Nasal sprays as a defense against Covid

Let’s start with some stuff that may be useful before we let ourselves have any fun. (Dessert comes last, kids. Eat your liver.) Some nasal sprays not only minimize the chance of catching Covid but may be also a useful treatment if you do get it.

New discovery? Only to me, it turns out. They’ve been around a while and the earliest study I found dates back to 2020–relatively early in the pandemic, when precious little in the way of protection was available and many front-line medical workers took to using them.

The sprays use iota-carrageenan. The bit I’m about to quote (it’s from the link just above) uses a brand name for the stuff. “Carragelose is a sulfated polymer from red seaweed and a unique, broadly active anti-viral compound. It is known as a gentle yet effective and safe prevention and treatment against respiratory infections. Several clinical and preclinical studies have shown that Carragelose® forms a layer on the mucosa wrapping entering viruses, thereby inactivating them, and preventing them from infecting cells.”

Got that? The useful words are “anti-viral,” “effective,” and “safe.”

Irrelevant photo: primroses

“Seaweed” isn’t particularly important but it is interesting. I’ve never squirted seaweed up my nose before. At least not while sober.

How often do you use it as a preventive? One study had medical workers using it four times a day, and it did decrease the odds of their catching Covid.

Another study had people using it three times a day and measured the number of people with Covid antibodies. By that standard, it was 62% effective. It also found that people who used the spray were less likely to develop symptoms than people in the control group. 

A third study reported the stuff to be 80% effective. It also describes Carragelose as a derivative of red algae. Don’t ask me. The article explains the mechanism this way: “The natural active ingredient forms a protective film as a physical barrier and prevents viruses from infecting the mucous membrane by introducing their genetic information into the membrane cells and propagating.”

The early studies were limited by the lack of testing early in the pandemic. They couldn’t be sure that they hadn’t included asymptomatic carriers or people already in the early stages of symptomatic Covid, leaving the numbers a bit wobbly.

The spray is effective against other viruses as well. It’s available under a number of brand names. Ask Lord Google about iota-carrageenan nasal sprays to find out what’s available wherever you live. 

Having read all that, I rushed out and bought a set of hers-and-hers nasal sprays for the household and started using mine in–well, in the random way that you (or at least I) do when you’re defending yourself against an invisible enemy. Is it here? Is it there? Is it under the piano? We don’t have a piano, but what level of human density demands that I shoot seaweed up my nose? I didn’t stop wearing a mask, since 60 to 80% is not 100%, although, damn, I was tempted. And as luck would have it, I now have Covid. That’s not what you’d call a ringing endorsement. It’s also a damn good example of irony. But I’m a sample of 1, which is to say, I’m not statistically significant, even if I am somewhat significant to my own self. I’m not sure where or when I caught it, so I don’t know if I was using the spray at the time. Quite possibly not.

I’m now using it in the hope that it’ll keep the case milder than it might be without it. I’m on the mend and expect to be in the clear  soon. I was pretty addled for the first couple of days (that still qualifies as a mild case) but I’m functional enough now to update and post this, although I’m not sure how competently I’ve done it. Whether nasal seaweed has anything to do with my rate of improvement  we’ll never know, since you don’t get to go back, pick a different path, and compare outcomes. 

Make your own decisions, folks. I’m not here to sell you anything.

 

Long Covid news

This is a bit tentative, but research suggests (sorry–we can’t use a stronger verb there) that vaccination may make long Covid shorter and less severe. The problem is that studies weren’t able to set up randomized trials. Too many people they had access to had already been vaccinated. But several studies hint that “Covid-19 vaccines might both protect against, and help treat, the symptoms of long COVID, with the proviso that more good quality evidence is needed.”

It’s not a smoking gun, but then we weren’t actually trying to shoot anyone.

A different study says that the omicron variant is less likely to lead to long Covid than the initial variant–what they call the wild-type virus, as if we’re in the process of domesticating this beast.

I don’t know. Maybe we are. 

The study has its limits, one being that long Covid can only be diagnosed by checking off a series of symptoms–there’s no test for it. The other is that the participants were mostly young and healthy. But for what it’s worth, where the initial version left people who had Covid 67% more likely to develop long Covid symptoms than the uninfected, omicron leaves the two groups equally prone to them.

Which if you read the fine print says other things can cause the symptoms of long Covid–another thing that makes it so damn hard to measure.

And finally, a study reports that having Covid can lead to face blindness–called prosopagnosia if you’re trying to impress someone. It’s counted as one of a range of neurological problems long Covid can cause. The good news for me is that I don’t have to worry about that one–I’ve had it for years.

Ha. Fooled you there, Covid.

 

And finally…

…for dessert, we get to have the fun I promised. Some genius has developed exactly the thing a pandemic-haunted world has been longing for–glow-in-the-dark Covid tests

Yes, kids, if your Covid test runs away, all you have to do is turn out the lights and there it’ll be, glowing away under the armchair. 

Life is good. Or if it isn’t, exactly, it usually beats hell out of the alternative.

Britain’s great salad crisis, and other news from Britain

As I write this, the UK’s in the midst of a salad shortage. The critics are talking mostly about the tomatoes, but if you listen carefully (keep the noise down out there, will you?), you can hear the lettuces and all their salady friends singing backup.

What’s happening is that tomatoes are scarce, and if you find any on the store shelves they’re expensive. They’re also, as Hawley’s Small and Unscientific Survey informs us, sorry looking specifmens. 

How short are the shortages? Not long ago, I was in my local supermarket looking for what I call an eggplant and the British call an aubergine. When I couldn’t find it, I asked a guy stocking sliced meats nearby if I could ask him a fruit-and-veg question.

“We haven’t got any,” he said wearily.

Since the fruit and veg section wasn’t completely empty, I told him what I was looking for anyway and he pointed them out. He seemed to be relieved to get rid of me without hearing any more moaning about tomatoes.

Irrelevant photo: Lesser celandine–one of the first wildflowers of the season, currently appearing at the base of a hedgerow near you. Or if not near you, at least near me.

So where’d the tomatoes go? As usual, the answer depends on who you ask. Everyone agrees that cold weather in Spain and Morocco are part of the problem. Most will add that growers in Britain didn’t plant much–or anything–this season because at this time of year they have to grow the tender little beasts in heated greenhouses and high energy prices have made that somewhere in between not economically viable and too depressing to even hallucinate about. 

You could add, if you like, that climate change will be doing this sort of thing regularly and we might want to, ahem, think about that. Or you could skip that and ask the weary guy in the supermarket what’s happened to the tomatoes, hoping to get an answer you like better. 

UK growers will add that they’re being put off not only by high fuel prices but by the low prices that supermarkets are willing to pay them. Consumers will choke on their turnips and ask what low prices the growers have in mind, exactly, because prices have gone up to maybe-I’ll-make-you-a-salad-for-your-birthday levels.

Why am I talking about turnips? We’ll get to that.

Some people will add that Brexit has a lot to do with the shortages. It’s made the UK more difficult and more expensive to export to, so sellers move it to the back of the line (or queue if you’re British), and when a product is scarce guess who drops off. Reports from France say they have no shortages of salad veg, although the prices have gone up. 

But as any British news addict can tell you, Brexit was supposed to let the country negotiate more favorable trade deals than it had in the EU. What happened? My impression is that it hasn’t been a screaming success. The new deal with Morocco has apparently made us harder to trade with, not easier, again moving us to the back of the line. 

Sorry, I don’t know the details of the deal and don’t have the oomph it would take to chase them down, that’s why I dropped in a well-worn apparently. I trust they’re suitably absurd.

Since we’ve been having shortages of fairly random products for some time now (I work at our village shop and it makes me aware of how random they are, and how frequent), we could expand the question and add that the just-in-time business model means any hiccup in the supply chain (Covid, anyone?) will lead to shortages of all sorts of products.

It wouldn’t be hard to find people who’ll add that it’s not a viable long-term strategy to depend as heavily as the UK does on India, China, and other countries that produce goods cheaply and ship them long distances. 

But back to our salad crisis: The environment minister, Therese Coffey, is trying to guide us through it by encouraging us to eat less imported food and cherish our turnips, which grow locally in whatever ridiculous weather we throw at them. 

Are we cherishihng them? Well, the head of an organic vegetable box delivery company is all for eating locally but said, “Winter turnips are an abomination. . . . We don’t grow them. Wouldn’t want to inflict them on our customers.”

Coffey’s intervention hasn’t quieted the tomatoratti, but that’s okay, she didn’t expect to. The government strategy is to keep us making jokes about turnips until warmer weather comes, when the government will claim credit for the victorious return of salad. Any day now, they’ll point that the shortage started under Tony Blair and was Labour’s fault. 

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To ease us through these trying times, the Guardian devoted a two-page spread to recipes that substitute everything short of socket wrenches for tomatoes. You can, it turns out, make a red pasta sauce out of carrots, celery, butternut squash, and beets–or as the British call them, beetroot. Add vinegar, olive oil, honey, onion, and garlic. Cook everything, blitz it, add fine herbs, and then, whatever you do, don’t serve it to me. I’d get as much joy out of cooking my spaghetti with red food coloring.

You could also forgo the redness and make a sauce involving butternut squash, egg yolks, and yogurt. Or one that uses onion, carrots, ground beef, toasted oats, and black pudding.

I know, I shouldn’t dismiss this stuff without trying it, but I’ve been cooking long enough and I’ve lived in Britain long enough to have learned–or to think I’ve learned–when to look a recipe in the eye and say, “Sorry, but the kitchen is closed for repairs.”

Is it a cheap shot to make fun of British cooks and their recipes? Probably, but they do seem to get carried away with themselves. I mean, surely there are a hundred non-tomato ways to serve noodles without resorting to beets or black pudding. And I don’t say that to diminish Britain as a nation. It’s a wonderful country and I hope it survives the current government, but that doesn’t mean I have to retire my taste buds.

I’d love to give you a link to the article but I couldn’t find it online. Do you suppose someone thought better of it?

 

And since we’re talking about British politics…

I haven’t written about the Monster Raving Loony Party since early in my blogging non-career, when I had only three followers. Now that I’m up to four, one of which is a lawnmower company that subscribed but never hits Like, so I have to assume they don’t read the posts–

Where were we? Surely it’s time to detour back to that most British of political parties.

The Monster Raving Loonies were formed 40 years ago, in, um, whatever year that was (it’s 2023 now, in case that helps), when David Sutch ran in a Bermondsey by-election under the name Screaming Lord Sutch. 

He’d been running since the 1960s, primarily as a way to publicize his music, although you could probably say that his political non-career eclipsed his musical one. 

Or skip the “probably. Of course you could say it. The question is, would you be right? I haven’t a clue. The point is that this time it was different: He wasn’t running as one lone loony, he was at the forefront of an entire party of loonies.

In its 40 years, the party’s run candidates in 76 by-elections (they’re the off-schedule ones that happen when an incumbent dies or is convicted of larceny and needs to be replaced) and in every general election. Its candidates have included R. U. Seerius, the Flying Brick, Bananaman Owen, Mad Cow-Girl, Sir Oink A-Lot and Lady Lily The Pink. Not one of them has won and the party’s current leader, Howling Laud Hope, says that any candidate getting too many votes will be kicked out.

Embarrassingly, some of its policies have become law, including pet passports (adopted in 2000), a change to pub opening hours (adopted in 2005), and giving the vote to 16-year-olds (okay, only in some elections and only in Scotland and Wales, but still). The last change must’ve been too much for the party, because it’s now calling for 5-year-olds to be given the vote. 

The country’s current political state doesn’t make a good argument for adult competence, so I could be won over on this one. 

Howling Laud Hope now describes his party as the official think tank of Parliament.

It’s proposing a high-speed rail line to the Falkland Islands and “a year off from listening to our politicians.”

In 1985, the Conservative government tried to shoo the Loonies off the national stage by making candidates put up a deposit that they’d only get back if they won 5% of the vote. The Monster Raving Loonies coughed up the cash. 

How seriously should we take the party? In 2019, one perennial candidate announced that he wouldn’t be running this time because December was “a bloody stupid time for a general election.” On the other hand, John Major described Screaming Lord Sutch as by far his most intelligent opponent.

What’s the party’s future looks like? Screaming Lord Sutch died in 199 and the current chair is in his 80s (which I have to say looks younger all the time), so it might be time to talk about a replacement.

“We might just elect someone’s parrot,” Howling Laud Hope said.

A possible treatment for long Covid brain fog 

A small study has identified two drugs, guanfacine and N-acetylcysteine, that may offer help for long Covid’s brain fog. In some cases they decreased it and in others flat-out eliminated it. And because  the drugs have already been approved for other uses (at least in the US, where the study was done; I’m not issuing guarantees about other countries), patients should be able to get them if they can find a doctor willing to prescribe them. 

Please note the if and the should in that sentence. It’s possible but not guaranteed. 

The results were strong enough that one of the researchers, Arman Fesharaki-Zadeh, went from researcher to advocate. 

“There’s a paucity of treatment out there for long Covid brain fog,” he said, “so when I kept seeing the benefits of this treatment in patients, I felt a sense of urgency to disseminate this information. You don’t need to wait to be part of a research trial. You can ask your physician—these drugs are affordable and widely available.” 

To confirm the findings, larger trials will have to be done, with a control group taking a placebo and lots of people in white lab coats looking important, but Fesharaki-Zadeh was convinced enough by the improvements that he’s gone on to use the combination with people whose symptoms are similar but were caused by Lyme disease and MS. He says the results are promising.

Irrelevant photo: Daffodils in February.

Other long Covid news

I’ve seen several articles lately about long Covid’s impact not on individuals but on society as a whole. The U.S. Government Accountability Office estimates that it has affected somewhere between 7.7 million to 23 million Americans. That’s a hell of a range, which probably testifies to how badly defined long Covid still is. 

A different study estimates that 500,000 people in the US aren’t working because of long Covid.

“It’s a pretty conservative estimate,” according to Gaurav Vasisht, a co-author of the second study. “It’s not capturing people who may have gone back to work and didn’t seek medical attention and may still be suffering, so you know, they’re just toughing it out.”

The good news is that the number of long Covid cases as a percentage of workers’ compensations has decreased. That change coincides with vaccines and treatments that can reduce the risk of long Covid becoming available.

What treatments? The article didn’t say, damn it. My best guess is they’re talking about antivirals.

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A different study reports that in people whose mild Cofid cases left them with long Covid, the “vast majority” of the symptoms clears up after a year, and that vaccinated patients had a lower risk of breathing problems. 

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Ah, but we have to balance out the good news, don’t we? A study that looked at a range of other studies saw that although most long Covid patients with mild cases recover, that’s not true of people with severe cases. 

Sorry.

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Yet another study shows a healthy lifestyle coinciding with an almost 50% reduction in the chances of women getting long Covid. That’s not proof that the two are linked, only a bit of statistical flag-waving that says these two things live together, eat supper together, and leave for work together, so we could maybe assume they’re in a relationship, not just roommates. 

The lifestyle (damn, I hate that word) factors they took into account were maintaining a healthy weight, getting enough sleep, not smoking, drinking only moderately, exercising, and eating a good diet. 

Swearing seems to have no impact, one way or another. 

The slightly-more-than-half the group who did get long Covid got milder cases. 

Why did the study focus on women? The article didn’t say, but women are somewhat more susceptible to long Covid. That may or may not explain it. 

 

Vaccine news

India has become the first country to approve a nasal Covid vaccine. It can be used as both a booster and a primary vaccine. Because the vaccine sets up shop in the nasal cavities, which is where Covid likes to set up its own shop, it could keep Covid from spreading. Could. Potentially.

Watch this space. Watch several other spaces. Watch your nasal cavities. We’ll see what happens.

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In China, researchers are at the animal testing stage of what they hope will be a universal Covid vaccine that targets a portion of the virus that has stayed stable across multiple mutations–11,650,487 of them if you’re counting. I’m not. I ran out of fingers somewhere around 12.

It needs more testing before it goes to human trials, but if I understand the article correctly, they’re hoping it will prevent breakthrough infections–the kind that dog people who’ve gotten the current vaccines. In other words, it could actually halt the spread of Covid–which (in spite of the way 90% of the people we all know are acting) ain’t over.

 

Non-vaccine news

We’ve got two items in this enticing little basket:

Number one is a spray that–if it works, of course–could keep Covid from getting any further than our breathing equipment. A group of engineers created “thin, thread-like strands of molecules called supramolecular filaments.” The idea is that you spray ‘em in your nose (or possibly mouth) and they block any virus from getting into your lungs.

Yes, you can still breathe through them.

The effect may only last an hour or two, but it would allow you to go into your nearest overcrowded venue and forget your worries for a while

How does it do that? Um, well, yeah. What do you say I quote?

“The filaments carry a receptor called angiotensin converting enzyme-2, or ACE2. These receptors are also found in cells in the nasal lining, the lung surface, and small intestine, and have many biological roles, such as regulating blood pressure and inflammation. The novel coronavirus enters our bodies primarily through interactions with this receptor. The virus’s characteristic spike protein clicks into this receptor, much like a key going into a lock, allowing it to enter the cell and replicate. Once the virus is locked into the cell, it prevents the cell from executing its normal functions, leading to and exacerbating infections.

“Researchers have long known that adding extra ACE2 into airways can block virus entry, essentially preventing the virus from binding with ACE2 in the lungs. However, since ACE2 has biological functions, simply delivering more ACE2 to the body may have unforeseeable complications. The research team’s newly engineered filament, called fACE2, serves as a decoy binding site for the virus, with each filament offering several receptors for the COVID-19 spike protein to attach to, and silences ACE2’s biological functions to avoid potential side effects.”

Like so many of the innovations I write about, though, it’s not yet ready for prime time.

Item number two in the basket is–oops, it’s very much the same but it’s coming from a different group. In fact, from more than one different group but still involving ACE2 receptors, decoys, all that stuff. 

Different delivery systems, different colors, slightly different mileage, but once you get past that they’re all related. Something seems to be happening here. Keep your eye on it.

 

Numbers

Statistically speaking, what do we know about the pandemic? 

  • That at least 6.8 million people died of Covid and 752 million caught it. 
    • That those numbers massively undercount what happened. Multiply them by 2 or 3 and you’ll get a more realistic number. 
  • That the global GDP dropped by 3.1% in 2020. Compare that to a 1.3% drop during the 2009 crisis. It bounced back by 5.9% worldwide in 2021.
  • That 135 million jobs were lost in 2020. 
  • That in 2022, 56 million more people were out of work than before the pandemic, and 37 million are expected to still be out of work in 2023. How those numbers square with the 5.9% bounceback in GDP is anyone’s guess.
  • That in the US, Covid is the eighth leading cause of death among people between 0 and 19 years old. If we limit that to disease-related deaths, it’s the fifth, and it’s first among infection or respiratory diseases.

Sorry about the wonky spacing of the bullet points. I’m sure there’s a way to even them out but I haven’t found it.

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A study of Covid in California prisons–do I need to mention that they’re crowded?–shows that vaccination and boosters reduced the spread of the omicron variant by 11% for each additional dose.

For the mathematically impaired, I’ll point out that 11% is not 100% but it’s also not 0%. That means breakthrough infections–the ones that push their nasty way in among the vaccinated–were common but they were less common than Covid cases would be without vaccinations. And the rate of serious illness was low.  In a bit more than five months, they clocked 22,334 confirmed omicron infections but only 31 hospitalizations and no Covid deaths.

People who’d been vaccinated were a bit less likely to transmit the disease–the number dropped from 36% to 28%–but the longer it had been since a person was vaccinated, the more the chances of transmitting the beast grew–6% every five weeks. People are at their least infections within two months of being vaccinated or getting a booster.

Having said all that, Covid was spreading widely in the prison population and Sophia Tan, the study’s first author, was calling for “new ideas. . . since the risk of infection in this vulnerable population remains so great.”

Has Britain moved on from Wallpapergate? 

Let’s follow up on what may be the least important story in recent British politics: Wallpapergate.

You remember Wallpapergate, right? That was when Boris Johnson & Wife redecorated the prime ministerial residence, which wasn’t up to their standards, with £840 a roll, hand-crafted wallpaper, complete with gold whatsits. The most diplomatic way to describe the stuff is to say it would appeal to a narrow audience. 

Of course, I never claimed to be a diplomat. The stuff’s so ugly you have to admire the courage of anyone who lives with it. 

What’s the update? I asked Lord Google if anyone had taken it down yet and he had nothing to offer me except the information that for a while there it kept falling down on its own, either because it was too heavy or because it was ashamed to be seen. Sadly, the Johnson’s had it rehung. Or re-whatever-it-is-you-do-to-wallpaper.   

So presumably the Sunaks are living with it. Maybe they think taking it down would offend the Boris-backing wing of the Conservative Party. With a party that fractious, you can’t afford to offend anyone. Or maybe they don’t think they’ll be there long enough for it to matter. Or maybe they’re living there in Johnson’s shadow, the way a history teacher once told my class to imagine Europe’s post-Roman barbarian hordes huddling in the shadows of the Roman coliseums and thinking about the greatness that was no more. 

We should also consider the possibility that they’re leaving it up because Rishi thinks it would be a great joke to stick Keir Starmer with the stuff after the next election. 

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Irrelevant photo: A frosty morning in January

For the sake of clarity, there’s a genuine scandal hidden under the wallpaper, but it’s nowhere near as much fun. It’s about who was going to pay for the redecorating. It was never supposed to be the Johnsons. A helpful donor was going to pick up the £200,000 tab, and I’m sure he was acting in the public interest and had nothing from it. Then the story went public and Johnson had to put his hand in his pocket.

And no, that wasn’t all for wallpaper. There was some furniture, a bit of this and that. You know how it is. These things add up and before you know it you have a couple of hundred thousand pounds. 

It could happen to anyone.

 

Spot the expert

A well-known writer wanted to update her Wikipedia entry. 

No problem, right? 

Wrong. Wikipedia rejected her changes, because what did she know about the subject?

The original entry said Emily St. John Mandel, author of Station Eleven, was married. No big deal to most of us. We don’t know her, don’t want to date her, and feel zero need to know about her private life. To Emily St. John Mandel, however, it did matter and she was of the opinion that she’d gotten divorced. Basically, she wanted to clear out the attic, the crawl space, and the Wikipedia entry after a breakup. So all she needed to do was make a simple correction, right? 

Not so fast, lady. To change a Wikipedia entry, you have to cite an authoritative source. First-hand knowledge doesn’t count.

So she went on social media and asked if any journalists would like to interview her about her marital status. The BBC and Slate figured she might actually be a reliable source raised, so they their hands–me, teacher, me!. When they published their interviews, they became something she could link to, proving that she really is divorced.

Her bio is now up to date. Let’s hope she doesn’t plan on marrying again. It’s not worth the hassle.

 

How not to start a war

Even before the spy balloon–or is it still an alleged spy balloon?–tensions have been high between the US and China over what bits of wet stuff lie in international waters and what bits are Chinese. Let’s not  go into the whys and why-nots of that, let’s just cut to an incident that happened back in 2015, when a US reconnaissance plane was patrolling a contested stretch of the South China Sea and got a radio message saying, “This is the Chinese Navy. Please go away quickly in order to wrong judgment.”

“I am a United States military aircraft,” a US officer said, “conducting lawful military activities outside national airspace.”

And what happened next? The voice that had introduced itself as the Chinese Navy said, “Meow.” That was followed by a series of beeps from the 1970s video game Space Invaders.

So we have a US military officer who introduced him- or herself as a plane and a (presumed) Chinese military officer who thinks he or she is a cat. 

World War III did not start that day. 

 

How not to write a headline

A recent article circulated by the news service Medical Xpress ran under the headline “Possible new way to reduce pain inspired by chickens.”

Do chickens inspire pain? I asked myself. 

Not in me, I answered myself. At least, not so far, and I’ve been around for a long time now. 

On the other hand, I reminded myself, they have beaks and pointy nails. And I haven’t spent a lot of time around chickens. Maybe they inspire pain in people who know them better.

Since this was a quick conversation and I’d run out of italics, I didn’t ask myself what it meant to inspire pain as opposed to causing it. Instead, I discovered that the article was about a way to reduce pain that was inspired by something involving chickens. 

From there on, the article was a disappointment.

 

Spot the chatbot

A chatbot passed a law school exam by  answering multiple choice questions and writing  essays on constitutional law and torts. Once you get past the headline, though, you learn that it was near the bottom of the class and didn’t do well with multiple-choice questions involving math or with open-ended questions. 

People marking the exams said they could could spot it because its grammar was perfect and it was repetitious.

 

Spot the restaurant

TripaAdvisor carried a listing for a nonexistent Montreal restaurant, Le Nouveau Duluth. By the time it was taken down, it had picked up 85 five-star reviews, including one that said, “Can’t believe this place really exists.”

Um, yes, there’s a reason for that, but it didn’t stop the place being at the top of the city’s ratings.

A careful reader might’ve picked up a hint that something was wrong by noticing the combination of valet and drive-through service. 

 

Spot the feelgood story

London will be giving the lowest-paid contract employees of Transport for London free travel on the network. That’s almost 6,000 workers, and none too soon: Fares are expected to go up by almost 6% in March and we’ve already got a cost-of-living crisis.

That story makes me feel so good that I won’t mention how underpaid they are and how that surely has something to do with why they need free transportation. They get the London living wage, which is higher than the minimum wage but not enough to live on. 

Covid, flu, and the fight against airborne viruses

Covid research has given us some unexpected insight into the flu: Contrary to what most of us have believed since forever, we’re not likely to catch the flu by touching contaminated surfaces. Yes, the viruses for flu and Covid can both survive on surfaces for some time, but the experiments demonstrating that used industrial strength amounts of virus–more than you’d find in real life–and that skewed the results. What’s more, a lot of the viral particles the experiments found were no longer infectious. It was viral RNA, which is “more like the corpse of the virus” than like the virus itself according to Emmanuel Goldman, of Rutgers University. 

Goldman was the first person to challenge the hygiene theater that had people sanitizing their groceries, washing their hands, and singing “Happy Birthday” to make sure they’d washed long enough. 

Or maybe it was only in Britain that people sang “Happy Birthday.” It was recommended by our then-prime minister–what was his name?–as a way to know you’d scrubbed for twenty seconds.

To be fair, that was relying on the medical advice available at the time. If he’d been marginally competent in other ways, I might forgive him.

Of course, I might not, but that’s a different post, and one I don’t plan to write. We could’ve skipped both the hand washing and the singing. Like Covid, the flu is airborne, and that’s how we’re most likely to catch it. During the first year of the pandemic, when people were still taking masks seriously (in spite of the people who hadn’t figured out that their noses were part of their breathing apparatus and that their chins weren’t), flu transmission went down to almost nothing.

Irrelevant photo: An azalea, now blooming indoors.

All that Covid-inspired hand washing did do one thing for us: It improved food safety.

Having called time on hygiene theater, Goldman is now pointing us toward a way out of the pandemic: 

Respiratory viruses like COVID-19 and the flu spread primarily indoors, so we need a safe virus-killing reagent that can be pre-deployed in occupied spaces. As it happens, we already have one.

“Triethylene glycol (TEG) is an air sanitizer that has been shown to be safe for humans to breathe at low concentrations. It’s also been found to kill viruses on surfaces and in the air at those same low concentrations. Given the science, regulatory agencies should fast-track approval of TEG-based air treatments.”

Will they? No idea.

A UK government study evaluates its safety this way: “There is some evidence that repeated exposures to a glycol-based aerosol may result in respiratory tract irritation, with cough, shortness of breath and tightness of the chest. However, it is not possible to extrapolate the findings to other workplaces/settings or to longer-term exposure impacts, without further research.” 

It’s generally used to make theatrical fog. That’s what the bit about “other workplaces” means.

 

A Report from the Department of Covid-Fighting Gizmos

This is going to sound like I’m wearing the proverbial tinfoil hat, but a gizmo that uses no batteries and no wires can detect the presence of Covid in air. It uses a “magnetostrictive clad plate composed of iron, cobalt and nickel, generating power via alternative magnetization caused by vibration.” I have no idea what that means, although I could define every last one of the words–or I could if I looked up magnetostrictive. Why bother when I still wouldn’t follow it? That’s why I’m quoting. 

I can’t give you a link on this, because it came as a download. The article’s title is the poetic “Batteryless and wireless device detects coronavirus with magnetostrictive composite plates.” If you ask Lord Google nicely, he may lead you to something at least vaguely related. 

Exactly what you do with the contraption once you have it is up to you. I imagine sending it into a roomful of people on the back of a small, dog-shaped robot and waiting for it to report back before I go in. If it’s not safe, I’ll just go home, thanks.

Why’s the robot dog shaped? To add a bit of charm to my tinfoil-hat look.

*

Another invention allows you–or if not you, at least someone–to watch viruses die as they try to make their way through masks. 

I know. I prefer a book myself. Or TV. Or, hell, social media if I get desperate. But still, the thing’s out there and someone wants to use it.

What does it do? It gets viruses to light up when they die, and by doing that they tell us that very few viruses get all the way through multilayered FP2 masks. That’s reassuring, but the process can also identify what materials are most effective at killing viruses. In other words, we don’t need the dog-shaped robot for this one. People who design masks will find it useful. The rest of us can give it a miss.

 

Coordinating information on long Covid

Worldwide, some 100 million people are believed to be living with long Covid, and a new questionnaire is trying to get a better picture of its impact, giving researchers better information. 

Existing questionnaires don’t cover the full spectrum of its symptoms. It’s not just fatigue; it can also be vomiting, incontinence, erectile dysfunction, hair loss, and so much other other fun stuff. The new questionnaire breaks the symptoms into 16 categories and uses a single scale to measure their severity, nad it can be “e-migrated, translated, and cross-culturally validated,” which I think means it’s set up to be translated into hundreds of languages. Accurately. Taking into account the cultural context in which it’ll be used. 

So far, it’s been approved for use in 50 countries.

 

New drugs in the works

A couple of Covid drugs look promising. Others are in the works, but let’s not spread ourselves too thin. We’ll look at two.

One of them is already used to treat a liver disease (primary biliary cholangitis, in case anyone asks), so its safety has already been tested and its patent has expired, which means it doesn’t cost a fortune. What’s more, it’s easy to store, it’s easy to ship, and it can carry a tune even when a symphony orchestra’s playing an entirely different one. It never loses its temper. What’s not to like?

Dr. Fotios Sampaziotis, of Cambridge University, explained it this way: “Vaccines protect us by boosting our immune system so that it can recognize the virus and clear it, or at least weaken it. But vaccines don’t work for everyone—for example patients with a weak immune system—and not everyone have access to them. Also, the virus can mutate to new vaccine-resistant variants.

“We’re interested in finding alternative ways to protect us from SARS-CoV-2 infection that are not dependent on the immune system and could complement vaccination. We’ve discovered a way to close the door to the virus, preventing it from getting into our cells in the first place and protecting us from infection.”

The timing’s good on this one, because the virus has out-evolved the antivirals we’ve relied on. And because it works on the human cell rather than aiming at Covid’s spike protein, it should be variant-proof.

It’s done well in small clinical trials and will be going into larger ones.

*

Another drug, in an earlier stage of development, also promises to be variant-proof. It’s called an ACE2 decoy, and it works by luring the virus to itself, so it ignores the cells’ ACE2 receptors, which is the normal route for infection. Once it’s done that, it takes off the top of Covid’s spike, which inactivates it.  

It sounds ugly, but there’s a microscopic war going on in there all the time. 

The drug could potentially be used against other coronaviruses, which enter human cells the same way. It hasn’t been tested in humans yet but they’re moving it in that direction.

Does Exeter Cathedral have the world’s oldest cat flap?

I can’t prove that Exeter Cathedral has the world’s oldest cat flap–no one seems to collect worldwide data on cat flaps–but it has one that was built sometime between 1598 and 1621. Or if not built, cut, since the hole doesn’t actually have a covering.

How authoritative are those dates? Dunno. Multiple sources use the same dates, but they could all quoting each other. Still, the door that the hole was cut in looks old enough to convince me, so let’s go with it.

The cat flap was to allow the cathedral cat (not the one in the picture, you understand) to get into the cathedral clock and catch the mice and rats drawn there by the animal fat that greased the clock’s workings. This may be the origin of the nursery rhyme “Hickory, dickory, dock/The mouse ran up the clock.”

Absolutely and completely relevant photo: The Exeter Cathedral cat door–with cat demonstrating that it’s still in working order.

The cathedral kept a series of cats on the payroll in the medieval era, spending 13 pence a quarter on each one in turn, which doubled for a few years in the fourteenth century. Maybe they had to add a second cat when the first one was overwhelmed. Maybe the first one took on an apprentice or insisted on a friend staying for a lifetime’s worth of suppers. The evidence is scant but tantalizing.

 

Want to buy Evelyn Waugh’s old house? 

From there, let’s go to the news: If you were in the market for an eight-bedroom, six-bathroom mansion, you’re too late to bid on the one Evelyn Waugh once owned. (He’s the guy who wrote Brideshead Revisited.) It came with a few small snags that looked like they’d keep the price down.

The asking price was £2.5 million, and yes, that’s down. In 2019, it sold for £2.9 million, and I’ll drop a hint here for the mathematically impaired: That’s more than this year’s asking price. The 2019 buyer was  a company controlled by a former BBC executive, Jason Blain, and it financed the deal with a £2.1 million bank loan, but the bank lost its sense of humor when the company that bought the mansion defaulted on the loan. 

To be fair to the BBC, Blain has also worked for Sony Entertainment. He seems to have a history with, um, I guess you’d say payment problems. The Mandarin Oriental Hotel took him to court when he paid only (only!) £508,500 of the £1.24 million he owed for an eight-month stay. The penthouse he was renting went for £4,725 a night, and his bill included £30,110 for valet parking and £25,497 for room service. 

I’ve seen enough movies to vaguely imagine how a person could rack up that kind of a bill on room service, but valet parking? Where were they parking that car? In a neighboring country? 

Never mind. Let’s talk about the sale’s snags instead. At some point after the 2019 sale, the mansion was rented to someone or other for £250 per year (I’d love to know the story there; all I’ve read is that they call themselves “Evelyn Waugh superfans”), and whoever they are, they’re refusing to leave and won’t let anyone in–no buyers, no real estate agents, and no photographers, so we won’t be able to go online and poke our snoopy old noses into the virtual rooms to see what we couldn’t have bought anyway. 

As the auctioneers explained the situation,  ““The property is occupied under a Common Law Tenancy at a rent of £250 per annum. A notice to quit was served on the occupant on 19 August 2022 and a copy of such notice was affixed to the property gate on 22 August 2022. Prospective purchasers should take their own legal advice regarding this and will be deemed to bid accordingly.”

I believe that means, “Don’t blame us when it all goes wrong.”

When the place was auctioned off, it sold for a mere £2.16 million. The occupants are still refusing the leave.

 

How much can you manage to spend on a train ticket?

British trains are expensive–complaining about the impenetrable pricing structure is a recognized indoor sport–but I can’t account for how much one passenger managed to spend.

The passenger was a drag queen who was booked for a private performance in Bangor but who lived in London. To be clear, that’s the Bangor in Wales, not the one in Maine. It would cost more to get from London to Bangor, Maine, but you’d need something more than a train ticket.

But back to business: She did what anyone would do and booked a train ticket–a first class ticket, which isn’t what anyone would do, but who could resist? I can only assume the client was paying but it’s not like I know that. It was supposed to include a Christmas dinner, even though this was well before Christmas. The British don’t believe in confining Christmas dinner to Christmas day. Christmas dinner, like the wine that was supposed to come with it, is a liquid, and it leaks into the surrounding month. The ticket cost £589

How could the ticket cost that much? It wouldn’t have been easy. After I’d stashed my credit card safely in the other room, I went online to see how far I could push up the cost of a similar ticket. A last-minute (you pay a lot more for a last-minute ticket) round trip came to £153.40. That doesn’t seem to have been first class, although I tried to upgrade myself in two different ways, and nothing mentioned Christmas dinner. Maybe I lack imagination, but I couldn’t get close to £589. 

Never mind. She paid a shitload of money for her ticket. I paid nothing for mine, but then I didn’t go anywhere.

On the way out, first class service was canceled and she was decanted into the ordinary cars. On the way back, the whole train was canceled, but not until two minutes after it was due to leave. 

She took to Twitter, which did at least shake loose a response from the train company, Avanti West Coast. It said, “We’re sorry to hear about this customer’s experience and we’re happy to look into their complaint. . . Our new timetable is based on a robust and sustainable roster for our people without reliance on overtime . . . ” and so forth, for at least two paragraphs of blither.

Merry Christmas. Would you like a side of cranberry sauce with that?

 

Could artificial intelligence write that?

I’ve been reading a lot lately about whether artificial intelligence is ready to replace writers. A new chatbot is–they say–impressing people with how fluent it is. Fluent enough that a Guardian columnist had it write the opening of his column and it produced a credible if boring paragraph. 

Academics report that it can give correct answers to questions they ask their students.  

It has certain limitations, as the columnist (once he took over for the chatbot) pointed out. It can’t see why a kilo of beef doesn’t weigh more than a kilo or compressed air or why crushed glass shouldn’t be a health supplement. It reproduces the biases of its human trainers and makes up facts, but then humans do the same things–more of them every day, it seems–so maybe it shouldn’t lose points for that. 

Humans, though, will bump up against the real world periodically, and that will give them a chance to correct some of their bullshit. Or we can hope it will. Mentioning no names, but I’m still waiting.

As time goes on, the chatbot will probably make fewer ground glass-type errors, but the bias it inherits from its humans is likely to continue. I also wouldn’t look for its prose to lift off the page and make us smile, and I wouldn’t expect creativity. Still, it could have written Avanti’s response to the passenger’s complaint as effectively as the human who (presumably) wrote it. Or more so, since it wouldn’t be bothered by any residual sense of shame. 

 

What about those pesky humans, though?

Humans, it turns out, are more likely to send hate-tweets when the weather turns nasty. The best available explanation is that we’re at our nicest, or at least our least horrible, when the temperature’s between 54 F (that’s 12 C) and 70 F (21 C). Outside of that, we get crabby.

The study tracked 75 million tweets from 773 US cities and found that the pattern held even in high-income areas, where people would be at least somewhat insulated from heat and cold. It couldn’t trace the demographics of hate tweeters but it could trace their targets: primarily members of the Black, Latino, and LGBTQetc. communities. 

Women aren’t on the target list. (Are women a community? Is any demographic group?) I’m not sure if that indicates a hole in the study’s design or a startling sociological insight. Seventy-five years of life experience (admittedly, I didn’t spend all of it on Twitter) says it’s a flaw in the study’s design.

The study–or at least the article on it–didn’t mention rain, snow, or other storms.

 

Your feel-good story for the week

A girl named Madeline (age not specified) sent a letter to her county government saying, “Dear LA County, I would like your approval if I can have a unicorn in my backyard if I can find one.”

The letter found its way to the department of animal care and control, and its director (or someone else on her behalf) sent Madeline a metal tag stamped “Permanent Unicorn License,” along with a fuzzy unicorn–white with pink ears, purple hooves, and a silver horn. The country did set some conditions though: Any sparkles or glitter sprinkled on the animal have to be nontoxic and biodegradable and the unicorn has be fed watermelon at least once a week.

Long Covid and the vaccines: do they give us any protection?

I come bearing a shred of good news about long Covid. Or at least it’ll look good to you if, like me, you worry about the prospect of long Covid. This comes from two doctors, Sarah Ryan and Lawrence Purpura, who’ve worked extensively with it. I’ll skip the details on their experience–just follow the link if you’re interested. It’s shortcut week here at Notes. In fact, the shortcuts are so short that I’m going to quote them interchangeably. They’ll never know–and if they do I’ll take no shortcuts in apologizing.

They say the long Covid cases they’re seeing have been less severe than the ones they used to see. They attribute that first to the omicron variants attacking the upper respiratory system, where they don’t cause as many of the heavy duty symptoms–lung complications, increased heart rate, lightheadedness, and chronic fatigue–and second to the vaccines being somewhat protective against long Covid. 

No, the vaccines don’t protect us completely, but “studies show that even one dose of a COVID vaccine reduces the odds of developing long COVID by seven to 10 times.”

Break out the ice cream so we can celebrate, will you? Or at least an M&M.

Irrelevant photo: Fields after a December frost.

Who’s most at risk? An article in Cell “identified four factors that correlate with greater risk of long Covid—type 2 diabetes, prior infection with Epstein-Barr virus, level of Sars-CoV-2 RNA detected in the blood, and the presence of autoantibodies.”

A different study sees being female as an increased risk. That same study saw people’s risk decrease by 30% if they’d have two doses of vaccine.

How likely are people with Covid to get long Covid? No one has a good answer to that. There’s no one definition of long Covid, which makes it next to impossible–or maybe that’s completely impossible–to compile statistics. 

Still, they estimate that something like 1% to 5% of Covid patients will go on to get moderate to severe long Covid. At twelve weeks, around 25% of them report fatigue, 25% report insomnia, 20% report increased heart rate or dizziness, and 15% report neurocognitive deficits–things like short-term memory problems. Some of those symptoms will be very mild to some disabling.

A different study came up with 1% of people who had Covid but weren’t hospitalized coming down with long Covid, 6% of people who were hospitalized, and 32% of people who ended up in intensive care units.

Many people will have what Ryan and Purpura call “profound recovery” in three to six months; 10% will have symptoms that go on for more than a year. An even smaller percentage will still have symptoms after a year and a half. 

So the news is far from an all-clear, but in a bad-news situation, this is good news.

 

Other long Covid news 

I’ve been stacking up articles on long Covid but never seem to get back to them. But here we are in shortcut week, so let’s do a few quick summaries and then run:

  • Covid’s associated with increased liver stiffness–a possible sign of liver injury–months after infection. Note the hesitancy in there: associated with; a possible sign. Nothing definite, just something worth looking into more.
  • Covid can affect the brain profoundly even months after infection.
  • A different study, from the early stages of the pandemic (I hope that’s significant), linked Covid to impaired reasoning, speed of thinking, and verbal abilities, comparing what they saw to the effects of sleep deprivation. The severity of the symptoms matched the severity of the infection.
  • A small study found Covid can damage the DNA in cardiac tissue. Compared to the 2009 flu, “Covid has led to more severe and long-term cardiovascular disease.”
  • Covid’s associated with increased chances of long-term brain problems, including strokes, cognitive and memory problems, depression, anxiety, and migraines. And if that doesn’t make you anxious, tremors, involuntary muscle contractions, epileptic seizures, brain fog, hearing and vision abnormalities, and balance and coordination problems–basically symptoms like the ones that come with Parkinson’s. Vaccines reduce the chances of having any of this joy land in your life by about 20%. Keep in mind, though, that a group of people who’ve had Covid are more likely to face these problems than a group that hasn’t, but that doesn’t mean all of them will.
  • Covid was associated with an increased chance of stroke and heart attack. If the study’s correct, over the course of a year, for every 1,000 people who had Covid, you’d expect to find five extra strokes, three extra heart attacks, and twelve extra cases of heart failure 

Those last two studies show a pattern but don’t show cause and effect so let’s not go off the deep end with them. 

 

Is Covid no worse than the flu?

The claim that Covid’s just like the flu translates to “Don’t get hysterical.” So an article from Australia has given us a comparison of the two. 

Between the beginning of 2022 and August 28, Australia had 44 times as many Covid cases as flu cases and 42 times as many Covid deaths. 

That makes the death rate from Covid lower, right? It looks that way to this number-phobe, but it also misses the point. The absolute numbers are higher. If you find yourself in the group of people who died, you’re not going to be consoled by the percentages. 

Okay, strictly speaking, if you find yourself in that group you’ll be dead and unlikely to care anymore, but still, you see my point: Some 1,700 people were hospitalized with the flu between the start of the year and some date in September–pick a number, any number, because here at Notes we don’t really care. Compare that to a single day in July 2022 when 5,429 people were hospitalized with Covid.

 

Life expectancy

I kind of ditched our good news theme there, didn’t I? Sorry. I had some, I spent it all in one place, and now it’s gone. To hell with it, let’s do more bad news. It’s cheaper.

The Covid pandemic lowered life expectancy worldwide. Or at least in the 29 countries included in one study. That leaves out a bunch, but close enough for our purposes.

Predictably, the losses aren’t evenly distributed. Countries with the most effective responses bounced back to pre-pandemic levels relatively quickly. Countries where the response was less effective may have what the study calls “a protracted health crisis.”

It’s another piece in the argument that Covid’s not just the flu in fancy clothes. Flu in the second half of the twentieth century caused smaller, less widespread drops in life expectancy. 

 

The new variant on the block

The new variant that’s emerged in China is BF.7, which is short for something more complicated, which we don’t need to bother with. It’s more infectious than earlier variants, has a shorter incubation time, and is better at infecting people who’ve already had Covid. The symptoms aren’t that different than we’re used to: fever, cough, sore throat, runny nose, and fatigue, but some people end up with vomiting and diarrhoea.

It’s been found in several countries other than China but doesn’t seem to be spreading as quickly in them, although (as I write this, in mid-December) it’s not clear why.

A US tradition invades Britain, and other news

The British are (generalization warning here) touchy about cultural imports from the US, and some people are downright sniffy about them. Halloween? I can’t get through the fall without someone telling me that not all that long ago kids wouldn’t have dreamed of going door to door asking for candy. So it’s interesting no one has yet felt the need to remind me about Black Friday’s roots in the US, although it was brought over far more recently than Halloween candy. Maybe that’s because it involve shopping, bargains, and adults, so it slots into the culture with fewer rough edges. But an import it is. 

Irrelevant photo: I almost remember the name of this, but that’s not quite enough. It’s a flower, and I didn’t grow it.

 

Black what?

The Black Friday tradition started in the 1950s, and it wasn’t until 2010 that the US shipped it to Britain. If you’re in the mood, you can blame Amazon for either the introduction or the delay. I’m always happy to blame Amazon–for anything. Still, it wasn’t until Asda joined the mayhem, in 2013 (or 2014 on other websites), that Black Friday really took off in Britain. 

The tradition–for you few happy souls who have no idea what I’m talking about–is that stores slash their prices massively on the day after Thanksgiving (that’s always a Friday), and when shoppers get a whiff of those bargains they go mad. Periodic post-Black Friday headlines in the US involve crowds breaking down doors or trampling innocent grannies in their frenzy to get to the discounted whatevers before they run out. 

What’s it like in the UK? Well, now that Black Friday’s safely in this year’s rearview mirror, let’s check in with a study by the oddly named British consumer group Which? that (or which) nibbled the numbers behind some 200 supposed Black Friday discounts and came back with the news that 86% of the items were either cheaper or no more expensive in the six months before they went on sale. To put that in simpler terms, they weren’t a bargain. A full 98% were either cheaper or no more expensive at other times of the year. None–0%–were cheaper on Black Friday alone.

Don’t you just love a deal? 

Some retailers raised their prices just before Black Friday so they’d be telling the truth when they claimed to have cut the price. 

Which?’s retail editor, Reena Sewraz, said, “It’s rarely the cheapest time to shop and you’ll probably find the things you want are the same price or cheaper as we head towards Christmas, the New Year and beyond.”

 

The history of Black Friday

If I’ve taken the fun out of bargain hunting, let’s talk about where the name Black Friday came from. 

Hawley’s Small and Unscientific Survey tells us that the most widespread explanation is this: The shopping day after Thanksgiving is when stores count on crossing over from the red (debt) into the black (profit). But Hawley’s Small and Unscientific etcetera also reports that this isn’t the only tale around.

An alternative explanation, from no less a source than the Britannica, is that it originated in Philadelphia in the 1960s, when the police used the phrase to describe the chaos created by masses of suburban shoppers descending on the city to start their Christmas shopping. 

It wasn’t a compliment.

But we can go back further than that and trace the history to the 1951 edition of that rivetingly titled magazine, Factory Management and Maintenance, which wrote about workers’ habit of calling in sick the day after Thanksgiving. 

“‘Friday-after-Thanksgiving-itis’ is a disease second only to the bubonic plague in its effects,” it said in an editorial. “At least that’s the feeling of those who have to get production out, when the ‘Black Friday’ comes along. The shop may be half empty, but every absentee was sick —and can prove it.” 

The editor recommended using the day as a bargaining chip in union negotiations, since employees were taking the day off anyway. 

“Shouldn’t cost too much,” he (and odds are a 1951 editor was a he) wrote.

For all you would-be union negotiators out there, there’s a lesson in this: If they’re happy to give you something you didn’t think to want, be suspicious. 

 

Another way to invade England

In France, a group called the La Mora Association is recreating one of the ships William the Conqueror sailed in. They plan to sail it across the channel in 2027, more or less the way William the C did in 1066.

William came over with (probably) 14 vassals–that’s vAssals–who brought an average of 60 vEssels each. Probably. One chronicler says W the C had 3,000 ships. Modern estimates are in the neighborhood of 700, 800, or 1,000. Still, that’s a lot of floating boatage.  

The ships would have been Viking-style longships–those long, narrow things with both a sail and oars, not to mention a dragon head. At least mostly. The Bayeux Tapestry shows a few, but it doesn’t show all 700, not to mention 3,000.  

Whatever they looked like, the ships carried something like 7,000 men and 200 horses, plus armor, weapons, shields, bacon (no, bacon was not used as a weapon; yes, bacon is the beginning of a new category), hard-baked bread, cheese, dried beans, and wine. Plus water and feed for the horses. 

The men were a mix of knights, foot soldiers, and servants. It would’ve taken a lot of servants to keep an army functioning. And a lot of beans.

When the recreation of W’s ship sails, it will leave the weaponry, the horses, and most of the men behind, along with the other 999 ships. And its crew will set a different tone than W’s did.

“We want this to be a symbol of Franco-British friendship,” the association’s president said.

Is he aware of how that worked out last time? 

Well, yes. He even knows about Brexit. But he thinks the ship can, “in the wake of Brexit . . . reunite our two countries,” although my best guess is that the rhetoric comes after the fascination with building an eleventh-century ship, using historic techniques, on the basis of not much more than a picture in a 230-foot-long tapestry and some reproductions of viking ships in a Danish museum. 

 

And in another story very marginally related to ships . . .

Want to vote on the word of the year? You’re too late, but Oxford Languages did open the contest to the public–sort of–so you had your chance.

Having learned from the Boaty McBoatface fiasco (or glorious success, depending on your point of view), in which the public voted in their gazillions to name a serious research ship Boaty McBoatface, forcing the serious research organization sponsoring the contest to publicly overrule them, this contest’s sponsors gave us three choices and only three choices:  metaverse, #IStandWith, and goblin mode. 

Zzzzzzzzzz.

But hey, after its snooze-making fashion, it is democratic. 

Drugs, denials, and British politics

It’s always fun when you can wring a denial out of a politician, and the denials are rolling in: Unspecified people who do equally unspecified work at Chevening–an estate used by Britain’s secretary of state–reported finding “suspected class A drugs” after parties thrown by Liz Truss, the lettuce who became prime minister but was then secretary of state.

Lettuce? Well, yes. Her tenure as prime minister was so short that a lettuce publicly outlasted her. She’ll never live it down. 

What kind of class A drugs? Something that registered as cocaine when it was tested with a swab that changes color when it gets high. Or, more accurately, when it comes into contact with cocaine.

Irrelevant photo: This is from our recent cold snap.

Is cocaine legal in Britain? Nope. Possession carries a sentence of up to seven years or an unlimited fine or both, and in July the government launched (or anyway, announced; I can’t swear that they did any more than that) a crackdown on casual users. 

Casual users? Yes. Those are the kind of users who have passports, because it was going to confiscate them. That’s a more fitting punishment for a high-end user than jail time, which is a better fit for the low-end, no-passport, no-invite-to-Chevening kind of drug user.

An unspecified insider says cocaine’s used widely in Whitehall (“Whitehall” being shorthand for British government offices) and around Parliament. And you know how it is: These are important people. You can’t just toss them in jail when they do something illegal.

During the ten minutes when Truss was prime minister, one of her spokes-salads said cracking down on illegal drugs was a priority. 

Cleaners report finding white powder at no less a residence than 10 Downing Street after two of the parties that were held during lockdown back when Boris Johnson was prime minister. Johnson outlasted many lettuces as well as a head of broccoli, and although several barbers are rumored to have attempted damage control on his hair he outran them all. 

No one’s saying either Truss or Johnson put the powder up their own personal noses. In fact, Johnson’s said not to have been at either of the No. 10 parties that left powder behind. But it does raise questions about the culture around them and what’s tolerated at high levels and not at lower ones. 

So what about those denials? 

When the Guardian, which broke the story, asked for a comment, Truss’s spokes-salad said, “If there were evidence that this alleged activity had occurred during her use of Chevening, Ms Truss would have expected to have been informed and for the relevant authorities to have properly investigated the matter. As it is, the Guardian has produced no evidence to support these spurious claims.”

A spokescomb for Boris Johnson said, “Boris Johnson is surprised by these allegations since he has not previously been made aware of any suggestions of drug use in 10 Downing Street and as far as he is aware no such claims were made to Sue Gray or to any other investigators.

“It was a feature of Mr Johnson’s premiership that he strongly campaigned against drug use, especially middle-class drug use. His government made huge investments in tougher policing to help roll up county lines drugs gangs, which cause so much misery. He repeatedly called for harsher punishments for the use and distribution of class A drugs.”

A spokesdriver for No 10’s current U-turn expert said, “The Guardian has provided no evidence to support these claims. If there were substantive claims, we would expect these to be reported to the police.”

So there you go. Move along, folks. Nothing to see here.

Larry the Cat refused to comment but is alleged to have a serious catnip habit. As for me, I don’t usually post in the middle of the week, but this was too much fun to ignore.

The future of mRNA vaccines

Covid may end up giving us an unexpected gift–a real one, not some snarky, I’m-saying-the-opposite-of-what-I-mean gift. All the work that went into developing the mRNA vaccines for Covid may soon translate into a flu vaccine that works against all 20 known subtypes of flu. It’s still in the testing stage, but it’s looking promising, and since flu can turn from annoying to lethal without having to file paperwork, this is no small thing.

In animal tests, it reduced symptoms as well as protected the little beasties against death. 

To be clear: protection against death is good. It’s not as good as 600% protection against illness, as we know from the Covid vaccines, which miss that 600% bullseye, but it’s a hell of a lot better than having zero protection against death.

The flu vaccines that are around now are seasonal: they protect against the recent versions but if some new strain that jumps unexpectedly from a bird or animal, adapts to humans, refuses to file paperwork, and turns out to be as potent as the 1918 flu–well, they’re not up to the job.

The 1918 flu? That’s the one those of us over a certain age learned to call the Spanish flu because it didn’t originate in Spain and because it’s important to have someone to blame, however inaccurately.

Thoroughly irrelevant photo: a neighbor’s dahlia

The developers of the new vaccine are currently designing human trials, and with luck the vaccine will be available by 2024.

Yeah, so what else can the technology do?

Since you asked, mRNA technology makes the creation of multivalent (be impressed with that word, please) vaccines relatively easy. 

Multivalent vaccines? They’re the ones like that flu vaccine that fore-arm us against bugs with pandemic potential, even when we’re not forewarned. 

The vaccine we really need these days is a pan-coronavirus vaccine, and one is moving into the human-trial stage. Or it’s fixin’ to get ready to think about moving into the human-trial stage. It’s close. In animal trials, three doses not only protected against severe disease, it also protected against infection and decreased the amount of virus the vaccinated animals shed, so they were less likely to pass it on.

Now we come to the hazy part: The article I read introduced it as a vaccine against coronaviruses in general, but the rest of the article focused on it as a Covid vaccine. I’ll leave you to figure out what that means. I’m short on time and can’t trace this one through the convolutions of the internet. 

The article did say, “The vaccine candidate is a combination of a nanoparticle antigen . . . along with an adjuvant—an ingredient that boosts a vaccine’s effects . . . . The adjuvant formulation, 3M-052-AF, significantly enhanced the immune responses in the animals when combined with the antigen.”

I’d translate that for you but I’m in so far over my head that not even the tips of my fingers reach the air. It does sound impressive, though.

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A Covid nasal vaccine is also in development, and it’s designed to piggyback on the immunity that previously vaccinated people carry. By coming in through the nose, it can work primarily on the mucus lining, which is where Covid likes to throw a housewarming party when it enters a body. If the vaccine works, it will be the emergency number you’ll want to call before the party starts, because you know what kind of neighbors Covid germs are. Loud music, fights, broken glass on the sidewalk. 

I could go on, but you get the picture.

In a trial, the spray protected previously vaccinated mice against both death and disease. It did zilch for unvaccinated mice. In hamster trials, it reduced transmission of the disease. It doesn’t use  live viruses, viral vectors, or adjuvants, and that may make the vaccine safer. 

Why? How much? No idea. Go do your own research.

So far, it hasn’t been tested in humans and the article I read was heavily spiced with the word may, so it’s not time to get too excited about this one. Although that hasn’t stopped me.

What about vitamin D and Covid?

Do vitamin D supplements protect against Covid? According to two studies, no. It makes sense that they would–vitamin D supports the immune system–but in a trial of 6,000 people vitamin D supplements made no difference in the number of either Covid or other respiratory tract infections. A second trial involved 35,000 people and tested vitamin D plus cod liver oil. Again, no noticeable difference emerged.

Both trials have their limits. In one, some people in the control group popped the occasional vitamin D supplement. In the other, most of the participants weren’t low on vitamin D at the start of the trial, so the real trial was with a much small group. And vaccines were rolled out during both trials, throwing the balance off. So don’t count them as conclusive, just suggestive.

The endless, depressing news about long Covid and (new word here) post-Covid

Having had Covid can–emphasis on can; it doesn’t always–leave people with nervous system  damage that messes with anything from their sense of smell to their ability to concentrate. It can increase their chances of having a stroke–not right away but eventually. 

It’s called neuro-Covid. Yes, folks, it’s another new word. Don’t say Covid hasn’t been generous with us.

A study that looked at the cerebrospinal fluid and blood plasma of people with neuro-Covid found an overblown immune response in the group with the most serious symptoms: impairments in the blood barrier that could have been caused by a cytokine storm; antibodies that had turned on the body’s own cells; and an overactivation of the microglia, which are immune cells responsible specifically for the brain. People with serious symptoms also had a smaller brain mass than healthy people, especially in the area responsible for the sense of smell.

“The virus triggers such a strong inflammatory response in the body that it spills over to the central nervous system,” Professor Gregor Hutter of the University Hospital of Basel said. “This can disrupt the cellular integrity of the brain.” 

The researchers are hoping to find a test that could predict long Covid and neuro-Covid before they strike, and to identify targets for drugs to attack–in other words, to identify the excessive immune response at an early stage so they can put the brakes on it. 

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A different study shows that having multiple Covid infections increases the risk of long Covid and of other post-Covid health risks. This was a massive study–5.8 million people in the US Veterans’ Affairs database. Its limitation is that this is a population primarily of older white males, so diverse it ain’t. 

The study showed that, compared to people who hadn’t been reinfected, people with repeat infections are twice as likely to die prematurely and three times more likely to be hospitalized. Heart and lung problems were more than three times more common, and reinfection also contributes to brain conditions, kidney disease, and diabetes.

The risk could increase with each infection.

Are you depressed yet? Sorry. It’s not pretty out there and I would have to open the damn curtains. But since I have . . . 

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Another study came at post-Covid brain problems from a different direction. 

To back up for a minute and state the obvious: The problem with studying brains is that as long as their owners are using them you have to accept some limits on the ways you study them. You only have access to certain information once their owners to die, which most people are reluctant to do, even in the interest of science. So this set of researchers created brain organoids–little clusters of brain cells the size of a pinhead. If the organoids object to being messed with, they have no way of letting us know, so it’s open season and the researchers infected them with Covid.

Sorry, guys. For the greater good and all that.

The researchers found that an unusual number of synapses were eliminated.

So what? Well, synapses are the social media of the brain. They allow the neurons to communicate with each other. In the normal wear and tear that goes on inside a brain, a number of synapses will be eliminated, which may explain why I can’t remember what I did five days ago, not to mention the fingering for an F chord on the guitar: The downsizing committee up there decided I no longer need to know those things and got rid of the relevant synapses in the name of efficiency. I might still want to know that stuff, but it’s austerity up there in my skull and something had to go. I should be grateful my brain didn’t ditch everything I know about commas, because, hey, that’s important.

I’m aware that that last paragraph implies that who- or whatever I am exists separately from my brain, but let’s stay out of that rabbithole while I remind you that austerity is what Britain’s government–or what passes for a government when it’s not tied up with more important business–calls cutting public services. Calling it austerity, though, makes it sound like it’s good for us. Think of it as the kale of the political world.

So what the researchers saw happening in the infected organoids was something like what’ll happen in austerity Britain 2.0, which is Sunakian austerity as opposed to Cameronian austerity. When the promised spending cuts kick in, it won’t just be the F chord that goes, it’ll be the smell of lilacs and where I put my car keys and the oomph I need to get from one end of the official looking letter that just came in the mail to the other so I can figure out if I’m being evicted or asked to serve as the next prime minister.

Did I lose you in that last paragraph? Sorry. I was having such fun–

I’ll summarize in a marginally sane way: In infected organoids, an excessive number of connections were downsized–or as serious people would put it, eliminated. That’s frighteningly like what happens in Alzheimers, Parkinsons, and schizophrenia. 

It’s true that our brains are bigger than organoids, and with luck, more complex. But post-mortems on Covid patients (post-mortems, I remind you, are carried out on people who are no longer using their brains), as well as brain imaging on live patients, show that the gray matter isn’t as thick in people who’ve been infected, which hints at a loss of synapses. 

Keep in mind that we’re still in the land of hints, though, not definitive conclusions, and also that I’m not clear on whether the post-mortems and scans were carried out on people who’d had serious cases of Covid or simply from people who’d been infected.

For the researchers, the next step is to look at whether various drugs will inhibit all that downsizing. 

Some of us living in Britain want to know if some drug can stop the government from downsizing services that have already been downsized so radically that they’re held together by nothing more than thread and newspaper headlines.

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Will you forgive me if I toss in a bit of good news? Paxlovid looks like it decreases the odds of developing long Covid.

Pax-what? It’s an antiviral pill that reduces the chances of hospitalization and death in people who’ve been infected–and reduces the chances of long Covid by 25%.

That’s from a preliminary study–it hasn’t been peer reviewed yet, and its study subjects were (again) mostly older white males in high-risk groups, but the US National Institutes of Health plan to study the drug’s effectiveness on people who already have long Covid to see if it works after the fact.