Self-checkouts, like many problems, seemed to be solved when I visited Japan. They have 3 stations, 1 where an employee scans your items and then puts them back into a new basket. They then direct you towards (one of many) terminals where you pay. There are then more spaces where you can bag your groceries.
Once you've seen it you'll be baffled as to why it isn't a global solution. No need for the employee or others to wait while you count your coins or bag up, and no need for anyone to wait behind you while you wait for the self-service checkout to weigh each item individually, fail to scan etc.
Aldis has a similar flow. One or two cashiers can handle the whole store as they just do scanning and collect payment. They’re also concerningly fast at scanning. It really baffles me why more stores don’t adopt some of their policies.
This is an excellent podcast around the Dunning-Kruger effect, how we can all be afflicted by it, and what it actually means. Setup around a (true) airline hijacking.
The demand for a Tesla at $25K is going to be huge. Given previous manufacturing delays, I wouldn't expect them to anywhere near keep up. Therefore although they could sell at $25K, due to the insane demand they may as well sell at $30K to reduce some demand, and then bring it down to $25K over a year or 2 as they work through those willing to pay a higher price.
For those (like me) who are looking for some more details of this new strain, I found 2 papers from the `COVID-19 Genomics Consortium UK (CoG-UK)` of great interest. It seems like the prime reasons for concern are increased frequency of mutations, increased proportion of cases, and possible change in immune response
> Several aspects of this cluster are noteworthy for epidemiological and biological reasons and we report preliminary findings below. In summary:
The B.1.1.7 lineage accounts for an increasing proportion of cases in parts of England. The number of B.1.1.7 cases, and the number of regions reporting B.1.1.7 infections, are growing.
B.1.1.7 has an unusually large number of genetic changes, particularly in the spike protein.
Three of these mutations have potential biological effects that have been described previously to varying extents:
> - Mutation N501Y is one of six key contact residues within the receptor-binding domain (RBD) and has been identified as increasing binding affinity to human and murine ACE2.
> - The spike deletion 69-70del has been described in the context of evasion to the human immune response but has also occurred a number of times in association with other RBD changes.
> - Mutation P681H is immediately adjacent to the furin cleavage site, a known location of biological significance.
> The rapid growth of this lineage indicates the need for enhanced genomic and epidemiological surveillance worldwide and laboratory investigations of antigenicity and infectivity.
Anecdotally I know a family where every member tested positive for COVID in the spring with severe symptoms at the time. They recovered, then over thanksgiving they started experiencing very mild symptoms (some none at all, others loss of taste and smell to more typical cold like symptoms), and all tested positive once again.
It might be that after you contracted COVID once, or a particular strain of COVID once, that you have a heightened immune response and less severe symptoms when you do catch the disease again. It is hard to say for sure what is going on from an isolated case, but this certainly doesn't bode well.
How doesn't it bode well? If you get one strain of covid, get over it, then catch another strain and your symptoms are much less than the first time due to your body having the proper defenses against covid, then that's your immune system working as intended.
Is it impossible to get a cold twice in one season? If so, why is catching covid twice a bad thing, especially if the second time is a lot milder than the first time, even for people who experience mild symptoms the first time?
Seemingly not at same rate tho. I guess some specialist can explain it better, but afaik there are some viruses and vaccines where you can spread and some you don’t.
For covid there’s no data yet, but my hunch says it reduces spread only slightly.
Does anyone have insight on how much / specific changes in the spike protein would be needed to render the mRNA vaccines - which to my understanding create only those spikes - would be render less effective or not effective?
The short answer is that 'The extent to which SARS-CoV-2 may evolve to escape immunity induced by infection or vaccination is not currently known'. However analysis has been carried out to work out how far from the receptor-binding site the mutations are, and how 'antibody-accessible' these are, with a few such as . No conclusions are drawn from this analysis.
Earlier on in the report (towards the end of page 1), this statement is given `One of these (the N501Y mutation) occurs in the region of the Spike protein, the receptor binding domain (RBD), that the virus uses to bind to the human ACE2 receptor. Changes in this region of the Spike protein can result in the virus changing its ACE2 binding specificity and alter antibody recognition`.
Saying all this, vaccines are designed to create a range of antibody responses, in order to stop this very fear of a single mutation rendering a whole vaccine useless. [https://www.nature.com/articles/d41586-020-02544-6] I also recall reading somewhere that adapting the vaccine to account for a mutation (much like is done yearly with the flue vaccine) is relatively easy, though I haven't managed to find that article again yet.
I've read that COVID-19 can sometimes be found inside the body even after testing negative for some time. This being a reason for continued weakness and impairment after infection.
Could this possibly continued infection lead to faster mutation, or is the amount of people infected the cause for the rapid mutations, or something else?
It's suspected that this mutation arose from a single patient who had a long case of COVID-19. Here's an interesting pre-print study on an individual (not the one from this mutation) who harboured many mutations over a 101-day period. [https://www.cogconsortium.uk/news_item/persistent-sars-cov-2...]
They didn’t reject the bidders because of the materials, they were rejected due to the overall bid price. They had a budget (£8 million iirc), most came in at ~£11 million except the winning bid which was at ~£9 million. They then engaged in some shady pre negotiation with them to reduce their bid before accepting it.
After accepting it the contractor realised some of their values were wrong so in addition to attempting to find hundreds of thousands of pounds of saving from the council, they were also trying to save hundreds of thousands due to their own misestimates.
Part of this led them to select aluminium cladding over the originally specified zinc cladding which was much less flammable but much more expensive.
Right, but a company that wouldn't have switched to the ACM rainscreen cladding could never have won the bidding process - because they had to agree to do a bunch of cost cutting to have a chance of winning the bid.
So even if the average standards in the industry are high, and 95% of companies wouldn't have suggested the use of dangerous cheap materials, those companies wouldn't have won the bidding.
So any change in the rules needs to improve the bottom end of the industry - it can't be a mere voluntary scheme that improves only the conscientious and competent.
Corporate witnesses who do testify are immune from having their own admissions used against them in a criminal proceeding. Though it’s worth noting things said about others can be used against said others.
https://www.standard.co.uk/news/uk/commuters-ordered-to-repa...