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00:07 Alright. 3rd Calibration. 3rd What were your thoughts? Good

00:17 Bad paper. It was a decent . Okay. So I heard a

00:26 for good paper. So tell me was good about it? What was

00:33 about it was mediocre about it? to follow. Okay. Was it

00:44 A. Maybe I heard. Real Confident in that one. All

00:59 . Did it, was it easy understand? Did you understand what they

01:02 trying to trying to tell you? they were did they follow the conventions

01:08 the paper or of the instructions? . Did they demonstrate what their topic

01:14 ? Very early on? Established in abstract. Established in the introduction.

01:21 they prove it? You know what mean? To prove it? You're

01:28 , I don't know. I mean guys seem real nervous about this,

01:33 ? And again the point is is they making claims and then being able

01:40 demonstrate that through their writing, presenting for that. So for example,

01:45 I was trying to prove that the are gonna win the world Series,

01:50 make that claim. I'd have to well let's look at their competition.

01:55 example. Let's look at the A. Dodgers. I saw you

01:59 your thumb down Children. Yeah. , he did. But no,

02:10 say. All right. Let's take look at the record. The record

02:13 the the Astros is 106 and something something. I don't know 60

02:18 So is that an indicator of astro . What do you think? Someone

02:25 doesn't care about baseball? What do think? I don't know.

02:35 fair enough. How about they completely their division series? How many losses

02:46 they have? Well zero the playoff lost? San Diego? Dude Padres

02:56 great Padres. Great Padres are We'll see. My point. Is

03:01 that all we gotta do is we got appointed to see what you're doing

03:04 now is he's actually he's creating argument ? And so I'm not creating strong

03:09 one because I don't follow baseball, know, So I don't have strong

03:13 for it. But the idea is are they making a case for their

03:18 if they're making a claim? Is evidence there to prove their claim?

03:22 what do you think we're talking about ? Yeah, that's not what we're

03:35 about right now. We're talking about . What we're talking specifically about the

03:39 . You guys just read All Remember this is not about grades were

03:44 . So you went through, you through the first time. How was

03:47 score the first time? Bad. ? I'm too harsh. Come

03:56 Get real. I'm too harsh. harsh. Come over to your house

04:00 beat you up and kick your Alright. So how do you think

04:04 too harsh? What did you What did you think was good about

04:07 paper? You thought it was? type of paper did you think it

04:10 make your case? Like what? , keep going. Alright. You

04:27 it? But then what was your the first time going through? Okay

04:34 20 not good because I mean you're not good and and other people are

04:38 gonna be very very different. All . So I mean were you like

04:41 , way off in your scores like the 20%ile? Was your score like

04:44 of off in the 60th%ile or you the 80th%ile and that made you feel

04:49 ? Okay, so so not entirely point with what I was saying.

04:55 anyone here like her, anyone like Yeah 11 person is willing to admit

05:00 to people 345. Okay. And when you went back the second

05:05 what happened, did you did you to guess your way into what my

05:09 were? Or did you kind of at it more with a with a

05:13 eye and say am I looking for that are R. O. I

05:19 know better or worse than what I in other words, Am I judging

05:24 not because I feel bad for the or I want them to do well

05:27 I judging it for what they presented that's really the hardest thing to do

05:32 I mean I'm gonna just tell you my perspective when I read other,

05:35 I read you guys works and stuff that, I'm rooting for you?

05:38 right, When I get personal statement this is where I do most of

05:41 reading, right? I get personal for all you guys playing school.

05:44 like, come on, let this let this one be the good

05:48 You know? So I said that this one be the good one.

05:50 it's like because what we're trying to is we're trying to communicate clearly.

05:57 that's the goal here. It's not the grade. And I know you

06:00 are still stuck on, it's about grade. It's not about the

06:02 Are they accomplishing what they're what they've out to do? And the rubric

06:07 what they're set out to do. are you meeting those particular standards?

06:11 , let's take a look. Let's what dr Wayne thought. Let's see

06:15 he was harsh. Is that the ? Harsh? Alright, So,

06:20 just gonna go down for the A four or three or three and

06:24 three. So, did they meet standards? Yeah. Okay. Doesn't

06:30 like I was harsh. Introduction. or 4 and four. Okay,

06:38 344333332 mm. In text citations. the text references are really excited using

06:48 correct format as laid out in the . So, they screwed up something

06:53 citations. Probably didn't use the proper . All right, general. So

07:00 conforms to the instructions on formatting four , tables figures. I can't remember

07:04 they had won game 333333 and So this was a three. It's

07:15 functional good paper. It's appropriate. is what I expected junior to

07:20 All right. So, it wasn't bad paper. I wasn't harsh.

07:23 was a good paper. So score basically uh right. Right. Smack

07:28 the mean, can't read my own , 77 points out of 110,

07:32 think is why I say here, comes out to about 77.3. It's

07:37 a bad paper. So, the isn't that It's that I'm I'm like

07:43 things. I thought this was a paper was in a great paper,

07:48 ? Not everything can be the great , You know, the hardest thing

07:53 science because you got a bunch of . That's what I'm gonna use.

08:01 right. Everyone wants to prove, their bona fides. And so when

08:05 right, they're gonna just slimy. critics mean evil nasty people who go

08:11 to the ego and they stab And that's gonna happen to you

08:16 All right? You're gonna get five and you're gonna see one of your

08:20 . It's gonna stand out as a thumb to the other four reviews that

08:23 gonna get and you're gonna focus heavily that one review. And you're gonna

08:28 ? Why did this person hate my ? They're jerks. All right.

08:34 people just great harshly. All But don't worry about that. Look

08:37 the other four. right? And am I meeting the standard? If

08:42 meeting the standard, you're in good . All right. Not everything is

08:46 be perfect. In fact, I I don't write perfect stuff,

08:51 In fact, every time I write guys an email back, I promise

08:54 I have to make at least six in that one sentence email. All

08:59 . Because I got fat fingers and hit like three keys at the same

09:02 . It's awful, right, tenses sorts of things. So,

09:09 with this. So ultimately, did come back and hit a score that

09:12 were happy with? I keep looking again real. But let's look at

09:16 rest. You guys ultimately How many got it right the first time.

09:23 45. Okay, good. You guys calibrated you guys are

09:30 right? Alright. And that's the you should be the rest of you

09:33 . You're gonna go in there, go in open minded for every

09:37 Even the one that pisces you off first time. Take that step

09:41 Go back into the second paper and , this is a new paper because

09:45 promise you the first time you read bad paper, you're gonna be mad

09:48 you're gonna want to take it out everybody else. You know, you're

09:51 probably if you have a pet you're kick You're gonna kick the pet.

09:54 right? But what we're trying to here is to make sure. So

10:00 of you have emailed me and said a second. I don't understand why

10:02 got these scores or blah blah Look, you guys are ultimately determine

10:06 other's grades. But I get to whether or not you grade it

10:13 right? That's what the calibration was us to make sure we're all on

10:16 same page and now we know what what the same page looks like.

10:21 , so when you guys grade each and there will be some of you

10:25 here. Actually probably not in here you guys are actually showing up for

10:28 of the people who don't show You're gonna look at the assignment.

10:30 crap. I gotta do write my and you're gonna click on you're gonna

10:33 here's my score. You're gonna just number and you're gonna go straight down

10:37 list. All right. So if receive that that review, how would

10:41 feel about that that make you happy ? Will that make you happy

10:46 No. So that's gonna make you one. Number two. It's not

10:50 be fair because you actually worked right? You read all five of

10:53 reviews, five of those papers and like come on. Right. So

10:58 job is to make sure everyone's doing reviews and I can do that because

11:02 can simply look at all five reviews determine whether or not you're way off

11:05 then I can look at all five your reviews and see how far off

11:08 are and all the other reviews. so I get to adjust your grade

11:12 , 95% of you, 98% of . Let's go 99% of you.

11:16 do everything right if you grade the honestly and if you're and I'm looking

11:22 you, Gabby, you know, if you grade the papers and you're

11:26 easy grader relative to other people, you're consistently grading the same way and

11:30 using the same sort of judgment. paper I can't subjectively say that you're

11:36 right? Because your opinion, in opinion, we're not gonna come come

11:41 an agreement mark. Are we going come to agreement which the better team

11:45 okay? Yeah. Because you're never to accept the fact that the Astros

11:50 have whooped the Dodgers. They would whipped the Dodgers would have would have

11:56 I can say that because I'm in top of the front of the

11:59 We would we would never know because not playing the game right? But

12:06 can have differing opinions, right? we have to look at it using

12:10 same lens. Alright. And it's fair for me to make an opinion

12:14 I'm not a big baseball follower. Dodgers had a deeper bullpen but offense

12:22 better for the Astros. Yeah. right. now having said all

12:30 We have a paper due monday you done with the paper yet one person

12:40 got a week of just sitting on butt. That's awesome, awesome.

12:45 rest of you guys. Do you that? Just think you could be

12:48 your butt doing nothing for a All you gotta do is get it

12:51 , turn it in, turn it will actually tell you what your uh

12:56 similarity score is. If you're not with that you can go and make

12:59 , you can keep doing that. the last paper you turned in before

13:02 actual deadline for the paper will be accepted. So whatever the last one

13:06 , that's the one that counts. so if you want to start turning

13:09 in right now And start affecting the scores you can think up to the

13:15 three you have to wait 24 But first three our first three are

13:19 . It's kind of like cocaine I . I don't know. It's trying

13:25 come with some silly drug reference. So we got that going on.

13:31 Anything else? You guys nervous? questions? I know you have a

13:36 we'll get to. Yeah it Well so let's say you're an easy

13:46 and you come across a paper that's crap and you give them an

13:49 And everyone else because it says it's crap. What do you think is

13:52 happen? I'll fix your score. that? Yeah. That's that's in

13:58 what it is. It's basically saying now again there's some subjectivity to

14:02 Right? So I know I've had graders in my class before and you'll

14:07 like four scores that will all be together. This is this is gonna

14:09 true. Everyone's gonna get if you all five of your reviews which my

14:14 is you will if you turn into you have five reviews to do.

14:16 you don't do those reviews just go and just start taking points off each

14:19 the for each of the reviews that miss. All right? You can

14:23 a zero on a paper even if turn on paper and if you don't

14:25 your reviews. Okay. Those two are tied together. Some people don't

14:30 that on this last assignment. I'm it clear right now. The two

14:34 are attached to one another. If don't know the instructions, go back

14:38 read them. Don't be like my who was ready to murder last night

14:41 missing several assignments. I didn't read instructions Professor for God's sakes. Follow

14:49 directions anyway. Sorry. Um So two things are tied together. All

14:59 ? You will get four. I you'll get five reviews. If you

15:02 get five you get four reviews. okay. That's just a function of

15:06 algorithm and dividing this number of people the number of reviews. But what

15:11 happen is you'll probably get if you all five reviews for the reviews will

15:15 clustered, one will be an it may be an outlier on the

15:18 end, it might be an outlier the front end but that's just very

15:22 typical of what happens just which is we have five reviews and basically it's

15:27 average of all five reviews will determine final grade on the paper and presuming

15:31 did your reviews, that's gonna be grade for the paper. But if

15:35 don't do your views and I'm gonna points off based on the number of

15:37 you don't do. So now your was that yeah, average of the

15:44 . Right and remember how many versions this paper do we have?

15:51 So can you have a perfect The first go round. Right,

15:55 want to see perfect scores. I be honest if it's a really good

15:59 , say it's a really good paper I don't wanna see perfect scores because

16:03 that person won't know know how to improvements for the 2nd 1. So

16:07 know try to see where you can them make improvement. So calibration number

16:14 is right in the middle good Not perfect. Okay. Okay.

16:27 first I think it's like three or days. I found that if I

16:31 you guys too much time, everyone to the last minute anyway so it's

16:35 easier to get it up at the end and everyone just do it and

16:38 you have plenty of time to do second one around and everyone knows how

16:41 read all their individual reviews. You figure it out, you go to

16:44 grade, click the grade and then can actually see you can cycle through

16:49 . But again it's not it's not to cycle through them. Right?

16:52 it a little tiny arrows? shows you bad design and what they

16:57 with it, wow. All This where we left off.

17:13 this is just an introduction of the slides. First slide when we talked

17:19 that uh When we talk about the and the heart pumping, the heart

17:24 a wave, right? It's a wave in the aorta. We have

17:29 and diastolic pressure which systolic represent maximum . Very good. Alright. Over

17:37 distance as you move away from both those values drop right as a

17:42 of search within our resistance and eventually end up with a nice smooth um

17:50 of blood. So the question is in order to get the blood back

17:55 the heart right? Then the atria the right side has to be the

18:02 point of pressure, right? Because gonna flow from an area of highest

18:06 to the area's lowest pressure, So you have to imagine then that

18:12 basically going high to low, my are not my lowest point alright,

18:17 pressure inside my feet that are still blood forward but there's also other types

18:23 pressures. So for example when the beats, what it's gonna do,

18:26 gonna squeeze and then squeezing, it creates pressure on the atria right?

18:31 creates back pressure onto the vena cava so on. And so you end

18:35 with these other sorts of pressure Now first year I thought this actually

18:40 to memorize this stuff. You need memorize these particular peaks and stuff like

18:43 . But what this is just trying show you is what that pressure actually

18:47 like in the jugular vein. And you can see it goes up and

18:51 you can see the pressure dropping but goes up again and it kind of

18:55 that and that's a function of the that the hardest creating as a function

18:59 its own beating backwards. Alright so it's a back pressure. Alright?

19:08 in doing that by increasing the pressure the jugular veins which is the vein

19:11 gonna mp into the vena cava. that gonna do if I increase the

19:15 there? What happens to the rate flow into the into the vena

19:22 It increases, right? So what doing is I'm I'm basically starting over

19:27 pressure that looks like this, A slope. It's pretty pretty shallow

19:32 . And what I'm doing is doing . So that drives blood quicker back

19:38 the atrium. Which is why the fills up so quickly, right?

19:42 it's like pushing and think of yourself a bathtub if I push the water

19:46 from where I am, is that gonna come rushing back faster at

19:50 Yeah. So that's what it's doing just a function of just the regular

19:57 . We also have what is called respiratory pump. Alright. Not very

20:01 . You see this being demonstrated while lying on your back and actually it's

20:05 easier to see that when you're lying your back. All right. But

20:08 you're not familiar with the anatomy just that you understand there's a muscle that

20:11 after thoracic cavity to the abdominal cavity the diaphragm, right? When you

20:16 in, what you do is you're your thoracic cage. We're gonna talk

20:20 about that in a couple of right? And that what you do

20:23 you're expanding the thoracic cage so the goes outward and the diaphragm pushes downwards

20:29 that the thoracic volume increases its volume what happens according to Boyle's law with

20:37 decreases. Alright. So now what done is I've created a a tilt

20:43 towards the abdomen from the abdominal cavity the thoracic cavity what you're doing is

20:48 dropping the thoracic pressure. So you're increasing the slope. So blood flows

20:54 the thoracic area as a function of just breathing in. It's actually sucking

21:00 up towards the thoracic region. similarly if your diaphragm is being pushed

21:06 into the abdomen, what's happening to pressure in the abdominal region? It's

21:12 . So I'm tipping the thoracic region . But I'm tipping the abdominal region

21:19 . So every time I breathe in creating abdominal pressure and decreasing thoracic

21:24 So the flow of blood is being towards the thoracic region faster. And

21:29 when I exhale I make my thoracic smaller diaphragm goes up. What happens

21:36 the pressure in the abdomen? It what happens to the pressure in the

21:41 cage and increases so it pushes the into the heart and then it pulls

21:46 from the lower limbs up into the . So what have I done that

21:50 created a bellows or a pump just a function of breathing, pull it

21:55 the legs, move it to the , breathe in push it from the

21:59 into the thoracic cage, breathe push from the thoracic cage pulled back

22:03 from the lower limbs. So you what I'm doing is not just the

22:08 doing all the work your muscles as function of breathing are doing the

22:14 Alright that's what all that says? we have the skeletal muscle pump.

22:18 you noticed that you can't sit still a chair. That's not because you

22:22 a. D. D. Although might be able to associate some

22:26 But you know that you wiggle a . You move around a lot

22:29 You kind of feel that uncomfortableness in lower limbs. Alright. Well what

22:34 doing is basically you're contracting muscles to blood. So most of your veins

22:40 Which is how we're returning blood back the heart are found deep within skeletal

22:47 . Alright. And if you can , all right. I I know

22:52 going to talk about this in a of lectures when we talk about the

22:54 vessels. So not this lecture, the next lecture uh within veins you

22:59 these valves and it forces blood to in one direction. Alright. But

23:03 for a moment you didn't have these . Alright. And so here you

23:06 standing in this is showing you where heart is and this this this is

23:10 the vasculature volume, the venus volume the heart. And so just like

23:16 any sort of cylinder, the pressure here at the bottom is going to

23:20 much much greater than the pressure up at the top? Because that volume

23:24 fluid is pushing down and being pulled gravity. Right. And so fluid

23:28 gonna have a tendency to pull in lowest point. But where does the

23:33 want to go? Let's go up the heart. So remember the pressure

23:39 this point in the venus system is very low. Right? Remember that

23:44 we we looked at where it showed here is the pressure over here in

23:47 aorta and it was dropping down the and elastic arteries and it went down

23:50 the resistance arteries and then it finally down to the capillaries where it's smoothed

23:54 . And then you're now over here the small veins and then you're into

23:57 venous return and then finally you're back here in the atrium. You remember

24:01 picture and it was just like kind a sigmoid curve. I'd have to

24:06 flip him back there about 30 slides find it. So you can imagine

24:09 slope down here on the venus return very, very low. It's like

24:14 15 millimeters down to like zero millimeters mercury. So that that return is

24:19 , very slow. And with gravity on all that fluid, it just

24:23 to stay down on the feet. . So part of that is arrested

24:28 a function of the valve that breaks that that wall alright? Or breaks

24:33 that column. But skeletal muscle does same thing. Skeletal muscle also breaks

24:40 the column by squeezing in particular so that you end up with these

24:45 columns or of blood in in you know, these regions. So

24:51 just trying to say look between the and the calf. So you can

24:53 in the space. So instead of a column, that is what do

24:56 think? 4.5 ft? four It's called four ft. So instead

25:01 a calming four ft tall, it's 8" tall. So the pressure at

25:06 bottom here is much much smaller than pressure of the volume there. And

25:12 of course you're resetting. So the here is almost nothing relative to the

25:18 there. And then if I'm squeezing tube, that's one way. If

25:24 squeeze here, what's the blood gonna to do? Think of a tube

25:28 toothpaste? All right. How many you have that horrible habit of screaming

25:32 from the middle. Alright. Just make sure when you have a

25:37 they do the same thing. All . Cause they're doing it from the

25:40 , they're gonna be really upset with . But if you squeeze in the

25:42 where the toothpaste gonna go, something out, some goes back. But

25:48 I put a valve in there where squeezing which way they're going to

25:52 Only the way that the valve allows . So, your skeletal muscles in

25:57 legs and in your limbs in general doing that. They are used as

26:02 pump to push blood to create that to help drive it back to the

26:08 , to oppose the activity of gravity to return blood to where it needs

26:12 go, kind of cool. So not just a function of your heart

26:17 that gets the blood back to where goes. You have all these mechanisms

26:21 create these very, very short term gradients that help push blood back to

26:27 heart, even though they're not technically of the system. Okay, this

26:38 kind of cool. A lot of here. Alright, so your skill

26:43 your cardiac muscle, this is your . You can see we kind of

26:46 through it now. What I want show you here is that if you

26:49 a slice through the heart, you see that the two sides of the

26:53 are differ in terms of their thickness density. All right. So,

26:59 some real simple logic, if I a big thick muscle, is that

27:02 stronger or weaker than a thin Stronger. Okay, good.

27:05 we're all on the same page, kind of understand this concept.

27:08 you can see right here, we the left and the right. Look

27:10 the right, right over on this , right, has a thin

27:14 left, has a thick wall. right. And so we're looking primary

27:18 the ventricle. So why would this ? Well, the blood from the

27:23 side of the heart goes into which ? Left side? Oh yeah,

27:28 sorry, I should have said right . I'm on the wrong side.

27:32 she's right, I'm wrong. Blood the right hand side goes into which

27:36 , pulmonary and the left goes into . Alright, looking at me and

27:42 me as an example how big is pulmonary system from here to where

27:48 I like that right about there. and so my systemic is everything

27:53 Right? So you can imagine the of blood that's being moved into both

27:58 is the exact same. But I more blood in the systemic system that

28:02 have that is resisting the blood coming right? So my left side of

28:08 heart has to work a lot harder inject blood into the systemic system than

28:12 right side of the heart has to to eject that same volume of blood

28:16 the pulmonary system. And that muscle that it's like sitting there lifting weights

28:22 all you're doing is you're sitting there curls all day long with your right

28:25 side and that muscle is gonna be whereas your left hand side is gonna

28:29 a little weak thing. Alright that's going on there. There's a high

28:33 of resistance in the systemic side. that heart muscle has to work harder

28:39 get that same volume of blood The other thing that's really kind of

28:43 . So I told you um I it was thursday about my friend had

28:47 upside down BCG right? So his . C. G. Was a

28:51 P. And then the Q. up and then the r. Went

28:56 and then the s came back up then he had a normal t.

29:00 how did this happen? You I didn't even know he says because

29:04 development his heart muscle didn't arrange the way. This is what your heart

29:10 looks like. All right. And can see it has this kind of

29:14 orientation. The green represents the muscle the atria. The red represents the

29:18 around the ventricles. So when your beats, yes it is propelling blood

29:22 the atria to the ventricles and the outward. But it's doing it like

29:26 wring a towel, it's going so if you've ever milked a goat

29:32 a cow how do you squeeze the out of the teat? Do you

29:37 pull straight down? That's gonna really the goat or the cow?

29:42 What do you do? Right. basically push it out in a sequence

29:52 the spiral representation this muscle does the thing. It pushes it downward and

29:58 it pushes it upward in in that of way. So when that signal

30:03 down through the septum and up through muscles on the outside, what it's

30:06 is it's causing the muscle itself to of ring that blood downward and back

30:12 out through the ventricles out through the of the of the simulator valves.

30:18 now in his case his muscles are flopped in the ventricles. So they

30:22 arrange this way they arranged backwards. what does the E. C.

30:26 . Represent the electrical activity of the . And so when the CG reads

30:32 it's reading the muscles were going backwards of forwards and that's why you got

30:37 really weird funky QRS way for Which is kind of cool. So

30:42 was a developmental thing. All Don't need to know anything on this

30:48 . Basically. What the slide basically says is that the two sides work

30:53 . But if you look really really they're not actually 100% in sync.

30:57 I never asked any questions about Alright so this is the other thing

31:02 trying to show you is how it its contractions. So the right side

31:06 the heart when it's contracting is acting like a bellows. So squeezing back

31:11 forth like this. Whereas when you're at the right side of the ventricle

31:16 it's more like a tube where it's from all sides. Alright. And

31:20 even though it still has that ring because of the size of the muscle

31:24 how it's arranged. It has kind a different sort of appearance. That's

31:29 early what all this stuff is talking . Yeah I think it actually matches

31:39 . Yeah. All right skeletal muscle muscle. Are they different? Yes

31:50 have different names. They have their alright but how they work is very

31:55 similar. The the primary difference here we saw the action potential in the

32:00 I'll muscle is more like that plateau like a table, right? And

32:04 said in this particular case yes calcium involved in both. But what we

32:08 here is the action potential that's being . The function of that sodium and

32:12 potassium later. And the calcium coming . And the calcium that's coming in

32:17 acting on the troponin in the same that it wouldn't skeletal muscle. Pulling

32:21 triple my son out of the way allowing the contraction to take place.

32:25 right now we have some regulators. . And the way that we regulate

32:29 regulators threw phosphor relation. So if go back and look at the picture

32:32 the first one is gonna be fossil . Let's see if I can find

32:35 . There it is. It's trying show you. So here's circa what

32:38 circa sorry, smooth muscle or not smooth smooth into plaza in

32:46 Um calcium channel. So what we're is to get calcium out. We're

32:50 be pumping calcium using circle to get into the circle plasma particular.

32:55 so um our molecule fossil Lamborn is molecule that inhibits the activity of circuits

33:02 break on circa. So when you fossil lamin around it slows down the

33:07 at which circuit pumps. So that allow circuit of pumps calcium. It

33:11 calcium out in the cytoplasm. But we phosphor elated, what we're doing

33:16 we're hitting we're inhibiting the break so putting a brake on the break.

33:19 two negatives make a positive. So doesn't once you phosphor relate basically circuit

33:24 at a normal rate. The other is Troponin has three sub units.

33:29 talked about those three subunits briefly saying there are three subunits. One binds

33:33 calcium. Can you guess which The one with the C.

33:36 That's real hard. What do you that binds to troubled mind?

33:41 it's all not that hard. I was the one that's binding to

33:46 acting. All right. So when phosphor relate the trope trope excuse

33:53 The troponin C component. What that's do is it's going to increase the

33:57 at which we release calcium when we calcium were no longer being pulled away

34:01 said we're now in a position where covering and protecting the acting. So

34:05 that's going to increase the rate at we are returning back to rest.

34:12 So both of these allow us to more relaxed quicker. So when there

34:18 no phosphor relation, the return back rest is um is shorter. Are

34:26 is is longer it takes longer to back to rest when phosphor relation is

34:30 . We're increasing the rate at which remove calcium or make that acting binding

34:36 available. So we returned to rest lot quicker. All right. Oh

34:45 we go. Alright back to the cardiac output is equal to.

34:52 ma'am. We need to go Um Yeah. All right.

35:02 I think in terms of All take all regulators out of the

35:05 Alright, so to come back to . What are the two things that

35:09 going to do? We want to rid of calcium? Right.

35:12 So whenever we get a contraction to back into relaxation, remove calcium.

35:17 calcium, no contraction. Right. , if I want to stay in

35:21 contracted state longer, I want to calcium more available. Right?

35:26 by by having fossil lamb in their Landman block circa circa pumps calcium.

35:34 , when fossil Lamborn is present. works slower. That help when I

35:40 for late Foster lam binh, I inhibiting the activity of Foster lemon.

35:47 circle works faster or at its normal . So calcium leaves faster when we're

35:53 with Troponin, troponin basically releases calcium a at a specific rate. But

35:59 I lost four late troponin, what gonna do is it's gonna release calcium

36:04 . And so that's gonna allow me get rid of the calcium so that

36:07 go back to my original position of . Help. Okay, Alright,

36:15 cardiac output said it had a formula output is equal to and heart

36:23 stroke volume and heart rate. All . So, if I want to

36:27 cardiac output, I can affect stroke or I can affect heart rate.

36:31 gonna deal with stroke volume right Alright, how do I affect stroke

36:35 . Alright, so, there are basic ways I can do this.

36:40 can affect pre load. I can affect after load, or I can

36:46 chemicals apply themselves to the heart that going to alter its contract illit

36:51 All right, So, that's how going to look at this. We're

36:53 to pre load first after load and you're gonna go there's a lot of

36:57 in there, that things make All right. So, we're using

37:01 words than we need to understand and I'm gonna try to keep it

37:05 for you and I need to go right direction. Alright, so,

37:09 can see there's a lot of words . See up there frank Starling,

37:12 you read frank Starling, was it to you? Was there a lot

37:15 blah, blah, blah. another head say yes, Okay,

37:19 Starling is really, really simple And Starling were to cardiologist and they

37:23 looking at how the heart works. what they described as essentially this the

37:28 of blood you give to the heart the amount of blood that the heart

37:30 pump. That's pretty simple. So, if I increase the amount

37:35 blood coming to the heart, the pumps more blood. If I take

37:40 blood, you know, in other , I don't return as much blood

37:43 the heart and the heart pumps All right. This is an intrinsic

37:48 of the heart. So the heart what you give it? All

37:52 So what we're really affecting when we're how the heart pumps is, we're

37:57 not what the heart is doing. affecting what is coming to the

38:02 Alright. So how do I How do I increase how much blood

38:06 coming to the heart? What do think I can do exactly? I

38:12 hear what she said. Well, resistance will be on the front

38:16 on the back end. I want increase resistance. In other words,

38:20 I wanna do is I want to want to go through a contraction.

38:24 ? So here I've got a it has a certain amount of blood

38:27 the tube. All right. So I want to get more blood out

38:32 the tube faster than what am I do, squeeze it? So when

38:37 have venus contraction, what that's gonna that squeezes the tube. That pushes

38:42 to the heart. All that blood up in the atria frank. Starling

38:46 the heart looks all that blood and I need to get this out of

38:49 heart. So it sends it to ventricles and the ventricles then contracts and

38:53 that blood outward. Alright? So I increase pre load I'm going to

39:00 the contract style activity of the I'm gonna increase SV now.

39:04 What I'm doing is I'm dealing with diastolic volume. Right? So what's

39:08 diastolic volume says it in the right? The max volume I get

39:16 rest. Right? So remember the contracts diagnostically we're here refers to the

39:23 . And so what happens is when contract and send all that blood into

39:28 ventricle before it contracts it still and that that volume that's inside the ventricle

39:35 the end diastolic volume. So, I'm doing is I'm increasing E.

39:41 . V. Okay. Here's the SV is equal to E D V

39:50 E. S P E S In systolic volume. Alright, So

39:56 I increase cTV and I keep PSV same, what's happened to SV?

40:05 increases. Right. Just making up number E D V is 100 E

40:10 V. Is 10. What's the ? So, SV would be

40:14 Okay. If I take a tv give it 50 more. So,

40:17 100 and 50 mg SV stays the . So 100 15 minus 10 equals

40:23 stroke volume has increased decreased same. by how much? 50.

40:30 truly 40 because SV is what we're how much is SV increased?

40:35 So do you see no, you're . 50. You get the gold

40:40 I get the minus f minus. right. So that's what we're dealing

40:44 you increase E. G b you're increase SV Because we're not talking about

40:49 right now. All right. I that's alphabet soup, but in diastolic

40:53 takes more time to say. All . Because frank. Starling observed

40:59 and Starling observed the heart pumps what pumps. Alright? You give

41:03 It does. Alright, so increase return. How do I increase venous

41:08 ? We have talked about that yet activity, we'll get to it.

41:13 will yield an increase in stroke So that's one way that we affected

41:17 in diastolic volume secondly, after after load is something you already understand

41:23 well. Alright? We we refer it as another term. We talk

41:28 blood pressure. If I have raised pressure, what am I doing?

41:33 increasing resistance to the blood being pumped of the heart. So, if

41:38 have greater after load, right? my arteries are saying don't give me

41:42 blood and my heart saying, but have to pump what I have to

41:47 , then what does the heart have do? It has to work

41:52 Right? So now what I'm doing I am increasing my E.

41:58 V. Right? Because the resistance you can't let out as much as

42:02 as you want to let out. still letting some out. But I'm

42:05 have more left over in the Alright? The SV is just the

42:09 left over the heart. So, I increase the SV and I'm not

42:12 about the E. D. At all. That stays constant

42:15 D. V minus E. And SV is increasing decreasing stroke

42:20 All right that makes sense. If if I'm being resisted against and I'm

42:28 increasing the amount of work I'm doing amount of stuff that's the amount of

42:33 that I'm accomplishing is less. So this case I'm moving blood volume so

42:38 I'm not able to move as much volume that means I have more left

42:41 on this side. So after load the end systolic volume and it results

42:48 an increase of that in systolic All right now for all of us

42:53 is pretty pretty constant. PsV stays or less constant. It's once you

42:58 developing pathologies like high blood pressure where see after load having a great

43:03 And so much of the medicines that do is there to reduce um the

43:09 load right? Because what we're concerned is not how much blood is leaving

43:15 heart but how much work the heart doing and if the heart works too

43:18 what's it gonna want to do? wants to rest too Just once it

43:28 . Doesn't really do much else after seizes up and dies. Alright I'm

43:35 tropic agents in a tropic refer to things that are going to change the

43:41 of calcium. Alright. Positive. know tropes increased calcium ability. Negative

43:46 decreased calcium availability so you can go read through all this stuff But if

43:51 increasing calcium availability? What's that? that gonna do to the activity of

43:56 heart? It's gonna increase the rate which it beats and it's gonna increase

44:04 strength. Alright. So examples again agonists. Alright. Anything that's going

44:11 make the heart beat harder? So think about it. Think about

44:16 adrenaline does. What does adrenaline due your heart faster and harder?

44:23 I mean you're saying that? All . That's extra calcium. So that's

44:29 a positive item trump does stronger increases the available of calcium. Plus

44:35 the number of cross bridges. So negative tropes do the opposite. So

44:40 have natural ones. Those things in bodies like what is listed here.

44:45 then there are things that are external are referred to as many trips as

44:49 . Alright. Which you'll get the of you are going to farm

44:52 get to learn the whole big All right. So this is just

44:57 example. So what we're doing is changing the force of contraction. So

45:04 do we change stroke volume? In pre load affecting pre load effects

45:10 D. V. After load effects . S. V. Right.

45:17 here what we're gonna do is we uh basically you're gonna increase stroke volume

45:24 decreasing SV basically those hard contractions causes blood to leave. All right in

45:31 response. So if I have more leaving the heart heart faster, what

45:35 that going to do to the V. What do you think I

45:41 more blood leaving the heart? What's to happen to the blood returning to

45:45 heart? It's going to increase as . So think about think about what

45:52 right when you are exercising right? hearts beating harder. More blood is

45:56 back to the heart. Hearts beating . It's basically a system that has

46:00 stay in constant motion. So what gonna do is you're gonna see that

46:05 come back on the on the back . That kind of makes sense.

46:13 right. Ready to do the easy . Ready to move away from the

46:20 stuff. All right. It's really that hard. Alright. What's

46:27 It's a fluid consisting of a whole of stuff. The fluid portion is

46:33 plasma has within it. A bunch molecules will get to what the most

46:37 ones are. Just minutes. So it's a fluid matrix is what

46:41 refer to it as. So it's plus stuff has specialized blood cells which

46:46 not entirely blood cells. These are called the formed elements because as we

46:50 see in just a moment of parasites the platelets is a term that we

46:55 in humans, other species we call but you'll see them every now and

46:59 elsewhere as homicide. But these two are not actually cells anymore. They

47:06 from cells but they're not cells any . Only sells here, the

47:11 So if you're not familiar with these sites, these are red blood

47:14 leukocyte or white blood cells. Platelets sometimes referred to as homicides.

47:19 if I just take all these things put them in a in a,

47:23 don't know a vial, let's just it that way. These formed elements

47:28 very, very heavy. So what they going to do? They're gonna

47:31 . Right. And so the cardiovascular ensures a constant motion and a constant

47:39 of this fluid informed elements. So these things are equally distributed.

47:43 so they're in constant distribution. The hematocrit is a term we use

47:53 refer to the packed cell volume. specifically, it refers to the percentage

47:59 sites I have seen in some textbooks in some places that they also include

48:04 Buffy coat because Buffy coats are really small and why not just include

48:10 . But for your purposes. And the exam, when you see

48:13 it's the original site percentage which comes between 42 and 45%. The Buffy

48:19 is represents the rest of the formed . So that the sites is that

48:25 cell volume and that Buffy coat is final 1%. So that's why most

48:31 kind of consider both together because like doesn't matter that 1% doesn't really change

48:36 Now. What you see here in hematocrit, It's gonna be dependent upon

48:41 whole bunch of factors primarily aging your . So, males typically have a

48:46 dramatic red and that's because testosterone is promoter of erythropoietin production, which is

48:52 for making red blood cells. And females have a slightly lower one about

48:57 , but they're close enough. Um what is plasma? Um I'm just

49:04 to show you here. It's kind clear ish, kind of It's really

49:06 clear. It's it's it's opaque kind of yellowish in nature. Um

49:11 makes about 55%. It's because it's made up of water about 90%.

49:16 does a really good job of distributing heat. Um with regard to

49:20 else is in there, about 68% plasma proteins. We'll look at some

49:25 the general ones in just a plus a whole bunch of other

49:28 And these are things we kind of about. So electrolytes, we don't

49:31 don't really count them in that We just know that their electrolytes

49:35 You're dissolved gasses that includes oxygen and dioxide and nitrogen. All those things

49:40 you find in your atmosphere in those concentrations roughly are going to be found

49:46 the plasma as well. But when talk about the lungs and what they

49:50 , that's not the fluid we're really or the gasses, we're talking

49:54 It's gonna be gasses that are being through the urethra sights. For the

49:57 part there's other organic molecules that aren't part of the plasma proteins. So

50:02 signaling molecule, any hormone and they're there as well. But because

50:07 not made in the liver and they're part of the plasma protein cohort,

50:10 just kind of ignore them. There percentage is so small. The term

50:15 , when you hear serum it is without fibrinogen, which is one of

50:19 plasma proteins and the other clotting factors are included in uh those plasma

50:25 Alright, so that's what serum ultimately very, very similar. What we're

50:32 at here is a western block. guys know what Western blot is.

50:36 people. Four people nodding your Alright. And really what they're trying

50:39 show you where these different plasma proteins located and so why we're interested in

50:45 plasma proteins is because of the effect they have on osmolarity and the effect

50:50 the movement of water through the interstitial back to the plaza and back and

50:56 again. Alright, so they're responsible creating an osmotic gradient. Alright,

51:01 those platinum proteins are too big to their way into the interstitial fluid.

51:04 only found in the plasma, hence name. And so they attract water

51:09 into the blood because of that osmotic . Alright, this is when we

51:16 concerned about blood pressure and blood Part of it has to do with

51:21 presence of these plasma proteins. So have to know of their existence and

51:23 going to see their effect Over the of the next couple of lectures,

51:28 of the most common ones albumin. guys heard albumin before? It's a

51:32 itsy bitsy teeny tiny protein. Um you go crack open an egg,

51:36 that clear stuff, not the The clear stuff is is is a

51:40 high concentration of albumin. It's actually the highest concentration, but it's one

51:45 where you can actually see it and it. You can see albumin is

51:48 of sticky. Right? Does a good job of binding things in a

51:52 , very non um specific manner That up almost 60 the globulin. Have

51:59 heard of globulin before? You've heard one in particular? Those are the

52:04 globulin. Gamma globulin. Those are antibodies. All right, so they're

52:09 but you'll have alpha globulin, beta . You have to have an alpha

52:12 a beta. So, these are transporters, they transport all sorts of

52:16 . Primary lipids and other ions primarily . For the most part they can

52:21 as regulators. And if you look the picture in here anything with an

52:26 , Right, Those are like the globulin. Let me see if I

52:29 find there's I g a gamma globulin there's a beta globulin for you.

52:34 right. You can see where the czar look look at that big old

52:38 . Right then we have fibrinogen. we'll get to that here at the

52:42 of class fibrinogen plays the main major role in homeostasis. That's blood

52:47 And you can see fibrinogen there it . Right, it's this peak that

52:56 trying to represent this red line. , so that's fibrinogen and then there's

53:00 proteins in there and you can kind go through there. It is

53:04 you can go through and kind of you know, oh what's this?

53:09 that? They're all sorts of fun in there. So there's a whole

53:12 of proteins is really what it boils to and they have varying roles in

53:16 plasma, primarily carriers but also play major role in clotting pronounce that word

53:24 me please. Oh I like that sis poetess is it's a fun word

53:33 say. So mad opposes. It could be you'll see uh him oppose

53:39 . So they they take out the and just called Hema polices refers to

53:44 production of these formed elements. So all originate from the same um origin

53:50 if you look at this you can here's my red blood cell um right

53:53 , that's the um mega carrier These are your lymphocytes all through here

54:01 the way down. And so you see they all start off as a

54:05 or from a progenitor. And so you need in order to get this

54:10 happen and to get these things as can see marked here in red?

54:14 are specific molecules that kind of direct particular uh pluripotent cell down a specific

54:22 . So what happens is you go this pluripotent cell, that can be

54:27 type of hematopoietic cell, which then of goes, okay, do I

54:30 down the lymphoid line or do I down the myeloid line? And then

54:33 I go down one of those lines what which way are you directing

54:37 So once you go down a particular you can't go back alright, you've

54:42 differentiated too far to uh go backwards really what it is. All

54:47 And so that's what this is just to tell you, is that there's

54:50 pathway of differentiation that's going to be upon the type of side of kind

54:55 type of signaling molecules that are available drive in a particular direction.

55:00 And so this is just kind of big list. Honestly, you

55:04 I'm not sure, I may ask question on this, but really this

55:08 what it boils down to the tells you what it is. So

55:10 is a granule site monta site, , colony stimulating factor. It basically

55:16 you down the Nile Lloyd line so you either produce a granule side arm

55:20 a site and that's what all these are right here? Right? And

55:23 this pushes you down specifically. Am going to become a granule site or

55:27 I becoming a mon a site? , So it's G CSF or

55:31 S. M CSF. Um Don't about the inner Lukens throw is gonna

55:38 you from this sort of stem Either down to the mega carrier site

55:42 if I have or it is going push me towards the red blood

55:48 So, the big picture here is I want to make a specific type

55:52 cell, I have to have specific that tell me what to do.

55:58 right. And so what I want show you here is the oasis.

56:02 right. We all need red blood . We agree with that.

56:06 Okay. So this is gonna occur the red bone marrow. All right

56:10 you don't always have red bone marrow utero. You have no red bone

56:15 . And so all your red blood are gonna be made primarily first initially

56:18 the yolk sac and then when you your liver and your spleen form very

56:22 on, that's when it takes over then eventually the bones form. And

56:25 when you have you you populate the um um cavities of the bones and

56:31 ends of the bones with this red . And so during most of childhood

56:35 have a whole bunch of red bone but then we get old and we

56:38 up that red those those spaces with is called yellow marrow, which lack

56:41 a better term is really just kind fat. All right now, it's

56:45 fat, but it's like fat and you can actually revert yellow marrow back

56:49 red marrow in dire needs. But essence, your red bone marrow is

56:54 to be found in some very, hard to reach places. So,

56:58 are not like when you talk about long bone, we're talking about the

57:02 head of the femur, for not easy to get to. You

57:05 to actually go digging through a whole of muscle and actually dig through the

57:09 koksal, which is your hip to to the head of the femur.

57:13 , not a fun place to go this stuff. Now, the way

57:17 decide how much red blood cell we're is dependent upon how much oxygen the

57:22 receives. So, our kidney is oxygen sensor. All right now,

57:27 your tissues are dependent upon the oxygen delivered to it. But only the

57:31 is the one that responds to the received. So, if it's not

57:34 enough oxygen and says, wait, , wait, wait, Where's my

57:37 ? Well, apparently, I don't enough red blood cells carrying enough

57:41 So, I'm going to tell the bone marrow to make more red blood

57:46 . That may not even be the , but that's how it determines

57:49 Yeah corn kidney. No, because still censoring, you're still monitoring is

57:56 kidney getting the oxygen needs? no, this is. So,

58:04 we're talking here, we're really talking big picture stuff. So, if

58:07 put you underwater and hold you underwater two minutes, your kidneys not going

58:10 my oxygen? I mean, it , but your brain is really kind

58:14 doing more of the where's my oxygen than your kidney is. Alright,

58:18 , we're talking about a long term , a long term hormonal response

58:22 Not minutes, minute. Yeah, , I think, and we may

58:33 it to another on another slide. so, yes, so, the

58:37 here is this is more representative of oxygen carrying capacity of the blood.

58:42 , the number of red blood cells how well the blood carries oxygen.

58:48 it represents the number of red blood . Because your red blood cells are

58:52 cell that carries oxygen. So, you don't, if your kidneys aren't

58:56 enough oxygen, it's got to be fault of the number of red blood

58:59 I have. Right. And using your example, if I go

59:04 a high altitude, which we know a higher altitude, the oxygen in

59:08 atmosphere is a lot lower kidney doesn't , oh, I'm sorry, I'm

59:12 colorado I'm at 10,000 ft. It's less auction around. It just

59:16 wait a second. Apparently, I have enough red blood cells.

59:19 what I'm gonna do is I'm going make more red blood cells so that

59:24 auction carrying capacity can increase. now there are a lot of steps

59:32 , you see here is that stem and you can see. So,

59:35 I want to point out here is is the step that requires us to

59:40 from that noncommittal step to the committed of producing the red blood cell.

59:46 , The original site. And what's here is that what we're gonna

59:49 We're modifying a cell from a functional that can divide to a cell that

59:55 is basically a bag of hemoglobin. right, so, you can see

59:59 what it says. Look, I'm go through a series of divisions

60:02 So I'm gonna still get a series divisions. But what I'm gonna start

60:06 is my machinery says, I need start making hemoglobin. And so it

60:10 making tons and tons of this protein it starts filling up the cytoplasm of

60:14 cell. And to the point where like, I don't want my other

60:18 , All I want is hemoglobin. so we extrude all our organelles,

60:23 extrude the nucleus. And at this , we're just basically a container full

60:29 hemoglobin. And there's still some steps need to take place. But what

60:34 do is we get to this immature called a particular site. And that

60:38 site can enter into the uh circulation serve as a red blood cell while

60:45 still goes through that last few steps organelles removal. And so once you

60:50 an original site, you're now using , very basic cellular activity to maintain

60:58 function. And that cell function is circulate and hold on oxygen. You

61:04 still do a little bit of glycol . But that's about it right.

61:09 not much else going on inside the . So massive, massive modification in

61:15 to the erythropoietin. Alright, erythropoietin produced by which structure starts with a

61:24 kidney kidney is monitoring how much oxygen need. It's the one that's sending

61:29 signal to the red marrow, it's a to make that signal.

61:35 how many retro sites do you You have about five times 10 cells

61:39 mill of blood. Adult males are 5.5 liters. Females are about 4.5

61:45 of blood. So, if you to do the math to figure out

61:47 many red blood cells are in circulation now, that kind of gives you

61:51 sense. And again, that's an . If you're smaller, you're gonna

61:54 fewer. If you're taller, you're have more or bigger. All

61:57 So, when we think of a sites, think transport of oxygen as

62:02 as the transport of carbon dioxide. is their function very flat. You

62:06 see here there by concave and the this shape allows them to uh navigate

62:13 the intricate structures of the capillaries. themselves are very very small. They're

62:19 as almost as big as the red cells themselves. And typically what will

62:23 is that you'll get a stack of blood cells that kind of jam up

62:27 , create this this kind of like of red blood cells, it's called

62:33 . And they kind of move together you can kind of see that in

62:36 picture. Alright now this shape does couple of things. It allows them

62:41 move very very easily in these blood . So think about a basketball basketball

62:46 round. Right think of it being at the proper P. S.

62:49 can you bend the basketball in No, so it would be very

62:53 difficult to go through a very very capillary that has a sharp turn.

62:58 if I deflate the basketball, remove the air from it. Could have

63:01 the basketball now. So that's kind what we've done here, It's the

63:04 volume inside. It's just now I a flexible structure. Second thing is

63:10 it also increases or decreases the distance the center of the cell to the

63:15 . So if I'm completely filled up hemoglobin, the rate at which oxygen

63:20 move in and out of the cell very very quick because the distance between

63:24 hemoglobin is and where the outside of cell is is very very short.

63:29 , so it's advantageous to the cell have this particular shape. So a

63:36 no, basically no organelles, about of 7% of its contents hemoglobin.

63:42 have about 280 times 10 to the million or 10 to 6 million.

63:46 to 10 to the six molecules per . Again, if you want to

63:50 the math, you can go back multiplying too much hemoglobin. You

63:56 you do make a teepee uses glycol . Why you guys like blue bell

64:02 cream? Do you remember the We eat what we can and we

64:07 the rest. Do you remember that that used to be their big ad

64:12 they had a listeria. In which I don't know what happened. I

64:15 there the week that they had the listeria problem. I was still eating

64:18 cream. I could care less. know, they'll kill me or it

64:22 either way I die happy. Anyway, so that used to be

64:27 , add it would be like this driver and says alright son, you

64:30 have whatever you want. And then finally gets to the destination, he's

64:33 all the ice cream in the right? And actually if you go

64:36 the factory and you should, if never been, it's not too far

64:40 Brenham. It's a weekend trip, can eat ice cream, they right

64:44 there. But they have you they you go by during the tour,

64:47 get to see the break room and whole wall of the break room is

64:51 and you basically, they have all points that all the workers have and

64:55 put their names on the pint and just sit there and that's their ice

64:58 . And then when they run out they go get another point and they

65:00 their name on it and that's there's a bad job if you don't mind

65:06 cream. All right. So, idea why do I tell this

65:10 Because it's the same thing. You not want yourselves to consume the oxygen

65:14 you're carrying. Otherwise your kidney is be really, really upset. And

65:19 the rest your body is gonna be as a function. And they stick

65:22 for about 100 and 20 days. about 100 and 20 days, they've

65:25 beat up enough that they're just kind basically barely being held together. And

65:28 when they arrive in the spleen. spleen is like this horse shows roller

65:33 for these places basically bust up the and causing the rupture and then you

65:38 recycle the hemoglobin and or really the the iron and you break everything

65:43 So the spleen is where we recycle . So here's a molecule you guys

65:49 seen ever since you've been freshmen. remember that first time you talked about

65:54 structure and show you a picture of . Yeah. So what do we

66:02 here? It's just a pigment. iron here in the center is capable

66:06 binding of oxygen. So there's two . We have 1234 globe and molecules

66:12 two pairs of different types of globe . All right in the center of

66:16 of you. That's where the heat . That's what the oxygen is

66:19 So each hemoglobin combined. How many 4? Which makes it really simple

66:26 if you find one you're 20% 25% to 50% saturated, 3, 75%

66:32 , 400% saturated. See how easy math is. I love things like

66:37 thing is hemoglobin. Doesn't just buy oxygen. Alright so one of the

66:42 so that option will bind the iron when it does it binds and we

66:46 that molecule now oxy hemoglobin. when you remove the oxygen, the

66:51 hemoglobin and then like I said you other things. So carbon dioxide can

66:56 to the globe and portion and when does so we refer to as carb

66:59 hemoglobin. Alright not carb oxy that's what you get when you bind

67:05 to the irreversible carbon monoxide. you can bind up two protons when

67:11 happens. And so this is a that hemoglobin can actually serve as a

67:15 to the blood. It binds up free protons combined. Up to nitric

67:20 serves as a vase, a dilator all this is to the hemoglobin.

67:24 molecules cyanide. Uh So fox side hydrogen sulfide. These are other things

67:31 can serve as a carrier for. , but we're gonna be really primarily

67:36 in the carbon dioxide, the protons well as the oxygen. There are

67:42 molecules that you need to be aware . The 1st 123 D faster Glycerin

67:48 a molecule released by cells that basically , hey give me your oxygen.

67:53 so what it does is that that fossil glycerin causes hemoglobin to say I'm

67:59 longer interested in binding up to the . So the oxygen is released and

68:03 that comes from the red blood Glutathione just helps against protect against oxidative

68:09 . Where we're gonna get oxidative damage . Not a trick question from the

68:16 . And it's carrying right? So um carbonic anhydrous, we're gonna learn

68:22 whole bunch about it helps to convert dioxide into bicarbonate. If you don't

68:26 that molecule right there should have a sign on top that bicarbonate is going

68:30 be like your best friend for the couple of weeks. Alright. Um

68:34 is really really important for carbon dioxide . We're gonna have a proton exchange

68:41 proton a chlorine by carbon exchanger. allows us to move these two uh

68:46 ions back and forth very very quickly the red blood cells wall. And

68:50 we have aqua porn's which can serve a carbon dioxide channel, which allows

68:54 to move carbon dioxide in and out the cell very very quickly in the

68:57 blood cell. It's interesting. That's aqua porn, isn't it?

69:04 All right. This is basic, , basic, basic basic immunology.

69:13 not even immunology. You need to your Lucas sites. All right.

69:16 what they do. Alright, we two basic types of Granules are two

69:20 types of sites and a granule Granule sites have Granules. Granules sites

69:27 . So basically, if you stain , you're going to see that those

69:31 staying with a di specific type of and that's where their name came

69:36 So, there's three types of granule , neutrophils get cinephiles and besa

69:40 All right. They don't really exist that long in the blood. They

69:44 of hang out there for a little , but then they arrive in their

69:47 and that's where they kind of hang . The a granule sites are the

69:50 that you primarily see in circulation. key feature between these, if you

69:56 at the granule sights, you're gonna that their nuclear nuclei look weird.

70:01 right. They look like they've been and pinched and so they have what

70:05 called lobes to them. So sometimes see um Lobular granule sites is sometimes

70:13 term that you'll see. All So neutral Phyllis feels the difference between

70:18 is which dye binds them. All . So we're gonna start with the

70:24 . The most common type. It's lobed. So you can see I've

70:29 done you're not gonna have to identify . Alright. I'm not gonna I'm

70:32 pointing them out so that you can in the spread which ones they

70:34 All right. They're fake acidic in . Alright. So what they're looking

70:38 is they're looking for that first line bacterial infection. Do you have a

70:43 inside you? I'm gonna kill All right. So that's what we're

70:47 to deal with. They play an role in your inflammatory response. The

70:52 to fill about 4%. Alright. job is to deal with parasites.

70:58 right. In the Western World. World Western World. Do you think

71:02 have to deal with a whole bunch parasites? So what do you think

71:06 see NFL counselor like. Low very . Very low. Alright. If

71:12 go to India or Southeast Asia, do you expect in that population?

71:18 . Okay. They also play a in allergic reactions to some degree.

71:22 right now they're called because they get by an acidic um a die.

71:28 you've heard of H. And Standing Standing standing okay. Don't worry

71:37 if you haven't taken microbiome then. haven't seen this stuff yet but this

71:43 and purple stuff H. And Alright. So the sn is the

71:48 stuff besa fills. Besa fills again smaller portion. They play a major

71:56 in um uh allergic reactions. But I was trying to get here is

72:01 a dilation and heparin. So you imagine here is when an infection occurs

72:06 if there's damage there these cells show and they say ah this is the

72:10 of damage starts releasing. The histamines starts releasing the heparin Heparin. Its

72:15 is to serve as an anticoagulants. it allows fluid to come into that

72:18 and not create a clot. The causes days of dilation and inflammation so

72:23 the fluid shows up. All You can remember what histamine is because

72:28 you get all topped up you take of that. Okay. Monitor sites

72:35 baby macrophages. So again is the largest population. Um They basically are

72:43 circulation. And then what will happen they'll differentiate into the macrophage. Macrophage

72:47 kind of like the neutrophils and that looking for bacteria but typically you'll have

72:52 different types of macrophages. One that as a population that doesn't migrate through

72:58 . It becomes a stationary macrophage and monitors its environment or what it can

73:03 is it can migrate from tissue to to tissue. It can also serve

73:06 an androgen presenting cell which is more we need to know. That's basically

73:11 you alert your other uh how you the lymphocytes lymphocytes um This is the

73:21 the second largest I should have said the the previous not the manga sites

73:27 most of these are hidden up. . They're they're they're kind of sequestered

73:32 a way away in um your lymphatic looking for the presence of pathogen.

73:40 . So you have two different populations cells and T cells and this is

73:45 specific line of defense against specific foreign . B cells are the antibody producing

73:52 . All right. So what they're is that each of these cells are

73:55 to a specific pathogen. They're just and if that specific pathogen comes along

74:01 to the B. Cell that causes B cell to differentiate become a plasma

74:05 and it starts producing that antibody that's that specific antigen, that specific pathogen

74:12 has that response to that particular Alright. So it plays a role

74:17 antibody mediated or what you'll see sometimes mediated defense. T cells on the

74:24 hand and their names come from the . And T. Come from where

74:28 where they mature. So B cells and bone marrow T cells are made

74:32 bone but then they go to the and that's where they're selected for

74:37 What they're doing is they recognize the themselves through their receptor recognizes the

74:44 So this is what is called cell immunity. Alright. There's different types

74:48 T cells T helper cells to killer um side of toxic T cells um

74:54 there's like three or four others that now that when I was in school

74:58 exist so. Alright. But their is they act directly they're not producing

75:03 to bind things up there recognizing the and then they say hey come kill

75:08 thing, this thing needs to be . And that's how um how they

75:13 work. That is your kindergarten exposure the immune system. Yes ma'am.

75:30 asking a question that has a 45 answer and I mean and it's a

75:35 good question. I'm not trying to . I mean it is an incredibly

75:39 question which is why all our topics to do with the immune system.

75:44 immune system is grossly complex. And essence what you have is for the

75:49 . Cell and T. Cell. each have their own specific receptor called

75:52 B cell receptor in the T. receptor. Very complex part right?

75:55 what this is is it's a piece D. N. A. That

75:59 these regions that are variable regions and reorganize themselves during the process of

76:05 And so every one of your T and every one of your B cells

76:09 unique in that they recognize a specific antigen. Right. And so this

76:17 a roll of the dice. Let's out um trying to be very careful

76:23 trying to go too far. It's basically a random process of what you're

76:28 to be able to recognize. So and I may be able to recognize

76:31 same pathogen. But the way that do our through different antigens,

76:36 determinants, different episodes. Alright. the way that we go to make

76:41 that the B. Cell and Cell they go through a process of

76:45 which basically says can you recognize something now? Are you recognizing self?

76:52 . Okay. We don't want you die go die in a fire.

76:55 we select away from those things that attack ourselves. And then those things

77:01 can both recognize uh an antigen and something that's not self are the ones

77:07 stick around and I can't remember what total number of combinations are. But

77:11 like ridiculously high. It's not But it's it's crazy now just to

77:17 you a sense. Alright, so For the vaccine that was for the

77:23 that we the COVID-19 right. What did was we created a a very

77:30 small molecule right, a very small genic piece of. Well it was

77:37 RNA that could make a small And so the idea was is do

77:42 have an antibody that can be produced can recognize that episode? And if

77:50 did then you created a monoclonal A single antibody that can recognize it

77:56 for those who got exposed to the virus has many many proteins, many

78:03 different shapes on those proteins. And we created a massive polyclonal attack.

78:11 , we basically created a defense that much, much greater than those that

78:16 just being exposed with that little tiny . And I went way too far

78:21 that. So, immunology is a of fun and very, very

78:26 I know. What do I Like zero seconds left. Two

78:29 Alright. I think this is the slide I'll do right here, I

78:37 . Yeah, well, we'll leave that. We're gonna stop here with

78:43 platelet one. All right. what is the platelet? A platelet

78:48 a portion of the mega carrier site off. All right. So,

78:53 make a carrier site. Remember was down the same path as the original

78:57 . And then you got it gave a different hormone. It's that causes

79:04 mega carrier site to start doing this of weird, shimmy shake. And

79:07 it's plasma membrane starts doing this kind weird stuff. And the sheer force

79:11 the blood going by that thrombosis site that mega carrier site rips off a

79:17 tiny piece of that plasma and within plasma void or within that plasma.

79:23 the plasma membrane within that structure are that the platelet needs in order to

79:29 its function. Alright. So, a whole bunch of Granules in there

79:33 you can see right here, here's little blab and they're they're being torn

79:36 . So this is the structure. what you're gonna have, you're gonna

79:39 these alpha Granules in these dense core . And what these do is within

79:44 structures, the alpha Granules. Those all the elements you're gonna need to

79:47 a blood clot and then you have molecules that regulate where those are gonna

79:54 how they work. So, the platelet plays a role in this process

79:59 homeostasis. Alright, Homeostasis is the word for saying, creating blood clots

80:05 scabs. Alright, They exist in blood for about 10 days. How

80:09 the red blood cells stay in the ? 120. So, I want

80:13 to see those two differences. Don't the two, once three months.

80:16 is just about a week. All . And then after about 10 days

80:19 kind of fall apart. Macrophages come and show them all up and get

80:22 of them. All right. And , what when we do we'll start

80:25 the most cases when we get back Thursday. All right. And so

80:30 kind of what this is the start . We get to talk about

80:36 You Yeah, don't talk to me the Dodgers going based on my email

80:46 yesterday? The reason I asked is I remember seeing on

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