cells are invaded and how harmful that is to the host organism.

In Omicron's case its just as virulent as previous strains of Covid but its adaptations for transmissibility make it more infectious of the brachia and upper respiratory system and not the lung alveoli. As mortality/severe outcomes are tied to auto-immune dysregulation ("Cytokine storms") the site of infection is critical in terms of the lethality of the resultant disease.
 

FireFly

Member
The essence of empiricism is the repeatability of an experimental induced phenomenon.

Using a control group to an actual test group and observing the outcomes will involve a statistical analysis, but if the placebo and the actual group end up being mixed then the analysis is always going to be flawed.
All experiments involve comparing two or more groups; one where the "intervention" or state we are testing for is present; and one where it is not. And in order to decide whether any differences between the two groups are "real" or simply due to experimental variability, we need to perform some kind of statistical analysis. So statistics is foundational to truth in science. When physicists announced they had discovered the Higgs Boson, they were not technically claiming to have "proved" that this particle exists. Rather they were claiming that given the accuracy of their data, they were able to reject the hypothesis that the Higgs Boson does not exist at the sigma 5 (1 in 3.5 million) significance level. In other words, that there was only a 1 in 3.5 million chance of achieving their tests results, if the particle did not in fact exist. But if there are an infinite number of universes, we would expect that in some of these universes, the Higgs Boson does not in fact exist, and these results are still produced. We may be living in such a universe, so the Higgs Boson may not actually exist!

You are conflating two subtly different points here. Virulence and lethality are not the same thing.
Virulence on a microbiological level relates purely to cytotoxicity, i.e. how effective the pathogen is at invading and damaging cells. However lethality actual depends greatly on which cells are invaded and how harmful that is to the host organism.
In Omicron's case its just as virulent as previous strains of Covid but its adaptations for transmissibility make it more infectious of the brachia and upper respiratory system and not the lung alveoli. As mortality/severe outcomes are tied to auto-immune dysregulation ("Cytokine storms") the site of infection is critical in terms of the lethality of the resultant disease.
Well, the definition of virulence that I see widely circulated online is is "Virulence is defined by the ability of a microorganism to cause disease in the host" (https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/virulence). But even if the degree of disease or damage to a host does not correspond to the lethality of the virus (seems like a strong claim), the underlying point remains: that if the evolutionary process does not select for lethality, then mutations that make the virus more transmissible may make it more or less lethal.

 
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Rentahamster

Rodent Whores
Basically it has evolved to multiply much more efficiently in the brachial portion of the upper respiratory tract, which is great for it because its the area of optimal airflow that an aerosol dispersed pathogen needs, but the consequence of that is it does far less well in the alveoli and deep lung tissue.
Maybe, but we don't know that for sure yet. The research that I think you're referencing was only done ex vivo for 48 hours, but it didn't study the upper respiratory tract, unless you're talking about something else that I'm unaware of.

With less deep lung infection the risk of cytokine-storms causing respiratory failure recedes (being an auto-immune syndrome it damages where the virus is) and therefore we get the reduced death-rates.
Not necessarily a good thing, if the reduced death rate doesn't cancel out the increased transmission rate. Contagiousness is exponential.

The really good news is if the research about the transmissibiity adaptation proves correct -and the signs are good because it conforms with the actual statistics for admissions/mortalities- then the virus will not need to mutate much more as its reached an optimal point in an evolutionary sense and this strain should drive all previous variants to extinction.

Whats more It doesn't serve the virus' evolutionary needs to regain its propensity for invading the lungs when all that would do is result in more death and actually hurt its ability to spread versus Omicron.
I'm not sure if we could label anything "optimal", evolutionarily speaking. Organisms can almost always increase their fitness. Death of the host is also not necessarily a source of negative selection pressure if the optimal window of transmission is separate from the death of the host. Furthermore, I'm not sure if SARSCOV2 as a whole would even be influenced that much by lethality, in terms of evolutionary fitness, since SARSCOV2 is already mostly non-lethal to begin with. If COVID19 was killing 80% of people within the infectious period, then sure I can see a fairly large selective pressure to not be so deadly, but as it is SARSCOV2 is already relatively non-lethal so I don't know if there is much selective pressure on that side of things anymore.

In Omicron's case its just as virulent as previous strains of Covid but its adaptations for transmissibility make it more infectious of the brachia and upper respiratory system and not the lung alveoli. As mortality/severe outcomes are tied to auto-immune dysregulation ("Cytokine storms") the site of infection is critical in terms of the lethality of the resultant disease.
I don't think we have enough data yet to make that case with a lot of confidence. We need to study more patients who actually have the disease in their body.
 

Clear

CliffyB's Cock Holster
Interesting discussion that this is, I think we're kinda getting stuck in the semantic weeds.

I guess my point is essentially the razor again: More complication results in more potential for distortion, hence asking the most atomic question results in the most stable, foundational "truths".

Personally speaking this is how I make judgement calls, especially understanding that statistics are mostly meaningless on an individual basis. 99.9% efficacy isn't much of a comfort if you happen to be in the .1 cohort after all!

I prefer observation to extrapolation is all. And the consequence of that is I prefer to try and maintain a positive outlook when at the end of the day I know this so much is entirely out of my control. I can control my own mind though.
 
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FireFly

Member
Interesting discussion that this is, I think we're kinda getting stuck in the semantic weeds.

I guess my point is essentially the razor again: More complication results in more potential for distortion, hence asking the most atomic question results in the most stable, foundational "truths".

Personally speaking this is how I make judgement calls, especially understanding that statistics are mostly meaningless on an individual basis. 99.9% efficacy isn't much of a comfort if you happen to be in the .1 cohort after all!

I prefer observation to extrapolation is all. And the consequence of that is I prefer to try and maintain a positive outlook when at the end of the day I know this so much is entirely out of my control. I can control my own mind though.
The basic question is what percentage of Omicron cases lead to hospitalisation and deaths, in various groups (vaccinated, non-vaccinated, per age group). The data for this is already being collected and I think is fairly well understood. We just need to wait until we have enough of it to draw meaningful conclusions.
 
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