تدريب Shadowing: Homeostasis - تعلم التحدث بالإنجليزية عبر الفيديو
جارٍ إنشاء الدرس...
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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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المفردات وملاحظات التحدث لهذا الدرس
يحتوي هذا الفيديو على 314 جملة و3594 كلمة للتدرب على الترديد. مدة الكلام 21:31. يتكلم المتحدث بسرعة طبيعية، نحو 167 كلمة في الدقيقة، قريبة من المحادثة اليومية. 80% فقط من الكلمات ضمن أكثر 3,000 كلمة شيوعًا في الإنجليزية، فالمفردات صعبة نسبيًا.
أهم المفردات في هذا الفيديو
15 كلمة من الفيديو تستحق التعلّم، مع النطق والمعنى:
| الكلمة | النطق | المعنى |
|---|---|---|
| glucose اسم | /ˈɡluː.kəʊz/ | جلوكوز |
| receptor اسم | /ɹɪˈsɛp.tə/ | مُسْتَقْبِل |
| feedback اسم | /ˈfiːdˌbæk/ | تَلْقِيم اِسْتِرْجَاعِيّ, تَقْيِيم |
| vessel اسم | /ˈvɛsəl/ | فُلْك |
| stretch فعل | /stɹɛt͡ʃ/ | تَمَدَّدَ |
| mechanism اسم | /ˈmɛk.ə.nɪ.zəm/ | آلِيَّة |
| sweat فعل | /swɛt/ | عَرِقَ, عِرِق |
| muscle اسم | /ˈmʌs.əl/ | عَضَلَة |
| breast اسم | /bɹɛst/ | ثَدْي, بز |
| insulin اسم | /ˈɪnsəlɪn/ | إِنْسُولِين |
| tissue اسم | /ˈtɪʃ.(j)u/ | مَنْدِيل, مِنْدِيل |
| hormone اسم | /ˈhoɹmoʊn/ | هُرْمُون |
| nerve اسم | /nɝv/ | عَصَب |
| organ اسم | /ˈɔːɡən/ | عُضْو, عِضْو |
| anterior صفة | /ænˈtɪɹ.i.ɚ/ | أَمَامِيّ |
الأفعال المركبة التي ستسمعها
| الكلمة | المعنى |
|---|---|
| go down فعل | نَزَلَ |
| pick up فعل | قَطَفَ |
| take off فعل | خَلَعَ |
نطق يحتاج إلى انتباه
يستخدم المتحدث 81 من الصيغ المختصرة، مثل I'm, don't, gonna. انطقها بصيغتها القصيرة كما تسمعها.
- أصوات “th”: sympathetic /ˌsɪm.pəˈθɛt.ɪk/, thalamus /ˈθæləməs/
- أصوات “sh” و“zh”: tissue /ˈtɪʃ.(j)u/, stimulation /stɪm.jʊˈleɪ.ʃən/, illustration /ˌɪləsˈtɹeɪ̯ʃən/, shuttle /ˈʃʌtəl/, examination /ɪɡˌzæm.ɪˈneɪ.ʃən/
- الكلمات الطويلة — انتبه لموضع النبر: mechanism /ˈmɛk.ə.nɪ.zəm/, stimulation /stɪm.jʊˈleɪ.ʃən/, anterior /ænˈtɪɹ.i.ɚ/, apologize /əˈpɑləˌd͡ʒaɪz/, illustration /ˌɪləsˈtɹeɪ̯ʃən/
كيف تتدرب بهذا الفيديو
- استمع إلى الفيديو كاملًا مرة واحدة دون أن تتكلم، ودوّن الكلمات التي لا تعرفها.
- ابدأ بسرعة 0.75×، وردّد جملة جملة، ثم عُد إلى السرعة العادية عندما يصبح الأمر سهلًا.
- سجّل صوتك وقارنه بالأصل، مع الانتباه إلى كلمات مثل glucose, receptor, feedback.
القواعد في هذا الفيديو
أكثر التراكيب التي يستخدمها المتحدث، مع العبارات نفسها من الفيديو:
| التركيب | في الفيديو |
|---|---|
| الجمل الشرطية if + جملة، will/would + فعل — شرط ونتيجته | if I inhibit shivering, I won't be · if I decrease the heat production, that'll decrease |
| المبني للمجهول be + اسم المفعول — التركيز على ما يحدث لا على من يفعله | is called · are coupled · be dilated |
| جمل الوصل who / which + جملة — معلومة إضافية عن شخص أو شيء | receptor, which is · Hypothalamus, which is · effectors, which is |
ما هي تقنية التظليل الصوتي؟
التظليل الصوتي (Shadowing) تقنية تعلم لغة مدعومة علمياً، طُورت أصلاً لتدريب المترجمين الفوريين المحترفين. الطريقة بسيطة لكنها قوية: تستمع لصوت إنجليزي أصلي وتكرره فوراً بصوت عالٍ — كظل يتبع المتحدث بتأخير 1-2 ثانية. تُظهر الأبحاث تحسناً كبيراً في دقة النطق والتنغيم والإيقاع وربط الأصوات والاستماع والطلاقة.