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00:05 Yes, hello. Hello. folks. Um let's get started

00:20 Uh ok. Uh So let me this. Uh So we're starting,

00:31 starting the last unit. Where's my at there? He is. Um

00:40 the banner say? What's the banner ? Oh, wow. Homecoming

00:50 Ok. Ok. Um So starting new unit. Last unit,

00:57 Um Another 12, 3.5 weeks. call it, right? So we

01:06 uh come half a week in Thanksgiving . Um So that's what 1234567,

01:16 6.5, I think I'll cover So, so yeah, same to

01:28 . Um The uh All right. we're starting the last unit. So

01:33 switching gears. So obviously the stuff week is not on the exam.

01:37 So exam three, right? This , Saturday um chapter 7 to

01:44 right? As always that review your guide. Um You have questions

01:51 minute questions I'm available this week, let me know. Um The drop

01:57 is next week. Ok. So gonna have the exam three to uh

02:04 know, make your final evaluation, ? Should I stay? Should I

02:08 . Ok. So, um and I'll address some of that on uh

02:28 inaccurate. But now there's this issue Chapter 10 from smart work can transfer

02:33 . So I, I and I those people. So there's multiple technical

02:36 working on these things, right? because you don't see a grade on

02:40 doesn't mean it's not there, Because I have access to smart

02:44 I can just download directly from smart everything. Uh uh And so uh

02:49 the clicker, the clicker points there accurate. Ok, that are on

02:54 , the um quiz quizzes are So, you know, um but

03:00 I don't know what's going on with the chap pretended transfer everything else is

03:03 , that's that happened. So it's, it's all being worked

03:07 The latest thing was video points wasn't to you or to me. And

03:12 that's I have a temporary fix on as of today. So uh m

03:17 technical issues going on which I So that's why I, I,

03:21 know, I sent out the the calculation, right? So follow

03:25 Ok, and you can go in go to smart work and get

03:30 if you're not sure about, if still uneasy about are these grades accurate

03:33 not? Or you can go to work and see your grades there,

03:36 can uh uh of course your quiz and click your grades. So use

03:41 formula to, to estimate your current . Ok. Um, there you

03:48 , the, the curriculum, which been in place since day one,

03:53 ? For exams each worth 17%. the, the, the smart

03:58 the, um, the smart the quizzes the clickers, you

04:03 that's what the grade is. There's a couple of extra credit

04:07 right? One is target clickers. is basically fill out the evaluation.

04:11 . So that, those are your , some are expecting a windfall of

04:16 to come raining down from above, . At the end of the semester

04:21 get them over the hump or whatever grade is. That's not happening,

04:25 . Ok. So really think hard , you know, after you take

04:31 three, whether to stay in or out. Ok? Everybody here is

04:42 the boat. Ok? And in boat, everybody is evaluated the same

04:48 . Ok? There's, there's I cannot, I will get emails

04:55 long right toward the end of the . Relaying all the trials and tribulations

05:00 person has undergone. Ok. I'm . They want points for this,

05:06 and the other. Ok, to . I've had people not graduate because

05:10 didn't get what they needed in this . That's nothing new to me.

05:14 ? It's not a lot over 20 but it has happened. Ok.

05:19 that could be the stark cold Ok? So just preparing you for

05:25 stuff, right? It's not just class you, you're taking other classes

05:28 well or it's, it's, it's the brink, so to speak.

05:32 . So um give this person 50 gets into the like out of

05:50 What about these other people? They would rightly create, yell at

05:57 , right. Which they should because not being treated the same way.

06:02 ? So while I sympathize with and realized shit happens during the semester,

06:07 ? Happens to me too. But you know, that's why communication

06:12 so important. Ok, email me something happens and then I can maybe

06:16 with you. But when I hear and that and I, then I

06:20 something on December 10th, there's nothing can do. Ok. So everybody

06:27 evaluated by that same curriculum that I . Ok. And so that,

06:34 what the greatest cap and that's what will be. Ok. There is

06:37 a curve possibly but historically, people make like an average of 50 in

06:44 course, they make an average of 70 ok. Overall average is around

06:49 . Ok? And so, you , curves as the way most people

06:54 do them, the overall class What sets kind of the CD?

07:04 . But yeah, you raise, curve up right to make that,

07:07 50 now becomes ac ok. But know, people don't, we don't

07:13 , I don't have bad grades like . So because the overall average is

07:23 7234 somewhere in there. Ok. don't rely on having a big curve

07:30 help you out either. Ok? you know, you want there to

07:35 a really low class average, you a lot of help and we

07:38 I just don't have that. so again, I'm just preparing you

07:42 what's coming up. Ok. So know there's gonna be some panicky

07:46 Ok. So let me just give reality check. Ok? And I

07:53 , he may go, yeah, guy is really an a hole.

07:56 . No, I just have everybody, I have 400 people in

08:00 . Everybody's got to be treated Ok? And yes, that happens

08:04 these people and doesn't happen to these a whole range of things.

08:09 But I can't, you know, I, I can't give points for

08:15 , right? Because if I if effort was all it took,

08:19 be one bar on my curve. makes 100. Ok. Has everybody

08:24 seen a great distribution curve with just bar that everybody made 100? I

08:28 think so. Ok, so, know, yes, I assume everybody

08:33 makes a good effort but it, ends up where it ends up.

08:39 . So again, hey, I , I've been here since day one

08:43 help. Ok. Come to the if you need help. Not a

08:48 . Ok. I can probably count two hands. The number of people

08:51 seen this entire semester. Ok. not sure I can, I can

08:56 help with the remaining, you exam, what's up with exam

09:00 That's right. I can help you exam four stuff material. Absolutely.

09:05 . But, um, I can't once we get to December,

09:10 November 30th right after that. Not I can do to help you with

09:15 four. Ok. So, that's, you know, and I

09:21 having said that I'll still get emails that's fine. I expect it.

09:25 know that I can't lift you up you need to go necessarily to

09:30 just based on having a good effort just not having a good semester.

09:36 . Is that, does anybody else with that? Yeah, I got

09:42 gonna be treated the same. So, and yes, there are

09:46 where things happen but, you you may have to just either take

09:51 the drop or you can have, the medical, um, withdrawal is

09:57 option that's through e colon building, that. Uh, because that,

10:01 know, you may have a legitimate concern that I did your entire

10:05 So certainly take advantage of those things will help you out that way.

10:11 . And if you're not sure I , I might be able to lead

10:13 to the right resource for that. , um, anyway, so,

10:19 , so, you know, think these things if you take exam three

10:23 , and, you know, really Ok, so if you want my

10:29 , that's fine too. Ok. , um, so let me get

10:33 soapbox. Any questions about anything? . Any questions? All right.

10:41 , um. Ok. Uh, see, the usual stuff,

10:45 We have a weekly quiz this Yes, I know you got the

10:49 just, just do a weekly quiz , on Monday. Ok, after

10:53 completed the exam, um, so gonna finish up to 23. So

10:59 kind of a what we've been talking 7 to 10 gonna be really changed

11:05 , in terms of what we're doing . So we're focusing on uh aspects

11:10 , I guess clinical slash medical And uh so we look at it

11:24 from the body's perspective, OK? immune system, right? Um Then

11:30 look at the pathogen, right? we see how the body's various defenses

11:36 , you know, can, can help to overcome an infectious disease.

11:50 then finally, it kind of kind all comes together. At the

11:55 we look at different microbial diseases, ? And there you see kind of

12:00 . Here's what your body does. how they respond in these particular

12:04 OK. And so chapter 26 there's a, there's like a select number

12:12 diseases we look at, OK. If you, if you look ahead

12:18 look at the lecture notes for 26 see a list, there's a list

12:22 pathogens to know um to me that's of really heavily memorization of stuff is

12:28 part? Ok. And, um, but, you know,

12:33 things to know like a pathogen and disease does it cause? What are

12:36 of the features? Yada, yada , we'll, I'll talk more about

12:39 as we get closer. Ok. , um, ok, where are

12:45 starting here? Right here. innate immune system, right. What

12:51 are born with? Right, right of the gate, right? You

12:55 the ability to fight disease. Although a newborn baby, you don't have

13:00 same level as you know, as will when you develop a little bit

13:06 , but you do have of a skin obviously that that's a

13:10 Um but the uh in terms of , right? One's own immunity is

13:18 whole host of factors, determine, know, your resistance or susceptibility.

13:24 . So you got your innate immune , your adaptive immune system, which

13:28 your microbiome, right? Um How you are a number of factors,

13:35 ? What's your health at the time have underlying medical conditions? Do

13:39 do you um many infectious diseases you know, can vary depending on

13:45 gender, male or female. Um occupation. Ok. You can be

13:52 predisposed to certain diseases. Uh The of the year or respiratory infections occur

13:58 winter months. Um uh uh Have traveled somewhere? Right. So a

14:04 of different things, there's just a a lot of different things play

14:07 you know, when you come down something or not. Ok, age

14:11 well. Like young versus young and . Whenever there is a, some

14:16 of disease outbreak, the ones inevitably first die are those that are either

14:22 old or very young. Right. of, most of humankind in the

14:28 , you know, uh, relatively , have a better chance typically.

14:34 . And so we know that just you get affected, you don't necessarily

14:38 down with disease, right? A carriers, right? Those people,

14:43 right, are carrying uh, the and don't have any signs, symptoms

14:48 disease. Ok. So, so we have to deal with those

14:53 well. Ok. And a number human diseases outbreaks that occur, you

15:00 trace back to a human who's carrying . It has no symptoms of the

15:05 , meningitis, what you got, , vaccinated for before coming to school

15:10 , right. That's one of those where half the population carries it in

15:15 throat. And if there is an of meningitis, it's somebody some human

15:21 in the vicinity, it was the . Ok. So let's look at

15:25 question. This is any kind of that one of those before and

15:29 right? We're gonna see it again the end, but just see if

15:33 as you look at this material. , at all. And so basically

15:38 bunch, a number of terms will through, we'll get through all these

15:42 , right? I mean, c neutrophils, lymphatic tissue mucociliary can say

15:51 escalator. What in the heck is , you know, uh natural killer

15:56 , third line defense opportunistic path. . Is there something here that might

16:03 false? Ok. So your best . Well, there has to be

16:11 false when there's no other option here it because here you said.

16:34 Mhm. Ok. Let's count down 10 Smith. Do do do.

16:52 , let's see the picture of that . Ok. So let's move

16:58 We'll come back to this one in few, well, several minutes.

17:05 . Ok. Wrong way. Here go. All right. So one

17:11 I mentioned over and over again this and at various times was Chipotle.

17:17 . So there's a nice, would that be a readable? I

17:23 know. Anyway, nice looking avocado top of that. Ok.

17:28 but as we know with Chipotle, this can happen to you,

17:33 Ok. So that's why they came with this phrase. You can't spell

17:39 , right? Cio le spells. . So, um, so with

17:52 it was, and more than once bone outbreak related to, uh,

17:58 , you know, you might think , uh, wouldn't it be like

18:01 meat or something like that? uh, no, actually with the

18:05 , we'll talk about that later. , um, and again, it

18:10 more than more than one time. . And not most recent outbreak wasn't

18:15 long ago. OK. So this , this is just an example scenario

18:21 a infectious disease. We could look any infectious disease, you know,

18:27 , and we're going to see a of similarities, right? So we

18:30 a person who's sick, right? this person ate a burrito bowl and

18:35 four days later with severe diarrhea. . So she's uh been experiencing bloody

18:42 , telltale sign of an E coli . Dual sample tested positive for Shiga

18:48 E coli. That's the uh OK. And so like with any

18:53 signs and symptoms, right? So can be uh measurable, right?

18:59 a fever, you can measure a uh or more subjective like you feel

19:04 , right? You really can't put , put a number on that,

19:08 ? So there's always gonna be those of things with any, any infectious

19:12 . Ok. Uh Of course, any kind of G I tract infection

19:17 we've all experienced at one time or . Um You know what the symptoms

19:22 you get, you know, um diarrhea, typical, right?

19:27 it can get more severe, Is we do see blood,

19:31 So that's typically when toxins produced or cells in the intestinal wall, your

19:37 have a lot of blood vessels associated it, right? Because that's where

19:42 body picks up nutrients to feed your your cells. So you have

19:46 lot of blood vessels there. And toxins that are produced can affect them

19:52 you can get um uh uh blood . Uh and you know, the

19:58 symptoms of these kind of diarrheal diseases if you have severe stomach cramps,

20:03 know, abdominal pain, right? things like dysentery, right,

20:09 can induce those real severe symptoms. . Um So the uh cause,

20:16 etiology, right? So, remember Coke's postulates, right? So uh

20:20 coli, so you have to, know, detect, right, detect

20:24 uh with e with this uh E , you don't necessarily have to culture

20:30 identify but you can use immi right? Um Ogen, right.

20:35 that, look for that um duration severity, right? Any disease has

20:41 duration, um severity of disease. and you know, with this one

20:49 course, can last for several Um now we can have the pathogen

20:55 the virulence factors, right? So goes to, to determining severity,

21:02 . And uh the collection of virulence , how dangerous is it is a

21:08 to think of virulence. Ok. so the um uh these are the

21:14 of different things, right? It could be flagella, it could

21:18 FMRI it could be a capsule, could be a number of things,

21:22 ? Anything that enables it to cause , whether it's sticking to your

21:27 whether it's um uh um damaging cells to get into your body and hide

21:35 from your immune system. Many different of factors. Go ahead the

21:40 that's where you go to find Right. I mentioned mumps,

21:45 um meningitis. These can be found other humans. Humans can be the

21:49 for many diseases. OK? Um it can be many other things as

21:55 . Air water, soil, Transmission you gotta get from the reservoir

22:00 you, right? Insects is often a uh vectors. Insect vectors are

22:06 transmit uh or the mode of transmission the air through the water,

22:12 Depends. OK. So when we at the, and this is kind

22:15 what we'll talk about in chapter 25 microbial pathogenicity is the route all about

22:24 pathogen. So there's a source for . And so just think of the

22:29 as OK. I want to study . X. OK. Where would

22:33 go to find it? Right? could be another human or could be

22:39 , air uh um not air, not that often but water or

22:46 OK. Um Animals very common. . So whatever it is, there

22:51 to be some way of transmitting it you in various ways. Sneeze

22:55 Um um um the uh an what have you to a susceptible

23:02 right? And you of course, various innate and adaptive immune systems to

23:09 against it. OK. So the , if it's successful, we'll have

23:15 obviously answer you, maintain itself there your body. Replicate and more than

23:22 um and cause damage. Right. course, this is all due to

23:27 V factor. Ok. And so seriousness of any disease really relates to

23:32 the pathogen, what are three And what's your level of immune health

23:39 you will? So all of that to determine the seriousness? Ok.

23:44 so again, pathology is really the process. Ok. Um Pathogenesis is

23:54 the micro pathogen causing disease and the factors. And of course, with

23:59 disease process, you have changes to body, you know. Not.

24:06 uh yeah, in terms of um mild symptoms, maybe very severe symptoms

24:11 depends. OK. So let's look this question. OK. So

24:18 what I've just gone through, you pretty much use to describe any infectious

24:25 , right? So it will be associated pathogen, viral material protozoan.

24:32 . And it will have its mode affection, produce symptoms of different

24:38 Whatnot. OK. So we're basically start with as humans and our innate

24:47 system. OK. So it is which responds faster. OK.

25:13 Mhm. Mm OK. So the immune system responds faster because it's simply

25:30 , right? We're ready to your is here a physical barrier, mucus

25:35 lining your body cavities. It's, there doesn't have to do anything.

25:40 . Um That immune system requires more , let's say, OK. And

25:47 will explain why here in a OK. So the specificity versus the

25:53 . OK. That relates to uh the, in the innate adaptive immune

26:01 relies on recognition. So you have detect and recognize antigen. OK.

26:08 that's not a, something that happens . OK. So there's gonna be

26:14 time component certainly for adaptive immune system respond and do something. OK?

26:21 of that specificity. Um, the and the immune system doesn't have that

26:26 . So you can uh break it into two lines of defense.

26:33 In your innate imm system, I of the pathogens out here and it's

26:37 into you, right? What are various various um barriers it's got to

26:43 ? OK. So obviously, all right, if you inhale it

26:48 through mucus membranes, right? It's become a contact to that or you

26:53 , right? Either of those is be in involved in associations with your

26:58 membranes. OK. Normal microbiota, things you already have in and on

27:03 body, right? Your own those provide a definite um defense because

27:08 very well adapted to your body to particular micro environment that they inhabit in

27:16 body, you know, in and your body. OK. So for

27:21 just to come in and get them of there, it was not an

27:24 thing. OK. So their presence you. OK? Um Second line

27:32 . OK. So I look at as more specific cells that come into

27:37 and processes inflammation fever compliment. Uh are all processes that occur, complement

27:45 . Ok. Um What involves And the other thing that shown

27:51 but what's a vital component, a of in different ways are what we

27:59 uh cytokines? Ok. The cytokines here are chemicals, generic name.

28:09 describe the various chemicals that tell different system cells to do stuff,

28:15 That relate to these processes, So, inflammation is brought about by

28:21 cytokines and then they do certain things the process. So uh so you're

28:26 see that a lot in the section cytokines. OK. Um Guess how

28:32 get your cells to do stuff. don't do it on their own.

28:34 have to talk to them through right? Cytokines is how you talk

28:38 your immune system. OK? And adaptive immune system. So the third

28:45 of defense, OK. So T and your B cells and B cells

28:52 antibodies. T cells are kind of different types. Uh certain of them

28:58 of control the overall adaptive immune OK? And antibodies are certainly part

29:05 that. OK? But there's also functions beside that. OK. And

29:11 , uh but first and foremost is doesn't work unless they detect an

29:18 That's what starts the whole thing. ? Um Detect it and then

29:24 that's why you get the specificity comes the binding, specific binding to

29:28 OK. That triggers a bunch of steps OK. So, um

29:36 So that's kind of the overview Uh we're gonna take each one in

29:41 little more detail, some more than . Um And we'll go first

29:47 second line, next week is third . Um Chapter 24. OK.

29:54 , is that immune system? So look at this question here. So

29:58 relates to your microbiome and its role your immune system. OK. So

30:07 can thank your who for providing your . OK. That's an easy

30:22 Yeah. You OK. All Yes. These people oops. This

31:05 , this one and she's, those the mothers, right? Mothers?

31:10 you're that, you get your micro through that birth canal. OK.

31:16 , once you're out in the universe you begin to inhale, you need

31:20 eat food uh et cetera, then micro bota builds up. OK?

31:27 uh just gives you an idea of here, right? So um you

31:33 need to memorize that table, but the amount of microbes you have in

31:38 skin mouth gug I tract you see in the fourth to sixth uh

31:44 So CF us is basically they call forming units. Um But for

31:50 I just think of that cells. ? So 10 to 4 CS per

31:54 land, right? That's per sweat . OK? G I tract not

31:59 , you know, 10 to the per cubic centimeter, that's astronomical.

32:04 tell you how loaded your gut is microbes. Ok. Um So

32:09 you see the, the, the source here at birth canal, birth

32:14 , uh gut track, um surrounding environment G I tract baby formula,

32:20 , you know, you're drinking mother's , um the uh uh you

32:26 contact with, um, you ingesting looking food and whatnot.

32:30 So, um, so you're set , you know, with a good

32:34 of microbes and they've done studies on studies, you know, uh raising

32:40 completely devoid of any microbes, You can put them in these settings

32:45 they, they're on antibiotics, they have any con any microbes inhabiting them

32:51 inside them. Of course, in laboratory setting, obviously, and those

32:55 are sickly, they're not, they live very long. OK? And

33:02 the point is that they have a , right? Because they interact uh

33:06 , with your immune system cells boosting in different ways. Um Now,

33:12 we'd say they're found everywhere, you shouldn't have microbes in your brain

33:17 in your liver or other b organs signals something is not, right?

33:22 obviously, they live in other spaces and on your body. OK.

33:27 so it can vary throughout life. may move somewhere geographically that can change

33:32 microbiome, uh you know, periods you're sick and maybe you're on antibiotics

33:37 maybe chemotherapy that can change the balance microbes. So there's different things that

33:42 occur that can kind of change the sometimes. And um uh you

33:48 but you do kind of have a group of microbes that are with you

33:53 much throughout your life. OK. so this, this is an ecological

33:58 here, right? You may have , well, actually this is the

34:01 term competitive exclusion, right? The thing we look at microbes means the

34:08 thing, right? So you have two species can occupy the same niche

34:14 like the textbook definition, right? so uh one gets kicked out or

34:21 , right? And so same microbial antagonism is that so no two

34:26 species are gonna be in the same . Um It's in competition,

34:31 So you have, you know, you look at your body, you've

34:36 lots of little micro environments, Your teeth, in your, in

34:40 mouth, your teeth and your skin microbiome here versus what's in your

34:48 is gonna be a little bit right? Because the environments are slightly

34:51 little different. So, and and microbes are kind of adapted their particular

34:56 environments. OK? And so that itself helps keep unwanted things out,

35:02 ? Because it's gonna take a lot kind of outcompete them because they're they

35:08 create their own micro environment, To be anaerobic um particular uh ph

35:13 whatnot. And so it's not an thing to be an outsider and kind

35:18 sort of shop there. OK. we look at symbiosis in different

35:23 I'm sure you're familiar with this, relationship between the two. So,

35:29 and, and for the most your microbiome is comprised of commences and

35:36 types. OK. Mutualistic types, , where you both benefit, there's

35:42 of benefits of uh your microbes. um um uh can digest certain foods

35:48 you couldn't, otherwise they can produce acids and vitamins that you wouldn't otherwise

35:54 . Uh That's just a very small tip of the iceberg a lot more

36:02 they do for you. Um Commences much are just you try them at

36:08 more or less. Uh They, don't uh you don't really benefit from

36:12 but they're not harming you and that's commenced relationship. They do benefit.

36:17 But you know, a parasite that may have, obviously, it's not

36:22 you, right? So that's that minus uh relationship. OK.

36:26 so again, it's these commences and types that are pretty much your

36:32 but sometimes some, the members in group of your microbiome can become

36:41 OK. And that's generally when um , when they get access to parts

36:49 your body, they don't normally c . Classic example of that Staph

36:56 right? Staph live on your skin mucous membranes in your nose and maybe

37:00 have a cut or something punctual and they can get in there and that

37:06 lead to a infection, OK? a gut uh a gut microbe,

37:12 have some kind of a issue in gut and maybe they gain access outside

37:18 gut and then they cause infection. it's typically when um they're in a

37:23 environment through some means or um you're compromised, you, maybe you're on

37:30 and you kind of upset the balance . And so maybe that can cause

37:34 to uh be more disruptive if you , than they normally would be

37:39 So, but again, the opportunistic are already on you. OK?

37:43 only show, show themselves under certain . OK? Normally they're kept in

37:50 . OK. But the primary that's not something that's not gonna arise

37:55 your, from your microbiome. That's that you acquire, right? It's

38:00 to cause problems. OK. extreme example, right? You Ebola

38:07 not gonna be part of your micro , right? You're gonna have required

38:10 and it's, it's there to cause . That's the nature of a primary

38:15 . OK? Um OK. So we get into these uh barriers,

38:25 like basic, it's a little bit because the physical barrier also has serves

38:33 a chemical barrier. OK. for example, right, your

38:37 OK. Um obviously is a actually pretty formidable barrier. You have keratin

38:47 and protein that's part of that Along with your skin cells, skin

38:52 are very tightly packed together. You see that here. All right,

38:57 full of just epithelial cells. Top , sloughs off dead skin cells,

39:02 off together all the time. Uh you do have natural openings in the

39:06 where pathogens might be able to get like sweat glands, hair follicle,

39:11 kind of thing. Ok. Um subcutaneous infection of course is when the

39:16 is broken and the infection results but your mucus membranes because of course,

39:23 can s you ingest food, you breathe in, right? So that's

39:29 contact mucous membranes, OK? And um the in the mucous membranes,

39:36 course, you have different types of . So mucus is there to kind

39:39 keep tissues moist. Um the um but they can also act to trap

39:46 that are there, OK? Your and saliva, tears, you're constantly

39:52 tears over your eyes, that kind mechanical action can kind of sweep stuff

39:58 . Um saliva, you're constantly, swallowing stuff is washing over your

40:04 So that kind of mechanical action can disrupt something that's trying to colonize

40:10 hairs in your nose and Celia uh your throat. Uh again,

40:16 trap uh microbes, trap particulates containing , uh your mucociliary escalator,

40:25 That's actually a very important defense you when you, when you contract things

40:30 pneumonia, um whooping cough, uh respiratory illnesses is is because that becomes

40:38 . Ok. So it's really a defense against respiratory microbes, ok?

40:43 really a combination of both the mucus produce uh as well as Celia that

40:49 constantly moving in your trachea. And the mucus traps microbes.

40:55 Celia just to expel them out, ? And things can go wrong if

41:01 Celia themselves are impaired and now can't . And the, the, the

41:07 you produce is not of the right . If you will thickness, if

41:13 will, if it gets too, dehydrated, right, it becomes very

41:19 and it doesn't work as well. ? And so those are kind of

41:23 that can happen if you have an that can, that can uh affect

41:28 . Ok. So um other things the um epiglottis, earwax and

41:36 right? E even earwax has a right? To trap microbes in your

41:40 on obviously, uh epics covers your um digestion. So your intestinal wall

41:47 constantly uh contracting, moving material OK. Now, so again,

41:55 mentioned, so skin and mucus membranes be a physical barrier, but they

41:58 secretions as well, right? And the skin typically oily kind of

42:04 right? Uh low ph that that itself is an environment that's not hospitable

42:10 many things. Um mucous membranes of , gastric juice, low ph force

42:18 , slightly acidic. Uh But what's among a number of these is this

42:25 ? OK. You see this in number of different secretions that degrades cell

42:31 . OK. Specific for cell wall peptic I can OK. Um The

42:37 the defenses So this is kind of catch all name where you peptides that

42:44 act like straws to kind of poke into the membrane contents leak out.

42:51 that's uh and if you do something , I don't know, hundreds of

42:56 things, there are hundreds of different of these, various of your cells

42:59 them and release them uh to The net result is to basically kill

43:06 path. OK. Through, OK. Um OK. So um

43:16 . So, chemical physical barriers. this is a feature of various of

43:25 immune system cells. All right. this term mps used to be called

43:30 , right? It's kind of a term. Um these are basically uh

43:38 on the periphery of the pat. . What you see on the outside

43:43 flagellum cell wall, a cap and are what bind to specific receptors.

43:57 here you can see one that's part a a cell here. OK.

44:02 the pathogen and these TLR um right. TLR is toll like

44:11 NLR nod like receptors. So these just names that they he's been

44:17 Uh they were found uh in function , in a different um different

44:23 but they're also involved in this process well. Think of this as pulling

44:30 fire alarm, these alarm system. . So these receptors don't kill

44:45 OK. But they bind to these , OK. That are part of

44:50 periphery of the pathogen. OK? the binding. So TLRS are on

44:56 surface. OK. NLRS are OK? Because pathogens, obviously

45:05 a viral infection is an obvious one they go inside yourself. But we'll

45:10 learn that bacterial types can do that . OK. Um They can produce

45:17 as well internally. And so and put them inside of cells.

45:21 so these are things that can be by these internal receptors. OK.

45:27 whatever the case of activation. So one, the net result is

45:34 it triggers formation of cytokines. And, and the cytokines are of

45:41 types. OK? This is just a few functions you associate with

45:48 OK? To keep attractants, brain system cells to the site of

45:56 basal active factors, manipulating blood vessels the area. Uh We'll see in

46:03 inflammatory response, you need to get stoy cell types out of your blood

46:09 the surrounding area. You gotta manipulate vessels. That's what vasoactive factors

46:14 OK? Activate T cells that their system macrophages. So and again,

46:21 could add several more things to the , but they all work in,

46:26 , in really activating cells or immune . OK? Get them going.

46:31 , hey, I'm detecting something. get, let's get going. Um

46:47 let's see here. OK. Any at this point like chemical barriers,

46:52 barriers um to like receptors, not receptors. OK? So again,

46:58 is the alarm system. OK. next we'll get into kind of the

47:06 , 2nd layer. OK. Second , different cell types. OK.

47:10 look at this question. Adaptive immune . Cell types are that um looking

47:30 the cells of the, of the immune system or representative? Ok.

48:12 down. OK. Mm. it's gonna be lymphocytes. OK.

48:30 T and B cells. Ok. actually um natural killer cells are in

48:37 too. No. Um so we'll at uh we're focused on adaptive immune

48:49 in chapter 25. So now we'll on or 24. Excuse me.

48:52 we'll focus mostly on these types OK. Um OK. So when

49:01 look at blood and we centrifuge spin it right in a centrifuge,

49:08 get uh fractions of plasma fraction that your proteins, antibodies compliments and lots

49:16 other stuff. To be honest. your uh what we call formed elements

49:23 basically cells in uh red blood Erythrocytes is the formal name um

49:32 these aren't cells but rather fragments, involved in clotting. And um then

49:41 of course, are your leukocytes, blood cells. And so the term

49:48 sites, a granular sites. So still use, it's really just that

49:55 comes from the appearance of these cells a light microscope. OK. Um

50:02 just means that these three neutrophils, , eosinophils have you see these little

50:09 dots, basically lots of them in cells that represent these Granules and the

50:13 contain different chemicals that they release. . They're not as visible in these

50:21 . Although they, although they do , they have granular, they're just

50:24 visible like they are in this So that's, that's where the terminology

50:29 . Ok. So a granulocytes are which develop in the macrophages, dendritic

50:35 and lymphocytes. Ok. So, OK, so we'll start with the

50:42 granular acidic types. Uh So, are kind of your primary infection fighters

50:51 on in an infection. Ok. Pig cytosis is their thing.

50:58 Um This term polymorphonuclear, you can the, this is the nucleus and

51:03 broken up. It's one continuous thing , but it's nucleus, it's a

51:09 that's kind of it has different lobes it's all connected, right? So

51:13 a very weird looking nucleus. Uh that's the nature of these kind of

51:18 , right? Hence this term Ok. It's a very weird looking

51:24 there. Uh Anyway, they, are of course high percentages in your

51:28 . Ok. Um And this mentioned , basal active factors and they blood

51:37 . These are what you're trying to out of your blood to fight an

51:41 . Ok. Um Basophils, their is not pig cytosis. Their thing

51:47 releasing chemicals with different types. If you have allergies, you can

51:53 these cells and mast cells, we of giving a hyper response to different

52:00 . Ok? Because they release different types, chemical cytokines might involve

52:05 inflammation, et cetera. Ok. in low quantities in your blood.

52:12 . The Ain fills a little bit . 3 to 5%. But

52:15 um, they're p acidic. but their job is really dealing with

52:20 , pass by large. What do mean? I mean, like something

52:25 a worm. Ok. A parasitic , right? Wouldn't have an eyeball

52:33 that or even a mouth. But large, there's a large kinds of

52:38 kinds of um uh parasitic worms uh there uh even large protozoans. And

52:45 they do is they collectively come are to the large pathogen. OK.

52:55 these are eosinophils. OK? And are brought actually brought there through the

53:04 of antibody. OK. And so , we, we write like that

53:11 the letter Y, OK. That be an antibody and A B is

53:16 for antibody. OK. And so a cell type that can interact with

53:25 . OK. And so that's how get these ails to the site,

53:30 bind to antibody and antibodies is combined two ways. They can buy

53:38 The antigen A G is short for . But then the here to the

53:46 and eosinophil, a macrophage, a cell, they can also buy

53:52 But it's a way to get the types. You want to two the

53:59 , right? Because they're now binding antibodies that are stuck to the

54:03 So now you've got all these eosinophils and then they can collectively dump out

54:09 chemicals, their toxins and kill the . Ok. So that's what,

54:14 why we say they deal with large types that requires a collective effort.

54:20 the Ain is not gonna do you're gonna get a bunch of there

54:22 you can do that through the action antibodies. Ok? We'll also see

54:27 macrophages and dendritic cells also work with too um in a different way.

54:36 so uh so you're a gran acidic we'll talk about this will come up

54:43 with eosinophils in chapter 24 uh in context of antibody engine interactions.

54:52 Um And so uh your monocytes, . So these are in your blood

55:02 then they come out of your blood lymphatic tissue. So your lymphatic

55:08 yeah, fluid, your lymphatic fluid moved through gravity and muscle contractions and

55:22 vessel contractions, right arteries, for . Um uh but the macrophages,

55:29 cells, T cells B cells, environment is really lymphatic tissue.

55:37 And so monocytes come out of the into lymphatic tissue and they develop into

55:44 cell to macrophages. So, these a type that work with the adaptive

55:50 system. OK. And so this here of being for short, we

55:56 that a PC antigen presenting cell. . And that's how dendritic cells and

56:06 work with the adaptive immune system. . Um We just saw how eosinophils

56:13 that on a limited basis. But macrophages and dendritic cells, it's a

56:19 part of their function to work with the adaptive immune system as well.

56:25 . But they are major phao cytic types, dendritic cells, macrophages and

56:33 . Phagocytosis is their thing. Um And so lymphocytes, um so

56:42 killer cells are in there uh as as T cells and B cells.

56:48 this concept of different types of you gotta fight, right? You

56:55 that right here, intercellular and So your immune system, it's gotta

57:03 a way to deal with both OK? And so uh natural killer

57:10 can also deal with these types as . They attach to a host and

57:24 inside to replicate. OK? But too do different bacterial types, do

57:30 not for the purpose of using the to replicate themselves, but using the

57:36 to hide out, right? To be seen, you know, in

57:41 extracellular environment, right? That's, much less uh it's harder to find

57:47 if they're hiding inside of a right? Versus walking around outside.

57:50 that's what the strategy is for some patterns. OK. Um So you

57:57 to have a way to find OK. And so of course,

58:00 c patterns, they do their whole outside the cell, of course,

58:05 ? And so you have antibodies and phytic cell types, they take

58:09 of them. OK. So you to be able to handle both

58:13 OK. So this will bring us to this topic. Um So natural

58:24 cells are a type that look for cells. Uh They can be cancerous

58:31 . Um What happens is an infected can have changes to the surface.

58:39 . The surface molecules, the infection can cause changes on the surface.

58:45 all infected cells respond this way, many do. Ok. And they

58:54 will these changes? Certain cell types programmed to see these changes.

59:01 And to have a response to OK. And one of those is

59:07 profile of MH C molecules on the . OK. They will change.

59:13 so that's what a natural killer cells the lookout for. OK. So

59:18 cells also produce these changes. And we can, and so what

59:24 do is in response, they buy it. So, so if

59:29 if they're seeing this, it's like get it out no good. It's

59:33 fact, we gotta get it out the population. So they kill it

59:37 um secretion, oops through preference. , perforin perfer. So the perforate

59:44 means to basically put a hole in , contents leak out cell dies.

59:51 ? And so grand enzymes similarly have these digestive enzymes. Apoptosis is a

59:57 . Your cells naturally do as they and they accumulate mutations, other

60:04 You wanna just get them out of population, they're no good. So

60:06 the apoptosis is the textbook definition is program cell death, right? So

60:13 a, it's a the natural thing occurs, but you can have processes

60:17 induce it to occur and this is way to do it. OK?

60:24 When you get, if you've got sunburn and you turn red, your

60:29 is turned red and eventually the skin off, that's essentially apoptosis. Your

60:35 is getting rid of those sun damaged cells because they've mutated, get them

60:41 . And so you, you induce cells to undergo apoptosis. OK.

60:47 uh back to this MH CCS So if um one who gets a

60:59 tissue graft uh receives uh an organ , what have you, you will

61:06 an analysis of these molecules between donor recipient. OK? You have um

61:17 are what we call self antigens. think of it as a barcode them

61:32 your own selves. OK? Like zip code, so to speak.

61:37 . So if you come outside the code, then you're gonna see this

61:42 seen as something that's not supposed to there. OK? You wanna get

61:47 of it. So that kind of sets up the, the an

61:50 for example, would not have a non self engine would not have

61:57 right barcode. So your body goes doesn't match, let's do something,

62:02 get rid of it. OK? , and you have to have something

62:05 that in place. So how else you gonna know if you're being infected

62:09 something that's not supposed to be there you have a system in place that

62:15 your cells, tissues as your right? That's what these do.

62:20 . So the basic surface cell surface , glycoproteins, OK? Of a

62:28 specific sequence. OK. And um these are heritable. So you can

62:35 that you're gonna have self engines very to siblings, parents, right?

62:42 the whole basis for you know, typing or matching up tissues in a

62:48 recipient kind of scenario. OK. When somebody needs a kidney, who

62:52 you look to first a brother or , parent, family member,

62:56 So more close, closer in terms self. OK. Um So what

63:03 different class, there are two classes . OK. So I always start

63:07 the second class because that's the smallest , it only has three types,

63:11 ? Macrophages, dendritic cells, B , OK. Mh C class

63:17 So these are all antigen presenting OK. Um So this works with

63:26 T cells, recognize class two. also have T cells that recognize MH

63:40 class one. OK. And so are what we call cytotoxic T

63:47 We'll talk about this next time. don't worry so much about it

63:50 but this is where it comes Uh you have what are called helper

63:55 cells that work with those types. ? So it kind of sets up

64:03 different differentiation between the T cell functions . OK. And so, and

64:09 actually look for infected cells. So of toxic T cells look for infected

64:18 , kind of like how the natural cells do it just a different

64:22 Ok. And so nucleated mammalian right? That's basically your body cells

64:34 art A B cell, dendritic cell macrophage. Ok. And are not

64:42 red blood cell, red blood cells have a nucleus, OK? And

64:47 blood cells have their own system, ? The A bo the A bo

64:51 system, that's the self engines for blood cells, right? For everything

64:58 , it's this system, the MH system. OK. So this diagram

65:06 is showing you just a cell, M ac ays the surface.

65:11 Um And again, work with different of T cells, right? So

65:15 example, if you have a skin , a liver cell, a a

65:24 uh uh a a neuron, you know, name any kind of

65:30 cell other than a red blood cell infected, right? Then it's possible

65:36 T cell type here could recognize it get rid of it, right?

65:42 remember this is the guy, these deal with infect cells, right?

65:50 pathogens, right? And so um can be virus infected, right?

65:58 are lacking, right? Lacking M . So you don't see them on

66:02 surface, but it's not a hard fast rule, not all virus infected

66:09 will do this. Some do some . Ok. So, um,

66:15 , but, but you do, can't recognize some of these and you

66:17 get rid of it. Ok. cancerous cells may have changes.

66:24 So, uh in fact, big of study right now is to,

66:30 to stimulate your immune system cells to recognize cancerous cells that are affected like

66:37 . Ok. And use your immune to better attack those those cancerous cell

66:43 because not all cancerous cells will do either. OK. So, uh

66:48 again, dealing with different types of . OK. Um Any questions about

66:54 MH C molecules like your self OK. The thing that is your

66:59 code for your cells. OK. All right, lymphatic tissue.

67:08 So this um the system of vessels associated with your blood vessels. Um

67:20 come together at certain parts of your in very dense structures like armpits growing

67:30 uh tonsils, for example, in spleen are very dense areas of lymphatic

67:36 and full of full of the cell you see here. OK. And

67:42 those cells, cell types in those tissues come into contact with um air

67:50 breathe, for example, in your , right? You can have this

67:53 tissue there. Um food you ingest into your intestine, you have your

67:59 has layers of these areas of these lymphatic tissues, right? And so

68:04 cells there can deal with any pathogens may be present. So things you

68:09 ingest, et cetera can be dealt that. They're in your blood,

68:13 goes through your spleen cells in Lymphatic tissue can, can protect against

68:19 . So, uh it's a vital . You have your lymphatic system.

68:25 um from another standpoint, your blood are, is exchange of material

68:43 Ok? So nutrients come in, comes out and so that fluid that

68:52 , we call it interstitial fluid, ? But it represents fluid that's

68:58 lost from your blood cells or from , from your blood and you wanna

69:03 that, ok? And so you to collect that material, ok?

69:12 it travels basically through muscle contractions. blood vessel arteries of course, pump

69:20 well um or contract and that kind action moves it along. They kind

69:26 feel dump, dumps back in your up here around your collar bone on

69:32 side, collects back and dumps back the blood vessel, ok. So

69:36 how you kind of maintain your blood , ok? But again, lymphatic

69:41 is gonna have a lot of these types here of the skin and in

69:53 intestinal wall. So here for tires patches, right? These purple

70:03 , ok? Or where this dense tissue is at, ok? And

70:10 kind of show you a different view what they do is they will collect

70:19 . All right on these M cells on the other side, you'll have

70:25 , et cetera that will absorb Ok. So it's a way

70:29 to, to round up, so speak these potential pathogens. Ok.

70:36 And you have it in your skin well. Skin areas of your skin

70:38 the same kind of areas to, uh deal with um, pathogens as

70:44 . Ok. Um, ok. , oh, I think we're just

70:52 done here. So let's, let's, that's a good place to

70:56 actually. Figure, is there any so you can come up? Uh

71:02 can let you know, uh talk you. Uh We'll see you all

71:06 time. Pick it up with

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