Not sure how a draught factors in over here, but yes, for those scenarios you also have plans. Floods are the boogie man of the Netherlands, so we absolutely have not only scenarios but regular 'practice sessions' for emergency services and such. I am sure states in the US that are at risk have the same for Tsunamis. As for war, I am pretty sure the US has allocated some money to that scenario. As in quite literally thousands upon thousands of times more than to a pandemic.
General / Off-Topic The safest place
- Thread starter Robin of Spiritwood
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Not sure how a draught factors in over here, but yes, for those scenarios you also have plans. Floods are the boogie man of the Netherlands, so we absolutely have not only scenarios but regular 'practice sessions' for emergency services and such. I am sure states in the US that are at risk have the same for Tsunamis. As for war, I am pretty sure the US has allocated some money to that scenario. As in quite literally thousands upon thousands of times more than to a pandemic.
sadly if humanity won't control it's population nature finds a way. Too many people, too much overcrowding, too much movement around the world = ripe conditions for pandemics. I'm hoping this all opens a few eyes to how the earths human population levels is a BIG problem.
I think we have to wait until the end of this, to learn what the best approach was. Here in Scandinavia, Sweden is running the minimum restrictions approach. They basically started of at a level of restriction they can afford continue with, for a very long time.
This has lead to about 4 times more deaths per capita, than in Norway and about twice as high as in Denmark. Norway and Denmark run similar programs.
On the surface the Swedish approach may look like a mistake but compared to for example Belgium (similar sized population), they are doing far better. As far as I know, Belgium have far tighter restrictions than even Norway and Denmark.
I think it's to early to have a strong opinion on what the best approach is, before all the broke eggs are counted. Perhaps it's to complex to tell, even then.
As long as China and other east Asian countries continue to completely ignore hygiene and animal well being in their food markets, these epidemics will come at a steady rate. Corona is particularly harsh, but it's not the first and it will not be the last.
Western agriculture have their own problems, as we found out with the Mad cow / Creutzfeldt Jakobs incident.
All this may turn out to be peanuts, when the overuse of antibiotics i food production tips the balance in favour of the bacteria.
As I said, there is always something
To provide some context, CCP has a tendency to respond to these things rather severely. During the SARS outbreak, when a link with civet cats was presumed, they went on a national extermination tour, killing every single on they could find. Most of the rare (and bizarre) animals (part of the so called 'era of wild flavor' trend) disappeared from the wet markets (and moved to black markets). COVID19 is going to have severe consequences for the wet markets. In surrounding countries a vast majority supports completely shutting their own similar versions of it.
The problem is that they usually have a huge, visible crack down and then when attention is elsewhere they turn a blind eye. The markets pop up again after a while and the government does not care.
It's not like these markets are small and can be hidden from local police. If they really cared, there wouldn't be any after SARS.
The effects and measures lasted till this outbreak. They didn't crack down on the concept of the market, merely aspects of them. I can see that change though.
Ok, so in English:
The virus particles have long poky bits. The S ( spike) proteins.
They stick to receptors on cells. The one we knew about was the ACE2 receptor, found in lung and gut.
Turns out they can also stick to the CD147 receptor, found in blood cells, both red ones and lymphocytes.
Hence it can infect the blood cells.
The CD147 receptor is involved in malaria transmission into red cells. We have been looking at that for years, and there's a medicine called meplazunab that can adhere to CD147 and block it off. Could that be useful in Covid 19 disease? It might, so they are trying it.
( Hydroxychloroquine is also antimalarial, but works a different way.)
If the virus gets into our T cells, it can shut down the immune response like AIDS does. That makes the infection much more severe.
So in the situation where people have almost no symptoms, it's possible that their version of CD147 is sufficiently weird enough that their T cells don't get infected at all.
One kind of T cell is the Natural Killer cell.
These antisocial cells find other ones they do not like, and kill them. So they are sort of like citizen vigilantes, suppressing crimes like Cancer and Infection. If you like, they are the Punisher, cruising the streets in the van. And those T cells are the last ones we want a virus to take over.
There is a very real possibility that Coronavirus might hide out inside the T cells, long after the illness is over, because what immune system can take out its own cells? They don't have a Police Internal Affairs Division.
That makes vaccines really difficult. Like the AIDS vaccine- oho, there isn't one.
To fix this problem, we need to change the CD147 receptor. It is a protein, coded for by the BSG gene.
( Big Space Gun)
Actually BSG is short for Basigin. Basigin also known as extracellular matrix metalloproteinase inducer or cluster of differentiation 147. But where's the fun in that?
We need to alter the code in the BSG gene, so that we make a resistant form of Basigin (CD147). And to do that we would need some sort of man made virus with a copy of somebody's resistant gene. Ha ha, yes I know.
Even if that works, the corona virus can still stick to the ACE2 receptor. But it might not cause much disease at all in most people. And our immune systems would work to provide immunity much better. So we wouldn't need a vaccine.
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@Robin, thanks for the fun explanation 
Last year I was reading up on how CRISPR and CAS9 works, and it really is remarkable what goes on at these scales!
I found these nice animations based upon actual best scientific understanding :
Source: https://youtu.be/B_zD3NxSsD8
Last year I was reading up on how CRISPR and CAS9 works, and it really is remarkable what goes on at these scales!
I found these nice animations based upon actual best scientific understanding :
That probably explains the clotting disorders with covid patients.
Good thing we have the 5G net, so that man made virus can be deployed quickly.
Ok, so in English:
The virus particles have long poky bits. The S ( spike) proteins.
They stick to receptors on cells. The one we knew about was the ACE2 receptor, found in lung and gut.
Turns out they can also stick to the CD147 receptor, found in blood cells, both red ones and lymphocytes.
Hence it can infect the blood cells.
The CD147 receptor is involved in malaria transmission into red cells. We have been looking at that for years, and there's a medicine called meplazunab that can adhere to CD147 and block it off. Could that be useful in Covid 19 disease? It might, so they are trying it.
( Hydroxychloroquine is also antimalarial, but works a different way.)
If the virus gets into our T cells, it can shut down the immune response like AIDS does. That makes the infection much more severe.
So in the situation where people have almost no symptoms, it's possible that their version of CD147 is sufficiently weird enough that their T cells don't get infected at all.
One kind of T cell is the Natural Killer cell.
These antisocial cells find other ones they do not like, and kill them. So they are sort of like citizen vigilantes, suppressing crimes like Cancer and Infection. If you like, they are the Punisher, cruising the streets in the van. And those T cells are the last ones we want a virus to take over.
There is a very real possibility that Coronavirus might hide out inside the T cells, long after the illness is over, because what immune system can take out its own cells? They don't have a Police Internal Affairs Division.
That makes vaccines really difficult. Like the AIDS vaccine- oho, there isn't one.
To fix this problem, we need to change the CD147 receptor. It is a protein, coded for by the BSG gene.
( Big Space Gun)
Actually BSG is short for Basigin. Basigin also known as extracellular matrix metalloproteinase inducer or cluster of differentiation 147. But where's the fun in that?
We need to alter the code in the BSG gene, so that we make a resistant form of Basigin (CD147). And to do that we would need some sort of man made virus with a copy of somebody's resistant gene. Ha ha, yes I know.
Even if that works, the corona virus can still stick to the ACE2 receptor. But it might not cause much disease at all in most people. And our immune systems would work to provide immunity much better. So we wouldn't need a vaccine.
A third of UK NHS caregivers tested positive for coronavirus.
The figure is given on Tuesday by CNN which quotes the British government: according to the latter, a third of the essential carers and staff of the NHS tested positive for coronavirus.
edition.cnn.com
---------------------------------------------------------
The figure is given on Tuesday by CNN which quotes the British government: according to the latter, a third of the essential carers and staff of the NHS tested positive for coronavirus.
One third of NHS staff and other key workers tested in UK have coronavirus
The coronavirus pandemic continues to spread across the world. Follow here for live updates on the Covid-19 outbreak.
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It explains why lymphocyte count drops for sure. (Infected lymphocyte makes a bazillion virus particles, and then explodes. Minus one. Repeat a zillion times and count has to drop.)
When you can't get a PCR swab test, doing a cheap quick blood count can pick up this change in 5 minutes. 40% case positive, not diagnostic but useful. This clues us in to how the story is going to go. Big drop = Big Trouble.
If it is increasing clottability in a person, that might be due to widespread inflammation in the vessel walls, so the blood clots on contact all over the place?
IDK for sure, but the ACE2 system is closely involved with vessel wall control, and blood pressure. Might be the regular receptor to blame?
Inadequate PPE supply. The obvious reason. And it will get worse.
Dramatic !
And 778 dead in 24 hours in the United Kingdom (around 760 in France in the last 24 hours).
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Stopped listening to that source on the matter in January. Obvious reasons, reinforced daily.
Ok, so in English:
The virus particles have long poky bits. The S ( spike) proteins.
They stick to receptors on cells. The one we knew about was the ACE2 receptor, found in lung and gut.
Turns out they can also stick to the CD147 receptor, found in blood cells, both red ones and lymphocytes.
Hence it can infect the blood cells.
The CD147 receptor is involved in malaria transmission into red cells. We have been looking at that for years, and there's a medicine called meplazunab that can adhere to CD147 and block it off. Could that be useful in Covid 19 disease? It might, so they are trying it.
( Hydroxychloroquine is also antimalarial, but works a different way.)
If the virus gets into our T cells, it can shut down the immune response like AIDS does. That makes the infection much more severe.
So in the situation where people have almost no symptoms, it's possible that their version of CD147 is sufficiently weird enough that their T cells don't get infected at all.
One kind of T cell is the Natural Killer cell.
These antisocial cells find other ones they do not like, and kill them. So they are sort of like citizen vigilantes, suppressing crimes like Cancer and Infection. If you like, they are the Punisher, cruising the streets in the van. And those T cells are the last ones we want a virus to take over.
There is a very real possibility that Coronavirus might hide out inside the T cells, long after the illness is over, because what immune system can take out its own cells? They don't have a Police Internal Affairs Division.
That makes vaccines really difficult. Like the AIDS vaccine- oho, there isn't one.
To fix this problem, we need to change the CD147 receptor. It is a protein, coded for by the BSG gene.
( Big Space Gun)
Actually BSG is short for Basigin. Basigin also known as extracellular matrix metalloproteinase inducer or cluster of differentiation 147. But where's the fun in that?
We need to alter the code in the BSG gene, so that we make a resistant form of Basigin (CD147). And to do that we would need some sort of man made virus with a copy of somebody's resistant gene. Ha ha, yes I know.
Even if that works, the corona virus can still stick to the ACE2 receptor. But it might not cause much disease at all in most people. And our immune systems would work to provide immunity much better. So we wouldn't need a vaccine.
Holy I-can-not-say-it-cos-filter . Bad news . Thanks for sharing .
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On the bright side, so many doctors are likely going to die that employment for me should be certain in the future.
Job creation! Opportunity! We need a Paul Verhoeven style recruitment advertisement.
Job creation! Opportunity! We need a Paul Verhoeven style recruitment advertisement.
Just out of curiosity : does the paper you linked above somehow validate some Information from a few weeks ago, when I dont recall where and who claimed there were "inserts" of HIV in SARS - CoV -2 genome ? Probably the wording then was wrong or misleading( iirc, it was one of the reasons ppl. thought it possible CoV -2 was human engineered ), but does the paper you linked effectively also mean parts of HIV and CoV -2 are identical ?
Might be this the explanation for some "cured" Covid-19 patients getting reinfected and testing positive again? Or am i going too far?
I decided to replace this post with a picture of a pair of boobies. An improvement, if I dare say so myself.
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