Shadowing Practice: Homeostasis - Learn English Speaking with Video
Les maken...
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What's up Ninja Nerds?
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In this video we're going to be talking about homeostasis.
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Before we get started, if you guys like this video, it makes sense to you, it truly benefits you, please support us.
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Also, if you guys want some awesome notes and illustrations to check out
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while we kind of go through this lecture together go down
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the description box below to take you to our website we have some great notes
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and illustrations but let's talk about homeostasis
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when we talk about homeostasis what is homeostasis it's basically the state of balance right
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so you want to be able to maintain a balance within our body systems
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and so one of the best ways
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that I think of kind of explaining homeostasis is utilizing examples
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I think it'll kind of give you the bare bones information
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it'll help you to be able to truly think about this in a very specific pathophysiological or physiological way.
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So when we talk about homeostasis is trying to be able to maintain a degree of balance.
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So whenever something is out of balance and we'll use two particular examples on something like glucose, the glucose levels are too low or they're too high.
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Well, that's a state of imbalance.
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How do we help to be able to maintain that balance?
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One of the ways that we help to be able to counteract the imbalance
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or to counteract the imbalance response is we use something called the negative feedback mechanism.
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So I want you to think about the negative feedback system or the mechanism as the counter response, the counter response, if you will.
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So in other words, there's some type of problem.
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In other words, there's a stimulus, if you will.
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What is this stimulus?
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The stimulus in this particular example that we're going to be referring to is glucose.
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So glucose, we obviously want it to be able to maintain a normal level.
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And that varies, but generally if the glucose levels are too high.
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So the glucose levels within the blood are too high.
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This is a particular stimulus for our body.
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And what happens is, this high glucose will then go to a particular organ in our body called the pancreas.
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And when it goes to the pancreas, there's different types of cells.
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We call them pancreatic alpha cells, right?
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And on these pancreatic alpha cells, they have these like little receptors on them.
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Some of these receptors here, we call them glut receptors.
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And what these glut receptors do is when glucose actually binds to them, they kind of move the glucose into the cell.
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And that's the signal to the cell.
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Hey, glucose levels are really, really high pancreas.
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I need you to respond to this high glucose level.
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And so the pancreas as a response to this high glucose level will make a very special type of hormone.
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And this hormone is called insulin.
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And what insulin does is, is insulin is the signal that then goes and binds onto these like little receptors on different cells in the body.
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When it binds onto these receptors, it tells this cell, hey,
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I need you to open up these like protein channels and start shuttling in glucose into the cell.
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And so what it does is, it opens up these channels and starts pulling glucose out of the blood and into the cell.
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Now, as a response to that, think about this, my friends.
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High glucose was the stimulus, okay?
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High glucose is going to be the stimulus.
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Then, a receptor has to pick up that signal.
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This will be the glut receptors.
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The glut receptors has to send signals to your pancreas.
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So it's gonna send afferent signals into your actual pancreas.
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It's gonna send information to the pancreas, say, hey, pancreas, that blood sugar will be high.
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I need you to make insulin.
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So then the pancreas will be the control center, if you will.
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The pancreas will then send an efferent signal via the insulin.
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The insulin is then going to go and act on an effector.
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In this case, these tissue cells.
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And when it acts on the effector, it's going to produce a particular response.
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And what is that response?
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To shuttle glucose into these cells.
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And what's the overall effect out of all of this?
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The overall effect is if I pull glucose out of the blood into the cells, I'm going to lower my blood glucose levels.
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And that's a homeostatic mechanism. And the same concept.
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What if the glucose levels are too low?
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So now we go to the opposite situation here where the glucose levels are too low.
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Well, this is an abnormal type of change within the body.
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Homeostasis, we want to try to maintain a balance.
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So the negative feedback system will develop a counter response.
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The glucose will then be what?
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The stimulus.
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It'll then go and do what?
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Tell these glut receptors that are present on the pancreas that, hey, glucose is low.
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If the glucose is low, then the pancreas will respond to that and say, oh, okay, if the glucose is really, really low, I need to be able to figure out a way to increase the glucose.
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So then what it does is it makes a hormone.
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And this hormone is called glucagon.
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Glucagon.
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And what glucagon does is it binds onto these little receptors on your liver.
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Tells the liver, hey, liver, we need some glucose in the bloodstream.
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So what the liver does is it breaks down big molecules present inside of the actual liver called glycogen,
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or takes other molecules like amino acids and lactate and fatty acids
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and turns it into glucose via a process called gluconeogenesis or glycogenolysis.
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and then pushes this glucose into the bloodstream.
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So if you think about it, the low glucose was the stimulus.
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It will then act on the glut receptor, which is going to be the receptor.
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The pancreas will be the control center, who will then release glucagon.
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Glucagon will then be the efferent signal to another particular target organ or an effector.
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That effector is going to be the liver.
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and the overall response is it's going to put more glucose into the bloodstream, and what will happen, my friends?
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The glucose will increase.
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So that is the concept that I want you guys to understand when we're talking about negative feedback mechanisms.
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But maybe you're still a little tough.
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It's still tough to kind of, okay, I get it, I get it, Zach, but I'm not there yet.
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Let me give you another example to really solidify it.
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So now what we're going to do is we're going to say, okay, I'm not going to talk about blood glucose now.
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I want to talk about body temperature because body temperature is a big thing as well.
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I really want to be able to maintain a normal body temperature.
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So let's say that I expose one person to very cold temperatures and I expose another person to very hot temperatures.
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Our body wants to be able to maintain a certain degree of homeostasis.
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We don't want to be too cold.
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We don't want to be too hot.
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We don't want to have too high glucose levels and we don't want to have too low glucose levels.
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So what happens is this cold temperature will stimulate something called thermoreceptors.
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So the cold temperature is the stimulus.
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The hot temperature is also a stimulus.
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It'll then hit these thermoreceptors in the skin.
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When you hit the thermoreceptors in the skin,
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these are coupled with nerves and it'll send signals toward your central nervous system.
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This is your afferent signals
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and it'll go to a very specific structure in your cns
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you know what this structure is called here it's called the hypothalamus
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so we're just going to represent this right here as your
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hypo thalamus it's going to be the same thing for this
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structure right here the hypothalamus will then respond to this particular signal that hey there's really cold temperatures
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And then what it'll do is it'll send efferent signals down through your spinal cord,
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out through particular nerves that go and send signals to these effectors to produce a clinical response.
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What are those effectors?
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Well, one of them is the blood vessels.
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If there's really cold temperatures, I don't want the blood vessels on my skin to be dilated because if they're dilated, a lot of blood flow goes there.
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And two things happen with increasing blood flow to the skin.
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One is it irradiates heat.
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So that's going to be a way of losing heat.
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I don't want to lose heat.
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So I don't want to vasodilate them.
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I want to vasoconstrict them.
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Second thing is if lots of blood flow go through here, it helps these glands to be able to make sweat.
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And sweat will then coat the skin and then allow for evaporative cooling.
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I don't want to cool my body.
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I'm already too cold.
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So what I want to do is, is I want to vasoconstrict this vessel.
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So I'm going to cause vasoconstriction of the cutaneous vessels.
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And then I'm going to inhibit sweat gland production.
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I'm going to cause a vasoconstriction response and I'm going to inhibit sweat production.
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So this will inhibit or reduce evaporative cooling.
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The other concept is I'm going to send signals to my muscles.
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You know my skeletal muscles?
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When they help them, you know whenever we shiver, you guys ever been in a cold temperature, do you shiver?
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When you shiver, it actually generates ATP.
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It's these incomplete kind of contractions.
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And so what I really want to do is I want to help to kind of cause an increased stimulation
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to these actual skeletal muscles.
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And I want to produce a very profound shivering response to counteract the cold temperatures.
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And what this will do is this will increase heat production.
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And this will help to counteract the cold temperature.
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And the same thing, a vasoconstriction and inhibiting of sweat production will do what?
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This effect will actually inhibit evaporative cooling.
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And again, that will do what?
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Inhibit the actual cold temperature.
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And that's the goal, is to counteract.
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In the same concept, my friends,
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hot temperatures hits the thermoreceptors, stimulates the thermoreceptors sends afferent signals up through the nerves to your hypothalamus.
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Hypothalamus, which is the control center, says, okay, body's way too hot.
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I'm going to send efferent signals down to the effector organs so that we can actually develop a clinical response.
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And then that clinical response will hopefully, Lord willing, counteract the stimulus, the hot temperatures.
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So now all I've got to do is do the opposite here.
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I want to vasodilate because if I vasodilate, I get a lot of blood flow through my skin, which radiates heat.
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That's good.
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So I want to cause vasodilation.
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And then if I vasodilate my blood vessels, also I'm going to get a lot of blood flow
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and I'm also getting a lot of sympathetic supply here to my glands.
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And so if that's the case, what I'm going to do is I'm going to increase my sweat production.
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And if I increase my sweat production, then what I'm going to do is I'm going to have this nice layer of sweat here.
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And whenever the air kind of hits that, it's going to allow for an evaporative cooling response.
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And so I want to stimulate sweat production.
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And the combination of these two particular processes will do what?
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It'll allow for stimulation of evaporative cooling.
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And that is a great thing because it's going to start cooling the body.
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And if I cool the body, what am I going to do?
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I'm going to inhibit my body's increase in the internal body temperature.
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Same concept, I'm actually going to do what to my muscles?
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Do I want them to shiver now to generate heat?
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No, I don't want them to shiver.
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So I'm going to inhibit the actual shivering response.
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So if I inhibit shivering, I won't be able to generate a lot of heat.
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So then that'll do what?
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That'll decrease the heat production from my muscles from my muscles.
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And if I decrease the heat production, that'll decrease the increase in the internal body temperature.
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And that's the counteractive response.
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It's the same concept.
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These are my stimulus.
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These are my receptors.
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The blue and red are the afferent signals.
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The signals coming up to this structure here, the hypothalamus, is my control center.
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The efferent signals going down to my actual effector organs from these points here is my efferent signals.
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Oops, efferent signals, apologize.
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And then the last point here is going to be my effectors, which is gonna be these particular structures here.
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And then this would be the last part here which would be the effectors, which would be the skin, the blood vessels, and the muscles.
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That's the concept that I want you guys to understand here with the negative feedback system
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but that's not the only thing that plays a role in homeostasis.
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We also have something that's kind of interesting called the positive feedback, let's talk about that.
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All right, so positive feedback mechanism.
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So when we talk about this again, homeostasis is maintaining a state of balance.
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Many different disease processes, right, they don't allow for that counterbalance.
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So in situations where maybe the glucose is too high, maybe the problem with them not being able to bring the glucose down is they have a problem with insulin, right?
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And so that's kind of the whole process.
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When there is a breakdown in the homeostatic mechanism, it's usually a disease process.
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Now, negative feedback is to counteract a response.
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So low glucose, high glucose, low temp, high temp, we get the point.
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You can continue to go down the list.
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High blood pressure, low blood pressure, high pH, low pH.
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We can go down a list of all types of abnormalities and how our body maintains that balance.
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Positive feedback is a little bit different.
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In this one, you're amplifying the initial response, which is odd, right?
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So you often don't really kind of want this type of response.
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So what situations which are actually truly helpful for you in your exam to remember positive feedback mechanisms,
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where actually amplifying the response to the initial stimulus would actually be a good thing?
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The first one is the birthing process.
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that baby be stretching the cervix, right?
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And so during the birthing process, you be stretching that cervix all the way out here, right?
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So there's a great degree of stretching during the birthing process.
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That stretching of the cervix is a very powerful stimulus that activates stretch receptors within the uterus.
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These stretch receptors then send afferent signals to your control center.
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And in this case, that control center, guess what it is?
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The hypothalamus and the posterior pituitary.
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So here in the control center, we have a structure here called the hypothalamus.
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And another really important structure that the hypothalamus influences is called the posterior pituitary.
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And what happens is the hypothalamus will stimulate the posterior pituitary who will then release something called oxytocin.
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That's our efferent signal.
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Oxytocin will then move down and bind onto particular types of receptors on the muscle of the uterus.
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Now if a baby is stretching the cervix of the uterus and you're getting ready to have birth, would you want to not contract and help to push the baby out?
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or would you want to contract up to push the baby out?
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That's the goal, right?
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So we actually don't want to kind of prevent any kind of like issues here.
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We actually want to continue to cause contraction of the uterus that'll push the baby further.
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And guess what it's gonna do?
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Stretch the cervix even more.
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That's amplifying the response.
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So what oxytocin will do is it'll stimulate uterine contraction and it'll try to propel the baby further down into the cervix,
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which is going to be jamming that cervix out even more.
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So you'll increase the stretch of the cervix.
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You'll increase the stimulation of the stretch receptors, increase the stimulation of the hypothalamus, the posterior pituitary, continue to increase more oxytocin,
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increase uterine contraction, and do this process until what?
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Until the baby is expelled, all right?
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That's the really important process for birth.
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There's two more examples that I think are really helpful.
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And again, just keep thinking about this process.
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You always have a stimulus, a receptor, an afferent signal, a control center, an efferent signal, and then the effector.
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It's been the same thing.
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We've kind of learned it throughout the process.
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But the next mechanism is here we have a baby.
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So here we have the breast tissue, right?
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Here's a baby who's suckling on the breast, right?
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So the stimulus is suckling.
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So this is usually during the lactation process, right?
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So the stimulus is suckling.
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What it does is the suckling activates certain types of tactile or mechanoreceptors around the breast.
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That then sends signals down the nerves connected to the actual mechanoreceptors to what?
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To the hypothalamus and the pituitary structures.
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What is this again?
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The hypothalamus and the anterior pituitary.
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I'm gonna put anterior pituitary here.
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And there's also another structure called the posterior pituitary.
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Now, anterior pituitary makes a very specific hormone.
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And this one is called prolactin.
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And the posterior pituitary, we already know which one that moan makes.
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Oxytocin.
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The difference here is there's two efferent signals.
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So the stimulus was the suckling.
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The receptor was the mechanoreceptor.
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The nerves going to the hypothalamus is going to be the afferent signal.
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The hypothalamus, anterior pituitary, posterior pituitary are the control center.
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The prolactin, the oxytocin are going to be the effectors.
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Or the efferent signal, I apologize, efferent signal.
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The effector will be the breast tissue.
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When prolactin is released, what does it do to the actual breast tissue to produce a response?
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It actually stimulates these glands to make milk.
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So it actually stimulates milk production.
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So now these glands here in the breast tissue are gonna fill up with the good old milk.
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Okay?
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The next thing is that oxytocin is going to stimulate milk ejection.
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So it's gonna stimulate milk ejection.
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We also call this the milk letdown reflex, or the letdown reflex.
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So now it's gonna stimulate myoepithelial cells around the gland and pa-poo!
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we're gonna shoot some of that milk right into the baby's gullet.
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And so from here, the actual response is gonna be prolactin and oxytocin stimulating what?
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These we're gonna draw with little dots here.
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Here's the prolactin, here's the oxytocin.
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Prolactin will stimulate the milk production.
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Oxytocin will stimulate milk ejection.
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And that's gonna be the response.
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The The effector is the actual mammary glands of the breast tissue.
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That's the concept there.
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Alright, if that's not enough, let's do one last one.
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Here we have a stimulus.
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The stimulus is there's a hole or a tear in a blood vessel.
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Whatever that reason may be, there's a hole in the blood vessel there.
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When the hole in the blood vessel occurs, certain chemicals are released that signal the platelets and tell the platelets, hey, platelets, there's an injury here.
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So the platelets then respond to that.
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And they have little receptors on them that kind of take off that information.
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They say, okay, I'm going to come and stick to you.
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So then the platelets stick to this actual hole in the blood vessel.
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When they stick to the hole in the blood vessel, the next thing that they do is they release more chemicals.
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And these chemicals tell more platelets, hey, there's a lot of kind of like injury over here, a lot of platelets sticking here.
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Can you come and stick to this platelet plug as well.
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And they come and stick.
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And again, more platelets will continue to stick here, and they'll release more chemicals that'll tell more platelets to, again, come and stick.
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And you see the whole point was there was a stimulus, but what did we do with each one of these particular scenarios?
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We amplified the response.
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That's another concept of a patient developing a positive feedback mechanism.
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And this is via what's called the platelet plug.
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So the platelet plug.
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And the same thing with the suckling mechanism.
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The trigger was the baby suckling.
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What is going to happen is it's going to cause this baby to do what?
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Send signals all the way up to the hypothalamus to produce hormones that will cause milk production.
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The milk will then be ejected into the baby's mouth.
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What's the baby going to continue to keep doing?
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Suckling.
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So that it can continue to stimulate these receptors, send more signals to make more milk.
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It's a constant amplifying process.
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That's the big thing to take away from this.
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And that finishes our discussion here on homeostasis.
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I hope that you guys liked it and hope it made sense.
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As always, until next time.
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Woordenschat en spreektips bij deze les
Deze video bevat 314 zinnen en 3594 woorden om na te spreken. Het gesproken deel duurt 21:31. De spreker praat in een natuurlijk tempo van ongeveer 167 woorden per minuut, dicht bij een alledaags gesprek. Slechts 80% van de woorden hoort bij de 3.000 meest gebruikte Engelse woorden, dus de woordenschat is pittig.
Belangrijke woorden in deze video
15 woorden uit de video die het leren waard zijn, met uitspraak en betekenis:
| Woord | Uitspraak | Betekenis |
|---|---|---|
| glucose zelfstandig naamwoord | /ˈɡluː.kəʊz/ | glucose, druivensuiker |
| stimulus zelfstandig naamwoord | /ˈstɪm.jə.ləs/ | prikkel, stimulus |
| stimulate werkwoord | /ˈstɪm.jəˌleɪt/ | stimuleren, aansporen |
| feedback zelfstandig naamwoord | /ˈfiːdˌbæk/ | terugkoppeling |
| vessel zelfstandig naamwoord | /ˈvɛsəl/ | vaartuig |
| stretch werkwoord | /stɹɛt͡ʃ/ | strekken |
| mechanism zelfstandig naamwoord | /ˈmɛk.ə.nɪ.zəm/ | mechanisme |
| sweat werkwoord | /swɛt/ | zweten, transpireren |
| muscle zelfstandig naamwoord | /ˈmʌs.əl/ | spier |
| breast zelfstandig naamwoord | /bɹɛst/ | borst |
| insulin zelfstandig naamwoord | /ˈɪnsəlɪn/ | insuline |
| tissue zelfstandig naamwoord | /ˈtɪʃ.(j)u/ | weefsel |
| hormone zelfstandig naamwoord | /ˈhoɹmoʊn/ | hormoon |
| nerve zelfstandig naamwoord | /nɝv/ | zenuw, neuronenbundel |
| organ zelfstandig naamwoord | /ˈɔːɡən/ | orgaan |
Phrasal verbs die je zult horen
| Woord | Betekenis |
|---|---|
| go down werkwoord | afdalen |
| break down werkwoord | stukgaan, kapot gaan |
| check out werkwoord | onderzoeken |
| figure out werkwoord | uitvogelen, er achter komen |
| pick up werkwoord | oppakken, optillen |
| take off werkwoord | uittrekken, afzetten |
Uitspraak om op te letten
De spreker gebruikt 81 samentrekkingen en verkorte vormen, zoals I'm, don't, gonna. Spreek ze kort uit, zoals je ze hoort.
- De “th”-klanken: sympathetic /ˌsɪm.pəˈθɛt.ɪk/, thalamus /ˈθæləməs/
- De klanken “sh” en “zh”: tissue /ˈtɪʃ.(j)u/, stimulation /stɪm.jʊˈleɪ.ʃən/, illustration /ˌɪləsˈtɹeɪ̯ʃən/, shuttle /ˈʃʌtəl/, examination /ɪɡˌzæm.ɪˈneɪ.ʃən/
- Lange woorden — let op de klemtoon: mechanism /ˈmɛk.ə.nɪ.zəm/, stimulation /stɪm.jʊˈleɪ.ʃən/, anterior /ænˈtɪɹ.i.ɚ/, apologize /əˈpɑləˌd͡ʒaɪz/, illustration /ˌɪləsˈtɹeɪ̯ʃən/
Zo oefen je met deze video
- Luister de hele video één keer zonder te spreken en noteer de woorden die je niet kent.
- Begin op 0,75× snelheid, spreek zin voor zin na en ga terug naar normale snelheid zodra het makkelijk gaat.
- Neem jezelf op en vergelijk met het origineel; let daarbij op woorden als glucose, stimulus, stimulate.
Grammatica in deze video
De structuren die de spreker het meest gebruikt, met de exacte woorden uit de video:
| Structuur | In de video |
|---|---|
| Voorwaardelijke zinnen if + zin, will/would + werkwoord — een voorwaarde en het gevolg | if I inhibit shivering, I won't be · if I decrease the heat production, that'll decrease |
| Lijdende vorm be + voltooid deelwoord — het gaat om wat er gebeurt, niet om wie het doet | is called · are coupled · be dilated |
| Betrekkelijke bijzinnen who / which + zin — extra informatie over een persoon of ding | receptor, which is · Hypothalamus, which is · effectors, which is |
Wat is de Shadowing-techniek?
Shadowing is een wetenschappelijk onderbouwde taalleermethode die oorspronkelijk is ontwikkeld voor professionele tolkentraining en gepopulariseerd door polyglot Dr. Alexander Arguelles. De methode is eenvoudig maar krachtig: je luistert naar native Engelse audio en herhaalt het onmiddellijk hardop — als een schaduw die de spreker volgt met slechts 1–2 seconden vertraging. In tegenstelling tot passief luisteren of grammaticadrills, dwingt shadowing je hersenen en mondspieren om echte spraakpatronen tegelijkertijd te verwerken en te reproduceren. Onderzoek toont aan dat het de uitspraaknauwkeurigheid, intonatie, ritme, verbonden spraak, luisterbegrip en spreekvaardigheid aanzienlijk verbetert — waardoor het een van de meest effectieve methoden is voor IELTS Speaking-voorbereiding en echte Engelse communicatie.