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When will this shit end?


Chrisp1986

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1 hour ago, squirrelarmy said:

The problem with PMQs has never been the questions or the person asking them. 
 

Its the vague responses from the right dishonourable gentleman opposite that are causing the issues

The thing I like with PMQ’s is the ability for the opposition leader to follow up during that first period. The questions switch between opposition and government each turn in Oz which makes it hard to keep momentum in the line of questioning. 
 

Unfortunately we’ve also copied the Westminster tradition of never answering the question. 

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6 minutes ago, Toilet Duck said:

Latest discovery in terms of therapeutics HERE

Published online in Cell in the last couple of days but basically is shows that in order for the virus to get into target cells, not only does it need to use ACE2, but it also needs to bind Heparan Sulfate (HS) first (which is part of the carbohydrate layer on the surface of the types of cells the virus infects). The first step, binding to HS opens up the receptor binding domain of the spike, allowing it to interact with ACE2 and get into our cells. Nicely conducted study and possibly a massive finding. The reason for that is we have drugs that we already use that can block the interaction with HS (namely the anti-coagulant heparin in various forms). In fact, there are already 64 different studies underway examining whether heparin or its derivatives might be useful therapeutically for COVID. The reason these studies were started was because coagulation problems were observed in a lot of patients that were having difficulty with the disease (and indeed in one study, disseminated intravascular coagulation was observed in a massive 74% of patients that didn't survive, whereas less than 1% of patients that survived had coagulation problems). However, in addition to treating the coagulation, heparin may actually impact upon the ability of the virus to enter cells and thus replicate. So, we already had an indication that anti-coagulants may help improve outcomes for COVID patients, but now it seems we have a key piece of the mechanism and they may do more. 

Sounds positive.

In reality how long would it take for the leap forward in terms of giving these drugs to those who need it?

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3 minutes ago, JoeyT said:

Sounds positive.

In reality how long would it take for the leap forward in terms of giving these drugs to those who need it?

There's already 64 clinical trials underway! In reality, anti-coagulant use has become a key part of managing COVID patients. There's a simple test for coagulation problems, which some hospitals are now doing on admission to check to see whether they should be considering this option. Rather than searching for something by screening loads of existing drugs and re-purposing them though, this was discovered by the symptoms of patients. But, if the findings in this study are true and the virus really does use this to get into cells, then it opens up using this approach for many more patients and poses the intriguing question of whether they might even have prophylactic utility (can be used as a preventative measure). 

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8 minutes ago, Quark said:

Could effective treatment prove to be just as, if not more, important that vaccinations?  Or is vaccine still the key?

If a proper cure could be found then that would be just as good as vaccines. On one hand, it’s less good because prevention is obviously better than curing someone who has become ill, but on the other hand if we could stop people dying then that’s great news. 

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24 minutes ago, Toilet Duck said:

Latest discovery in terms of therapeutics HERE

Published online in Cell in the last couple of days but basically is shows that in order for the virus to get into target cells, not only does it need to use ACE2, but it also needs to bind Heparan Sulfate (HS) first (which is part of the carbohydrate layer on the surface of the types of cells the virus infects). The first step, binding to HS opens up the receptor binding domain of the spike, allowing it to interact with ACE2 and get into our cells. Nicely conducted study and possibly a massive finding. The reason for that is we have drugs that we already use that can block the interaction with HS (namely the anti-coagulant heparin in various forms). In fact, there are already 64 different studies underway examining whether heparin or its derivatives might be useful therapeutically for COVID. The reason these studies were started was because coagulation problems were observed in a lot of patients that were having difficulty with the disease (and indeed in one study, disseminated intravascular coagulation was observed in a massive 74% of patients that didn't survive, whereas less than 1% of patients that survived had coagulation problems). However, in addition to treating the coagulation, heparin may actually impact upon the ability of the virus to enter cells and thus replicate. So, we already had an indication that anti-coagulants may help improve outcomes for COVID patients, but now it seems we have a key piece of the mechanism and they may do more. 

No idea what any of that means...but I think it's potentially good news. Thanks TD.

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9 minutes ago, Toilet Duck said:

There's already 64 clinical trials underway! In reality, anti-coagulant use has become a key part of managing COVID patients. There's a simple test for coagulation problems, which some hospitals are now doing on admission to check to see whether they should be considering this option. Rather than searching for something by screening loads of existing drugs and re-purposing them though, this was discovered by the symptoms of patients. But, if the findings in this study are true and the virus really does use this to get into cells, then it opens up using this approach for many more patients and poses the intriguing question of whether they might even have prophylactic utility (can be used as a preventative measure). 

So are you thinking as simple as positive test -> here's some blood thinners to take at home type scenario? 

Are these relatively easy to get hold of/stockpiled already or would we run into the China/Brexit supply problem? 

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3 minutes ago, steviewevie said:

No idea what any of that means...but I think it's potentially good news. Thanks TD.

Basically, if ACE2 is the doorknob that the virus uses to open our cells and get inside, then Heparan Sulphate is the key that unlocks it...and it just so happens we have drugs that can hide the key!

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5 hours ago, crazyfool1 said:

edging towards more unlikely id say based on the feelings the last couple of weeks with the increase in cases this early and the testing shambles that needs rapidly sorting before the winter kicks in ....  55/45 ... not happening . but I like to edge on the side of positive 

Thanks for the update!

I’m in two minds now, the wife is pregnant and due in March. We have tickets so not sure whether I want it to go ahead or selfishly delay another year!

 

I see ToiletDuck is still providing excellent scientific updates!

Edited by Jack The Stripper
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12 minutes ago, efcfanwirral said:

So are you thinking as simple as positive test -> here's some blood thinners to take at home type scenario? 

Are these relatively easy to get hold of/stockpiled already or would we run into the China/Brexit supply problem? 

There's tons of anti-coagulants knocking about, but this finding may make heparin-derivatives the version of choice (some of the trials are looking at nebulized heparin so it goes straight into the lungs). Don't know necessarily about handing blood thinners out to all and sundry, as use of these types of drugs usually needs quite a bit of monitoring (warfarin for example, has longer effects than heparin, but can interact with lots of things so is checked regularly...that's why they made new versions that don't need this, but whether they are effective for the viral entry part being discussed is not known yet)..obviously more work needed, but it's another positive development. I have to say, the amount of work the research world is getting through on COVID is phenomenal...never seen anything like it.  

Edited by Toilet Duck
typos!
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1 minute ago, FestivalJamie said:

Just went past a fish and chip shop, 5 teenagers in there without masks and staff without masks on either.

No wonder numbers are spiking as much as they are.

I wouldn't get so stressed about seeing people on your day to day walks. It'll just stress you out.

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56 minutes ago, Toilet Duck said:

There's tons of anti-coagulants knocking about, but this finding may make heparin-derivatives the version of choice (some of the trials are looking at nebulized heparin so it goes straight into the lungs). Don't know necessarily about handing blood thinners out to all and sundry, as use of these types of drugs usually needs quite a bit of monitoring (warfarin for example, has longer effects than heparin, but can interact with lots of things so is checked regularly...that's why they made new versions that don't need this, but whether they are effective for the viral entry part being discussed is not known yet)..obviously more work needed, but it's another positive development. I have to say, the amount of work the research world is getting through on COVID is phenomenal...never seen anything like it.  

Is there any likelihood that individuals that regularly take low dose aspirin could be less at risk to infection, or at least severity of disease? 

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On 9/9/2020 at 1:23 PM, ace56blaa said:

Someone said Johnson was up against the select committee today is that still happening  and when, cant find info about it anywhere 

Hi mate you asked about this last week, it's on now.

Edited by Ozanne
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1 minute ago, parsonjack said:

Is there any likelihood that individuals that regularly take low dose aspirin could be less at risk to infection, or at least severity of disease? 

So, it hasn't been proven, but strangely enough, it was the first thing we thought of just before we shut down! We've been doing a study on low-dose aspirin and breast cancer outcomes (turns out if you have been taking it for a while and then get breast cancer, you do much better and the cancer doesn't spread as much, but there's no point in taking it once diagnosed). So, very early on we wondered if low-dose aspirin would give some protection. The counter argument was that the anti-inflammatory effect of it would dampen down the immune system...the second part has been examined and seems that NSAIDs like aspirin and ibuprofen don't hamper the immune response sufficiently to make outcomes worse (and therefore remain safe to use), but the other study, whether long-term prior use has any effect if you happen to get infected still needs to be done. Ireland is actually a good place to do this as it's one of the only countries where low-dose aspirin is prescription only (it's over the counter in massive bottles in the US!), so we can link the prescribing database with hospital records and see if this indeed is true. So, it's something that we actually plan to look into (since we already have the aspirin prescribing database for our other studies), but the ethics approval to link the databases takes ages and funding for epidemiology studies at the moment is taking second place to other types of COVID research...the short answer is, I don't know, but suspect it might enough to look into it!

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