Crap from Facebook for March 21st, 2021

 

This has what appears to be a headline: "Snowflake students claim Frankenstein's monster was 'misunderstood' — and is in fact a VICTIM"

Someone responds with, "but that's........that's the book. that's what the book is about"

Unlike most of my "Crap from Facebook" blog posts, I actually commented when I saw this one. My initial response was...

He murdered a five-year old child and framed the babysitter for it because the kid happened to be related to his creator.

It was before I went to bed this morning. I was tired. It seemed like a suitable response at the time. No one replied to me, so don't worry about me having gotten into an argument on this one. But I thought about it again and it bugs me. Mostly, it bugs me that I can't get away from Frankenstein. I find myself impelled to think about this book more than almost any other book, and it's a pretty bad book!

I mentioned it in another Crap from Facebook entry, back in May of last year, but I'll always associate this book with poor Hank Galmish, who picked it for variety as part of the curriculum in a college class about novels. I watched it dawn on him that he'd messed up, that he'd forgotten just how bad of a read Frankenstein actually is. And he just wanted to escape. He was bored out of his mind reading the book himself and possibly even felt like he owed the class an apology for picking it as one of the books we'd all read that quarter.

If I remember correctly, the post last year dealt with the idea that Frankenstein was "the first science fiction story." What I didn't talk about then was the idea that "it's a tragedy." On the one hand, this could be less annoying because it's true. Frankenstein definitely uses tragic elements. It's fair to classify the story as a tragedy. On the other hand, at least the "it was the first science fiction story" is mostly unique to Frankenstein, and not a tired excuse trotted out for lots of other shitty "classics."

Without regurgitating everything I can remember about the plot of Frankenstein, I'll note that it involves a lot of stupid decisions by both Victor Frankenstein and his creation. Some of those are morally wicked things too (like the bit I mentioned in the Facebook comment), but mostly, they're just foolish approaches to situations that could have been mitigated with even a jot of forethought. The book is about bad people doing bad things and having bad things happen to them for it. Some innocent victims get caught in the crossfire, but they're not the focus of the story anyway.

The whole structure of the narrative, in the first place, is superfluous and annoying. The plot is tedious. The prose is bland. The characters have essentially no development and behave strangely. Reading this book for any reason, even in the most cursory and clinical sort of way for literary analysis, is a dull experience. However, the genre classification in this case is correct: Frankenstein is a tragedy. Well spotted indeed. The parallels to tragic tales already well-known in the literary canon at the time are evident. The book tells a tragic story and Mary Shelley wrote it that way on purpose. So good job: you figured it out. It's a tragedy.

You wanna know what else is a tragedy? That anyone ever had to read the damn thing. By the way, I'm not mad at Mary Shelley. She was 20 when she wrote the book. If some crap I'd written at 20 were touted as a great classic, it would be crappy too. No one is a great writer at 20. Developing those skills takes time, practice, and experience.

Big impromptu influenza things from my dad's Facebook...

A little over a week ago, as a result of something kind of stupid that my dad shared on Facebook, he sincerely asked a scientific question about viruses.

You have me curious as to the major differences in the Flu Vaccine, and these (now at least 4) Covid-19 Vaccine? I would assume their are similarities--- and of course I wonder and even can speculate some of the differences.

That was a surprisingly reasonable way for him to ask about this topic, given the usual crap I see on Facebook. So I wrote a long answer. Since I spent a bit of time just typing the answer up, I decided to save a copy of it here, where it will be easier to find if I ever want to look at it again in the future. Also, if anyone happens to read this blog post and spots an error in my description, please let me know! I was typing most of this up from memory and my biology classes are many years behind me. Anyway, I thought I did a decent job of explaining these concepts to someone like my dad, and while that won't necessarily translate to an explanation that would work for someone else, maybe it could work? I don't know. I found it worth preserving. So deal with it...

There are some pretty big differences. To start with, I need to recapitulate something you might have learned a long time ago.

 

In our cells and (most of) the cells of any animal, there are different membranes holding structures, and all those little bits are made out of mostly proteins and lipids, with smaller components made up of sugars and of certain kinds of RNA. There's a big membrane in the middle of a cell called the nucleus, and that's where the DNA for the cell is stored, bundled up around little balls of special proteins. In order for cells to live, they need to make lots of different proteins and each protein has to have its own shape, which is very specific. It's the DNA that stores the information for which building blocks to use, and in which order, for making those proteins.

 

The nucleus uses chemical signals to control which parts of that bundled up mess of DNA gets unwound, and then special proteins follow the DNA like a track. As the protein moves along the DNA, it puts a building block of the corresponding RNA up and makes a new track out of RNA. So remember how the building blocks in DNA are A, C, G, and T? The proteins that move along the DNA do a process called transcription, and for every C they put down a G, for every G they put down a C, for every T they put down an A, and for every A they put down a U (not a T, for reasons I won't get into right now). Once the segment of DNA has been transcribed, you have a segment of what's called mRNA (short for messenger RNA). The DNA stays in the nucleus, but proteins ship the RNA out of the nucleus, where it gets fed into globs of rRNA (ribosomal RNA) and protein called ribosomes. The As the mRNA is fed through the ribosome, sections of it get matched up to sections of tRNA (transfer RNA), with A matching to U, U matching to A, C matching to G, and G matching to C.

Each piece of tRNA has two business ends. One end has three building blocks (AAG, CUA, etc.) and the other end fits onto a specific nucleic acid. As the tRNA gets lined up on a ribosome, it forms a sequence of amino acids in a specific order, and that string of amino acids is the first step in building a new protein. This process is called translation. Generally the mRNA will also present signals that cause certain parts to get trimmed or other parts to be fitted onto the protein, but that depends on what you're building.

 

That's a long refresher, but I needed to explain transcription and translation because different viruses hijack these systems in different ways. Some viruses have DNA. Other viruses have RNA. All viruses have protein because they need to do three things...

Step 1: Get inside the right kind of cell. Not just any cell will do. The proteins in a virus are adapted to do their own in a specific environment, and might not work properly in the wrong kind of cell. Each virus has proteins on the outside of it that are shaped in a way to hijack receptors on the outside of a certain kind of cell. It simply "docks" onto a receptor. Once docked, there are a few different ways in, which I'll gloss over for now.

Step 2: Hijack the proteins and ribosomes of the host cell and use those to build the proteins of the virus instead. The DNA or RNA in the middle of the virus stores the information for what it will hijack the host cell into building. It will also cause copies to be made of its own DNA or RNA, and those copies get assembled into new copies of the virus.

Step 3: Get the new copies of the virus out of the host cell so that they can spread out and infect more cells. There are a few different ways to do this. Just like there are different ways to get into a cell, there are different ways to get out, but I'll gloss over those for now.

 

Coronaviruses and influenzaviruses are both RNA viruses. They don't make their own DNA. Some viruses do, but we can ignore those for now and focus on RNA viruses only. So they both use RNA, but right from the start, there's a huge difference in how they use it. A coronavirus has what's called "+ssRNA." Basically, once proteins in the coronavirus sneak their own RNA into a host cell, is masqueraded as regular old mRNA, like what would normally have come out of the nucleus of the cell. That RNA, which is viral +ssRNA but is being presented as mRNA, gets translated and the proteins that the RNA codes for get built in the same way that a regular protein would get built, but these are proteins that the virus uses instead. Ultimately, the new viruses exit the host cell. This doesn't kill the host cell right away, but it's an energy-intensive process.

 

Like a lot of viruses, coronaviruses use a little trick to lock down the ribosomes that the are translating their RNA. So those ribosomes would normally get refreshed and prepared to receive new mRNA, but the viral RNA keeps them jammed up, copying viral RNA over and over. That means lots of new viruses. The process that coronaviruses use to exits host cells (called exocytosis) is energy-intensive. The host cell uses its own energy to build a membrane around the viruses, transport that membrane to the outer membrane of the cell, and then push those packets from the inside of the cell to the outside. Cells can only keep doing that for so long before they break down.

Now, coronaviruses use +ssRNA, but influenzaviruses have -ssRNA instead. Unlike a coronavirus, an influenzavirus contains RNA that cannot be fed directly into a ribosome as mRNA. Influenzaviruses take a different approach. While a coronavirus would have a mechanism to enter, and then try to get its proteins hooked up to the parts of the cell that have the most ribosomes, influenzaviruses have a two-stage entry sytem. They enter the cell membrane, then the parts that are left over form a new package that itself gets inside the nucleus. Remember how the nucleus is where mRNA first gets made? Well, the proteins in the influenzavirus snag some of that, and then have their own RNA tag along for the ride. They form a complex that makes strands of mRNA by stealing mRNA that the host cell was making, and those strands get exported by the normal systems to the ribosomes, which dutifully read them and inadvertently build new viruses.

 

In some ways, the proteins that the influenzavirus makes are quite aggressive. They don't just passively form new viruses, but start breaking down RNA that cell was using for other things, so that more material will be available for making new viruses. They also line the cell membrane with proteins to build the outside layers for new viruses, and a whole bunch of viruses start budding off from the host cell, which kills it.

 

So you see, even though coronaviruses and influenzaviruses have some things in common, and even though both of them contain single-stranded RNA, they also have some pretty extreme differences. Most of what I've said has to do with what the viruses do while inside a cell. But the outsides of the two viruses also look different from each other, because the systems they use for docking and entering host cells are different too. Coronaviruses got their name because under an electron microscope, their spike proteins look like a halo, and people thought that it looked like the corona around the sun. The outside of the virus is a lipid membrane with three different types of protein embedded in that membrane. The "spike" proteins are the ones that stick out the furthest and form the "corona", and they're the ones that dock onto host cells.

 

Influenza viruses are bigger and more oblong than coronaviruses (sometimes only a little oblong and sometimes they can be very oblong). It has a protein-based shell that sits inside a larger membrane. Compared to the size of the overall virus, its spike proteins don't stick out as far, but they're embedded in that outer membrane in a similar manner.

 

As you might imagine, these differences have some implications for vaccines. There are two big issues I'll get to when it comes to vaccines specifically. But for now, I'm out of time. More later.

 

At this point I took a break. So my dad responded.

It’s nice having a Scientist in the Family. Who can also write and explain that even a high school educated good looking guy can understand. I appreciate it!

You and I have talked about this before... I had a friend who is a doctor, who also served in the Coast Guard Reserves, who wrote his Thesis on the Swine Flu Epidemic in the early 70s ...I think around 74... Anyway, he made a case for only getting essential Vaccines because of (either I am not sure— White Cell memory or T Cell memory) has set capacity. And if you get every flu shot annually and a ton of low risk Vaccines introduced into your body’s defense system you are actually compromising your body’s defenses.

I personally believe there is logic to it. However, I would think anybody at a High Risk should protect themselves. But Don’t Believe Everything You Read....especially is Sound Bites!

Thanks Again! You Are Awesome—- like your Dad

The Compromise of the Defense System... His point was because you have already committed those cells and now have a lower Threshold.

Now back to me...

 

So, T-cells are a kind of "white cells." There are lots of different specialized cells in the immune system, and some of them have very specialized functions. Some cells are part of the "innate" immune system and others are part of the "adaptive" immune system, which can grow cells targeted at specific things called "antigens." An antigen is usually a molecular structure on the outside of a cell or virus, and the adaptive immune system can learn to recognize those structures and target them. Generally, these are the B-cells and the T-cells. B-cells produce immunoglobulin antibodies, and those have business ends that form shapes to match the shapes of antigens, like little molecular jigsaw puzzle pieces. The antibodies latch onto their antigens. On a virus like an influenzavirus or a coronavirus, the antigens that you want to get targeted are those spike proteins that I mentioned earlier. This does two things. Firstly, the spike proteins that have antibodies latched onto them cannot dock onto a cell. So once a virus gets hit by enough antibodies, it loses its tool to invade cells. Secondly, this tags the virus, which makes it easy for other cells in the immune system to recognize it as a threat.

 

T-cells use lots of little proteins called "cytokines" that act as signals to control other cells in the immune system. They'll send signals like "these are the wrong B-cells for this infection, bring me different B-cells" or "there are a lot of antibodies tagging invaders here, bring in the big eaters to come eat these invaders." Scientists still aren't sure what all of the functions are for every kind of T-cell, but they've figured out a lot of this. Sadly, one of the main reasons that they've figured so much of this because HIV messes with the function of T-cells and it also mutates a lot, so there is a large population of human subjects who have had their T-cells messed with by a virus. That has let researchers see the effects that happen when T-cells aren't doing their jobs correctly.

 

The question has come up as to whether the adaptive immune system can become "overloaded" or run out of memory. There are B-cells and T-cells that are called "memory cells" and they do store information on their own unique antigens. Do we eventually run out of those? The answer seems to be no, not really. At least, not under normal circumstances. The vast majority of memory cells that get created have nothing to do with vaccines, nor with when you're very sick fighting off a severe infection. They're just part of day-to-day life, and they barely take up any room. Your immune system doesn't store huge amounts of cells targeting every kind of virus, bacteria, or parasite you've ever been exposed to. Instead, it keeps tiny reserve amounts of those memory cells, and then when it find it needs a certain kind, it sends signals to clone a whole bunch of that one kind. And then, once the infection is gone, it decommissions most of those cells. It turns out that healthy people, even ones who are super-old like you, have plenty of spare memory cells ready to be activated in response to new antigens. Like other parts of the body, the immune system does start having problems with age, but that isn't because the immune system is running out of cells! In fact, it's kind of the opposite problem. Most of the age-related problems with the immune system are because some kind of physiological breakdown means that there are too many of the wrong kind of cell, and the aging immune system stops correcting for this in the way that it used to.

 

This is a matter that has been very well-studied, by the way. There's been some concern in medicine over whether vaccines need to be spaced out or if they'd interfere with each other. That doesn't seem to happen. There can be problems with vaccines (mostly allergic reactions), but none of that seems to be linked to scheduling too many vaccines.

 

Now, there are two traditional types of vaccines that have been in use for a long time. The first kind is a dead virus vaccine (also called an inactivated virus vaccine). To make that, a pharmaceutical company grows a bunch of viruses and then kills them, usually by heating them up, but sometimes by exposing them to chemicals. The second traditional kind of vaccine is a live attenuated virus vaccine (also called a weakened virus vaccine). To make that, a pharmaceutical company grows a bunch of viruses in a medium (usually eggs, but sometimes animals) that causes it to basically breed viruses that are weaker versions. Once they get a strain that can infect human cells without doing much damage, they use that to make the attenuated virus vaccine. Influenza vaccines used to be made with both approaches, but it turned out that the influenzavirus was a poor candidate for an attenuated virus vaccine. So flu shots are made using dead viruses.

 

Dead virus vaccines are pretty common, but they've had issues that have been known for a long time. Here are some issues with these vaccines...

 

1. The immune system might not respond at all. These aren't active viruses, so once they get into your body, they're just rapidly degrading clumps of protein. They'll get broken down on their own. If that happens, it can't hurt you, but it also means you don't get any immunity.

2. The innate immune system might respond before the adaptive immune system formulates a strong response itself. If cells in the innate immune system (such as phagocytes) destroy the dead viruses before the adaptive immune system finishes working on them, then you might not get immunity.

3. Because these are dead viruses, they tend to get broken up. There's a chance that the adaptive immune system might pick the wrong thing as an antigen. If you had a real infection, then that response wouldn't work and the adaptive immune system would keep trying until it got it right (or until you died). But since this isn't the real thing, your adaptive immune system might start working on the wrong protein or on a broken version of the right protein. It will most likely select the correct antigen, but might also generate antibodies that don't properly stick to that antigen. In a real infection, you'd be making a lot more of the cells that produce the immune response, so you'd get the right kind of memory cells eventually. But with a vaccine, your T-cells and B-cells might create a less effective response.

4. In a real infection, your T-cells can learn to target not just viruses themselves, but cells that are infected with viruses. You don't get that kind of immunity from a vaccine. If you get an immune response so good that it's killing the viruses before the have a chance to infect very many cells, that's not a problem. But if your response is too weak, then this issue compounds that.

 

Despite these issues, it's sometimes better to use dead viruses than weakened ones. They've tried making influenza vaccines using live attenuated viruses, but it didn't work very well. Also, even though these issues mean that a dead virus vaccine might not always work, that doesn't mean the vaccine is no good. For one thing, vaccine researchers have come up with better techniques to make influenza vaccines have a better rate of success than they used to. The flu shots in the last few years have been better flu shots than what used to come out every year. For another thing, vaccines that are only mostly successful can help create herd immunity. That's the reason I get the flu shot. If I became infected with an influenzavirus, I'd probably be fine. But if we have lots of healthy people getting the vaccine, then people who are immunocompromised or vulnerable to the virus are less likely to ever come in contact with it. Until relatively recently, we'd wiped out measles in this country with a live attentuated virus vaccine. The vaccine didn't work on 100% of the people who got it, but it does work about 97% of the time. And if almost everyone who could get the vaccine got it, there'd be no way for the virus to spread, even if someone from another country brought measles here, there wouldn't be enough non-immune people coming into contact with that person for it to spread through our population. That was true for a long time, but by 2018, antivaxxers had made it so that there were enough unvaccinated children for measles outbreaks to happen in the U.S.

 

There's one more issue with vaccines that's specific to influenza and doesn't apply to most other viruses, and unfortunately it's a big one. Remember how I said that the genome of the influenzavirus is made up of -ssRNA? Well, in some viruses, the genome would be "circular." In an influenzavirus, the RNA in its genome comes in eight separate strings. You could almost think of them as being like chromosomes. What sometimes happens is that a person or animal gets infected by two totally different strains of influenzavirus at the same time, and that two viruses with two different genomes both infect the same cells. So a string of RNA from one influenzavirus can get swapped into copies of another influenzavirus that is being built in a cell. Sometimes, this makes a new virus with different features. Whenever you've heard about issues with swine flu, that's why. You might get a virus that is really nasty, but it can't spread from birds into humans, so it's not a threat to us. And then you might get another virus that isn't as deadly, but is better at jumping between species. If a pig gets infected with both viruses and lots of its cells are being exposed to them, you could get a new virus that can jump to humans and is also deadly to humans. This is called "antigenic shift." It has happened before, and it caused the 1968 "Hong Kong flu." After the deaths from that flu, it was something doctors were really worried about, which led to an event you probably remember: the 1976 "swine flu scare." In that year, there was a vaccine that was poorly tested and its administration was poorly documented, so it was blamed for bad side effects in the elderly. There's been a lot of debate since then as to whether that 1976 vaccine actually killed anyone or not, but it became controversial anyway. For many years, it was believed that antigenic shift caused the 1918 flu pandemic. But in 2005, studies on a frozen body that had been exhumed in Alaska proved that it wasn't antigenic shift, but that instead a more normal type of mutation or "antigenic drift" had caused that pandemic.

 

Birds, migratory waterfowl in particular, have lots more strains of influenzaviruses than other animal populations. Part of the improvement in flu vaccines has been related to tracking what kind of viruses are dominant in those waterfowl before they make their way to the biggest areas where humans and chickens live together (southern Asia). In some past years, researchers developing vaccines had poor information or guessed wrong, and flu vaccines didn't really do anything because they were to the wrong strains of flu. Those were bad seasons for flu and more people died from it. But the past couple of years have been pretty good, mostly because researchers learned from the mistakes of the past.

 

Making new vaccines is part science, part art. The researchers who do this work have different tools and apply them in patterns based on what has worked in the past. So if a virus is similar to one that researchers have been able to make very strong vaccines to in the past, there's a good chance they'll be able to apply their techniques and make a good vaccine to this new virus. They've been making influenzaviruses for a long time and they've gotten pretty good at it. But even though coronaviruses have been around for a long time, there hadn't really been successful vaccines against them, at least not in humans. The tools that worked on other viruses weren't as effective with coronaviruses. So how do the coronavirus vaccines work and what are the differences between them? Well, because of how big of a deal COVID-19 has been, different companies have been trying some different approaches, and a few of them work pretty well. But let's focus on the approaches that have actually been through clinical trials and have been approved.

 

The ModernaTX vaccine and the Pfizer-BioNTech vaccine are both mRNA vaccines. This is a different type of vaccines that was pioneered in the 1980's, but abandoned back then for human use because it didn't seem to work very well in humans back then. Why not and what changed? Well, the idea behind an mRNA vaccine is that you make a string of mRNA that only contains the protein in the virus that you want, the antigen. So you'd get a sequence of mRNA that, when fed through ribosomes, would make the spike protein of a virus and only the spike protein. This is tricky, though: cells have other parts besides just ribosomes. There are proteins that act as gatekeepers and regulate what kind of mRNA gets fed through ribosomes. A real virus defeats those safeguards in some way. Influenzavirus does it by hijacking real mRNA in the nucleus of a cell, then replacing it partway through with is own RNA. Coronaviruses have built in disguises that gets past the safeguards inside a cell. So in order to make an mRNA vaccine, you have to modify the RNA to similarly protect it from these safeguards. A set of laboratory techniques called "nucleoside modification" is used to accomplish this. Fortunately, these techniques have been improved since since when researchers were trying to use them to make vaccines back in the 1980's. And just like a real virus, you need to get it into cells in the first place. One way to do this is to wrap the mRNA up in a package that can easily be recognized by the innate immune system. Cells called phagocytes (eater cells) gobble up the package, which then releases the specially modifed RNA. Phagocytes have their own ribosomes for making their own proteins, and the vaccine basically hijacks that like a virus would. But instead of making all the parts for viruses, it only has the RNA to make the spike protein on the outside, the antigen. So lots and lots of spike proteins get made inside these cells.

 

As we've gone over, a real virus would need a mechanism to exit from its host cell. Thankfully, the vaccine doesn't actually need to do that. Part of the natural life cycle of phagocytes is called "antigen presentation." They basically show the T-cells and B-cells some examples of what they've eaten, so the adaptive immune system can build countermeasures against antigens, if phagocytes provide correcte examples of those antigens. In a real infection, they gobble up some viruses present bits of gobbled-up virus to the T-cells and B-cells. But by the time the adaptive immune system grows the right kind of cells to fight the virus, there are already lots of infected cells, so the immune system has to do a lot of work to fight back. If pharmaceutical companies tried to make a vaccine out of inactivated viruses, as they've been able to do with some other viruses, the antigen presentation wouldn't work well enough for there to be a good chance that you'd get a good response against the spike protein. These new vaccines are different: they've had the very cells that are doing the presentation to your immune system being used as stooges to make loads and loads of the exact protein that you want to protect against. Instead of having to puzzle over molecular detritus that phagocytes scooped up and exposed to digestive proteins, they're getting large quantities of pristine antigen to work with. And because there's so much of it coming in, they get extra chances to form a good response. So the new mRNA vaccines to COVID-19 are very effective. They're a lot more effective than the dead virus vaccines used against influenza and almost as effective as the live attenuated virus vaccines used against measles.

 

Most of the technology used to make the mRNA for these vaccines has been around for a while, but the lipid package that makes protects the mRNA and gets it into the right cells so that it can work as an effective vaccine requires some pretty specialized and expensive new facilities that there aren't a lot of yet. So while those vaccines were being developed, other companies tried other approaches. The Oxford-AstraZeneca vaccine and the Johnson & Johnson vaccine are not mRNA vaccines. They're another type of vaccine called a "viral vector vaccine." This type of vaccine uses the techniques developed for gene therapy: they build their own virus-like structure. It's modified from a small type of virus called an adenovirus. This is yet another kind of virus, very different from influenzaviruses and coronaviruses. Much like an influenzavirus, an adenovirus gets its genetic material into the nucleus of a host cell. But the genetic material in an adenovirus is DNA, rather than -ssRNA. Instead of stealing mRNA from its host, an adenovirus simply has the proteins in the nucleus of the host cell build RNA for it. But while a real adenovirus would have DNA that would get transcripted into RNA that would then be translated to build its own proteins, this modified viral vector only has the DNA that corresponds to an antigen. It makes that same spike protein. Even aside from COVID-19, viral vector vaccines have become more popular with biotech companies in recent years, and some other companies around the world are working on their own versions, but the Oxford-Astrazeneca version and the Johnson & Johnson version are the two big ones for this.

 

There have also been attempts at getting a regular old dead virus vaccine to work with COVID-19. Nothing in the U.S. yet, but some Chinese companies are trying this, and there are also versions in India and one in France. So a dead virus vaccine could be considered the third major type of coronavirus vaccine. There are some other companies trying more exotic approaches, but nothing so far that looks to compete with these ones. So, to return to your original question about the difference between the different coronavirus vaccines: ModernaTX and Pfizer-BioNTech use mRNA vaccine technology, Oxford-AstraZeneca and Johnson & Johnson use viral vector technology (so does the Russian vaccine if you've heard about that one, as well as some vaccines made by smaller companies), while Sinovac Biotech and Bharat Biotech as well as the new French Valneva vaccine use inactivated (dead) virus.

Token

About six and half years ago, I wrote a blog post about a family dog dying. I got more time with Token than I ever did with Scout, which probably means that I'll miss him even more. I'd been spending time with my family, so I put this one off for a couple of days. But it's time. I wish I had something more pleasant to write about. Well, here we are.

In 2008, my brother Josh got a puppy. He named his new puppy "Token" after the character on South Park, although it became apparent that he didn't actually have a good grasp on what the word "token" meant, nor why the South Park character was given that name. Also, he didn't know how to spell it, so the first name tag that the dog had read "Tokin." If I'm making Josh sound like a dumbass here, I'm maybe a tiny bit sorry for that, but he kind of was. He's doing better now, though.

Token was Josh's dog, but was more reliably looked after by our mother, who referred to him as her "grandpuppy." She spent a lot of time with him. Her dog, Asiak, was still young and healthy enough at the time to be a playmate to the tiny puppy. My mom would also take Token with her on car rides. When I was working on finishing my A.S. degree at Green River and was going to have my mom pick me up from campus to take me to my first day at my new job at the Covington library, my mom was late showing up and I was freaking out. She pulled up to the curb with Token in the passenger seat of her car, explaining that she'd had to make a detour home because she couldn't bear the thought of leaving the puppy at home with no companionship. I was livid, but then it turned out that some minor incident at the library had management so distracted they didn't even notice that I was late, and shrugged it off when I brought it up myself and apologized.

Later that year, when Josh brought Token to his girlfriend's house, her cat ambushed Token. Josh punted the cat. I had Token home with me before my shift at work and noticed some residue around his eye. I called Josh and told him that I thought his puppy might have an eye infection. Then I learned about the cat attack. Perhaps because the first veterinarian to inspect the eye mistook the wound for a shallow laceration and prescribed medicine that was insufficient for a deep puncture wound, or perhaps because the puncture was just too severe anyway, the eye grew worse and had to be removed. In the same visit when Token was neutered, his left eye was removed. It was at this point that Token became the Dreaded Cyclops Puppy.

Token was naturally skittish and afraid of strangers. We'd take him on walks and people would see this terrified pit bull missing an eye, so they sometimes asked if he'd been rescued from a dog-fighting operation or something. Nope. He was just a spoiled dog that lost an eye when he was a baby and also might have been slightly schizophrenic or something. Seriously, sometimes he'd bark at nothing observable.

Whenever Josh wasn't home and didn't have Token with him, Token would snuggle with me and sleep on or near my bed. But usually, Token wanted to be wherever Josh was. So I'd try to get Scout to snuggle with me instead, but my teddy bear was extremely fluffy and preferred cooling his body on the coldest floor tiles that he could find. I forget when, but Josh's path in life took him across the country. He moved to Florida and then moved to New Jersey to be with Alex (they're married now and still live over there). He did not take his dog with him, so I became Token's full-time snuggle-buddy until my mom moved out of the house and took the dogs with her. We were reunited when I moved over to Rachel's house, and again when my mom moved in to my house and brought the dogs (Token and Chief) with her.

The last time (so far) that Josh visited Washington was in July of 2019, for Rachel's wedding. I took Josh to my place so that he could visit Token for a bit. About a month later, Matt moved in with me, so Token didn't have Josh, but my mom, my youngest brother, and I were all living with him. In September of 2020, Matt and my mom got a house together and moved out. They took Chief, but left Token with me. We remained snuggle-buddies and went on walks together around Les Gove Park.

Token was born on February 29th, 2008. So he was about to turn 13. I knew that age would catch up to him at some point, but I hoped that I could give him a good life in the meantime. And it seemed to be going really well. A week ago, I took him to visit my mom and we walked with Chief around part of Pipe Lake. Token seemed perfectly healthy at that time. He'd devoured Chief's food, so my mom convinced me to get a bag of that same food at the store where she got Chief's food. On Monday, he ate a bunch more of that food, but seemed agitated in the evening and I was worried that he was sick. After we went to bed, it was clear that something was wrong. He kept crying and wanting to go outside. I let him out three or four times and eventually he climbed into the recliner in my living room and fell asleep. Later that morning, I texted my mom. She came and picked Token up, then scheduled him for a vet appointment the next day. She speculated that maybe he was allergic to the new food. Token had his appointment on Wednesday, and we got the bad news on Thursday: cancer in his prostate and lymph nodes.

I'll miss him. Or rather, I'm missing him. Partway through typing this, I absentmindedly turned and looked at my bed to check on the dog. I've been randomly finding myself thinking to check if he has enough water in his dish or if he needs to go out. This sucks.

Crap from Facebook: February 18th, 2021

 

This was posted with the notion that the comment in black text on a white background is silly and unscientific, while the comment in white text on a black background is a rebuttal. However, both comments are a bit weird and lacking in nuance. In case I lose the image, here's what was said...

First person: "It's a bit cold outside this morning in middle America... Aren't you glad you aren't heating your home with a solar panel like nitwit Socialist @AOC is demanding?"
Second person: "Do Solar Panels work in the cold? YES! Solar Panels work by absorbing LIGHT from the sun, not heat. In fact, the chemical reactions that occur w/i the solar panels are more efficient at cooler temperatures. Also, white snow can act like a mirror to reflect MORE light onto them"
My friend: "The war on science"

So, the first comment seems to conflate rooftop solar with ground-based solar facilities. Most people don't have rooftop arrays on their houses, and people who heat their homes with electricity can get that electricity from anywhere on the grid. Also, AOC is a U.S. representative from New York's 14th district. She's not in "middle America" and attempting to mobilize "middle America" against a representative from another part of the country is just bullshit political drama, and has no bearing on the facts here.

The second comment does get one thing right. It is true that solar panels are more efficient at cooler temperatures. Solar panels work using the optical bandgap of semiconducting materials to excite electrons in their photovoltaic cells. For every material, the bandgap has a temperature coefficient. Material gets hotter, fewer electrons can cross the bandgap. Material gets colder, more electrons can cross the bandgap. So far, so good. But the materials selected for making PV cells in commercial solar arrays are selected, in part, because they're less sensitive to this effect.

We could make solar panels that would only worked in super-cold temperatures, but they wouldn't do us much good. Also, solar arrays use passive systems (and sometimes active systems) to keep panels cool. In some cases, those technologies falter in major heat waves, but ordinarily, they get the job done. I can assure you that if you're standing outside in the desert sun next to a working solar array, the insides of the panels are nowhere near as hot as the air around you. That's kind of the point.

Remember: solar panels need light. In severe winter weather, there's way less of it. Even a regular cloudy day can ruin the electricity yield of a solar facility. Snowstorms are worse still. Panels can become buried in snow or accumulate a layer of ice, either of which render them useless. Blizzards can also permanently damage these facilities, necessitating expensive repairs. When power providers know that a major snowstorm is coming in, they're not counting on solar facilities to keep the grid electrified, and for good reasons. It doesn't work that way. We're talking about some extreme cold here. -16 °F? That's -26 °C! If it's that cold, we can be sure that not a lot of sunlight is reaching the surface. I don't know if our second person in this exchange understands or remembers this fact, but light the light reaching the surface that causes solar panels to function is the very same light that causes the surface to warm up. Ergo, there ain't as much of it as normal. Ipso facto, solar panels are fucked in this situation. Q.E.D.

As for snow acting like a mirror and reflecting light onto solar panels, there are two major problems with that idea. Firstly, commerical solar panels are purpose-built to capture direct sunlight. They can absorb reflected light too, but there's a drop in efficiency there. Secondly, and more obviously, solar panels are at their most efficient when they're pointed at the sun. If they're tracking the sun properly (not a guarantee in winter storm conditions, by the way), then they're not going to be oriented to capture much reflected light.

It seems that almost everyone who saw this exchange interpreted the second comment as a strong takedown of the first one. In reality, both are pretty bad.

Grandpa Rose

A couple months ago, I found out that my maternal grandfather had terminal pancreatic cancer. He died on December 24th. I'd been wanting to write something about it here ever since, but I kept procrastinating on that. I'm at a loss trying to come up with anything meaningful to really say, and I guess I didn't really know the man very well, and that most of my memories of him kind of blur together and don't make much sense. I think that's because I saw a lot more of him as a kid and only spoke with him a handful of times once I got older, and also because he was generally pretty quiet anyway. Maybe it's just the way my brain works. I don't know. Recently, my mom and my sister were talking about something and it occurred to me that a story I thought was about my grandpa was actually about my mom's grandpa, my great-grandpa. So that was something I probably had mixed up in my head for years.

After the news sunk in, I had some strange vivid recollections of reading Robert Heinlein's "Future History" stories and seeing the plot point about how the Howard Foundation had been orchestrating matchmaking between people who had four living grandparents, something that wasn't as common back in the 19th century. I remember musing that I still had four living grandparents, and that I was older than the characters they were talking about. It's a totally meaningless distinction related to something that wasn't even important in the stories I was reading, but it was the first thing that popped into my head immediately on learning that my grandpa had died. So that's weird? I'm weird.

His name was Earl Thomas Ashton Junior. At first, I only knew of him as "Grandpa." Looking back, I wonder how well I understood the various relationships and individuals in my extended family. My paternal grandparents were "Nonny and Papa" by their own choosing, and that was all I knew them as. I think I only ever met one great-grandparent on my father's side, and she was "Grandma Vi" to me. My maternal grandmother was (and is) "Grandma Mickey." My maternal grandfather was "Grandpa", but his parents were "Grandma and Grandpa." That meant two different men (father and son) were, in my childhood, known simply as "Grandpa" to me. But I think that if there was ever a need for clarification, the elder of the two was stipulated to be "Great Grandpa." My maternal grandparents divorced while my mom was still a child, and at different points she lived with each of them and a step-parent, and with her grandparents (the same ones that were "Grandma and Grandpa" to me). Grandpa had two children with my mom's step-mother (I met my mom's half-siblings, but never met their mother). But by the time I showed up, Grandpa had divorced and remarried again. At least I think it was before I was born? I can't remember. It would have been in the 1980's, anyway. Since Grandpa's wife's name was Rose and since there was already a "Grandma" and a "Grandma Mickey" and a "Grandma Vi", it made sense that I knew her as "Grandma Rose." That was the way of things for me and for my sister, Rachel, going into the early 1990's. But then our little brother, Josh, heard about "Grandpa and Grandma Rose" and assumed that this meant "Grandpa Rose and Grandma Rose." He was corrected, but Grandpa thought it was hilarious and just kind of rolled with it, so it became a thing. He was "Tom" or "Tommy" to most people, but within my family, he was "Grandpa Rose."

As a kid, I remember seeing him hanging out with my dad a lot. I remember that he was always the one with a video camera at family functions, and that I got to see a tape of a party for my own first birthday, with lots of friends and relatives present, but not Grandpa (because he was the one holding the camera, of course).

In 1999, my Uncle Troy (Grandma Rose's son) started having kids. When I was in high school, they moved to Port Townsend, so they weren't close to where I was living, but still within driving distance (it was probably a 2.5-hour drive). On multiple occasions, Grandpa and Grandma Rose drove all the way up from San Bernardino to Port Townsend to visit their grandkids there, without me seeing them or even knowing they'd been in Washington until after the fact. I remember acting like it didn't bother me at the time, and reasoning that it's not like I was entitled to anything. But really, it did bother me. And I guess I kind of thought, "I'm not in their lives anymore." So I wasn't. And maybe that's part of why this is weird. They couldn't be bothered to keep in touch with me, so I couldn't be bothered to keep in touch with them. Perhaps that says something about me, though. Rachel seemed to maintain a lot more contact with them. They visited Rachel's apartment and I saw them there, probably some time in the late 2000's. I was going to say that was the last time I saw him, but I suspect that we were both at the same family reunion once or twice in the early 2010's, briefly. In fact, I remember that there was one in Oregon where I showed up with Rachel, and Grandpa and Grandma Rose were there when we arrived, but they left soon after so that they could drive up to Port Townsend to see their grandkids there. Yikes, this makes me sound bitter, but I promise I'm only just now even recalling this! I hadn't even given it any thought for years and years.

Well, this is awkward and I can't think of a good conclusion, so I'm going to quit while I'm not ahead.