SGU Episode 959: Difference between revisions

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== News Items ==
== News Items ==
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'''S:''' Jay, tell us about 3D printing soft robots.
'''J:''' I've been waiting for this. 3D printing has been making battery technology. Nice, steady advancements or whatever, but this one is pretty significant, what this team developed. So there's researchers from ETH, Zurich, and a US company, they're called InkBit, and they are a spinoff from an MIT group, and they've developed a groundbreaking 3D printing technology. And this is gonna fundamentally change the capabilities of 3D printing. I haven't seen the printer. I tried to find what it looks like, but the bottom line is that the real thing here is the engineering and what they were capable of achieving with the materials that they're using. So 3D printers today, they're limited. Most of them, if you're not using a resin printer, you're using a certain kind of plastic, and it's a fast-curing plastic, which means that the head of the printer basically softens it, puts it into position, and then it hardens pretty quickly. It's called a fast-curing plastic. The team's approach that they came to was that they wanted to accommodate slow-curing polymers, and this is a big difference because the slow-curing polymers take more time. They're a much trickier material to work with, and I guess historically, people just couldn't really get there. So what they were able to do, at its core, they were able to increase the number of usable materials, different types of plastics and polymers that their 3D printer can use compared to traditional 3D printers. So the slow-curing plastics have superior elastic properties, and of course, this enhances the durability, enhances the strength of the printed objects, and they can also, and this is probably the most important part, is that they can bend and go back to their original position, which, if you've used a standard 3D printer, with the basic plastics that you get for that, they're super rigid. There's no flexibility there, which means that they don't move. They really shouldn't be moved, because they'll tear apart. This technology that they came up with, it enables a seamless 3D printing of intricate and resilient robots using a variety of their high-quality materials, all these different types of materials that they've come up with, in a single operation, meaning that their printhead can print multiple polymers and plastics that have different temperatures, and of course, that would have a different curing time. They can print them at the same time. So one of the standouts is the team accomplished the creation of a robotic hand. The hand has bones, ligaments, tendons, and they're all crafted, like I said, from different polymers in one single printing session. Anyone that's used a 3D printer knows that this is pretty significant. The team was able to do this with fast-curing polyacrylates. These are traditionally employed in 3D printing, and they also, they shifted to using slow-curing theolene polymers, known for their, they're basically exceptionally elastic, and their rapid return to their original state or position that they were after bending, that's a big deal. The flexibility of theolene polymers also allows the researchers to fine-tune things like stiffness, and printing each part of the robot to its specific needs. Now, this is a soft robot. They're considering this to be in the category of soft robots, and these types of robots have advantages over traditional metal robots, right? Their pliability does a couple of things. It reduces the risk of injuring a human who works beside them, which this is a situation that is becoming more and more common. You have people, like on a warehouse floor, working beside robots, and they're also more adept at handling delicate objects, and that's another big thing to consider. You know, think about a company like Amazon, who wants a pack-and-pick robot to go in and pick up all sorts of different objects. You know, they want a robot that can pick up anything that a human hand can pick up, and this is a significant step closer in that direction. The researchers also use a 3D laser scanner, and this is really cool, because this inspects each printed layer for surface irregularities in real time, and the reason why this is important is it gives the printer dynamic feedback, and it adjusts the amount of material that's being printed as it's going, and it's compensating on the fly for any irregularities. Again, if you've done any 3D printing, irregularities, like you don't even know what's going on on the inside of your print job, unless you're gonna stand there. Some print jobs that Ian and I did took a day, days, whatever. They could take so long, like you're not. So having a laser be able to inspect the print job and give feedback instantly to basically the head of the printer, which is doing all the heavy lifting to make a fix immediately is huge. It's just a huge advancement. Typical 3D printers are error prone. They have unexpected results, and this solves that problem. So looking ahead, ETH Zurich researchers, they're planning to find new applications for their technology. InkBit, on the other hand, plans to leverage this innovation right away by offering a 3D printing service to customers and introducing new printers to the market. Now this, again, this is a big deal, and it's gonna significantly upgrade 3D printing products and parts that are gonna be available to all of us. You know, right now, there's a lot of 3D printing going on out there, and a lot of custom parts being made with 3D printers. We use 3D printers for prototyping. We use 3D printers to make props for movies, the applications are getting to the point now with the technology that we have today. It's huge, but this advancement actually is gonna bring a lot of nuance to 3D printing. You know, like I said, they're printing a robot arm in one piece, and it's made out of different materials, and it functions. That's a breakthrough.
'''S:''' Yeah, and I wonder, I mean, you would think that this technology could also be applied to prosthetics, printing a prosthetic.
'''C:''' Right, yeah, because those all have to be custom.
'''S:''' Yeah. Yeah. And, of course, you want them to be soft. You want them to be as human as possible.
'''J:''' Yeah, I think this is just a huge breakthrough in 3D printing. You know, the bottom line is, once this gets out to the market, and people are using it, and then people are gonna be even refining it further and further, it just doesn't end, you know? People that do a lot of 3D printing end up becoming innovators themselves because of their specific needs. And giving people access to something that can print soft materials with more complexity inside the print job is just a huge, huge leap forward.
'''S:''' Thank you, Jay.


=== First CRISPR Treatment Approved <small>(17:12)</small> ===
=== First CRISPR Treatment Approved <small>(17:12)</small> ===
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'''S:''' We're gonna, yeah, we're starting the show this week with a couple of upbeat news items. I'm gonna be talking to you guys about the first regulatory-approved CRISPR-based treatment for a disease. So, yeah, we started talking about CRISPR back in 2017, I believe, and here we are six years later, we have an approved therapy. That's fast, to go from working out the basic science of a new technology to having this kind of application. So, in the UK, a drug, a CRISPR-based drug, it's really a whole procedure but the drug itself is called CASGEVY, C-A-S-G-E-V-Y, the generic name is almost unpronounceable, exagamglogene autotemcel.
'''C:''' Sure. Rolls off the tongue.
'''S:''' So, it was approved for the treatment of {{w|sickle cell disease}} and transfusion-dependent beta {{w|thalassemia}}. So, you guys, just to give you a quick background on this, sickle cell is a harmful mutation of the hemoglobin gene that causes a conformational change in the red blood cells. So, the red blood cells, instead of being round, like discus-shaped and flexible, become sickle-shaped and rigid. And those abnormal or sickle-shaped red blood cells tend to clog up the capillaries, which impairs blood flow, and then the tissue gets ischemic, and it's extremely painful. Patients with sickle cell disease get these sickle cell crises, and that can be extremely painful and cause tissue damage. They have to be admitted to the hospital, they're treated with morphine, they're given transfusions, it's very serious. And then there's beta thalassemia. So, these are also hemoglobin genetic mutation-based diseases. So, the hemoglobin has four components, two alpha and two beta. And so, beta thalassemia is when you have a mutation in the beta globin component of the hemoglobin. There are about 1,000 different mutations that cause beta thalassemia.
'''C:''' Oh, wow.
'''S:''' Yeah, so it's a very, very heterogeneous set of mutations. Basically, anything that degrades the beta globin component of the hemoglobin. And it could be anything from asymptomatic to what we call transfusion-dependent. These are people who need to get blood transfusions every two to three weeks to stay alive, because their blood does not carry oxygen, and so they need to constantly replenish their red blood cells. The treatment's approved for transfusion-dependent beta thalassemia. So, any beta thalassemia that's bad enough that you need to treat it with transfusions. Now, at this point, you might be asking yourself, how can one drug, one CRISPR drug, treat two different diseases, one of which has thousands of mutations? So, what do you think the CRISPR-based treatment is doing? Think about that for a minute.
'''C:''' Something about the oxygen.
'''S:''' Think about that for a minute. Let me remind everybody what CRISPR is. This is Clustered Regularly Interspaced Short Palindromic Repeats. It is a mechanism that was derived from bacteria. Essentially, it is being used to target a, you can basically attach to it a sequence of RNA, and then it will basically find the matching sequence, right, in DNA, and then you attach an enzyme to it, which can, for example, cut the DNA at the location that you targeted with your target RNA. Now, you could do a couple of things. You could do lots of things with that, but they've already demonstrated that they can, for example, silence a gene by clipping it, just by cutting both strands, or they can turn a gene off, and then they can later use CRISPR to turn it back on again. So, they could reversibly turn it off, right? They could irreversibly turn it off, they could reversibly turn it off, or they can make a slice and then have the cells repair machinery, make repair the cut, but insert a new gene while they're at it, right? So, you could basically insert a gene into a specified location. So, you could use this for for genetic modification, for genetic engineering.
'''C:''' So, they must be engineering regular hemoglobin. Like, is it-
'''S:''' That's a reasonable thought, is that they're giving a normal hemoglobin gene to replace the bad one.
'''C:''' Or some sort of, like, repairing is, because is it the same error that causes? Yeah, it's, like, very different.
'''S:''' So, that's not a bad thought, but that's not how this works.
'''C:''' Okay.
'''S:''' It's actually pretty cool. So, in order to understand how this works, you have to understand something else about human physiology, and that is that the fetus has different hemoglobin than adults. And the reason for that is because fetal hemoglobin has to take oxygen away from the maternal hemoglobin, right? So, it has to have, under at least some conditions, it needs to be able to have a higher affinity for oxygen than adult hemoglobin does. Does that make sense?
'''C:''' Yeah.
'''B:''' Yeah, sure.
'''S:''' Because you know how hemoglobin works, is that it basically has an iron molecule in the middle, and then when it gets exposed to high oxygen tension in the lung, it binds oxygen from the air, and then when it goes to low oxygen tissue, it gives up the oxygen, right? So, it either binds to or release the oxygen based upon the oxygen tension, like how much oxygen is there. So, the fetal hemoglobin has to be able to steal the oxygen away from the maternal hemoglobin, and then still give it up to the fetus's tissue.
'''C:''' Right, so, like a higher affinity.
'''S:''' Right, and so we make fetal hemoglobin when we're a fetus, and then it dominates until we're about six months old, right, and then after six months old, we stop making fetal hemoglobin, we start making adult hemoglobin. So, all you gotta do is stop the process of turning off the fetal hemoglobin.
'''C:''' Oh, so kids with sickle cell don't develop sickle cell until they produce adult hemoglobin.
'''S:''' Yes, because it's a mutation in the beta subunit.
'''C:''' Right, so their fetal hemoglobin's fine.
'''S:''' Fetal hemoglobin has the alpha, so adult hemoglobin is alpha subunits and beta subunits. Fetal hemoglobin is alpha subunits and gamma subunits. So, if you have beta thalassemia, or if you have a mutation of the beta globin, then the fetal hemoglobin is fine. Now, it turns out, yeah, very interesting, right? So, it turns out that how does the adult hemoglobin take over for the fetal hemoglobin? Well, there's one gene, BCL11A, that turns off the production of gamma globin subunits
'''C:''' That's crazy.
'''S:''' So, all you have to do is silence that one gene, and we start making fetal hemoglobin again. And there you go.
'''C:''' And there must be people out there for whom, I mean, I feel like any time there's a single gene doing something, somebody out there already has a mutation. So, I mean, there must be people walking amongst us who just still are using their fetal hemoglobin, and that's a real problem. That's fascinating.
'''B:''' Yeah, but don't you see the problem with this?
'''C:''' What?
'''B:''' Can't they just go up to people and steal their oxygen? ''(laughter)'' Come on, people, think about it.
'''S:''' They'd have to hook up their blood vessels to your blood vessels.
'''B:''' Yeah, so what?
'''C:''' Yeah, you'd need to connect belly buttons somehow.
'''E:''' Over Bluetooth or something, you know?
'''J:''' Steve, the end result is, though, this literally fixes the problem.
'''S:''' Yes.
'''C:''' Yeah, oh my God, a lifetime of, wow.
'''S:''' Clinical trials that were used as a basis for the approval. So in a clinical trial with sickle cell patients, 28 of 29 subjects who were treated were free of sickle cell crisis episodes for at least a year. And in the transfusion-dependent thalassemia patients, 39 of 42 subjects treated did not need a transfusion for at least a year. Remember, these are people who were getting transfusions every two to three weeks. They were able to go more than a year without needing a transfusion. So it didn't work in 100%. You know, we could ask, why that one patient out of 29, or was it three patients out of 42, why didn't it work? Because the CRISPR, I guess, didn't get in.
'''C:''' Right, is it an uptake problem?
'''S:''' Didn't affect, yeah, it didn't affect enough of the cells. So this is how-
'''C:''' But maybe you'd have more doses or more refined.
'''S:''' This is how the treatment works. Well, let me tell you something. This is how the treatment works. So you take bone marrow out of the patient, right? And then you CRISPR the progenitor cells, the stem cells that make the red blood cells, so that they make the fetal hemoglobin. And then you have to treat the patient to prepare their bone marrow for an auto-transfusion. Then you give them back their treated, their CRISPR-treated bone marrow stem cells. So the whole process has to work. You have to be able to change enough of the stem cells that you took out, and enough of them have to survive and take up shop in the new bone marrow that you give back to the patient. So I guess for some of them, they're not making enough of the fetal hemoglobin to prevent the clinical, the negative clinical outcomes. But still, 20 out of 29, and 39 out of 42, that's pretty good.
'''B:''' That's pretty awesome. Question, if you have this treatment, and then you have alpha gamma, and you're an adult, and you're a woman, can you still have a baby?
'''S:''' Yeah, that's a good question.
'''B:''' I would think no. The hemoglobins would duke it out, each trying to get oxygen from the other.
'''S:''' So the short answer is yes, it's a potential problem. And there actually, it has been studied, because people can make fetal hemoglobin into adulthood naturally, without being CRISPR-ed. So this is already a thing. There was a study a few years ago that looked at women, 43 pregnancies of women who had persistence of fetal hemoglobin between 11 and 100%. And what they found was, is for those mothers whose fetal hemoglobin levels were 70% or higher of their hemoglobin, they did have an increased risk of intrauterine growth restrictions, right? So their babies did not grow as well, if their fetal hemoglobin was over 70%, greater than or equal to 70%. So yeah, in these patients, it would be a problem if they became pregnant. And then we'd have to see if there's something that could be done about it. I don't know if there's any treatment for it right now. Okay, one more thing. So how much do you think this whole treatment costs?
'''J:''' That's the scary part. I would hope that insurance companies are gonna cover it, but that might take a while.
'''S:''' Either way, so this is approved in the UK.
'''B:''' 500,000 a year.
'''S:''' The FDA is considering it. They'll probably the application's accepted. They're probably gonna make a decision in December or January. And the European health agencies also accepted the application. So it may be approved in the UK, Europe, and the US before long. But this is a single treatment. It's not per year. This is a single treatment. And then it's a one-off.
'''C:''' It involves?
'''S:''' Bone marrow transplant.
'''C:''' Bone marrow transplant, yeah. And bone marrow patients are in the hospital for a while.
'''S:''' Once you're done with the whole thing.
'''B:''' And it hurts.
'''S:''' Then you might be good for your life. You know what I mean? That could be it.
'''J:''' I'm gonna guess $50,000.
'''S:''' $50,000? So in the UK, the estimated cost is 1.5 million pounds. In the US, the estimated cost is $2 million. But here's the thing. There was a study that looked at the cost-effectiveness of the treatment. And they found that the treatment would be cost-effective, meaning that it would save more money than it would cost in healthcare dollars. This is not even including quality of life or anything else, just healthcare dollars. It would be cost-effective at a treatment cost of 1.5 million pounds or $1.9 million. That's because, as Cara said, getting hospitalized for sickle cell crisis is damn expensive.
'''C:''' Yeah, and it can happen a lot. And that is, you do. You land in the hospital when it happens.
'''S:''' Right. Yeah, so even though the sticker price is shocking, it's like $2 million. But it's actually cost-effective because it costs more than that to treat somebody over the course of their lifetime for sickle cell disease or to get transfusions every three weeks for life. It's expensive.
'''B:''' So the younger you are, the more willing they would be to foot the bill?
'''C:''' I hope not.
'''S:''' Yeah, I hope. That would be ageism. But it's still cost-effective.
'''C:''' The younger you are, the more quality of life you'll probably get.
'''S:''' And then, yeah, that's not even including the quality of life, you know?
'''C:''' But sickle cell is something, I mean, this is a genetic problem. It's something that happens from the time you develop hemoglobin, right? Or do people develop sickle? Yeah, you don't develop sickle cell later in life.
'''S:''' No, it's genetic and you start.
'''C:''' Yeah, you just have it.
'''S:''' As soon as you start developing the dominant adult hemoglobin.
'''B:''' So six months then.
'''C:''' Yeah, exactly. So that's why it's really sad to see a lot of these crises are happening. And of course, we know that sickle cell is more prevalent in African-American population right here in the US. And it's just really sad that you see very often these young children, some of whom have a lower SES, who are just in so much pain. And there's a lot of, I think, misinformation, disinformation, confusion around it. They often are labeled as drug-seeking because they have to, basically, for some of these kids, all they can do is take pain meds. They go in, they're monitored, and then they just have to put them on pain meds so that they can get through the crisis.
'''S:''' Well, you say pain meds. It's opiates.
'''C:''' It's opiates. It's specifically opiates. Yeah, so then there becomes this whole fear around addiction or is this kid drug-seeking?
'''S:''' Yeah, I've cared for a lot of sickle cell patients in the hospital, and they're in a lot of pain.
'''C:''' Yeah. These crises are brutal.
'''S:''' Yeah, they're brutal. But yeah, so these treatments could make a massive difference in the lives of a lot of people.
'''E:''' Oh boy, could it ever.
'''S:''' And then hopefully, like when, assuming the drugs get approved everywhere, the UK, the US, and Europe, this will fund further research, hopefully bring the cost down, subsidize it, hopefully, for less wealthy nations. There are 20 million people in the world living with sickle cell disease. And yeah, it's a lot of people. For beta thalassemia, it's not as many. /*It's about 100,000 in the US, 15,000 in the UK. For sickle cell and then for thalassemia, it's 100,000 people in the world, 1,200 in the US, 1,000 in the UK. That's a lot of people.
'''E:''' Worldwide, sure, yeah.
'''S:''' Yeah, so but yay for CRISPR. Yeah, so we're seeing a first approved treatment.
'''C:''' And what a great one. It's pretty exciting. Like what an innovative and brilliant approach.
'''S:''' The other thing about, one more thing to note about this is that, and we've talked about this before, that targeting the place, the location in the DNA and being able to do stuff there, like insert a gene, turn a gene off, silence a gene, et cetera, is great. But you have to get the CRISPR cast, whatever, to the right cells. Now with bone marrow-based diseases like this, we're actually bringing the cells to the CRISPR, right?
'''C:''' Yeah, yeah.
'''S:''' As opposed to bringing the CRISPR to the cells. That's harder, because then once you, if you're trying to bring the CRISPR to the cells in an adult, now you need a vector. And we have lots of options for vectors, but none of them are great. And that's still a limiting factor. So I'm not surprised that the first diseases that are being targeted like this are ones where we can take the cells out of the body and then do it outside the body and then put them back. So that's the low-hanging fruit. I think the next level will be ones where we can inject it into a specific place, like inject it into the eye, let's say, or something like that. But doing it, like getting it to go to certain tissues in the body is tricky. That's gonna be tricky. The viral vectors are more of a tricky technology at this point than the genetic engineering itself.


=== Omicron Update <small>(34:08)</small> ===
=== Omicron Update <small>(34:08)</small> ===
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'''S:''' All right, Cara, give us an update on that nasty Omicron virus.
'''C:''' Yeah, so I didn't even realize, Carl Zimmer wrote a really great piece in the New York Times. I don't know if you guys have read any of Carl Zimmer's work, I believe, personally. Yeah, but he's one of the greatest science writers of our time, has a lot of wonderful books. But he just wrote kind of a longish form piece for the New York Times, kind of giving us an update on Omicron. And I guess I didn't really realize, because of course, all of our concept of time has been so distorted by COVID, but we are coming up on four years of COVID, and we're almost to the day coming up on two years of Omicron. So Omicron first erupted, or at least we first identified it the day after Thanksgiving in 2021. And that was, if you guys remember, the Botswana and South Africa variants. That's what we were calling them at the beginning. We didn't know exactly what was going on, but there was this highly mutated version. This was post-alpha and delta variant. And it quickly overtook, like it quickly spread across the globe and became the dominant variant. It still is the dominant overarching variant to this day. And Omicron, of course, is pretty different from the alpha and delta variants because of the changes that we saw on the spike protein. Omicron has proven to sort of be this immune evader. It's this variant that is very, very good at infecting people, even people who have had COVID before, even people who are vaccinated. But Omicron also has resulted in fewer hospitalizations and fewer deaths. Now, it does seem to be the case that the reason Omicron has resulted in fewer hospitalizations and deaths is not because of anything specific to Omicron, but more because of the public health efforts that we've seen. People had already had the virus by this point and or were mostly vaccinated against the virus. And so we just saw fewer severe infections. But let's be fair. I mean, we've been in Omicron land for, like I said, we're coming up on two years, or actually as of this airing, over two years. The U.S. Centers for Disease Control and Prevention found that between October 2022, so last October, and September of this year, so two months ago, more than 80,000 people died of COVID. So we're looking at an eightfold increase over flu deaths. That's what we're still dealing with. Like we know that COVID has become somewhat endemic. We know that we are looking at potentially annual vaccinations or at least regular boosters, but we're still looking at eight times more deaths than influenza. So this is still happening. A lot of us are sort of acting as though it's not, but it is still happening. We're also seeing that Omicron is continuing to evolve. And as it evolves, we're seeing that vaccines continue to be our strongest line of defense. So when we look at Omicron, it itself has had lots of variations within it. Now we're looking at something called XBB. XBB is a hybrid. It's a hybrid. And that occurred when two different Omicrons wound up in the same cell. Here's something that's kind of interesting that I realized or that I learned, and I guess it kind of makes sense, but I never thought about it before. Most of the virologists who are on the case believe, and I don't think that anybody's been able to prove this at this point, but it seems highly likely that the quick kind of inflection point mutations that have occurred, when we first saw Omicron come on the scene, when we first saw specific sub-variants that are kind of different enough to be their own category come onto the scene, they believe that those occurred in single hosts, that single individuals who were likely very immune suppressed, got an infection, either took medication or didn't, but their body's immune system just wasn't capable of fighting the virus off totally. So some of those viral particles were still staying inside of them, mutating away, and then they were able to pass that new mutated virus on. And so it is kind of interesting that, and this will be important for the second part of the story tonight, that immunosuppressed individuals are really up against it. And we have to remember that because not only are they individuals who are more likely to be hospitalized, more likely to die from these infections, but they're also individuals that are more likely to be the kind of sources of mutations. And so we really do need to be paying like special attention to make sure that individuals with suppressed immune systems are really, really cared for. So I mentioned XBB, which was that hybrid, very, very infectious, even if you had been previously infected. It was dominant earlier this year. XBB is the one that the new shot, the shot here in the US at least, that just came out a couple of months ago, targets. But we're already seeing a new version of Omicron coming up in the ranks, mostly in France, but very likely it'll spread to other countries, and it's called JN1. That's what we're calling it right now. These are all part of the BA.2.86 lineage that we saw kind of coming onto the scene last year. But across the board, one of the things that everybody agrees upon is that vaccines are necessary, that vaccines do save lives. And a recent projection from the University of North Carolina showed that annual vaccination campaigns could save around 49,000 lives per year. So let's talk about the second half of what I wanted to mention tonight, and that is that in Texas, the state from whence I came, from where I came, a new ban was just implemented on COVID-19 vaccine mandates. This applies to hospitals. It is now, hospitals are now banned from requiring, from mandating that their workers be vaccinated against COVID-19. It applies to all private businesses, including hospitals. And we were just talking about these sensitive individuals, immunocompromised individuals. We know that kind of across the board, we're seeing that people aren't wearing masks in most places and many hospitals have already dropped their mask mandates. Now that Texas has completely banned COVID-19 vaccine mandates, there's kind of a lot of pushback, a lot of fear from both Republicans and Democrats in the state to specific, there's an Undark article, actually it was pulled from the Texas Tribune, where they specifically cited both a Republican and a Democratic legislator who are on immunosuppressants for their kidney transplants, who have been really pushing back and speaking out about how dangerous this ban is. And now they did get written to the bill kind of at the last minute that hospital workers who choose not to be vaccinated would be required to wear PPE. But a lot of people-
'''S:''' Can be required.
'''C:''' Oh, can be, there you go. Yeah, they can be required.
'''S:''' Hospitals are allowed to require their employees who do not get vaccinated to wear PPE.
'''C:''' So in some cases they won't be required, clearly. And in other cases, even if they are, people are really concerned that like, that's hard to implement. How do you know? So yeah, this bill was just signed into law this past Friday, and a lot of people are really concerned, specifically about transplant patients, cancer patients, individuals with underlying conditions, and whether or not this sets a precedent for other places to follow suit.
'''S:''' It's completely inappropriate legislative overreach. Let hospitals decide, make medical decisions for themselves. They're telling a hospital, can't make a medical decision about how to protect their own patients and employees. It's ridiculous.
'''C:''' That they're literally not allowed to.
'''S:''' It's a dumb decision because, yeah, hospitals are full of sick people, some of whom are very vulnerable to infection.
'''C:''' And I mean, you're used to this, right? You and I both-
'''S:''' It's the standard.
'''C:''' Yeah, it's standard. We have to be vaccinated against COVID to show up to work. The badge has the little thing on it that says, I had my flu vaccine, I had my COVID vaccine. I am approved to come to work because of that.
'''S:''' Yeah, so yeah, we are what's called a patient-facing employee, right? I interact with patients, and therefore I have a lot of requirements that I have to do in order to make sure that I'm not going to be, or at least minimize the chance that I'm gonna be a disease vector.
'''C:''' Right, yeah, you can't have hepatitis. You can't have, yeah, we've gotta get tested for this stuff, yeah.
'''S:''' This is all culture war bullshit. This is, you know what I mean? That's what this is. This is not based on anything rational.
'''C:''' This is anti-vax bullshit making its way into the legislation, and people are going to die because of it. That's the thing that's so incredible.
'''E:''' Well, there come the lawsuits, right?
'''C:''' Yeah, people are going to die.
'''E:''' And then what happens, right, when?
'''C:''' Oh yeah, I mean, yeah, then you're just talking about trying to recoup financial equivalence of lives lost, which is so devastating.
'''S:''' But I wonder if what will happen first is that a hospital will ignore it, ignore the law, do what they think is in the interest of their own patients.
'''E:''' Yeah, and then stand court.
'''C:''' Yeah, and then work with the ACLU, yeah, exactly.
'''S:''' You see, if one of their employees sues the hospital for violating the law, and then it'll work its way through the courts. That may be how it unfolds.
'''E:''' Right. And how will that look politically for whomever is in support of that at that point? Then you'll probably have some initiative to repeal this law.
'''S:''' Well, they're playing to their base with that.
'''C:''' The saddest thing is that we're even talking about it. That's the thing, because this is such an example of when we talk all the time on the show about whether or not we wanna get into politics or just stick to the science. This is a beautiful example of why this is such a sticky situation. This is a public health issue. It is, like you said, Steve, it is one best left to the experts to decide what is the safest and healthiest for their institutions. And when you expressly ban or forbid them from making decisions to ensure the health and safety of their employees and their patients, their hands are tied behind their back.
'''S:''' It's micromanaging. Any time, in my experience, any time a legislature tries to micromanage medical decisions, it's bad. It's always some ideological bullshit thing, yeah.
'''C:''' People got sick and die.
'''S:''' It's never like, because they don't, think about a situation in which a legislature is going to know better than medical experts, or like, what's the right thing to do?
'''E:''' It's like trying to make a law telling NASA how to build rockets. It's so ridiculous, it's so crazy.
'''S:''' As opposed to just saying, you have to be licensed, you have to be certified, that's fine. But saying this, that's why I say micromanaging, but saying like this specific decision we're gonna make at a legislative level rather than letting experts make it. The other thing is, is that legislatures move way too slow to keep up with the data, right? So what if so they're going to change their laws, their micromanagement when new studies come in as opposed to just letting experts decide based on change their recommendations on a dime if a new study gets published. It's just ridiculous, it makes absolutely no sense. It's always for ideological reasons. It's it's never for, it's never actually for patients or for people or because it's the right thing to do. It's always bullshit ideology. And this is no exception at all. There's no legitimate reason for them to get involved with that kind of decision-making. You know, whether or not a hospital, what hospitals do to defend their own employees and patients, it's terrible. All right.
'''C:''' Yep, I know, we're all like pissed. We're all like, grumble, grumble.
'''J:''' We're all pissed off.
'''E:''' It's not good. And like you said, Cara you don't have to be of one affiliation or the other. I think a lot of people can see this as not good.
'''C:''' Oh yeah, completely.


=== Lunar Library <small>(48:25)</small> ===
=== Lunar Library <small>(48:25)</small> ===
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}}
}}
'''S:''' All right, Bob, tell us about the Lunar Library. This is cool.
'''J:''' Ooh.
'''E:''' Ooh.
'''B:''' I found out on the SGU subreddit recently from user mem_somerville about the Arch Mission Foundation, which essentially wants to back up our civilization in case of a mega global disaster. It's a fascinating idea, and the tech they're using is even more interesting, in my opinion. The Ark Mission Foundation, it's a nonprofit organization, and they want to create many of these redundant repositories of human knowledge and seed them throughout Earth and the entirety of the solar system.
'''E:''' Sure.
'''B:''' Founded by Nova Spivack and Nick Slavin in 2015. So what do you think their inspiration was for this?
'''S:''' 2001?
'''E:''' 2012, the movie.
'''J:''' No, Bob, whatchamacallit.
'''B:''' Say it.
'''J:''' Isaac Asimov's book series.
'''B:''' Yes. Yep, right, Jay. Isaac Asimov fans should know this. It's the Asimov {{w|Foundation series}} in which the predicted collapse of humanity's galaxy-wide civilization, is they deal with it essentially by creating this archive of our accomplishments to minimize the coming dark ages and all that stuff to basically reboot humanity.
'''S:''' Although that was all a fake-out.
'''B:''' Well, you don't need to go into that level of detail. So on their website, on their website they say, it's funny, their website is like, humanity, we have a problem. Our modern civilization, the most technically advanced in human history has no backup. They say if a global catastrophe occurred today, most of our collective knowledge would be gone within a decade and it would take centuries to rebuild. So yeah, that's basically the line that they were talking about at the beginning of the foundation. They continue, we build and maintain ultra-long-term data storage archives called ARC libraries. Arch libraries are the most durable records of human civilization ever built. Using new technologies, they preserve more knowledge for more time than anything ever created. So that's definitely the plan and they seem to be well on their way to achieving at least some of that stuff. This is called the Arch Mission Billion Year Archive Initiative. It's a hell of initiative. The first proof of concept for this is called the Foundation Library. And I bet many of you saw it launch in 2018. The location of this library, Arch, surprised me. I wasn't aware of it back then. I don't remember reading about it. Can you guess what I'm talking about? Where was this ARC library that everybody saw? Everybody saw that famous image. I'll give you a hint. It was in a glove compartment. All right, you punks. That red Tesla Roadster that went into space.
'''J:''' Oh, cool. Yeah, yeah.
'''B:''' It's now orbiting the sun for the next, say, 30 million years. And there was actually one of those Arch libraries in the glove compartment.
'''E:''' Yeah, but they lost the key, so.


==== The ark itself <small>(55:57)</small> ====
==== The ark itself <small>(55:57)</small> ====
'''B:''' Yeah. They built this as the first library in space. And this Arch, though, was a proof of concept. It basically contained one thing, or three things. Isaac Asimov's Foundation Trilogy is in there. And it's claimed that this Arch could last for, get this, billions of years and still be readable. That's what the claim was. To me, that sounded way, way too optimistic. I mean, can you, backing up data that lasts for billions of years, like they said, like 14 billion years. I mean, I have-
'''E:''' What medium lasts that long?
'''B:''' I have eight-year-old hard drives that have crapped the bed, and they're saying they're gonna go 14 billion years. Well, I looked at the tech, and it is fascinating, and I wasn't able to spot any red flags. And I mean, I wouldn't be shocked if this really can last for hundreds of millions or billions of years. The claim was basically made by Peter Kazansky. He's a professor of optical electronics at the University of Southampton. And he got his PhD under the supervision of a Nobel Laureate for the invention of the laser. So yeah, he's got-
'''C:''' Oh, wow.
'''B:''' That would go on my resume. Yeah, my supervisor, yeah, he invented the laser, or one of the guys that developed the laser. So Kazansky brought this technology to its current state of the art. It was proved in 2010. But in the past few years, he's brought it to the current state of the art in terms of like speed and density and everything. And he created five disks, each one holding Asimov's trilogy. Now, these disks are considered actually the longest lasting storage objects ever created by humanity. Because if it does last billions of years, and yeah, that would be true. It uses a technique called 5D laser optical data storage. If you Google that, you are gonna come across many, many articles that call it essentially the Superman memory crystal. Remember Superman II with those crystals?
'''E:''' I do.
'''B:''' It kind of works so, because this medium is essentially fused quartz, which seems pretty similar to those Kryptonian memory crystals that Superman has in his fortress of solitude. So, but these non-fictional crystals will reportedly remain readable for up to 14 billion years, and they resist cosmic radiation, and they can withstand temperatures up to a thousand degrees Celsius. The tech is really cool. They use a femtosecond. That was one of Kazansky's breakthroughs, a femtosecond laser to create these different layers of tiny nanoscale patterns in the quartz. That's kind of redundant, tiny nanoscale. So you've got these nanoscale patterns in the quartz created by this femtosecond laser. So they call it 5D storage because the information is encoded in five different dimensions. Now they're not spatial dimensions. They're just three that we know of, right? Height, length, and width, plus orientation and position are considered dimensions of well in this context. So if you look at one of these disks, now imagine you've got this quartz, you're looking at it, and you're looking at it from a very specific angle and a very specific magnification, and then you would see an image or whatever.You'll see a layer of data that's encoded. But if you look at a different angle or magnification, you would see a completely different set of data. So the result that you could imagine is that there's this amazing storage density. It's 10,000 times denser than Blu-ray optical disks, assuming anybody even remembers what the hell that is. It could hold 500 terabytes on one disk. That's a half a petabyte. So that's huge. One little disk, one little CD-like disk holding a half a petabyte, big. That's pretty dense. And so if you wanna actually see the solar system with massive data backups, this technique ticks two of the biggest boxes. It's super high density, and it will last a stupidly long time. Kazansky sais this technology can secure the last evidence of our civilization. All we've learned will not be forgotten.


==== Reading the discs <small>(57:41)</small> ====
==== Reading the discs <small>(57:41)</small> ====
'''J:''' Well, how do you read it?
'''B:''' Well, that's a good question, Jay. You need some tech. You need some tech to do it, and that segues nicely into my next section here. But I wanted to say before I do that is that there are, of course, more immediate applications for this tech, right? National archives, museums, libraries, private organizations. You don't need to backup humanity and throw it into the solar system only. You could also use this for these things that will be incredibly important over the next 10, 20, 30, 40 years, not 14 billion. So the next phase here was the LEO Arch library. LEO stands for Low Earth Orbit. They launched that in 2018. It's piggybacking on a satellite. It contains a copy of Wikipedia. But I'm gonna jump to the next stage because this is taking a long time. The next stage is the LUNAR library, launched in 2019. So this was a lander from the Israel Aerospace Industries hosted this Arch, this LUNAR Arch, which contains lots of things like 30 million page library of books, data, images, all sorts of the scientific, historic, and cultural information. Wikipedia, of course, was there in English. And it also had a secret vault of content, including things like David Copperfield's magic secrets.
'''E:''' That's right, Copperfield.
'''B:''' His secrets revealed are on the moon. They actually, yeah, so if you can get there, you could find out all his tricks. But there's a caveat. Unfortunately, to slow the lander's descent to the moon, the braking method that they had to employ was litho-braking. Now, litho-braking is short for lithospheric braking. Does anyone know what the lithosphere of a planet or moon is? It's essentially the ground. So litho-braking ''(Cara laughs)'' is just a geeky-
'''C:''' It's just slamming into the ground.
'''B:''' Yes, it's just a geeky euphemism for crash landing. Now, remember, though, crash landing, or litho-braking, as we call it, it does have the benefit of being the quickest and cheapest way to stop. So there is that. So it hit the ground at like 300 miles an hour.
'''E:''' 300.
'''J:''' 300.
'''B:''' Pretty fast, but there's actually some hope that some of the data, or maybe even potentially all of it, survived, but they don't know. They don't know. Probably, they're not sure, but there's actually some hope that some of it actually survived. That's how hardy that is. But even though it was probably destroyed in a crash, the technology they used was very interesting. It was not the 5D optical laser storage that's in the Roadster's glove box. And Jay, back to you now. You mentioned that you need some fairly advanced technology to read those 5D optical laser storage disks, right? But if you want people, or even potentially aliens, I assume, in the distant future, if you want them to be able to read this data, the simpler the tech required, the better. It's just like a, keep it simple, stupid. That seems obvious. So that's why these people wanted to go with something, a storage technology that was more analog. And that's why they're using NanoFiche. Now, that should be ringing some bells when you-
'''C:''' MicroFiche?
'''B:''' Old guys out there, NanoFiche. Remember looking at archived images of newspapers using MicroFiche?
'''E:''' Absolutely.
'''B:''' Remember in those buildings we called libraries? Remember those days?
'''C:''' Yeah. With card catalogs.
'''E:''' We have a library in town. My family's all have library. We have library cards.
'''C:''' Oh, yeah.
'''E:''' We're still there.
'''B:''' Weirdos. ''(laughter)'' So I remember looking at old magazines and old science magazines and newspapers using MicroFiche. It was really cool. Basically, really tiny images, direct images, of the media that you were interested in. And then you had a machine and you read it. Well, now we have NanoFiche, which is created by etching these super high resolution, microscopic images on 25 micron thin layers of nickel. So nickel is used in this case because it's an amazing material. It doesn't degrade. It doesn't oxidize. It can handle electromagnetic radiation, heat, cold, microbes, chemicals. And it could do all of that for many thousands of years. So it's an amazing material for this type of storage. And the data density is pretty amazing. Imagine if you have a NanoFiche and if it was as big as a letter, I guess, eight and a half by 11, it could hold 300,000 analog photos, each one of them at 300 DPI. 300,000 fairly decent resolution photos on one eight and a half by 11, typical letter sized piece of paper. That's the kind of size we're talking about. If the NanoFiche contains just analog text and images, it could hold 1.2 million pages on one page. So it's extremely, extremely dense. It just essentially is shrinking it down, but it's not really encoded really in any way. Imagine the lunar library that now crashed and is probably in pieces on the moon. If you could look at that and if you could put it back together and fix it, what you would see is you'd see these 25 layers. The first four layers is all, tells you everything you need to know about how to go farther, how to decode and do things to the 21 layers below that, that has all the information that you want. It has the Wikipedia, it has the classic literature on it. Thousands and thousands of books of classic literature, David Copperfield's magic tricks are all on those lower 21 layers. And the top four layers will tell you, it's got like 60,000 high res images. It has book pages, language instructions, and the keys to decoding everything else below it. So that's what it had. It's not as dense as the 5D technique, but all you need to do, Jay, all you need to do to read this is a hundred magnification microscope to see it, a hundred times, that's it. You don't need a fancy electron microscope for this. This can be done with optical microscopes and optical microscopes were invented, what, 1590. So that's more ideal. It's maybe, it's not as hardy as the 5D optical storage. It's not gonna last for billions of years, but it's very easy. Any of us could put together a device from scratch that could read this. Whereas if you wanted to read that 5D optical stuff, forget it, forget it. You need specialized equipment to do that and the know-how to actually use it. So, okay, so that's kind of where we are. So after the crash, they're gonna go back to the moon for a second try in 2024. And of course, what they're gonna bring to the moon in 2024 is even bigger and better than what they tried in that crash. There's 60 million pages instead of 30 million. There's an internet archive. There's linguistic keys to 5,000 languages. There's archives of music. It's an amazing repository at this point. And they're really just getting started with this. But it's really a huge amount of information.
'''J:''' Is it even possible to measure how complete it is?
'''B:''' You'd have to define what complete is.
'''C:''' Yeah, right.
'''B:''' What does complete mean?
'''C:''' What percentage of all of the things does it have?
'''E:''' I don't know that anything's ever complete.
'''J:''' If you take categories, right? All the world's music, all the world's literature, all the world's art, all the world's technology, engineering, and all these categories, you know?
'''E:''' Wow, that changes every second.
'''B:''' You would need something at the range of 175 zettabytes. So Jay, that's the amount of data created, captured, copied, and consumed in the world by 2025. That's the estimate for 2025. So it would be, I would think, something in the range of zettabytes. And hey, man, that's a hell of a project. It's beyond reason, I think, to probably try to archive all of that. I think you'd have to pick and choose. You know, what would be the most important stuff?
'''E:''' Charlie bit my fingers.
'''B:''' I'm sure we don't need to back up everybody's email, you know? And that kind of stuff. But yeah, it's a lot. And we're just scratching the surface at this point.
'''S:''' What we need to do is put them all into a big black obelisk and bury that on the moon.
'''B:''' Ah.
'''E:''' Yes.
'''B:''' Interesting. I like this.
'''S:''' All right, thanks, Bob.
'''B:''' Mr. Clark.


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SGU Episode 959
November 25th 2023
959 Lunar Library.jpg

The first major installation of the Lunar Library is a 30 million page archive that flew on the SpaceIL Beresheet Moon lander, in 2019: It is now believed to be intact on the Moon.[1]

SGU 958                      SGU 960

Skeptical Rogues
S: Steven Novella

B: Bob Novella

C: Cara Santa Maria

J: Jay Novella

E: Evan Bernstein

Quote of the Week

Science has the answer to every question that can be asked. However, science reserves the right to change that answer should additional data become available.

Mary Roach, American author

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Introduction, Thanksgiving plans

Voice-over: You're listening to the Skeptics' Guide to the Universe, your escape to reality.

S: Hello and welcome to the Skeptics' Guide to the Universe. Today is Wednesday, November 22nd, 2023, and this is your host, Steven Novella. Joining me this week are Bob Novella...

B: Hey, everybody!

S: Cara Santa Maria...

C: Howdy.

S: Jay Novella...

J: Hey guys.

S: ...and Evan Bernstein.

E: Good evening everyone.

S: So this is our Thanksgiving episode. We're recording the day before Thanksgiving, but it won't come out until a couple of days after Thanksgiving. So when you're hearing this, we will have had our Thanksgiving in podcasting time. What's everybody doing?

J: Well, as usual, I'm in Colorado with my wife's family out here, and we are cooking for two days. And I'm telling you what, I'm like, I've eaten more in the last two days than I have in the last two weeks.

B: Shocker.

J: And this is just the prep for the big meal.

B: It's a warm-up, man.

E: That's right.

B: Wow.

E: Getting ready. It's like a competition, what, food eater. They have to get themselves, it takes weeks to build it up to the time of competition.

S: Have you guys ever eaten so much Thanksgiving that you couldn't move?

C: No.

J: Bob, remember that year that you and I ate so much that we couldn't bend over?

B: Jay and I, not just bend over, Jay. Jay and I couldn't sit. We couldn't sit. We had to stretch out because sitting was bending too much. It was historic.

J: Yeah, right? That was pretty serious eat right there, man.

B: This year, Liz and I are having our first Thanksgiving at the house, at the homestead.

E: Nice.

B: And Steve and Joss and their daughter Autumn is coming. We're very excited. And Liz invited her parents, but her mom got COVID.

C: Oh no.

B: So that's not happening. But this year, it's cool because this is the first time ever that my house is now decorated for Christmas, Thanksgiving, and Halloween at the same time.

J: Oh my god Bob, new level man.

E: Oh my gosh, a new milestone.

B: It's so exciting. So I had to take down, of course, 90% of the Halloween decorations that happened.

E: What?

S: Which still leaves behind more Halloween decorations than most people have.

E: Most people own. Yeah.

B: True. So the TV room is Christmas. It's looking real good. It's going to look even better once I do some more work tomorrow.

S: Well, but Christmas is coming and all.

B: And then the dining room is Thanksgiving-ish. It's got definitely no Christmas in there. It's Thanksgiving. And then the library, it's Halloween, but it's Christmas Halloween. So I just left it up because that's how I had it decorated for Halloween. And it's got a Christmas tree. It's all creepy decorations and everything. It looks great. So I was like, hey, I'm going to leave it up there. So it's three holidays, one house, and I love it.

C: I am up in the Pacific Northwest. I came up to Oregon, drove up here a couple of weeks ago in my camper, camped on the way up.

J: How's that going?

B: Cool. How'd that go?

C: Amazing.

J: Tell me about your camper.

C: It's been so fun. I mean, it's been super cold ever since I got it, so I've only really winter camped. But it's been lovely, and I'm actually doing even more work on it while I'm here. I'm putting some roof rack bars and a solar tray, so it'll be solar ready, which means my panel on the roof will feed energy into my thousand kilowatt hour battery that is in the bed of my truck so that I can power my refrigerator and my lights and my heated blanket and anything else I need. Yeah, it's great.

E: I have a question. When somebody is mobile, portable like that, how does one order things and have it get to them?

C: Yeah. So lots of orders going to, as my friend calls it, her shipping and receiving station, which is their dining room table. I've just been shipping things to my friends up here. I've got two very, very dear friends up here in Oregon, one of whom just had a baby. So lots of domestic things going on around here. And oh, so for Thanksgiving, it's going to be really fun. I've been invited to a friend's friend's house and there will be, I think they said 20 people.

B: Whoa.

C: So it's going to be a really big dinner.

S: That's big.

C: Yeah.

E: That's nice.

C: And we're all contributing different things. I'm making my sweet potato casserole.

E: Cara, the casserole you're going to make, are you going to use your solar powered kilowatt generator to actually cook that up?

C: If it was stove top, I could because I have a whole hookup for that too. But no, I wouldn't be, I would be using propane for that. But no, I don't have a, I don't have a camper oven, just a stove, just like a burners and a jet boil. So no, I will be making it in my best friend's kitchen.

S: I'm going to be making the stuffing for Thanksgiving, which I've never made before. So we'll see how that goes.

E: What sort of bread, what sort of bread will be the base of the stuffing?

S: Cornbread.

E: Oh, cornbread.

B: Really?

S: Yeah.

E: So good.

B: Is that common?

E: Oh my gosh.

S: Well, we'll see how it goes.

E: Have you never had it, Bob?

B: I probably did, but it just doesn't, it's not ringing any bells.

E: You're in for a treat. Steve, don't make it well, okay?

S: I mean, I could follow a recipe.

E: You'll be the hero.

S: Yeah, it'll be fine.

C: And you're not actually supposed to put stuffing in the bird while you cook it, right?

B: No.

S: No.

C: You have to make stuffing separately.

S: Yeah. It's not hygienic.

C: It's a salmonella-ing.

S: Yeah. It's basically an incubator for bacteria.

B: That was a thing. Remember that? Geez.

E: Oh boy.

S: Why do they call it stuffing?

E: That's a good point.

C: What about you, Ev? You haven't given us your plans.

E: Oh, I will be with family. I'll be with my wife, Jennifer, her two sisters in town, and some other close relatives. Obviously, Rachel will be there too. And it'll be traditional Thanksgiving fare, which we love.

S: Yeah.

C: Who doesn't?

S: Going traditional. No typical Novella family three-course meal, starting with lasagne.

E: Right.

S: Back in the day, that's what I used to do.

J: Back in the day, yeah.

S: It was really three full meals. It was like three four-day worth of calories.

E: Oh my gosh.

B: It was nuts, man. We got to the point where we just started taking a three-hour break between courses. Like, how do you go from lasagne to...

E: Three-hour break between courses.

C: How do you have a lasagne as a starter?

J: Let's cut this shit here. We were never hungry after the first course. You just eat. You're sitting there. You're eating. You know what I mean?

S: Let's move on with the show.

What's the Word? (6:39)

S: Cara, you're gonna start us off with the, what's the word?

C: Actually, this is, yeah, this is a pretty great word given that we're talking about stretching one's stomach full of food. So this word was recommended by Casey Soska, listener Casey from Pittsburgh. "Hi, Cara, my wife and I were talking about the weird little bumpy ridges our dog has on her lips and realized not only did we not know what they're for, but what they're called. We found that they're called rugae or rugal folds and they help when gripping and manipulating food, but apparently rugae are in many parts of the body. Thought it might be interesting to see what the root is nd if the term is used elsewhere." So you heard me, I don't do this enough, I'm gonna spell it. So the singular of this word is ruga, R-U-G-A, and the plural is rugae or rugay. You'll sometimes even hear people pronounce it rugi or rugay. These are all American pronunciations, by the way. I feel like I need to be really clear about that after the last time when we talked about epochs.

S: After the epic travesty.

C: Yeah, after the epic tragedy, which in the UK is pronounced epoch, or I think it's epoch, yeah, and in Australia as well.

E: Yes, but we forgive them, right?

C: Well, we're the ones who changed it probably.

E: Oh, then you're welcome.

C: You're right, exactly. So ruga, R-U-G-A-E, which is the plural of ruga.

J: Aruga.

E: That's that old horn noise, that's right.

C: So this is a word that you often see in anatomy, but you also see it in botany, sometimes in, or not sometimes, often in zoology as well. This is a fold, a crease, or a wrinkle. And you'll even see it, the adjective form will be rugate. So something that is wrinkled, folded, or creased. And I first came across this word, I don't know about you, Steve, but I first came across it in my biology lessons when I was learning about the interior lining of the stomach. Because when the stomach shrinks down, it's got all these different rugae. And when it gets really, really full, they kind of stretch out and it doesn't look nearly as folded anymore. But we do see rugae throughout different portions of the body, like Casey mentioned when speaking about the bumpy ridges on their dog's lips. You sometimes see it in different plant matter, in botany. And so let's talk a little bit about the root of the word. So rugae is Latin. It comes from the Latin word ruga. So it's actually, the root of it is its definition, which is a wrinkle. They think it's like proto-Italian or Italic, but there's something interesting when we start looking at other words that are related, like rugged, because the words for wrinkle and crease seem to be related to rugged. So like a rugged landscape is also very similar to rugae. And then I love this. I never even thought about this, but here's another word that's related. It uses the same root, corrugate, corrugate, right? The rugated part of the cardboard. The corrugation is very, very similar in its root to rugae. But usually you do see that word mostly as listener Casey wrote about it in anatomy textbooks. And when you're learning about different parts of the body, especially parts that have, want to have a higher surface area than is allowed, you'll see a lot of different kind of folds and wrinkles, and that's where many receptors might be so that the surface area can be increased for absorption.

S: Yeah, I learned about it in anatomy, obviously. A lot of things in the body have rugae. Your palate does, right?

C: Yeah, yeah, yeah, true.

S: The roof of your mouth. All right, thanks, Cara.

News Items

3D Printing Soft Robots (10:26)


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S: Jay, tell us about 3D printing soft robots.

J: I've been waiting for this. 3D printing has been making battery technology. Nice, steady advancements or whatever, but this one is pretty significant, what this team developed. So there's researchers from ETH, Zurich, and a US company, they're called InkBit, and they are a spinoff from an MIT group, and they've developed a groundbreaking 3D printing technology. And this is gonna fundamentally change the capabilities of 3D printing. I haven't seen the printer. I tried to find what it looks like, but the bottom line is that the real thing here is the engineering and what they were capable of achieving with the materials that they're using. So 3D printers today, they're limited. Most of them, if you're not using a resin printer, you're using a certain kind of plastic, and it's a fast-curing plastic, which means that the head of the printer basically softens it, puts it into position, and then it hardens pretty quickly. It's called a fast-curing plastic. The team's approach that they came to was that they wanted to accommodate slow-curing polymers, and this is a big difference because the slow-curing polymers take more time. They're a much trickier material to work with, and I guess historically, people just couldn't really get there. So what they were able to do, at its core, they were able to increase the number of usable materials, different types of plastics and polymers that their 3D printer can use compared to traditional 3D printers. So the slow-curing plastics have superior elastic properties, and of course, this enhances the durability, enhances the strength of the printed objects, and they can also, and this is probably the most important part, is that they can bend and go back to their original position, which, if you've used a standard 3D printer, with the basic plastics that you get for that, they're super rigid. There's no flexibility there, which means that they don't move. They really shouldn't be moved, because they'll tear apart. This technology that they came up with, it enables a seamless 3D printing of intricate and resilient robots using a variety of their high-quality materials, all these different types of materials that they've come up with, in a single operation, meaning that their printhead can print multiple polymers and plastics that have different temperatures, and of course, that would have a different curing time. They can print them at the same time. So one of the standouts is the team accomplished the creation of a robotic hand. The hand has bones, ligaments, tendons, and they're all crafted, like I said, from different polymers in one single printing session. Anyone that's used a 3D printer knows that this is pretty significant. The team was able to do this with fast-curing polyacrylates. These are traditionally employed in 3D printing, and they also, they shifted to using slow-curing theolene polymers, known for their, they're basically exceptionally elastic, and their rapid return to their original state or position that they were after bending, that's a big deal. The flexibility of theolene polymers also allows the researchers to fine-tune things like stiffness, and printing each part of the robot to its specific needs. Now, this is a soft robot. They're considering this to be in the category of soft robots, and these types of robots have advantages over traditional metal robots, right? Their pliability does a couple of things. It reduces the risk of injuring a human who works beside them, which this is a situation that is becoming more and more common. You have people, like on a warehouse floor, working beside robots, and they're also more adept at handling delicate objects, and that's another big thing to consider. You know, think about a company like Amazon, who wants a pack-and-pick robot to go in and pick up all sorts of different objects. You know, they want a robot that can pick up anything that a human hand can pick up, and this is a significant step closer in that direction. The researchers also use a 3D laser scanner, and this is really cool, because this inspects each printed layer for surface irregularities in real time, and the reason why this is important is it gives the printer dynamic feedback, and it adjusts the amount of material that's being printed as it's going, and it's compensating on the fly for any irregularities. Again, if you've done any 3D printing, irregularities, like you don't even know what's going on on the inside of your print job, unless you're gonna stand there. Some print jobs that Ian and I did took a day, days, whatever. They could take so long, like you're not. So having a laser be able to inspect the print job and give feedback instantly to basically the head of the printer, which is doing all the heavy lifting to make a fix immediately is huge. It's just a huge advancement. Typical 3D printers are error prone. They have unexpected results, and this solves that problem. So looking ahead, ETH Zurich researchers, they're planning to find new applications for their technology. InkBit, on the other hand, plans to leverage this innovation right away by offering a 3D printing service to customers and introducing new printers to the market. Now this, again, this is a big deal, and it's gonna significantly upgrade 3D printing products and parts that are gonna be available to all of us. You know, right now, there's a lot of 3D printing going on out there, and a lot of custom parts being made with 3D printers. We use 3D printers for prototyping. We use 3D printers to make props for movies, the applications are getting to the point now with the technology that we have today. It's huge, but this advancement actually is gonna bring a lot of nuance to 3D printing. You know, like I said, they're printing a robot arm in one piece, and it's made out of different materials, and it functions. That's a breakthrough.

S: Yeah, and I wonder, I mean, you would think that this technology could also be applied to prosthetics, printing a prosthetic.

C: Right, yeah, because those all have to be custom.

S: Yeah. Yeah. And, of course, you want them to be soft. You want them to be as human as possible.

J: Yeah, I think this is just a huge breakthrough in 3D printing. You know, the bottom line is, once this gets out to the market, and people are using it, and then people are gonna be even refining it further and further, it just doesn't end, you know? People that do a lot of 3D printing end up becoming innovators themselves because of their specific needs. And giving people access to something that can print soft materials with more complexity inside the print job is just a huge, huge leap forward.

S: Thank you, Jay.

First CRISPR Treatment Approved (17:12)


S: We're gonna, yeah, we're starting the show this week with a couple of upbeat news items. I'm gonna be talking to you guys about the first regulatory-approved CRISPR-based treatment for a disease. So, yeah, we started talking about CRISPR back in 2017, I believe, and here we are six years later, we have an approved therapy. That's fast, to go from working out the basic science of a new technology to having this kind of application. So, in the UK, a drug, a CRISPR-based drug, it's really a whole procedure but the drug itself is called CASGEVY, C-A-S-G-E-V-Y, the generic name is almost unpronounceable, exagamglogene autotemcel.

C: Sure. Rolls off the tongue.

S: So, it was approved for the treatment of sickle cell disease and transfusion-dependent beta thalassemia. So, you guys, just to give you a quick background on this, sickle cell is a harmful mutation of the hemoglobin gene that causes a conformational change in the red blood cells. So, the red blood cells, instead of being round, like discus-shaped and flexible, become sickle-shaped and rigid. And those abnormal or sickle-shaped red blood cells tend to clog up the capillaries, which impairs blood flow, and then the tissue gets ischemic, and it's extremely painful. Patients with sickle cell disease get these sickle cell crises, and that can be extremely painful and cause tissue damage. They have to be admitted to the hospital, they're treated with morphine, they're given transfusions, it's very serious. And then there's beta thalassemia. So, these are also hemoglobin genetic mutation-based diseases. So, the hemoglobin has four components, two alpha and two beta. And so, beta thalassemia is when you have a mutation in the beta globin component of the hemoglobin. There are about 1,000 different mutations that cause beta thalassemia.

C: Oh, wow.

S: Yeah, so it's a very, very heterogeneous set of mutations. Basically, anything that degrades the beta globin component of the hemoglobin. And it could be anything from asymptomatic to what we call transfusion-dependent. These are people who need to get blood transfusions every two to three weeks to stay alive, because their blood does not carry oxygen, and so they need to constantly replenish their red blood cells. The treatment's approved for transfusion-dependent beta thalassemia. So, any beta thalassemia that's bad enough that you need to treat it with transfusions. Now, at this point, you might be asking yourself, how can one drug, one CRISPR drug, treat two different diseases, one of which has thousands of mutations? So, what do you think the CRISPR-based treatment is doing? Think about that for a minute.

C: Something about the oxygen.

S: Think about that for a minute. Let me remind everybody what CRISPR is. This is Clustered Regularly Interspaced Short Palindromic Repeats. It is a mechanism that was derived from bacteria. Essentially, it is being used to target a, you can basically attach to it a sequence of RNA, and then it will basically find the matching sequence, right, in DNA, and then you attach an enzyme to it, which can, for example, cut the DNA at the location that you targeted with your target RNA. Now, you could do a couple of things. You could do lots of things with that, but they've already demonstrated that they can, for example, silence a gene by clipping it, just by cutting both strands, or they can turn a gene off, and then they can later use CRISPR to turn it back on again. So, they could reversibly turn it off, right? They could irreversibly turn it off, they could reversibly turn it off, or they can make a slice and then have the cells repair machinery, make repair the cut, but insert a new gene while they're at it, right? So, you could basically insert a gene into a specified location. So, you could use this for for genetic modification, for genetic engineering.

C: So, they must be engineering regular hemoglobin. Like, is it-

S: That's a reasonable thought, is that they're giving a normal hemoglobin gene to replace the bad one.

C: Or some sort of, like, repairing is, because is it the same error that causes? Yeah, it's, like, very different.

S: So, that's not a bad thought, but that's not how this works.

C: Okay.

S: It's actually pretty cool. So, in order to understand how this works, you have to understand something else about human physiology, and that is that the fetus has different hemoglobin than adults. And the reason for that is because fetal hemoglobin has to take oxygen away from the maternal hemoglobin, right? So, it has to have, under at least some conditions, it needs to be able to have a higher affinity for oxygen than adult hemoglobin does. Does that make sense?

C: Yeah.

B: Yeah, sure.

S: Because you know how hemoglobin works, is that it basically has an iron molecule in the middle, and then when it gets exposed to high oxygen tension in the lung, it binds oxygen from the air, and then when it goes to low oxygen tissue, it gives up the oxygen, right? So, it either binds to or release the oxygen based upon the oxygen tension, like how much oxygen is there. So, the fetal hemoglobin has to be able to steal the oxygen away from the maternal hemoglobin, and then still give it up to the fetus's tissue.

C: Right, so, like a higher affinity.

S: Right, and so we make fetal hemoglobin when we're a fetus, and then it dominates until we're about six months old, right, and then after six months old, we stop making fetal hemoglobin, we start making adult hemoglobin. So, all you gotta do is stop the process of turning off the fetal hemoglobin.

C: Oh, so kids with sickle cell don't develop sickle cell until they produce adult hemoglobin.

S: Yes, because it's a mutation in the beta subunit.

C: Right, so their fetal hemoglobin's fine.

S: Fetal hemoglobin has the alpha, so adult hemoglobin is alpha subunits and beta subunits. Fetal hemoglobin is alpha subunits and gamma subunits. So, if you have beta thalassemia, or if you have a mutation of the beta globin, then the fetal hemoglobin is fine. Now, it turns out, yeah, very interesting, right? So, it turns out that how does the adult hemoglobin take over for the fetal hemoglobin? Well, there's one gene, BCL11A, that turns off the production of gamma globin subunits

C: That's crazy.

S: So, all you have to do is silence that one gene, and we start making fetal hemoglobin again. And there you go.

C: And there must be people out there for whom, I mean, I feel like any time there's a single gene doing something, somebody out there already has a mutation. So, I mean, there must be people walking amongst us who just still are using their fetal hemoglobin, and that's a real problem. That's fascinating.

B: Yeah, but don't you see the problem with this?

C: What?

B: Can't they just go up to people and steal their oxygen? (laughter) Come on, people, think about it.

S: They'd have to hook up their blood vessels to your blood vessels.

B: Yeah, so what?

C: Yeah, you'd need to connect belly buttons somehow.

E: Over Bluetooth or something, you know?

J: Steve, the end result is, though, this literally fixes the problem.

S: Yes.

C: Yeah, oh my God, a lifetime of, wow.

S: Clinical trials that were used as a basis for the approval. So in a clinical trial with sickle cell patients, 28 of 29 subjects who were treated were free of sickle cell crisis episodes for at least a year. And in the transfusion-dependent thalassemia patients, 39 of 42 subjects treated did not need a transfusion for at least a year. Remember, these are people who were getting transfusions every two to three weeks. They were able to go more than a year without needing a transfusion. So it didn't work in 100%. You know, we could ask, why that one patient out of 29, or was it three patients out of 42, why didn't it work? Because the CRISPR, I guess, didn't get in.

C: Right, is it an uptake problem?

S: Didn't affect, yeah, it didn't affect enough of the cells. So this is how-

C: But maybe you'd have more doses or more refined.

S: This is how the treatment works. Well, let me tell you something. This is how the treatment works. So you take bone marrow out of the patient, right? And then you CRISPR the progenitor cells, the stem cells that make the red blood cells, so that they make the fetal hemoglobin. And then you have to treat the patient to prepare their bone marrow for an auto-transfusion. Then you give them back their treated, their CRISPR-treated bone marrow stem cells. So the whole process has to work. You have to be able to change enough of the stem cells that you took out, and enough of them have to survive and take up shop in the new bone marrow that you give back to the patient. So I guess for some of them, they're not making enough of the fetal hemoglobin to prevent the clinical, the negative clinical outcomes. But still, 20 out of 29, and 39 out of 42, that's pretty good.

B: That's pretty awesome. Question, if you have this treatment, and then you have alpha gamma, and you're an adult, and you're a woman, can you still have a baby?

S: Yeah, that's a good question.

B: I would think no. The hemoglobins would duke it out, each trying to get oxygen from the other.

S: So the short answer is yes, it's a potential problem. And there actually, it has been studied, because people can make fetal hemoglobin into adulthood naturally, without being CRISPR-ed. So this is already a thing. There was a study a few years ago that looked at women, 43 pregnancies of women who had persistence of fetal hemoglobin between 11 and 100%. And what they found was, is for those mothers whose fetal hemoglobin levels were 70% or higher of their hemoglobin, they did have an increased risk of intrauterine growth restrictions, right? So their babies did not grow as well, if their fetal hemoglobin was over 70%, greater than or equal to 70%. So yeah, in these patients, it would be a problem if they became pregnant. And then we'd have to see if there's something that could be done about it. I don't know if there's any treatment for it right now. Okay, one more thing. So how much do you think this whole treatment costs?

J: That's the scary part. I would hope that insurance companies are gonna cover it, but that might take a while.

S: Either way, so this is approved in the UK.

B: 500,000 a year.

S: The FDA is considering it. They'll probably the application's accepted. They're probably gonna make a decision in December or January. And the European health agencies also accepted the application. So it may be approved in the UK, Europe, and the US before long. But this is a single treatment. It's not per year. This is a single treatment. And then it's a one-off.

C: It involves?

S: Bone marrow transplant.

C: Bone marrow transplant, yeah. And bone marrow patients are in the hospital for a while.

S: Once you're done with the whole thing.

B: And it hurts.

S: Then you might be good for your life. You know what I mean? That could be it.

J: I'm gonna guess $50,000.

S: $50,000? So in the UK, the estimated cost is 1.5 million pounds. In the US, the estimated cost is $2 million. But here's the thing. There was a study that looked at the cost-effectiveness of the treatment. And they found that the treatment would be cost-effective, meaning that it would save more money than it would cost in healthcare dollars. This is not even including quality of life or anything else, just healthcare dollars. It would be cost-effective at a treatment cost of 1.5 million pounds or $1.9 million. That's because, as Cara said, getting hospitalized for sickle cell crisis is damn expensive.

C: Yeah, and it can happen a lot. And that is, you do. You land in the hospital when it happens.

S: Right. Yeah, so even though the sticker price is shocking, it's like $2 million. But it's actually cost-effective because it costs more than that to treat somebody over the course of their lifetime for sickle cell disease or to get transfusions every three weeks for life. It's expensive.

B: So the younger you are, the more willing they would be to foot the bill?

C: I hope not.

S: Yeah, I hope. That would be ageism. But it's still cost-effective.

C: The younger you are, the more quality of life you'll probably get.

S: And then, yeah, that's not even including the quality of life, you know?

C: But sickle cell is something, I mean, this is a genetic problem. It's something that happens from the time you develop hemoglobin, right? Or do people develop sickle? Yeah, you don't develop sickle cell later in life.

S: No, it's genetic and you start.

C: Yeah, you just have it.

S: As soon as you start developing the dominant adult hemoglobin.

B: So six months then.

C: Yeah, exactly. So that's why it's really sad to see a lot of these crises are happening. And of course, we know that sickle cell is more prevalent in African-American population right here in the US. And it's just really sad that you see very often these young children, some of whom have a lower SES, who are just in so much pain. And there's a lot of, I think, misinformation, disinformation, confusion around it. They often are labeled as drug-seeking because they have to, basically, for some of these kids, all they can do is take pain meds. They go in, they're monitored, and then they just have to put them on pain meds so that they can get through the crisis.

S: Well, you say pain meds. It's opiates.

C: It's opiates. It's specifically opiates. Yeah, so then there becomes this whole fear around addiction or is this kid drug-seeking?

S: Yeah, I've cared for a lot of sickle cell patients in the hospital, and they're in a lot of pain.

C: Yeah. These crises are brutal.

S: Yeah, they're brutal. But yeah, so these treatments could make a massive difference in the lives of a lot of people.

E: Oh boy, could it ever.

S: And then hopefully, like when, assuming the drugs get approved everywhere, the UK, the US, and Europe, this will fund further research, hopefully bring the cost down, subsidize it, hopefully, for less wealthy nations. There are 20 million people in the world living with sickle cell disease. And yeah, it's a lot of people. For beta thalassemia, it's not as many. /*It's about 100,000 in the US, 15,000 in the UK. For sickle cell and then for thalassemia, it's 100,000 people in the world, 1,200 in the US, 1,000 in the UK. That's a lot of people.

E: Worldwide, sure, yeah.

S: Yeah, so but yay for CRISPR. Yeah, so we're seeing a first approved treatment.

C: And what a great one. It's pretty exciting. Like what an innovative and brilliant approach.

S: The other thing about, one more thing to note about this is that, and we've talked about this before, that targeting the place, the location in the DNA and being able to do stuff there, like insert a gene, turn a gene off, silence a gene, et cetera, is great. But you have to get the CRISPR cast, whatever, to the right cells. Now with bone marrow-based diseases like this, we're actually bringing the cells to the CRISPR, right?

C: Yeah, yeah.

S: As opposed to bringing the CRISPR to the cells. That's harder, because then once you, if you're trying to bring the CRISPR to the cells in an adult, now you need a vector. And we have lots of options for vectors, but none of them are great. And that's still a limiting factor. So I'm not surprised that the first diseases that are being targeted like this are ones where we can take the cells out of the body and then do it outside the body and then put them back. So that's the low-hanging fruit. I think the next level will be ones where we can inject it into a specific place, like inject it into the eye, let's say, or something like that. But doing it, like getting it to go to certain tissues in the body is tricky. That's gonna be tricky. The viral vectors are more of a tricky technology at this point than the genetic engineering itself.

Omicron Update (34:08)

S: All right, Cara, give us an update on that nasty Omicron virus.

C: Yeah, so I didn't even realize, Carl Zimmer wrote a really great piece in the New York Times. I don't know if you guys have read any of Carl Zimmer's work, I believe, personally. Yeah, but he's one of the greatest science writers of our time, has a lot of wonderful books. But he just wrote kind of a longish form piece for the New York Times, kind of giving us an update on Omicron. And I guess I didn't really realize, because of course, all of our concept of time has been so distorted by COVID, but we are coming up on four years of COVID, and we're almost to the day coming up on two years of Omicron. So Omicron first erupted, or at least we first identified it the day after Thanksgiving in 2021. And that was, if you guys remember, the Botswana and South Africa variants. That's what we were calling them at the beginning. We didn't know exactly what was going on, but there was this highly mutated version. This was post-alpha and delta variant. And it quickly overtook, like it quickly spread across the globe and became the dominant variant. It still is the dominant overarching variant to this day. And Omicron, of course, is pretty different from the alpha and delta variants because of the changes that we saw on the spike protein. Omicron has proven to sort of be this immune evader. It's this variant that is very, very good at infecting people, even people who have had COVID before, even people who are vaccinated. But Omicron also has resulted in fewer hospitalizations and fewer deaths. Now, it does seem to be the case that the reason Omicron has resulted in fewer hospitalizations and deaths is not because of anything specific to Omicron, but more because of the public health efforts that we've seen. People had already had the virus by this point and or were mostly vaccinated against the virus. And so we just saw fewer severe infections. But let's be fair. I mean, we've been in Omicron land for, like I said, we're coming up on two years, or actually as of this airing, over two years. The U.S. Centers for Disease Control and Prevention found that between October 2022, so last October, and September of this year, so two months ago, more than 80,000 people died of COVID. So we're looking at an eightfold increase over flu deaths. That's what we're still dealing with. Like we know that COVID has become somewhat endemic. We know that we are looking at potentially annual vaccinations or at least regular boosters, but we're still looking at eight times more deaths than influenza. So this is still happening. A lot of us are sort of acting as though it's not, but it is still happening. We're also seeing that Omicron is continuing to evolve. And as it evolves, we're seeing that vaccines continue to be our strongest line of defense. So when we look at Omicron, it itself has had lots of variations within it. Now we're looking at something called XBB. XBB is a hybrid. It's a hybrid. And that occurred when two different Omicrons wound up in the same cell. Here's something that's kind of interesting that I realized or that I learned, and I guess it kind of makes sense, but I never thought about it before. Most of the virologists who are on the case believe, and I don't think that anybody's been able to prove this at this point, but it seems highly likely that the quick kind of inflection point mutations that have occurred, when we first saw Omicron come on the scene, when we first saw specific sub-variants that are kind of different enough to be their own category come onto the scene, they believe that those occurred in single hosts, that single individuals who were likely very immune suppressed, got an infection, either took medication or didn't, but their body's immune system just wasn't capable of fighting the virus off totally. So some of those viral particles were still staying inside of them, mutating away, and then they were able to pass that new mutated virus on. And so it is kind of interesting that, and this will be important for the second part of the story tonight, that immunosuppressed individuals are really up against it. And we have to remember that because not only are they individuals who are more likely to be hospitalized, more likely to die from these infections, but they're also individuals that are more likely to be the kind of sources of mutations. And so we really do need to be paying like special attention to make sure that individuals with suppressed immune systems are really, really cared for. So I mentioned XBB, which was that hybrid, very, very infectious, even if you had been previously infected. It was dominant earlier this year. XBB is the one that the new shot, the shot here in the US at least, that just came out a couple of months ago, targets. But we're already seeing a new version of Omicron coming up in the ranks, mostly in France, but very likely it'll spread to other countries, and it's called JN1. That's what we're calling it right now. These are all part of the BA.2.86 lineage that we saw kind of coming onto the scene last year. But across the board, one of the things that everybody agrees upon is that vaccines are necessary, that vaccines do save lives. And a recent projection from the University of North Carolina showed that annual vaccination campaigns could save around 49,000 lives per year. So let's talk about the second half of what I wanted to mention tonight, and that is that in Texas, the state from whence I came, from where I came, a new ban was just implemented on COVID-19 vaccine mandates. This applies to hospitals. It is now, hospitals are now banned from requiring, from mandating that their workers be vaccinated against COVID-19. It applies to all private businesses, including hospitals. And we were just talking about these sensitive individuals, immunocompromised individuals. We know that kind of across the board, we're seeing that people aren't wearing masks in most places and many hospitals have already dropped their mask mandates. Now that Texas has completely banned COVID-19 vaccine mandates, there's kind of a lot of pushback, a lot of fear from both Republicans and Democrats in the state to specific, there's an Undark article, actually it was pulled from the Texas Tribune, where they specifically cited both a Republican and a Democratic legislator who are on immunosuppressants for their kidney transplants, who have been really pushing back and speaking out about how dangerous this ban is. And now they did get written to the bill kind of at the last minute that hospital workers who choose not to be vaccinated would be required to wear PPE. But a lot of people-

S: Can be required.

C: Oh, can be, there you go. Yeah, they can be required.

S: Hospitals are allowed to require their employees who do not get vaccinated to wear PPE.

C: So in some cases they won't be required, clearly. And in other cases, even if they are, people are really concerned that like, that's hard to implement. How do you know? So yeah, this bill was just signed into law this past Friday, and a lot of people are really concerned, specifically about transplant patients, cancer patients, individuals with underlying conditions, and whether or not this sets a precedent for other places to follow suit.

S: It's completely inappropriate legislative overreach. Let hospitals decide, make medical decisions for themselves. They're telling a hospital, can't make a medical decision about how to protect their own patients and employees. It's ridiculous.

C: That they're literally not allowed to.

S: It's a dumb decision because, yeah, hospitals are full of sick people, some of whom are very vulnerable to infection.

C: And I mean, you're used to this, right? You and I both-

S: It's the standard.

C: Yeah, it's standard. We have to be vaccinated against COVID to show up to work. The badge has the little thing on it that says, I had my flu vaccine, I had my COVID vaccine. I am approved to come to work because of that.

S: Yeah, so yeah, we are what's called a patient-facing employee, right? I interact with patients, and therefore I have a lot of requirements that I have to do in order to make sure that I'm not going to be, or at least minimize the chance that I'm gonna be a disease vector.

C: Right, yeah, you can't have hepatitis. You can't have, yeah, we've gotta get tested for this stuff, yeah.

S: This is all culture war bullshit. This is, you know what I mean? That's what this is. This is not based on anything rational.

C: This is anti-vax bullshit making its way into the legislation, and people are going to die because of it. That's the thing that's so incredible.

E: Well, there come the lawsuits, right?

C: Yeah, people are going to die.

E: And then what happens, right, when?

C: Oh yeah, I mean, yeah, then you're just talking about trying to recoup financial equivalence of lives lost, which is so devastating.

S: But I wonder if what will happen first is that a hospital will ignore it, ignore the law, do what they think is in the interest of their own patients.

E: Yeah, and then stand court.

C: Yeah, and then work with the ACLU, yeah, exactly.

S: You see, if one of their employees sues the hospital for violating the law, and then it'll work its way through the courts. That may be how it unfolds.

E: Right. And how will that look politically for whomever is in support of that at that point? Then you'll probably have some initiative to repeal this law.

S: Well, they're playing to their base with that.

C: The saddest thing is that we're even talking about it. That's the thing, because this is such an example of when we talk all the time on the show about whether or not we wanna get into politics or just stick to the science. This is a beautiful example of why this is such a sticky situation. This is a public health issue. It is, like you said, Steve, it is one best left to the experts to decide what is the safest and healthiest for their institutions. And when you expressly ban or forbid them from making decisions to ensure the health and safety of their employees and their patients, their hands are tied behind their back.

S: It's micromanaging. Any time, in my experience, any time a legislature tries to micromanage medical decisions, it's bad. It's always some ideological bullshit thing, yeah.

C: People got sick and die.

S: It's never like, because they don't, think about a situation in which a legislature is going to know better than medical experts, or like, what's the right thing to do?

E: It's like trying to make a law telling NASA how to build rockets. It's so ridiculous, it's so crazy.

S: As opposed to just saying, you have to be licensed, you have to be certified, that's fine. But saying this, that's why I say micromanaging, but saying like this specific decision we're gonna make at a legislative level rather than letting experts make it. The other thing is, is that legislatures move way too slow to keep up with the data, right? So what if so they're going to change their laws, their micromanagement when new studies come in as opposed to just letting experts decide based on change their recommendations on a dime if a new study gets published. It's just ridiculous, it makes absolutely no sense. It's always for ideological reasons. It's it's never for, it's never actually for patients or for people or because it's the right thing to do. It's always bullshit ideology. And this is no exception at all. There's no legitimate reason for them to get involved with that kind of decision-making. You know, whether or not a hospital, what hospitals do to defend their own employees and patients, it's terrible. All right.

C: Yep, I know, we're all like pissed. We're all like, grumble, grumble.

J: We're all pissed off.

E: It's not good. And like you said, Cara you don't have to be of one affiliation or the other. I think a lot of people can see this as not good.

C: Oh yeah, completely.

Lunar Library (48:25)


(click to create redirect page)

S: All right, Bob, tell us about the Lunar Library. This is cool.

J: Ooh.

E: Ooh.

B: I found out on the SGU subreddit recently from user mem_somerville about the Arch Mission Foundation, which essentially wants to back up our civilization in case of a mega global disaster. It's a fascinating idea, and the tech they're using is even more interesting, in my opinion. The Ark Mission Foundation, it's a nonprofit organization, and they want to create many of these redundant repositories of human knowledge and seed them throughout Earth and the entirety of the solar system.

E: Sure.

B: Founded by Nova Spivack and Nick Slavin in 2015. So what do you think their inspiration was for this?

S: 2001?

E: 2012, the movie.

J: No, Bob, whatchamacallit.

B: Say it.

J: Isaac Asimov's book series.

B: Yes. Yep, right, Jay. Isaac Asimov fans should know this. It's the Asimov Foundation series in which the predicted collapse of humanity's galaxy-wide civilization, is they deal with it essentially by creating this archive of our accomplishments to minimize the coming dark ages and all that stuff to basically reboot humanity.

S: Although that was all a fake-out.

B: Well, you don't need to go into that level of detail. So on their website, on their website they say, it's funny, their website is like, humanity, we have a problem. Our modern civilization, the most technically advanced in human history has no backup. They say if a global catastrophe occurred today, most of our collective knowledge would be gone within a decade and it would take centuries to rebuild. So yeah, that's basically the line that they were talking about at the beginning of the foundation. They continue, we build and maintain ultra-long-term data storage archives called ARC libraries. Arch libraries are the most durable records of human civilization ever built. Using new technologies, they preserve more knowledge for more time than anything ever created. So that's definitely the plan and they seem to be well on their way to achieving at least some of that stuff. This is called the Arch Mission Billion Year Archive Initiative. It's a hell of initiative. The first proof of concept for this is called the Foundation Library. And I bet many of you saw it launch in 2018. The location of this library, Arch, surprised me. I wasn't aware of it back then. I don't remember reading about it. Can you guess what I'm talking about? Where was this ARC library that everybody saw? Everybody saw that famous image. I'll give you a hint. It was in a glove compartment. All right, you punks. That red Tesla Roadster that went into space.

J: Oh, cool. Yeah, yeah.

B: It's now orbiting the sun for the next, say, 30 million years. And there was actually one of those Arch libraries in the glove compartment.

E: Yeah, but they lost the key, so.

The ark itself (55:57)

B: Yeah. They built this as the first library in space. And this Arch, though, was a proof of concept. It basically contained one thing, or three things. Isaac Asimov's Foundation Trilogy is in there. And it's claimed that this Arch could last for, get this, billions of years and still be readable. That's what the claim was. To me, that sounded way, way too optimistic. I mean, can you, backing up data that lasts for billions of years, like they said, like 14 billion years. I mean, I have-

E: What medium lasts that long?

B: I have eight-year-old hard drives that have crapped the bed, and they're saying they're gonna go 14 billion years. Well, I looked at the tech, and it is fascinating, and I wasn't able to spot any red flags. And I mean, I wouldn't be shocked if this really can last for hundreds of millions or billions of years. The claim was basically made by Peter Kazansky. He's a professor of optical electronics at the University of Southampton. And he got his PhD under the supervision of a Nobel Laureate for the invention of the laser. So yeah, he's got-

C: Oh, wow.

B: That would go on my resume. Yeah, my supervisor, yeah, he invented the laser, or one of the guys that developed the laser. So Kazansky brought this technology to its current state of the art. It was proved in 2010. But in the past few years, he's brought it to the current state of the art in terms of like speed and density and everything. And he created five disks, each one holding Asimov's trilogy. Now, these disks are considered actually the longest lasting storage objects ever created by humanity. Because if it does last billions of years, and yeah, that would be true. It uses a technique called 5D laser optical data storage. If you Google that, you are gonna come across many, many articles that call it essentially the Superman memory crystal. Remember Superman II with those crystals?

E: I do.

B: It kind of works so, because this medium is essentially fused quartz, which seems pretty similar to those Kryptonian memory crystals that Superman has in his fortress of solitude. So, but these non-fictional crystals will reportedly remain readable for up to 14 billion years, and they resist cosmic radiation, and they can withstand temperatures up to a thousand degrees Celsius. The tech is really cool. They use a femtosecond. That was one of Kazansky's breakthroughs, a femtosecond laser to create these different layers of tiny nanoscale patterns in the quartz. That's kind of redundant, tiny nanoscale. So you've got these nanoscale patterns in the quartz created by this femtosecond laser. So they call it 5D storage because the information is encoded in five different dimensions. Now they're not spatial dimensions. They're just three that we know of, right? Height, length, and width, plus orientation and position are considered dimensions of well in this context. So if you look at one of these disks, now imagine you've got this quartz, you're looking at it, and you're looking at it from a very specific angle and a very specific magnification, and then you would see an image or whatever.You'll see a layer of data that's encoded. But if you look at a different angle or magnification, you would see a completely different set of data. So the result that you could imagine is that there's this amazing storage density. It's 10,000 times denser than Blu-ray optical disks, assuming anybody even remembers what the hell that is. It could hold 500 terabytes on one disk. That's a half a petabyte. So that's huge. One little disk, one little CD-like disk holding a half a petabyte, big. That's pretty dense. And so if you wanna actually see the solar system with massive data backups, this technique ticks two of the biggest boxes. It's super high density, and it will last a stupidly long time. Kazansky sais this technology can secure the last evidence of our civilization. All we've learned will not be forgotten.

Reading the discs (57:41)

J: Well, how do you read it?

B: Well, that's a good question, Jay. You need some tech. You need some tech to do it, and that segues nicely into my next section here. But I wanted to say before I do that is that there are, of course, more immediate applications for this tech, right? National archives, museums, libraries, private organizations. You don't need to backup humanity and throw it into the solar system only. You could also use this for these things that will be incredibly important over the next 10, 20, 30, 40 years, not 14 billion. So the next phase here was the LEO Arch library. LEO stands for Low Earth Orbit. They launched that in 2018. It's piggybacking on a satellite. It contains a copy of Wikipedia. But I'm gonna jump to the next stage because this is taking a long time. The next stage is the LUNAR library, launched in 2019. So this was a lander from the Israel Aerospace Industries hosted this Arch, this LUNAR Arch, which contains lots of things like 30 million page library of books, data, images, all sorts of the scientific, historic, and cultural information. Wikipedia, of course, was there in English. And it also had a secret vault of content, including things like David Copperfield's magic secrets.

E: That's right, Copperfield.

B: His secrets revealed are on the moon. They actually, yeah, so if you can get there, you could find out all his tricks. But there's a caveat. Unfortunately, to slow the lander's descent to the moon, the braking method that they had to employ was litho-braking. Now, litho-braking is short for lithospheric braking. Does anyone know what the lithosphere of a planet or moon is? It's essentially the ground. So litho-braking (Cara laughs) is just a geeky-

C: It's just slamming into the ground.

B: Yes, it's just a geeky euphemism for crash landing. Now, remember, though, crash landing, or litho-braking, as we call it, it does have the benefit of being the quickest and cheapest way to stop. So there is that. So it hit the ground at like 300 miles an hour.

E: 300.

J: 300.

B: Pretty fast, but there's actually some hope that some of the data, or maybe even potentially all of it, survived, but they don't know. They don't know. Probably, they're not sure, but there's actually some hope that some of it actually survived. That's how hardy that is. But even though it was probably destroyed in a crash, the technology they used was very interesting. It was not the 5D optical laser storage that's in the Roadster's glove box. And Jay, back to you now. You mentioned that you need some fairly advanced technology to read those 5D optical laser storage disks, right? But if you want people, or even potentially aliens, I assume, in the distant future, if you want them to be able to read this data, the simpler the tech required, the better. It's just like a, keep it simple, stupid. That seems obvious. So that's why these people wanted to go with something, a storage technology that was more analog. And that's why they're using NanoFiche. Now, that should be ringing some bells when you-

C: MicroFiche?

B: Old guys out there, NanoFiche. Remember looking at archived images of newspapers using MicroFiche?

E: Absolutely.

B: Remember in those buildings we called libraries? Remember those days?

C: Yeah. With card catalogs.

E: We have a library in town. My family's all have library. We have library cards.

C: Oh, yeah.

E: We're still there.

B: Weirdos. (laughter) So I remember looking at old magazines and old science magazines and newspapers using MicroFiche. It was really cool. Basically, really tiny images, direct images, of the media that you were interested in. And then you had a machine and you read it. Well, now we have NanoFiche, which is created by etching these super high resolution, microscopic images on 25 micron thin layers of nickel. So nickel is used in this case because it's an amazing material. It doesn't degrade. It doesn't oxidize. It can handle electromagnetic radiation, heat, cold, microbes, chemicals. And it could do all of that for many thousands of years. So it's an amazing material for this type of storage. And the data density is pretty amazing. Imagine if you have a NanoFiche and if it was as big as a letter, I guess, eight and a half by 11, it could hold 300,000 analog photos, each one of them at 300 DPI. 300,000 fairly decent resolution photos on one eight and a half by 11, typical letter sized piece of paper. That's the kind of size we're talking about. If the NanoFiche contains just analog text and images, it could hold 1.2 million pages on one page. So it's extremely, extremely dense. It just essentially is shrinking it down, but it's not really encoded really in any way. Imagine the lunar library that now crashed and is probably in pieces on the moon. If you could look at that and if you could put it back together and fix it, what you would see is you'd see these 25 layers. The first four layers is all, tells you everything you need to know about how to go farther, how to decode and do things to the 21 layers below that, that has all the information that you want. It has the Wikipedia, it has the classic literature on it. Thousands and thousands of books of classic literature, David Copperfield's magic tricks are all on those lower 21 layers. And the top four layers will tell you, it's got like 60,000 high res images. It has book pages, language instructions, and the keys to decoding everything else below it. So that's what it had. It's not as dense as the 5D technique, but all you need to do, Jay, all you need to do to read this is a hundred magnification microscope to see it, a hundred times, that's it. You don't need a fancy electron microscope for this. This can be done with optical microscopes and optical microscopes were invented, what, 1590. So that's more ideal. It's maybe, it's not as hardy as the 5D optical storage. It's not gonna last for billions of years, but it's very easy. Any of us could put together a device from scratch that could read this. Whereas if you wanted to read that 5D optical stuff, forget it, forget it. You need specialized equipment to do that and the know-how to actually use it. So, okay, so that's kind of where we are. So after the crash, they're gonna go back to the moon for a second try in 2024. And of course, what they're gonna bring to the moon in 2024 is even bigger and better than what they tried in that crash. There's 60 million pages instead of 30 million. There's an internet archive. There's linguistic keys to 5,000 languages. There's archives of music. It's an amazing repository at this point. And they're really just getting started with this. But it's really a huge amount of information.

J: Is it even possible to measure how complete it is?

B: You'd have to define what complete is.

C: Yeah, right.

B: What does complete mean?

C: What percentage of all of the things does it have?

E: I don't know that anything's ever complete.

J: If you take categories, right? All the world's music, all the world's literature, all the world's art, all the world's technology, engineering, and all these categories, you know?

E: Wow, that changes every second.

B: You would need something at the range of 175 zettabytes. So Jay, that's the amount of data created, captured, copied, and consumed in the world by 2025. That's the estimate for 2025. So it would be, I would think, something in the range of zettabytes. And hey, man, that's a hell of a project. It's beyond reason, I think, to probably try to archive all of that. I think you'd have to pick and choose. You know, what would be the most important stuff?

E: Charlie bit my fingers.

B: I'm sure we don't need to back up everybody's email, you know? And that kind of stuff. But yeah, it's a lot. And we're just scratching the surface at this point.

S: What we need to do is put them all into a big black obelisk and bury that on the moon.

B: Ah.

E: Yes.

B: Interesting. I like this.

S: All right, thanks, Bob.

B: Mr. Clark.

Who's That Noisy? (1:03:19)

Answer to previous Noisy:
Scientists' estimate of T-rex sounds

New Noisy (1:06:51)

[mechanical/instrumental musical warbling with background scratching/fingering]

what this week's Noisy is

Questions/Emails/Corrections/Follow-ups

Email #1: Trust in Science (1:08:30)

Follow-up #1: Fashion (1:21:17)

[top]                        

Science or Fiction (1:31:47)

Item #1: Researchers have developed a hydrogel that will allow people with diabetes to inject their insulin once every several months, rather than every day.[7]
Item #2: Scientists find that the eyes communicate to the ears, causing the ears to make a sound which can be used to track eye movements.[8]
Item #3: A new study finds solar wind-derived molecular hydrogen trapped in Apollo lunar regolith samples.[9]

Answer Item
Fiction Insulin-injecting hydrogel
Science Eyes communicate to the ears
Science
Hydrogen in lunar regolith
Host Result
Steve win
Rogue Guess
Jay
 Eyes communicate to the ears
Bob
 Insulin-injecting hydrogel
Evan
 Insulin-injecting hydrogel
Cara
 Insulin-injecting hydrogel

Voice-over: It's time for Science or Fiction.

Jay's Response

Bob's Response

Evan's Response

Cara's Response

Steve Explains Item #3

Steve Explains Item #1

Steve Explains Item #2

Skeptical Quote of the Week (1:45:15)


Science has the answer to every question that can be asked. However, science reserves the right to change that answer should additional data become available.

 – Mary Roach (1959-present), American popular science and humor author 


Signoff

S: —and until next week, this is your Skeptics' Guide to the Universe.

S: Skeptics' Guide to the Universe is produced by SGU Productions, dedicated to promoting science and critical thinking. For more information, visit us at theskepticsguide.org. Send your questions to info@theskepticsguide.org. And, if you would like to support the show and all the work that we do, go to patreon.com/SkepticsGuide and consider becoming a patron and becoming part of the SGU community. Our listeners and supporters are what make SGU possible.

[top]                        

Today I Learned

  • Fact/Description, possibly with an article reference[10]
  • Fact/Description
  • Fact/Description

References

  1. ↑ Arch Mission Foundation: Lunar Library I
  2. ↑ ETH Zurich: Printed robots with bones, ligaments, and tendons
  3. ↑ Science-Based Medicine: First CRISPR Treatment Approval
  4. ↑ Undark: Texas Implements a New Ban on Covid-19 Vaccine Mandates
  5. ↑ NYT: Omicron, Now 2 Years Old, Is Not Done With Us Yet
  6. ↑ AMF: Arch Mission Foundation Prepares Lunar Library II for December 2023 Launch
  7. ↑ Cell Reports Medicine: Use of a biomimetic hydrogel depot technology for sustained delivery of GLP-1 receptor agonists reduces burden of diabetes management
  8. ↑ PNAS: Parametric information about eye movements is sent to the ears
  9. ↑ Nature: Hydrogen-bearing vesicles in space weathered lunar calcium-phosphates
  10. ↑ [url_for_TIL publication: title]

Vocabulary

  1. ↑ Wiktionary: ruga
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