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The Wallenda Model of HomeostasisTAPP Radio Ep. 46 TRANSCRIPT

The A&P Professor podcast (TAPP radio) episodes are made for listening, not reading. This transcript is provided for your convenience, but hey, it’s just not possible to capture the emphasis and dramatic delivery of the audio version. Or the cool theme music.  Or laughs and snorts. And because it’s generated by a combo of machine and human transcription, it may not be exactly right. So I strongly recommend listening by clicking the LISTEN button provided.

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Episode 46 Transcript

The Wallenda Model of Homeostasis

Kevin Patton: The novelist, Philip Pullman, once wrote, “After nourishment, shelter and companionship, stories are the thing we need most in the world.”

Aileen: Welcome to the A&P Professor, a few minutes to focus on teaching human anatomy and physiology with host, Kevin Patton.

Kevin Patton: In this episode, I’m talking about measles and the loss of immune memory, a possible new mechanism for bone growth, and the Wallenda model of homeostasis. We already know that measles is a very serious condition. I don’t think I would have imagined that a discussion of measles would have been very relevant to helping me be a better prepared A&P teacher just a few years ago because it was eradicated in the United States and was not a serious public health concern, at least in this part of the world. But look what has happened with so many people skipping their measles vaccines or skipping their child’s measles vaccines, I should say, and now we’re in a situation where we’re having outbreak after outbreak of measles. There’s something I recently learned about measles that I didn’t know before. I think it’s very important and maybe you haven’t heard about this either, so let’s talk about the measles.

Kevin Patton: First of all, the measles virus often just called MV for short, is a single stranded RNA virus and it really only shows up in one host and that is humans. It’s very, very, very contagious because you can catch it just by aerosol droplets that are being breathed into the air by people. You don’t have to come into direct contact with someone with the measles. As a matter of fact, they say that in a room full of exposed people, 90% of those who are unvaccinated will develop the measles. Now, they’ll have various levels of disease, but 90% of them only smoke. 90% of people exposed are going to get the measles if they don’t have the vaccination. To make it even worse, measles virus, MV can hang around in the air for up to two hours after the person with measles is gone from the room. Wow, that is not a disease to play around with, is it? And it can have some very, very dangerous side effects.

Kevin Patton: I grew up in the time of measles. I had the measles when I was a little kid. Luckily mine was a pretty mild case. I wouldn’t wish it on anybody. I felt pretty miserable and I remember resenting, hearing my mother talking on the phone to her sister saying, “Oh, his case isn’t very bad.” And I just thought, well, [inaudible 00:03:08] inside my body, it feels pretty bad to me. But I didn’t realize being a little kid that it could be so much worse, even life threatening than the case that I had. But here’s something pretty weird that I didn’t know about before, and it has to do with the way measles works. When you breathe in the MV virus and it gets into your respiratory tract, it’s going to come in contact with those macrophages that live in your alveoli that are helping in part some of the immune protection that is keeping you from getting diseases in the first place. That makes sense. That’s pretty basic idea of immunology, right?

Kevin Patton: When the MV virus gets there, it’s going to latch on to a glycoprotein that’s in the membrane, that’s called SLAM, which is signaling lymphocytic activation molecule. You break that down, that makes some sense. Signaling lymphocytic activation molecule, but SLAM is just easier to say. That has a high affinity for the MV virus, and MV uses that to connect directly to the cell membrane of the alveoli macrophage and it can thereby bypass phagocytosis and go right into the macrophage. Then those infected macrophages, they’re going to travel through the lymphatic system to a lymph node. And you know what that means, if they’re not destroyed there and some of them may not be, they can then travel to many parts of the body. That’s what gets measles started in our body and it does so through the respiratory tract as we ready.

Kevin Patton: Now, one of the things that happens though is it gets into the body and it comes in contact with all kinds of memory cells there. Now, you know that memory cells, that is the various kinds of B-cells and T-cells and so on, that have developed a memory for something that you’ve been exposed to before and they stand ready to mount a very vigorous attack against whatever pathogen it was that triggered the formation of those memory cells in the past to ready to attack them again, ready to protect you again.

Kevin Patton: But all of those memory cells, they have those SLAM receptors on their surface too. That means that MV binds to them. Even though they’re not there to attack the MV, MV, I guess you could say, is going to attack them. It’s going to connect to them and that’s going to be a direct link to getting inside the cell and infecting the cell. So all of these memory cells, memory cells against the flu, against smallpox, against whatever it is that you’ve been exposed to one way or the other before, they get infected. And we know that during a measles infection, the population of your lymphocytes goes down, including these memory cells. Assuming that you survive the measles infection, then you eventually rebuild those populations of lymphocytes. But guess what? Now they’ve lost their memory. And that is sometimes called immune amnesia. Meaning you had the memory, you had the immune memory, but then you lost the immune memory. And how did you lose it? Well, in this case, the measles destroyed those memory cells by infecting them.

Kevin Patton: So they’ve done some studies that involves statistical models going even back in time over the various population studies that have been done before and after measles vaccinations became widely available. And they estimate that it takes somewhere around two to three years after a measles infection for your immune memory to be restored. Of course, it’s not necessarily going to be completely restored because you’re not necessarily going to be exposed to all the kinds of things that you had been exposed to before. So, wow. That’s crazy. That’s like the kind of amnesia you get when you get knocked in the head and lose your memory if it’s actually gone. If that memory is gone and it’s not recoverable, that means you have to relearn everything that you had remembered and there are probably going to be some memories that you lost that you’ll never get back because you’ll never relearn them, because you’ll never experience whatever that thing is again that caused the memory to be formed in the first place.

Kevin Patton: That is analogous to what’s going on in the immune system. That’s pretty huge. I mean, not only does measles make you vulnerable to secondary infections because they’re messing with your immune cells anyway. And not only is it a serious infection in and of itself anyway, so you’ve got two big strikes against you. Now, here’s the third big strike against you and that is it’s going to wipe out much of your immune system for the next few years. So please folks, encourage everyone around you to make sure that they are getting their measles vaccine, that their kids are getting their measles vaccine, that strangers and relatives alike are getting their measles vaccine. It’s really very safe and the alternative is very, very, very dangerous.

Kevin Patton: This podcast is sponsored by HAPS, the Human Anatomy and Physiology Society. Promoting excellence in the teaching of human anatomy and physiology for over 30 years. Go visit HAPS at theAPprofessor.org/haps. While you’re there, check out the slate of one day regional HAPS conferences. There’s probably going to be one near you this year.

Kevin Patton: I just saw some recent news in how we understand how the growth of long bones occurs. I think we all in our courses talk about the fact that there are these epiphyseal plates near the ends of long bones between the diaphysis and each epiphysis. That’s made up mostly of cartilage cells, that is chondrocytes, and that cartilage access framework within which we do ossification. So bone formation occurs within the cartilage. To oversimplify it, we basically make cartilage turn into bone as we make more cartilage and then turn that to bone as we make more cartilage and turn that to bone. Eventually we run out of cartilage, and that’s the end of the kind of growth at the epiphyseal plate that’s going to extend the length of the long bone. Our current understanding is that the chondrocytes are being produced by cells that we call progenitor cells. Progenitor cells, you may recall from our discussion about this in the preview episode, are stem cell like cells that are dedicated to a particular sound, this case chondrocytes. So we call those, chondroprogenitor cells.

Kevin Patton: The thinking all along has been that during embryonic development, we make a bunch of these chondroprogenitor cells. Then when we’re born, they’re limited in number and we’re not going to be making a bunch more chondroprogenitor cells. We have enough to make cartilage cells and then make more and then make more during that growth phase of the human life cycle. But eventually we do run out because we run out of chondroprogenitor cells and therefore we run out of chondrocytes. Well, some research has been done in mice. Now, not in humans yet, but in mice at the Karolinska Institutet where they were investigating this and they found that something else was happening. That after birth there were some big changes in the cell dynamics and that there were large stable groups of chondroprogenitor cells that were being produced that we didn’t think that was happening, but they acquired the ability to regenerate apparently.

Kevin Patton: So potentially, we can continue to grow our long bones longer than the usual case. Now, we don’t do that, but apparently we’re capable of doing that. At least mice are. And mice are, in many ways are a lot like human. But of course in many ways they’re not like us. So we still have to verify this in humans. We also need to figure out what’s really going on because if we have these additional progenitor cells, chondroprogenitor cells, why aren’t our bones just getting bigger and bigger and bigger? Well, there are some rare cases where that does happen. There are some rare disorders where that happens and maybe that’s what’s going on. So there must be something to regulate that in the rest of us who have normal growth. And of course we know that some people fail to grow as long as maybe they otherwise would because of some other kind of growth disorder.

Kevin Patton: So maybe if we can figure out what’s going on here with these chondroprogenitor cells and how they’re regulated, we might be able to fix both kinds of disorders or at least help out a little bit with the kinds of growth disorders in children that prevent them from growing normally or growing enough. Also, maybe it’ll help us understand these very rare cases where the bones overgrow and get too large. So something to keep an eye on. I do have links to the related articles in both the show notes and the episode page at theAPprofessor.org, so go check it out. See what you think.

Kevin Patton: A searchable transcript and captions for the audio gram of this episode are funded by AAA, the American Association of Anatomists at anatomy.org. AAA has a lot of resources to help A&P teachers. One of my favorites is their journal, Anatomical Sciences Education. I encourage you to check out this and other benefits of membership in AAA at anatomy.org.

Kevin Patton: In episode 45 of this podcast, I mentioned that when I’m teaching homeostasis, one of the central concepts of physiology that we all teach in our A&P courses, I use three different analogies as my primary starting point for helping students understand this very important concept. One of those models is the engineered control system model, the one that most of us use and is in most of the textbooks. An example would be using a thermostatic control the temperature inside a building like a home. I also use a different analogy and one that I spent some time explaining in the previous episode, that is episode 45, which I usually call the fishbowl model or the aquarium model of homeostasis. Where we think of the internal fluid environment of the body in much the same way we think of the internal fluid environment of a fish tank, but instead of supporting cells, a fish tank is supporting fish. And like the organs of the body, the fishbowl or aquarium needs a variety of machines that keep the internal fluid environment of the fishbowl in a relatively stable condition.

Kevin Patton: So you would use filters and heaters and automatic feeders and things like that to make sure those fish stay alive. The human body is like that, only we’re using organs instead of those fish ball assessors. There’s another really huge difference and that is, our bodies are jammed packed with cells with very little fluid in between them and so it’s a lot more fragile system than your typical aquarium, which has lots of water and very few fish rather than our body, which has lots of fish in very little water. I hinted, no, I didn’t hint, I came out and said there’s a third analogy, a third model that I use, but I didn’t tell you what it is.

Kevin Patton: I’m going to tell you what it is now and I’m going to explain it. I call it the Wallenda model of homeostasis. What is that word, Wallenda, mean? Well, it’s not just a word, it’s a name. It’s the name of a family of highwire performers in the circus. They go back many generations. Now, a guy named Karl Wallenda is the one who got them into the highwire business. As a youth in Europe, he made money by going around the streets of his home town and doing acrobatics and head stance and so on for coins. He eventually got into highwire work and he became so very good at it that he became world famous. He eventually immigrated to the United States and many of his descendants are still in the circus industry and most of them that are still working in the circus are doing highwire work or something related to highwire work. Not all of them but most of them.

Kevin Patton: So that idea of not just of a highwire walker being a model for homeostasis, the Wallendas in particular have some characteristics that make them an especially good model for homeostasis. And you’ll see what I mean by that as I walk you through it. So let’s go back to Karl Wallenda, the original patriarch of the family in terms of highwire artistry. One of the things that really made him famous and that he made famous were what are often called skywalks among highwire artists. A skywalk is a highwire walk that is especially high and/or especially long. Now, ordinarily a highwire in a circus tent is somewhere around 30, 40 feet high, 30, 40 feet long, somewhere in that range. It varies a little bit, but somewhere like that.

Kevin Patton: But a skywalk is like when you put a cable between two high rise buildings. Or the very first time I saw a skywalk was in the old Busch Stadium in St. Louis where a cable was strong all the way across the stadium. And Karl Wallenda, who was very popular when I was a kid, he got on at one end and walked all the way across and he was rigged up with a microphone so we could hear him talk as he went across because well, that just adds a little bit to it. He would throw in some jokes and he would talk about whether the wind was blowing hard or not and whether, sometimes he’d give instructions like hold it steady because some of the guide wires were actually being held by people down on the baseball field rather than being anchored in the ground. Somewhere anchored in the ground, but some of them were being held onto.

Kevin Patton: A skywalk is especially difficult and especially dangerous. And when you see that single artist walking across a single wire that’s very high and very long, you can see negative feedback inaction. And these skywalks are still done. The current family patriarch, Tino Wallenda, has done a number of these skywalks, and his nephew who’s become very popular recently, Nic Wallenda, you may have seen the TV specials where he’s walked across a cable strung across Niagara Falls and he did another one across the Grand Canyon and he’s done them at other locations. So when you watch these skywalks, one of the things you’ll notice is a lot of negative feedback going on because there is a set point that needs to be maintained or at least you need to stay close to it. So what’s the variable here and what’s the set point?

Kevin Patton: Well, the variable is the position of the highwire artist over the wire. The center of gravity of a highwire artist has to be over that cable because if it’s not exactly over that cable, then that person is going to fall. And if it’s a skywalk, they’re going to fall to their death. That’s like what happens in the human body when we do homeostasis. We have a variable that has to stay at or near that set point and if not, then we figuratively metaphorically fall off the cable, we fall off the wire and we die. The highwire artist, first of all, is going to, there is a few tricks they have up their sleeve. Your typical center of gravity is not very wide, so it’s very, very difficult to keep that over that cable, the position of that cable.

Kevin Patton: One thing that you can do to help yourself a little bit is to carry a very heavy pole. When you’re carrying that poll, that poll is now part of the weight of your body, but it’s a weight that is spread out now. So your center of gravity likewise and proportionally widens out. That means you have more room to sway back and forth before you begin to actually fall off the wire. That’s why high wire artists, especially when they do a skywalk, are carrying a very heavy pole. Sometimes they’re 80 pounds or more depending on the individual highwire artist and what their goals are and what the circumstances are. That’s a really heavy pole. It’s a lot heavier than it looks. I’ve lifted up one of those poles and it’s hard. I mean, those things are heavy. But the heaviness is actually what helps keep them on the wire.

  • NOTE: The balance pole is normally up to about 30 pounds or so. The 80-pound figure given in this episode would be unusually heavy.

Kevin Patton: Of course, that also means it’s going to take that much more energy to stay on the wire, having to carry not only your body, but to carry that poll as well. But even with that pole, there are various perturbing factors such as wind and well, there’s even shifts in the cable a little bit, hopefully just a little bit. There’s distractions you have and other kinds of things and you’re going to start to fall. So what you do is negative feedback. Your sensors that are in your body, and there are many of them. There’s your various proprioceptors throughout your body that are monitoring your body position. There’s your eyes and your sense of balance in your ears and lots of information coming in and being integrated in your brain and comparing all of that information to each other as well as to the set point position.

Kevin Patton: Where am I relative to that wire? It better be close to the middle. And if I’m not, if I’m off to the left, then what am I going to do? There’s going to be a signal sent to my metaphorical effectors, not metaphorical, they’re actually effectors. My skeletal muscles are going to pull me to the right if I’m falling left. And I’m falling to the right, I’m going to pull back left. I have to be very careful here because if you’ve listened to previous episodes, you know that once I start talking left and right, I get confused easily. Even I think I’m going to be okay for this one. That’s negative feedback. We’re always negating the disturbance. We’re reversing the disturbance.

Kevin Patton: If we’re falling left, we pull right. If we’re falling right, we pull left. Well, not we. I would never do that. It’s the Wallendas. It’s the Wallenda who’s doing the skywalk. And if we were standing right underneath them, which is not something I would suggest you do because sometimes they fall and you don’t want to be there when they fall. But if you were underneath them or better yet, let’s put a remote camera there directly underneath him, you would notice them swaying back and forth and back and forth as they’re recovering back to that set point position in dead center where their center gravity is over the wire. The variable is their position as I mentioned. What happens when they lose the ability to do that? What happens when things get out of hand? Well, unfortunately and tragically, that happened to Karl Wallenda. He was doing a skywalk in Puerto Rico, I think it was in San Juan, Puerto Rico, and it was between two fairly tall buildings. I think it was a hotel in a parking garage, and he got partway out. I’ll never forget this.

Kevin Patton: I remember the day he had this tragic accident. I came home from school, I was in college at the time, and I came home and I turned on the TV because I wanted to watch The Three Stooges or something or Jeopardy probably, and a news break came on and said, “World famous highwire artist, Karl Wallenda, has just died.” And they showed a video tape of him falling off the wire and they played it five minutes before the hour, every hour leading up to the news cast to the day. And many times afterward, It was very dramatic. He got partway out on the wire and it was very, very windy. You could see it was very windy. And if you’ve ever seen these skywalks before, something you would have noticed is the wire was more wobbly than it really should have been.

Kevin Patton: And looking back, the Wallenda family believes that that’s what caused the accident. It was not stabilized properly. So he really didn’t have a good chance of pulling back because the set point kept moving from under him. And when your set point flips back and forth, that limits your ability to stay near that set point. And that’s what happened to him. He fell off the wire and he passed away. But the thing about that is, and the reason why I bring it up here, and I also bring it up in my class is well, number one, to emphasize that a lot of these circus acts aren’t illusions. They are actual risks to people’s lives when they’re doing these things. They’re risks that are mitigated by safety procedures and safety equipment, but they’re still risks.

Kevin Patton: But the main reason I bring it up is because it illustrates how we are all going to die. Everyone who has died, has died in the same way that Karl Wallenda did. And that is by losing their balance. Now, he lost his balance of position on the wire and that’s what killed him. But I might lose my balance of pH and that might be what kills me. I might lose my oxygen balance, my CO2 balance. It might be a result of my heart stopping or not working properly or it might be the result of some other kind of condition. But in some way or the other, we all lose our homeostatic balance and that’s what kills us. It might happen fast, it might happen slow, it might happen somewhere in-between, but it’s all a loss of balance and yes, that’s dramatic, but it’s dramatic when anyone dies and we’re all dying from a loss of homeostatic balance.

Kevin Patton: Now, another thing about the Wallendas that I think is useful in terms of understanding homeostasis is something else they’re very famous for and that is their pyramids. Now, other highwire artists do pyramids, but Wallendas were the ones that really pushed the envelope on that and still continue to set the bar in terms of stacking themselves on top of one another and producing these really high pyramids. And I don’t know if you’ve ever tried to make a human pyramid, I remember trying to do it as a kid. Some of you may have been professional or semi professionals and done it in cheerleading or squad or something like that or gymnastics. But we were just goofing around as kids and we tried to see how big of a pyramid we could build and it wasn’t very big because it’s very unstable. Not only that, it takes a lot of energy especially if you’re on the lower [inaudible 00:29:43], which I never was because I was always among the shortest kids among my friends. So I got to be on top. But that has its own dangers involved.

Kevin Patton: You have the issue of having multiple people all trying to keep their own balance. So if I get a little off balance, that could throw everybody else off balance, even if they otherwise were doing pretty good themselves. We have an interrelationship, a balance. It’s not only that, there’s the great effort it takes to hold up all those people, especially if you’re on the bottom. One of the Wallenda pyramid performances that have made them very famous in well, in history period, but it’s certainly in the history of the circus, is the famous seven-person pyramid where they had four people on the bottom, two people in the middle row, one person on the top. And very often that person on the top, actually they were sitting on a chair.

Kevin Patton: And when they got to the middle of the wire, that person would then climb up on the chair, hold their balance, pull above them, and then sit back down. Then the whole pyramid would go to the other end of the wire and they’d unstack everybody. If you ever see one of those very complex pyramids being performed, and I’ve seen them performed a number of times, it takes a long time to build a pyramid because you have to be careful and there’s a lot of people involved. Then they’re going to move slowly to the middle, then as they get to the end, they’re going to have to unbuild the pyramid, so that takes some time as well. That’s one reason why not a lot of people in this business do pyramids because it slows things down a little bit. But when you do it, boys it’s impressive and it’s also very, very difficult and very, very dangerous.

Kevin Patton: One of the things that makes the seven-person pyramid so famous is that most highwire artists felt that it was impossible to get to seven people until the early 1960s when the Wallenda family under the direction of Karl Wallenda, put together a seven-person pyramid and it made it out of practice. Sometimes they’re able to do these things in practice but is never stable enough or they’re never good enough [inaudible 00:32:02] that they feel confident to perform it on a regular basis. But they did. They were doing it in a regular performance. In 1962, they were at a shrine circus in Detroit performing this and the artist way out in the front, in the lower level of the pyramid, lost his grip on the balance of pole. Probably because he was ill that day and didn’t give up his spot, but stayed in the pyramid and he lost his grip on the balance pole.

Kevin Patton: What they think happened is that he let go of it for an instant to try and rebalance it in his hands. And once you let go of that pole, your center of gravity goes from maybe several feet wide to suddenly like six inches wide. And with all that weight on his shoulders, it just basically pushed him off the wire. What that meant was that all seven people lost their balance. So the whole thing came tumbling down. A couple of them were able to grab onto the pole. They were injured, but they were able to hold onto, excuse me, not the pole, but the wire until they were rescued. But two people died in that accident and a third one was permanently paralyzed from the waist down and all of them had some kind of an injury, most of them serious injuries.

Kevin Patton: That was a very tragic accident there as well. And that’s what made it famous because for many years, nobody attempted the seven-person pyramid again. Then in the late 1990s, the Wallenda family decided to bring it back and they worked very hard on it and they premiered it at Detroit in homage of that original accident and they performed it in Saint Louis in a circus I was involved in, Circus Flora. They performed that many times there and they have attempted, various groups of individual Wallendas have put together pyramids over the years and they’ve attempted and succeeded in doing eight-person pyramids. In 2001, they achieved a 10-person pyramid. That’s not something that’s performed regularly, but they did perform it.

Kevin Patton: When you do these very complex, very large pyramids, it’s a lot more like what’s going on in the human body than when you’re watching a skywalk. Why? Because there isn’t one homeostatic balance that we have going on in our body. While our pH is being maintained in balance, our oxygen is being maintained in balance. And you know what? They’re related to one another. If one gets knocked out of whack, the other one’s going to get knocked out of whack. And the same thing with the CO2 balance. Boy, pH and CO2, they’re very closely linked, aren’t they? There’s all kinds of different balances in our body that are all interrelated. So when we lose our balance of any one of those things, that’s not the only problem we have because it’s going to knock other things out of balance. And the more things get out of balance, the harder it is to recover. That’s what makes a seven-person pyramid so darn dangerous. A lot more dangerous than a single highwire artist, which, believe me, is dangerous enough and I’m not going to ever try it.

Kevin Patton: It makes me scared just watching it. I’d barely survive that. I don’t think I could ever get close to getting on a highwire. Even a low wire, I think would terrify me. But my point here is that we’re all in danger. We’re all living on the edge all the time. We just don’t realize it because we’re doing it all the time and it’s a good thing we don’t realize it because we would all live in terror constantly, but we’re all in danger of dying. Why? Same reason that those folks in the seven-person pyramid who passed away, the same reason they died, the same reason Karl Wallenda died when he was doing his skywalk. It’s because of a loss of homeostatic balance.

Kevin Patton: When you watch the seven-person pyramid or an eight-person pyramid or even a three-person pyramid, you’re going to see those balance poles going back and forth and back and forth. And they’re not always in sync with one another. They’re each maintaining their own separate balance. But as a unit, they’re overall maintaining that pyramid in balance and that’s how it’s operating in our body. Another thing that I’ll mention is they’re really using a lot of energy to do it even though they’re moving slowly. Remember they’re carrying those heavy balance poles. If they’re in a pyramid, they’re also carrying a bunch of people on their shoulders who are also carrying heavy balanced polls and they are constantly pulling back and forth and back and forth to maintain that constancy. So even though they make it look nice and smooth, it is exhausting. And when you talk to them afterward, which sometimes you can because the Wallendas especially, they like to meet the circus fans at the end of a performance. So you’ll often see them at the exits as you leave the circus and they’re drenched in sweat and they’re tired and you can imagine why.

Kevin Patton: Imagine what they just did and of course they’re always conditioning themselves so that they’re able to do that. But it is an exhausting thing and that’s true of us too. Maintaining our oxygen balance is exhausting. Maintaining our pH balance is exhausting. Maintaining all these different kinds of temperature balance, it’s exhausting. That’s why I think I’m going to go sit on the couch after I’m done recording here because I’m exhausted by just standing here and recording this podcast. But I am using energy. I mean, not just for the speaking and thinking a little bit of what I do while I’m doing a podcast, it’s not just that, just living. Just sitting there on the couch uses energy and a lot of that energy is being used to maintain our homeostatic balance, maintain our temperature, maintain our oxygen level, maintain all of these things within their setpoint range that is as close to the set point as possible.

Kevin Patton: So putting this all together, the Wallenda model, the model of a highwire artist, but in particular highwire artists capable of doing these pyramids and so on, is that it involves generally negative feedback to maintain a variable that we can see in this model. That homeostasis is dynamic, that means it’s moving, it’s not static. Constantly moving, constantly recovering back toward the set point. We can also see that it’s an energy consuming process. Another thing the Wallenda model teaches us is that homeostatic balance is vital to healthy survival and when you lose it, you die. And we’ve seen that unfortunately with highwire artists. With the pyramid especially, we can also see in the Wallenda model that the balance of one homeostatic variable is often interdependent with the balance of other homeostatically controlled variables. So there’s the Wallenda model in a nutshell.

Kevin Patton: I’m sure there’s a lot of nuances to that that you can see. And what I do with all three of these models is I will recall them. I tell the story, I build the visual image in the minds of my students at the beginning of the course. And then we can always refer back to it over the remaining two semesters. I can always recall what’s going on with a highwire artist and with these other models. We can visualize how that applies in the kidneys, in the cardiovascular system when we talk about acid base balance, when we talk about the respiratory system and how important it is in acid base balance and oxygen balance and so on. So these models are not exactly going to define homeostasis, but they’re good tools for helping students imagine something abstract but looking at concrete things that represent these abstract notions.

Kevin Patton: Use these models if you like. If not, don’t. But they might give you some ideas for how to approach homeostasis or even other concepts in your teaching of A&P. I do have, as usual, some links to various resources that might help you with this in the show notes and at the episode page at theAPprofessor.org.

Kevin Patton: Distribution of this podcast is sponsored by the Master of Science in Human Anatomy & Physiology Instruction. The HAPI degree. Yeah, I know. You already have a degree related to A&P, but did it fully prepare you for the broad range of concepts and both anatomy and physiology? Did it fully prepare you in the theory and practice of teaching and learning? Did you get training in specific strategies? Okay, let’s face it. We can all benefit by learning more. Check out this online graduate program at nycc.edu/hapi. That’s H-A-P-I. Or click the link in the show notes or episode page.

Kevin Patton: Hey, don’t forget that I always put links in the show notes and at the episode page at theAPprofessor.org in case you want to further explore any ideas mentioned in this podcast. For other options and how to be a regular listener to this podcast, just go to theAPprofessor.org/listen. And don’t forget to call in with your questions, comments and ideas at the podcast hotline. It’s 1-833-LION-DEN. That’s 1-833-546-6336. Or send a recording or a written message to podcast@theAPprofessor.org. I’m on Twitter, Facebook, and Instagram using the handle, @theAPprofessor. I’ll talk to you later, okay?

Aileen: The A&P Professor is hosted by Kevin Patton. Professor, blogger and textbook author in human anatomy and physiology.

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Preview of Episode 47

 


Kevin Patton: Hi there. This is Kevin Patton with a brief audio introduction to episode number 47 of the A&P Professor podcast, also known as TAPP Radio, an oral history and epic saga for teachers of human anatomy and physiology.

Kevin Patton: In the upcoming full episode, that is episode number 47, I’m going to be talking about the fact that artificial intelligence is coming to teaching. Yes, even in higher ed. And I’ll discuss tips on how to prevent robots from taking your teaching job. And I’m going to talk about the human microbial system, that is the human microbiome and how we approach it in teaching A&P. And I’m also going to introduce a series of special episodes that I’ll be releasing this summer.

Kevin Patton: The free distribution of this podcast is sponsored by the Master of Science in Human Anatomy & Physiology Instruction, the HAPI degree. Looking to power up your game in teaching A&P? Or maybe you have colleagues that could benefit from more training. Or maybe you could benefit from more training. Can’t we all? Check out this online graduate program at nycc.edu/hapi. That’s H-A-P-I. Or click the link in the show notes or episode page.

Kevin Patton: It’s word dissection time. And the first term that I’m going to dissect is one that we’ve been hearing a lot about lately, but not necessarily related to the teaching of A&P. And that is artificial intelligence or AI for short. So let’s tackle the first part of the term, the word artificial.

Kevin Patton: Now, this isn’t a term that we normally break down the way we break down scientific terms. But we can. I mean, it’s built that way. Even though it’s an ordinary English word, that hasn’t stopped us before, has it? We’re going to dissect it anyway.

Kevin Patton: The first part of artificial is art. And you know what art is. That’s hard to define. I mean, that’s like classically hard to define. What is art? I don’t know what art is, but I know it when I see it, right? But we could define it, I guess, at least in very simplistic way as a craft or something you make. And then the F-I-C part of that, the fish part or fic would be to make or do. And then the al ending we’ve seen a million times before. And that means relating to. It’s an adjective ending.

Kevin Patton: So if you put all those pieces together, you’re talking about a word that describes something that’s crafted or made. Presumably it’s made by people. So that relates to the actual dictionary definition, which is something along the lines of a thing made by humans or something made by humans rather than just appearing in nature. So that’s artificial.

Kevin Patton: And now the intelligence part of that term, artificial intelligence, let’s break that one down too. So, again, it’s just an ordinary English word, but it can be broken down into word parts like our scientific terms. Intel, the first part, is actually derived from another word part that we see a lot. And that is inter. That means between or among or something equivalent to that. So between or among is the intel part. And then the lig part means to pick up or choose. It comes from actually a word part L-E-G, and that means to pick up or choose. And then the E-N-C-E ending is again, a very common word part that we see even in our A&P terms. And that is a state or a condition or inability.

Kevin Patton: We put that all together and what we get is, if we literally translate these word parts as sort of a phrase, it’s the ability to pick up from among things or between different things. And that kind of fits with how we understand what intelligence is, right? I mean, again, a very simplified dictionary definition of intelligence would be something along the lines of a capacity for learning and understanding. That’s what intelligence is. So yeah, that makes sense, an ability to pick from among things or between different things. Sure, makes sense.

Kevin Patton: Okay, let’s move on to our next term. And that is microbe, M-I-C-R-O-B-E, microbe. That’s a term that of course would come up ordinarily in A&P, right? But let’s break it down because that’s what we do. The first part, micro, very common word part, means very small or tiny. And the obe ending actually it’s really just the B that we need there. That’s the active part. That’s the active word part there in this term. B is actually a shortened form of bio, which you already know means life. I hope you know that because we’re all teaching biology so we ought to know at least that one.

Kevin Patton: And so you put that together, microbe, and it refers to a very tiny organism. Another way of defining that would be to translate that as microorganism. But I don’t want to do that because then you’re taking micro and translating it as micro, and that doesn’t make any sense. But the B or bio part means, refers to an organism here.

Kevin Patton: We look in a medical dictionary or scientific dictionary and we see that microbe is defined something along the lines of an organism that’s too small to be viewed by the unaided eye. That is, you need a microscope or at least some kind of a magnifier. The examples often given are things like bacteria and protozoa and maybe even some of the smaller fungi and algae and things like that. And even though a lot of us don’t really classify these technically as organisms, I would include viruses in there because the microbes we’re going to be talking about in the full episode are part of the human microbiome, and that does include viruses. So at least in that sense we’re including them as organisms.

Kevin Patton: That leads us to the last term that we’re going to dissect in this preview episode, and that is microbiome. That’s very much related to microbe, right? So again, the word part micro means smaller, tiny. The bi part of biome is once again from bio, which means life or something living. And then we have the ome ending, and we see that a lot in A&P, especially these days, like genome and proteome and all that stuff. And ome means an entire collection of something, usually a collection of similar things.

Kevin Patton: So put that all together, micro, bi, and ome, and it translates as an entire collection of microorganisms. And that’s what a microbiome is, right? It’s an entire set of microorganisms that’s living and interacting in a particular area. Of course, that’s derived from an ecological term, biome, which talks about a set of organisms, different communities that are living together in an interactive way, in a particular kind of situation in nature. And we call that the biome.

Kevin Patton: This podcast is sponsored by HAPS, the Human Anatomy & Physiology Society, promoting excellence in the teaching of human anatomy and physiology for over 30 years. Go visit HAPS at theAPprofessor.org/haps. That’s H-A-P-S.

Kevin Patton: It’s time once again for a recommendation from the A&P Professor Book Club. And this time we have long time listener Mindi Fried, whose voice you’ve heard before in this podcast. And she’s the first to call in with not one but two Book Club recommendations. You’ll hear her other recommendation, which is actually for a series of books in a future preview episode. The one I’m giving you now though is one that I’d never have looked at if not for Mindi’s recommendation. Here she is.

Mindi Fried: Hey Kevin. It’s Mindi again. My other book recommendation is the book Do Zombies Dream of Undead Sheep? It is by Timothy Verstynen and Bradley Voytek, and I probably massacred both of their names and I deeply apologize if that was the case. The subtitle to this is A Neuroscientific View of the Zombie Brain. I love this book. It is written in a very engaging way, and this book was what sparked the idea for my zombie project, which if you were at HAPS and into my workshop this year, you learned a little bit more about. Basically trying to use the idea of zombies and what’s working in zombies and what’s not working in zombies to teach A&P. This book really goes into different parts of the brain and why they are working or not working in a zombie. It is a fantastic book. It’s a really good read. I recommend it highly.

Kevin Patton: Well, thanks Mindi. This book is definitely on my reading list now, and I’m going to admit, it’s the only zombie book on my list at the moment, or ever.

Kevin Patton: Now, Mindi is going to get a $25 Amazon gift certificate for each book recommendation that gets into the A&P Professor Book Club. So there’s her first certificate right there. And because she’s among the first five contributors of a Book Club recommendation, her name is in the hat to receive a free Kindle Fire HD 10 tablet. Yes, free, a tablet. And you can join in on this too by calling in with your book recommendation at 1-833-LION-DEN, or sending an audio recording to podcast@theAPprofessor.org.

Kevin Patton: Now, there’s still room in the first five drawing, so it’s not too late. But it might be too late soon. So why not do it now while you’re thinking about it? For more details on this or any other recommendation in the A&P Professor Book Club, just go to theAPprofessor.org/bookclub. If you click on the link there or in the show notes or episode page, you’ll go to even more details at amazon.com where any purchase you make through the link will add a few cents to keeping this podcast freely available.

Kevin Patton: A searchable transcript and the captioned audiogram of this preview episode are funded by AAA, the American Association of Anatomists at anatomy.org.

Kevin Patton: Well, this is Kevin Patton signing off for now, and reminding you to keep your questions and comments coming, and those book club recommendations. Don’t forget about those. Why not call the podcast hotline right now at 1-833-LION-DEN? That’s 1-833-546-6336. Or visit us at theAPprofessor.org. I’ll see you down the road.

Last updated: July 3, 2019 at 17:14 pm

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