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00:10 | Mhm. Hey, oops. Um get started here. He um, |
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00:30 | see. So I sent out an um, yesterday, basically tell you |
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00:37 | you do. So we got the quiz again this week, mastering next |
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00:43 | . Uh Let's see, what else gonna finish up 16 today. Um |
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00:48 | the second part of the in eight system, Thursday is the adaptive immune |
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00:54 | and we'll do a bunch of uh questions around that discussion. We'll |
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00:58 | we'll start with the very beginning of 17 at the end today. This |
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01:03 | kind of what you um the uh . So remember the Sky Group opens |
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01:11 | Friday. Ok. So we can a spot. Um, the exams |
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01:17 | , uh still a couple of weeks , two plus weeks away. |
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01:21 | um, certainly if you have questions , you know, material, |
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01:26 | let me know combining office hours, . What have you? Ok. |
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01:32 | Then, uh let's see, next we'll finish up, um, eat |
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01:38 | three and start, you know, the following week. Ok. Um |
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01:44 | we may, may start some of here depending on, you know, |
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01:51 | , I'm thinking that we only have come. So, class ends on |
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01:55 | , December 1st. I think We may not have to have class |
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01:59 | day if we keep on schedule. , uh, anyway, um, |
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02:07 | , oh, the other thing was grade. So I have calculated that |
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02:12 | be posted in the morning. I'm just about that but it'll be |
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02:16 | in the morning. So, I didn't do all the heavy lifting |
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02:20 | would do if it was a final , but it's good. It's, |
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02:22 | a fairly close estimate. Ok. I didn't go through and so like |
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02:29 | , like the, um, forget top, the top something, clicker |
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02:34 | or whatever a game. I didn't all that, but it's still, |
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02:37 | gonna be a close enough estimate for you need, what you need. |
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02:41 | uh it also includes the extra credit the, I assume I was gonna |
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02:46 | out the survey. I have to until you get extra credit for |
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02:49 | So that's figured in uh the isn't figured in, but you can |
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02:53 | just add a point or something to grade. So anyway, it will |
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02:56 | a close up for you now and , and the, you can look |
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03:00 | , I'll put it in the, email ahead of time where I post |
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03:04 | . Um But it just captured it really like exactly what it's written |
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03:08 | the sys, right? Just taking point on black board and just following |
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03:12 | 1234. OK. Um And uh was the other thing? The uh |
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03:20 | um I can't remember but uh um the scale. So it's a numerical |
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03:30 | obviously. And so you're gonna compare number to the scale that's in the |
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03:34 | on, on the, we talked the grade and stuff. I also |
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03:38 | to that scale in the email as . So that's what you're gonna compare |
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03:41 | two to get a Testament of your grade. Ok. Um All |
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03:47 | So, yeah, so watch out that and like I said, I'll |
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03:49 | an email out because of that, , in the morning. So, |
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03:54 | , let's see. So, I don't think the drop eight is |
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03:57 | 16th. Is that right? I the 16th don't hold me to |
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04:01 | but, uh, I just wanna you that information to make a decision |
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04:06 | you are, if you're thinking about . Ok. Um, and so |
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04:11 | can easily figure out because the question becomes, what do I need to |
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04:15 | on exam? Three and four, , blah, blah, blah, |
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04:18 | ? So you can do that you just plug in the plug in |
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04:21 | right? And that will give you least the upper upper range, |
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04:25 | So that's easy to do and just the steps that are in the, |
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04:30 | , that are in the exam, mean, in the. So, |
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04:33 | , so, uh, the, , ok, if you have questions |
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04:38 | let me know. So let's, , so we're gonna do, we'll |
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04:43 | with two questions and then uh a bit of a, it's a recap |
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04:50 | last time. OK. So let's here. So we talked about all |
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04:56 | these last time. Ok. uh take a look, um, |
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05:04 | is the true statement. OK. it's not 80 D obviously, it's |
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05:12 | F yes. And on, on , on F there, you're not |
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05:49 | see that on an exam, You have to identify visually what cell |
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05:53 | , but I just threw it in grins. OK. Cut them |
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06:30 | You. All right. Coming down six buy for your, it's gonna |
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06:52 | Yes, it is. C uh basophils, the primary foci excel type |
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06:59 | neutrophils initially, then followed up by um to like receptors. They don't |
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07:07 | anything, right? They're not a , they're a surface molecule that binds |
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07:13 | a pamp, right? And that cytokine release and the alarm bell. |
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07:18 | like receptors are the alarm system, to speak. Uh pamp is |
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07:23 | Um That's what that is the um um that's involved in think of that |
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07:31 | facilitated pags. So it's when it PAP is coated with antibodies are complemented |
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07:38 | that's taken in and it's for cells pathogens that aren't easily fis OKS are |
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07:45 | to them and C molecules. So , that's your, your barcode on |
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07:50 | cell and tissues. It's your self . OK. So we'll clarify that |
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07:55 | here in a second, just as recap uh leptos. These are actually |
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08:00 | uh neutrophils. They have that weird um nucleus. OK. So those |
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08:08 | blobs are uh it's DNA are Um But again, I'm not |
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08:15 | I just do this in just for . It's not, you're not gonna |
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08:18 | images where you have to identify the type based on just the image. |
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08:23 | don't worry about that, but uh a nursing kill, you have to |
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08:27 | that, but not here. Um . One more question before we do |
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08:32 | content here. So which virus infected might be dealt with by. So |
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08:38 | remember the extracellular pathos, intracellular pathos systems systems to deal with that, |
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09:12 | . OK. OK. Put the on. OK. Counting down six |
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09:52 | that it is going to be natural cells. OK. So those and |
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10:01 | up we haven't really now I talked little bit about it but uh certain |
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10:08 | cell types uh what are called cytotoxic cells. Uh but them and natural |
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10:15 | cells deal with infected cells. Um OK. So a little bit |
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10:20 | a recap here. So innate So that's what we're doing talking about |
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10:24 | 16, right? So think about . 1st and 2nd line defenses, |
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10:28 | line physical chemical barriers to remember your barriers like your skin because membranes also |
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10:35 | secretions and those serve as chemical They can take lysozyme is very |
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10:41 | Um The simply the the nature of secretion or maybe salt to your city |
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10:48 | , that it can be a Um second line defense. But also |
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10:53 | the first line I remember is is microbiota. So that also is part |
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10:58 | second line are typically cell types Um So inflammation we'll talk about |
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11:05 | Uh fever, these are processes of , can involve cell types for |
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11:10 | Um But uh no specific cells uh like they use of or release toxins |
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11:19 | things like that. So various types um um defenses to, to counteract |
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11:26 | pathogens. And so we talked in question about PMS, right? So |
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11:31 | are, these are the peripheral features pats, uh outer membrane. So |
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11:39 | flagellum. So things on the external of this um pathogen. OK. |
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11:46 | to the sector combined. Uh and effect is to cause these of cytokines |
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11:51 | these are gonna alert cells, they're bring cells to cy of infection. |
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11:55 | can uh have varied effects. Um uh The uh we'll talk a |
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12:02 | about cytokines today in the context of response. There's a lot of those |
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12:07 | here in the inflammatory response to, do different things. OK. Um |
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12:14 | there's uh OK. These are the types. We went through these |
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12:19 | Uh each have different roles and basal are mostly um kind of releasing release |
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12:24 | different types of chemicals and cytokines. involving the inflammation and other processes. |
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12:32 | and figures at times. But their is also toxin producers. But to |
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12:36 | uh to really deal with large monocytes differentiate the macrophages uh in lymphatic |
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12:44 | . So, lymphatic system is about pro protecting against inhaled ingested microbes. |
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12:51 | your tissue can be quite dense in parts of your body and these are |
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12:57 | of macrophages, uh B cells, cells to, to help fight |
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13:02 | Um And then uh let's see what ? Oh Here. So then uh |
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13:09 | aosis oxidization, right? So we'll about these today. We haven't gotten |
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13:13 | yet but uh just quickly on the C. So this is important because |
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13:20 | your ability to recognize something has an that shouldn't be in your body can |
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13:28 | occur if your body knows and differentiate what's yours and what shouldn't be |
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13:37 | And of course, it occurs through occurs through biology occurs through molecules of |
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13:41 | type. And so self antigens are of like your barcode to identify yourselves |
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13:47 | your own. OK. So if comes in that doesn't have that same |
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13:50 | code and that's a trigger. And that's what can um uh alert |
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13:56 | immune system cause different effects. So have that system is broken down into |
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14:04 | types depending on the subtype. So I always do two first because |
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14:10 | the easiest, it only has three , right? It has B cells |
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14:14 | and dendritic cells. So the cell that are called antigen antigen presenting |
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14:19 | they show antigens to the body. . That can then respond different |
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14:25 | respond to them. Uh So everything that's not in that group is am |
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14:31 | one is basically all your body Ok. Uh Not red blood |
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14:36 | they have their own system. That's A bo system, their system. |
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14:41 | ? But everything else that's not a two is a type one. |
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14:45 | And so, um and so we'll , as we get into the adaptive |
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14:50 | system, you have certain of those interact with these types of C |
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14:57 | others interact with these. OK. that's what kind of differentiates their function |
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15:03 | talking about different types of T cells with these two. In fact. |
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15:09 | it, it'll, you know, keep repeating this and it will become |
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15:12 | as we go through. Um but then we see engines uh here |
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15:16 | just on the surface of the they originate inside the cell. Of |
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15:20 | , they can, then they can we can see molecules inside that are |
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15:26 | and they combined a viral piece, ? That's a piece of a virus |
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15:35 | of uh another bacterium. Sometimes bacteria enter into the cell and, and |
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15:43 | out. So maybe it's a piece that and it goes to the |
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15:46 | right? And now the immune system detect a G is for an |
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15:53 | can detect. Oh, here, it goes to the surface and now |
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15:57 | shown to the body, well, inside, it's invisible, but once |
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16:00 | gets in the outside then other immune cells can respond. A T cell |
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16:04 | respond or what have you. And that's how you can find out |
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16:09 | going on in terms of your immune . Uh, or you can have |
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16:13 | like this. Right? And um, you know, infected |
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16:18 | cancer cells can have different appearances on surface. OK? Maybe they lack |
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16:24 | C molecules altogether. That's what natural cells look for. So they, |
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16:29 | that tells the body, it's, not normal, it's abnormal not to |
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16:32 | MH CS on your surface. So infections like a viral infection, not |
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16:38 | but some can cause these changes to surface. Certain cancers, certain cancers |
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16:43 | do that. And so that's what metro curro cell looks for. Uh |
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16:48 | another type, don't worry about Now, what, what's called the |
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16:54 | T cell? OK. These two for uh um uh infected cells are |
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17:01 | showing antigen, OK, through their C one mole. And that's the |
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17:09 | there. And so it, it varies and an affected. So |
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17:15 | depending on the viral type and it will um have different responses. |
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17:21 | may be like this where a lax now cytotoxic natural killer cell may be |
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17:25 | the lookout for it or maybe it have that response and it, and |
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17:29 | does have MH C ANS on but they show a, a part |
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17:35 | that infecting organism as in on the . So you have cyto toxic T |
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17:41 | , I can recognize that we'll talk that in 17. But this over |
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17:45 | worth mentioning. So the point is got multiple ways to deal with different |
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17:50 | of infections. OK. But there a, so this is a, |
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17:54 | an intra cellular. Yeah. So on the inside in try cellular |
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18:13 | So you have to have a way deal with those and those that are |
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18:15 | the outside. So I need coli here foodborne illness, right? So |
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18:22 | have both, obviously, both can you and we have ways to deal |
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18:25 | those. And we do, we specialized cells that can deal with each |
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18:29 | . OK? So you do have lot of defenses. I mean, |
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18:34 | mentioned what I did earlier, the chemical bears etcetera. So we got |
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18:37 | lot of stuff going on that can happens. Uh it's gonna happen that |
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18:41 | be triggered in the course of an . OK. Which is all good |
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18:45 | you. Um Any questions about So engines OK. Um OK. |
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18:53 | then lastly ptosis optimization. Uh so remember, you know a a |
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19:00 | macrophage uh as part of the process also have. So this is a |
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19:06 | of tiny writing but that's a total receptor TLR for short, right? |
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19:10 | so that can the macrophage can not engulf and ingest and break it |
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19:17 | but in the binding part, it , you know, have a tool |
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19:21 | receptor and cines to alert more cell um these uh once it gets crunched |
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19:29 | , right? So this is the zone, then fuses with a Lysa |
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19:33 | , right? And so then it digested, that material can exit. |
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19:38 | , but also we have, this have MH C molecules, OK. |
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19:43 | A macrophage, if that's what it , would be a type two. |
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19:47 | . And so it will bind to of these particles. OK, then |
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19:52 | it c two antigen and then this be um, the, a part |
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20:03 | a virus or whatever crunched up in and show it to the body and |
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20:08 | it's visible to the cells of the system. OK? That's what |
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20:13 | that's what the antigen presenting cell OK? Shows whatever digested to the |
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20:19 | . So the immune system can respond needed. May, maybe it's |
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20:22 | maybe it's, if there's no response it's not, not a threat, |
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20:25 | maybe it is. So that's, to be determined by the cells that |
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20:30 | with it. OK. And then is the ization. All right, |
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20:35 | have the pathogen here and it's coated these little yy shaped thingies or |
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20:44 | OK. So, antibodies by antigen that's what it's doing. And so |
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20:49 | have these, these parts of the bind to the pathogen, right. |
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20:59 | part combined to a cell like a to different body parts. And so |
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21:09 | so optimization accounts for those pathogens that easily fit because they're slippery like a |
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21:16 | a thick capsule or something. So have antibodies to it or complement is |
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21:21 | other one. So are both s complement and antibodies coat the cell that |
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21:27 | it easier to bring in the The fig cytic cell can bind to |
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21:32 | antibody or complement and bring the whole and digest it up. OK? |
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21:39 | OK. I think that was most the stuff. Any questions? |
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21:44 | So a little bit of a Um All right. So here's so |
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21:51 | first process I guess you'd call it gonna talk about is uh inflammation. |
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21:57 | ? And there is a stepwise process that. So take a look |
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22:01 | So what should be, it's really first and all these occur in |
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22:06 | But there's one thing, it's really happen first and it's gonna trigger each |
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22:11 | the next steps. OK? The are going, all right. Count |
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23:15 | from 321. Yeah, it's set kind of release is gonna be first |
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23:25 | sets everything else in motion, So let's see. Set of kind |
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23:30 | is one, any guests on number or let her at me d that |
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23:46 | , yep, it's deep. Then get mm Let's see which one is |
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23:56 | better before they can exit. They to stick. All right, give |
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24:04 | three. They're not exit. Then actually the egg actually contributes, contributes |
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24:12 | the swelling and then we fix everything , repair. It could be like |
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24:17 | scab or something like that. So, uh so we'll go through |
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24:22 | . So obviously, um a lot cytokines are involved in inflammation. |
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24:27 | And so as we look at um we've all had this at some |
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24:33 | or other, maybe we have it now. We have inflammation right |
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24:37 | ok. Um The um, it be fairly simple from, you |
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24:43 | you had a splinter in your finger something or a paper cut maybe and |
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24:47 | slightly infected. And so now it , right? Makes a red, |
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24:51 | blotch and it kind of hurts and the warm to the touch or is |
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24:54 | normal part of the inflammation. So, um, so first inflammation |
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25:02 | meant to the response is meant to the infection where it is encountered, |
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25:09 | ? So, again, if we the example of a splinter, |
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25:12 | it gets infected. So the inflammatory is meant to contain it right there |
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25:17 | that spot that it spread. Two is the um the main infection |
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25:26 | cells in the beginning are your right? So, neutrophils are circulating |
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25:31 | your blood. So the the infecting aren't gonna be in the blood. |
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25:37 | , they're gonna be somewhere in the tissue. Ok. So that means |
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25:41 | have to get the cells neutrophils out the blood into the surrounding tissue. |
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25:47 | , a big part of inflammation is is getting that to happen. |
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25:51 | Which means you're going to um make vessels more in the area. So |
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25:57 | , it's a local thing, you're make blood vessels in that area more |
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26:01 | , more permeable, so they can out, ok? So that's what |
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26:05 | to a number of things the redness see in your inflammation, the the |
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26:12 | that occurs because of course, not does red blood cells come out but |
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26:16 | fluid of the blood comes down as . That's why it causes the swelling |
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26:20 | uh it feels warm to touch, , often pains associated with it. |
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26:24 | these all these are all normal Ok? So, of course, |
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26:29 | last step is let's depending on the of the damage, fix it right |
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26:34 | blood um to form a scab perhaps kind of things. Ok. |
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26:40 | um the chronic, we're talking this is about a acute, the acute |
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26:47 | response which means, you know, occurs over a period of 5 to |
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26:51 | days. Ok. Then you're done there. Chronic is when it |
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26:55 | over and over again. Ok. like a very typical is intestinal |
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27:02 | So, if you have food um uh these can constantly be triggered |
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27:07 | inflammations in your, in, in gut and you get these, this |
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27:12 | occurred over and over again, over periods of time. So, uh |
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27:15 | , that can take its toll on body, of course. Um But |
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27:19 | focused on the acute observatory response So, uh among the, a |
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27:25 | of cytokines are at least, um you're bringing together a number of different |
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27:31 | , you have to work on the vessels to make them more permeable. |
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27:35 | make them bigger generally as well. have to get various cell types to |
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27:39 | site. So a lot of these are involved in doing that. |
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27:43 | The tinary process factor is one of a cell that's damaged will release this |
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27:48 | that can be often be the first of. OK. Uh Something's not |
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27:53 | here. Let's let's cause let's get going. So we can take care |
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27:56 | this potential infection perhaps, right? the uh in two necrosis factor works |
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28:03 | different parts of the body, especially the liver and it causes liver to |
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28:07 | things that are called acute phase Among these actually is compliment. Um |
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28:13 | one of those as well as some . Um And so the stages, |
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28:18 | , as we look through this vasodilation the manipulation of blood vessels. |
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28:24 | To make them bigger, actually dilate bang uh py migration. So getting |
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28:32 | out of the bug into the tissue fatties pathogens and then of course |
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28:39 | Ok. So um sure example, again, this is kind of the |
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28:45 | example of a uh a puncture a splinter or something where uh there's |
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28:51 | on it that are infecting. So call subcutaneous um infection. Um And |
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28:59 | here's a section of the skin, see, and we're gonna involve different |
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29:03 | types. OK. So again, one of histamine and kinds, |
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29:07 | So histamine is one of those that on the blood vessel. OK? |
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29:12 | what that means is we are going take a blood vessel in the area |
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29:17 | initially looks like that. Ok. this would be the, this top |
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29:21 | is the skin, the upper layer skin, ok. Skin surface |
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29:28 | Ok. And there's a blood vessel . Ok. So the action of |
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29:32 | among others used to dilate it, gonna make it bigger, right? |
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29:38 | it gets closer to the skin surface the skin. And that's where you |
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29:41 | the reddish kind of color comes from it feels warm to the touch, |
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29:45 | ? And so what it also does it will increase the volume of blood |
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29:51 | that area. So, remember remember is local, localized response, |
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29:56 | So with blood vessels in that area will die. And then, so |
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30:01 | of uh a water hose and you your finger on top of the |
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30:07 | your, your resist resistance to right? You're, you're decreasing G |
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30:11 | if the water can come out. if you make the hose bigger if |
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30:15 | could, right, you'd be slowing the flow of blood in that |
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30:21 | Uh, plus being bigger, more volume in the air. Ok. |
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30:26 | so, uh, and you need slow down the blood flow in the |
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30:30 | because remember you're trying to pluck out neutrophils that are coming through, so |
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30:35 | wanna slow down, they make them they'll begin to, uh, stick |
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30:40 | the blood vessel wall and squeeze OK. So that's reasonable for, |
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30:45 | , you know, in the local to, to increase blood flow by |
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30:49 | it bigger and slow and consequently slow flow down. OK? To facilitate |
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30:54 | exit of these neutrophils. OK? so uh kind itself also part of |
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30:59 | process is to um take the cells make up the blood vessel, |
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31:07 | And kind of pry them apart. ? Because remember that's you gotta mix |
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31:12 | between the cells so you first can out, ok? And so that's |
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31:16 | kinds do, OK? Um You other leo trying and things that kind |
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31:22 | contribute to the same process because there's just histamine, but the other chemicals |
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31:26 | act as what we call vasodilation That's what we're talking about and we're |
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31:31 | it big right up here is His toy can do that as well |
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31:37 | other, other side. OK. so um prostate glands. Ok. |
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31:45 | , uh so here up here, foot actually damaged, physically damaged cells |
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31:50 | the area and that can trigger release that tumor necrosis factor. Then it |
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31:56 | travel, getting the blood travel to liver and then cause uh formation of |
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32:01 | other specific proteins. But also you have macrophages just floating around here that |
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32:07 | , that can bind to these right PMS and that can elicit cytokine production |
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32:11 | well. And so that all all get cells to the site uh to |
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32:16 | histamines, et cetera. And so not sure you animation show this as |
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32:21 | . Um So prostate madness though uh , are, are are released and |
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32:28 | were my nerve end engineering, Because you wanted to be alerted to |
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32:31 | something's happened to you, right? you know that oh I'm having an |
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32:35 | , I need to clean this We so alert you to that there |
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32:38 | something going on there. OK? what happens is these um these uh |
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32:49 | area so I can't get hit But, but what happens is let's |
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32:53 | show the picture here. OK. here is the blood vessel in the |
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32:59 | . So we we would have they were gonna kind of pull the |
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33:04 | that make up the blood vessel apart little bit. So they can squeeze |
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33:07 | . As you see, this neutrophil rolling down along the side of the |
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33:12 | . There's actually little um uh uh help promote the uh release of these |
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33:20 | surface molecules that kind of act like to kind of stop the neutrophils to |
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33:26 | them down. Those are rolling Ok. And then, then the |
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33:32 | uh cytokines kind of pull apart the of the blood vessel and that's how |
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33:35 | squeeze through. So the um the uh squeezing through is the diapedesis. |
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33:43 | . The kind of slowing down while stick to the surface before then is |
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33:47 | margination. So, margination is kind , they stick to the cell wall |
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33:51 | they squeeze out. That's the ok? Um Now, uh so |
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33:59 | it's so, so as the neutrophils , right, exit the blood |
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34:03 | of course, you're gonna have other come with it. It's not like |
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34:06 | filter where only, only the neutrophils out, other stuff comes with it |
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34:10 | that's what contributes to the, the . Ok? And uh then of |
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34:15 | they're there in fighting infection. So have ptosis. So after a while |
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34:20 | have what conforms pus pus is basically your white blood cells, some of |
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34:26 | are still alive from the dead, cells that they, they die. |
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|
34:30 | it's kind of collection of all that . Ok. Um And then uh |
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34:35 | that's followed, of course, by and you may have some, depending |
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34:40 | the severity of the injury. You have some lack of movement, maybe |
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34:45 | your movements impaired in the area or functions impaired until repair occurs. The |
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34:51 | part is basically uh can be um cell division to replace the cells, |
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34:58 | blood, uh scab formation, these of things. And so that leads |
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35:03 | a what you see right here, can only lead eventually gets it clears |
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35:08 | and back to normal. OK. let's um I'm gonna show this |
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35:16 | Uh I'll come to this one in second. Uh Let's look here. |
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35:26 | . So there we go. So is that's gonna be the same splinter |
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35:33 | of uh example here. So you your vocabulary in the area. Villa |
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35:38 | super tiny, uh one cell your red blood cells and mixed in |
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35:43 | you see some neutrophils there, all white blood cells. So here's macrophage |
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35:48 | here's the subcutaneous wound pathogens, here macrophages in the area. So remember |
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35:56 | fixed macrophages, right? These these be sitting here just hanging out. |
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36:01 | they have release of cyto contrast. that's the PTLR effect, right? |
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36:06 | among the cytokines will be histamines et cetera. So we'll blow that |
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36:13 | up. So here are cells that up the buzz vessel, OK? |
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36:17 | for endothelial cell, then you have uh uh white blood cells will have |
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36:23 | cells have these kind of glycoprotein of on the surface. And some of |
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36:27 | are meant to, here's how it it down, right? It's rolling |
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36:30 | , all right. And um then we have to break apart these |
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36:36 | right? So don't worry about the here integra. Uh but these are |
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36:41 | molecules and they interact with blood cell called ICANN to kind of help slow |
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36:46 | down. Kind of analogous the velcro to those cells. And um then |
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36:55 | have the effect of a Brady Yeah, that helps break apart the |
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37:00 | between these cells uh temporarily, at so that they can uh slip |
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37:06 | So the sticking part is kind of margination that what you just saw is |
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37:11 | diapedesis or squeezes through. Ok. now they can get into the surrounding |
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37:16 | and they can do their thing. use the size. OK. |
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37:21 | and then of course, uh or come out and so you have more |
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37:27 | , more histamine to kind of continue dilation effect and the, and the |
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37:33 | and they have mass cells in the that all are triggered the youth hisam |
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37:36 | , all to work on a blood causing dilation it. But then you |
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37:40 | the background kind of fill up, a flu. So it's growing up |
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37:44 | the area. Um And so the but again, this is classic |
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37:52 | right? They work on the nerve to heighten the sense of pain in |
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37:56 | area. And so you get your basic signs like redness, warmth, |
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38:03 | , swelling, you can all the . So uh that's like inflammatory |
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38:10 | acute inflammatory response, right? Um uh any questions about that? So |
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38:23 | when this, when this can become uh bad for you. OK? |
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38:28 | if um you have a, so talked about endotoxin before I grab negative |
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38:34 | so that they lice and that materials that the material that cause a |
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38:40 | Uh It's when you have a a think it has an inflammatory response that's |
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38:44 | , not just they look less area body wide, right? So if |
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38:47 | have a very negative infection in the , right, then potentially all the |
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38:52 | in the much more cells in the can respond to this thing rather than |
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38:56 | being a local effect, right? so knowing the effects of inflammatory |
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39:01 | dying in blood vessels, right? If that happens on the body wide |
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39:06 | , now you have blood vessels that gonna be, you know, being |
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39:10 | and it's the flu coming out and blood volume will go down as a |
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39:14 | because it's happening body wide, not locally and that's when you can go |
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39:18 | the shot. And now you're using blood volume from numerous blood vessels in |
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39:23 | body and uh blood pressure goes Um et cetera. So not a |
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39:29 | thing. So, so a body inflammatory clots is something that's very dangerous |
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39:33 | that happens. Ok. Um and endotoxin is one of those that can |
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39:38 | this um ok, uh fever, ? So, fever is again something |
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39:49 | all experienced. Um So it's really a resetting of a temporary resetting of |
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39:58 | body's thermostat. Ok. So, , hypothalamus is what controls your body |
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40:05 | . And, um, the, thing that will adjust the, |
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40:12 | um, set point. So normally set point is at around 3738 or |
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40:19 | , plus or my half a degree so, uh, we're all a |
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40:24 | bit different but, uh, it's within that range. Um, |
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40:29 | uh, and so what happens is triggers it to, to, to |
|
|
40:35 | ? Ok. And so pyrogens are chemicals that cause fever. Ok. |
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|
40:40 | can have what's called endogenous or exogenous . Ok. So outside the |
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40:46 | these are things like bacteria, viruses , they come into your body and |
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40:50 | trigger endo endogenous pyrogens. So, you produce like introducing one or IO |
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40:59 | , please act directly in the OK? And turn the set point |
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41:04 | up and so, so a psych cycle if we take 37 C as |
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41:12 | set point. Ok. Um So of pyrogens, uh can elevate |
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41:19 | Ok. So if we go up say 40 give or take, um |
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41:25 | shift to a higher set point. . So much like if um your |
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|
41:32 | , when you go in front of house and you turn your thermostat. |
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41:36 | . Um Are you going to immediately capable? You're gonna feel cool for |
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41:43 | while, right? Until you're, that temperature gets to, to the |
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41:49 | , temperature gets to what you said , right? So, So the |
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41:52 | in your body, it's not So you turn a thermostat up in |
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41:56 | body, it takes a bit for body to catch up with that new |
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42:02 | point. And so until you you're gonna feel chilled. Ok. |
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42:08 | Typically what happens is you kind of between chills and sweats, chills and |
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42:14 | . Um because that, um that points kind of going up if you |
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42:21 | of feel, feel the effects of as it goes down, your body |
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42:25 | not, your body is at this set point, but it goes down |
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42:28 | little bit and it takes a while readjust, you're gonna feel hot until |
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42:32 | get to that new set point. that's why you go kind of typically |
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42:35 | through oscillating high and low chills, and uh and uh sweats, |
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42:41 | Until finally, you, you overcome infection, fewer breaks and you go |
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42:48 | to your normal set point. Um Now you obviously, even, |
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42:54 | though you o up your, when uh set point is increased and your |
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43:00 | catches up with that temperature, you don't feel it obviously. Um but |
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43:05 | is serving a purpose. OK. the most obvious is probably, you |
|
|
43:10 | , pathogens that affect our bodies, pathogens. Um You grow them at |
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43:16 | degrees in, in the lab, ? So that's your body, that's |
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43:19 | they're used to. So if you that, that that will affect their |
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|
43:23 | growth rate. OK. So it that, but probably more importantly, |
|
|
43:29 | uh helps your immune system. So uh increases T cell activity. |
|
|
43:34 | one of the things about your adaptive system, right B cells and T |
|
|
43:39 | , they, they, they take , OK. So they have to |
|
|
43:46 | and, and they have to respond antigen and that's, there's a time |
|
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43:51 | to that. OK. And so you can buy time to help them |
|
|
43:57 | , that's in your favor. And slowing down pathogen growth, retriver is |
|
|
44:01 | of those ways. So it, slows them down but enables your T |
|
|
44:06 | and B cells to find them and the engine and then do their |
|
|
44:10 | OK. So T cells as we , um a particular T cell type |
|
|
44:16 | very, it's kind of the master the whole, the whole thing, |
|
|
44:20 | ? Because there are B cells that to activated by T cells. B |
|
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44:23 | make antibodies and T cells kind of with in intercellular pathogens. So, |
|
|
44:29 | the whole system is kind of regulated certain T cell types and you increase |
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44:33 | activity to do this during fever. . And then iron uh again, |
|
|
44:40 | really goes back to thinking about right? What's needed for growth. |
|
|
44:44 | . Iron turns out to be a essential element for pathogens. OK? |
|
|
44:50 | for all life. But I uh you kind of fight with them |
|
|
44:54 | , over um the, the availability iron, right? You, you |
|
|
44:58 | many different ways, certainly through right. Hemoglobin, finding oxygen is |
|
|
45:04 | big source of iron, but also types as well. So you have |
|
|
45:08 | definite need for it and you need hold on to it. So, |
|
|
45:11 | you keep it away from pathogens that's affect their, grows as well? |
|
|
45:17 | , um, so fever does uh, definitely has a, a |
|
|
45:23 | in, in your innate immune which is still down to growth and |
|
|
45:26 | mobilize your adaptive immune system. Um, you know, too high |
|
|
45:32 | t, too high A T is not, that is detrimental. |
|
|
45:37 | ? Because your body can't sustain that something that's like 101102, you |
|
|
45:41 | that's sustainable. But uh but not you go with a 405 that's |
|
|
45:46 | your body can't function uh very well that. Ok. And obviously you |
|
|
45:50 | do something about that. But for of us that go through a typical |
|
|
45:55 | , you know, it's one that fever 101102 is, is typical. |
|
|
46:02 | . Uh For so compliment, so , um, is our protein factors |
|
|
46:12 | are not complement, are not a type? Ok. They're, they're |
|
|
46:17 | just proteins that are floating around in blood. Ok. And uh unless |
|
|
46:22 | until you're, until you have an , compliment is in an inactive |
|
|
46:29 | Ok. So there's ways to activate to make it do its functions. |
|
|
46:36 | ? And there are three ways that be triggered. Now, there are |
|
|
46:40 | bunch of proteins that make up OK? Uh But it really boils |
|
|
46:46 | to these, the C three and five, those when those get |
|
|
46:53 | that's generally when most of the action a compliment. OK. So |
|
|
46:59 | there's like 20 of these things that inactive and it's like a cascade |
|
|
47:04 | So, uh for example, C , you see there is inactive, |
|
|
47:09 | activated by I think C two, is from C three A and B |
|
|
47:15 | then activates five right into C five and B and it kind of goes |
|
|
47:21 | going. So C six activated in and 89. So that's, that's |
|
|
47:25 | you mean by cascade chain reaction. it's when these are activated. Like |
|
|
47:31 | said, that's when most of the occurs. OK. So um like |
|
|
47:37 | you have certain cell types that work the adaptive system, macrophages Andri cells |
|
|
47:43 | also work with the immune system. . So remember uh well, complement |
|
|
47:50 | classical path. This is the first bound. OK. So simply binding |
|
|
47:57 | uh a uh an antibodies activated. . You see antibodies bound here. |
|
|
48:04 | . And there's a compliment factor. so anybody binding to a pathogen, |
|
|
48:09 | compliment that activates the uh antibodies Now the effects you see here. |
|
|
48:15 | . Optimization cytolysis inflammation, those three when the compliments activated are the |
|
|
48:24 | But however, it is activated. are the three outcomes. OK. |
|
|
48:28 | , antibodies is one way to Um another way is to bind to |
|
|
48:34 | cell surface glyco lid. So, um have these old on surface. |
|
|
48:44 | . And complement can, can bind these. OK? And that in |
|
|
48:49 | can trigger the activation. OK. And then lastly is what I called |
|
|
48:56 | . OK. So, lectins are one of those Uh I mentioned |
|
|
49:03 | , tumor necrosis factor uh can go the liver and that can create the |
|
|
49:08 | to produce one of these c reactive . And, and uh lectin is |
|
|
49:14 | of those. OK. So, by it's very common uh nanos and |
|
|
49:21 | types of sugars are, are commonly on bacterial surfaces. OK? So |
|
|
49:27 | , that's what they find. And so uh that they can trigger |
|
|
49:33 | activation. OK. So um and again, the outcomes, you see |
|
|
49:38 | three outcomes here, ization, cytosis . So it's the same, the |
|
|
49:42 | three outcomes occur regardless of how it's . OK. So what are |
|
|
49:46 | what we know optimizations? OK. the, it's just uh like antibody |
|
|
49:52 | be a cell, the cell and cells can take up the pig cytic |
|
|
49:58 | can take it up. OK? cytolysis. So this you see here |
|
|
50:08 | complement proteins come together to form these channels in the cell membrane. |
|
|
50:14 | And basically the stuff leaks out of cell killing it OK. That's what |
|
|
50:17 | call a membrane attack complex. Maybe I put these complement proteins. |
|
|
50:23 | This is more effective with gram uh . OK? Because gram positive we |
|
|
50:32 | a couple of lighting cell wall OK? And so these don't really |
|
|
50:38 | into a cell wall, they fit a membrane. And so remember that |
|
|
50:43 | have a outer membrane layer. That's they're more susceptible to this kind of |
|
|
50:47 | . OK. And then uh is the uh inflammatory response. So |
|
|
50:54 | can um bind two cells in involved inflammatory response, releasing a histamine. |
|
|
51:02 | kind of enhance the uh th for response by producing these, triggering the |
|
|
51:08 | of these cytokines. OK. So , all three of these are are |
|
|
51:14 | of activating compliment no matter how it's . OK. Um And then uh |
|
|
51:21 | see interference. So, interferons uh think we talked a little bit about |
|
|
51:27 | in uh but they're a defense against . OK. Anti viral defense. |
|
|
51:33 | so we have different classes. Type is the one that's anti viral. |
|
|
51:40 | . And so how it works is this. OK. So you have |
|
|
51:46 | virus infected cell, OK. And have uh um that infection itself is |
|
|
51:55 | triggers the formation of uh interferon, . Iron effect and triggers that and |
|
|
52:07 | any neighboring cells OK. Cells in nearby nearby will, if they had |
|
|
52:14 | receptor for it will bind the, OK. Then those cells take it |
|
|
52:19 | and that acts as a activator to uh viral anti proteins. OK. |
|
|
52:27 | again, these are cells in the of this infected cell. OK. |
|
|
52:34 | um and the net result is the infection basically stops, right? Because |
|
|
52:39 | these uh cells uh have these antiviral that the virus comes in. They |
|
|
52:46 | block the infection. OK. So , the cell that starts infected is |
|
|
52:52 | likely succumb the infection. But the cells are then protected by uh by |
|
|
52:58 | action of interferon that they take Ok. So uh this was |
|
|
53:07 | I think. Um So it's like of the first biotechnology products to mass |
|
|
53:12 | to appear on it, anti viral . Um It didn't prove to be |
|
|
53:19 | because of the toxicity of it. in large doses, it's toxic. |
|
|
53:23 | it's not long lasting. Uh but is still effective um in the, |
|
|
53:29 | you go to the hospital and you a background infection, they do give |
|
|
53:33 | a neuron, a shot of neuron it is effective in kind of that |
|
|
53:38 | that setting, in a more local kind of way in a uh uh |
|
|
53:42 | , in and then start it uh small doses that works, it's affected |
|
|
53:47 | not as a marketing as a pill mass consumption. Doesn't, that doesn't |
|
|
53:52 | work. Ok. Nonetheless, it's, it's still it is effective |
|
|
53:56 | its its role. OK. Um other type of interfering is one that |
|
|
54:04 | neutrophils and macrophages. OK. So that means to activate a macrophage or |
|
|
54:13 | is it may initially look. So the key is that um it may |
|
|
54:19 | like this initially. OK. Then it's activated, it will have the |
|
|
54:27 | of these pseudopods. So that's an macrophage, for example. OK? |
|
|
54:41 | creating a pseudopod, he helps bind , and take things in, |
|
|
54:47 | To be creating more of those, really through the action of uh it's |
|
|
54:51 | that actually causes that. But that when you activate a ma, |
|
|
54:55 | there's different ways to activate, you do with interferon, you can do |
|
|
54:58 | with certain T cells. But that all the same. You create more |
|
|
55:02 | these pseudopods and that enhances vig. . Um So the uh antimicrobial |
|
|
55:14 | OK. Let's see. This yeah, this is the last last |
|
|
55:19 | the innate immune system that passes. . Um So these uh take different |
|
|
55:27 | . OK. So iron binding So remember that iron is a big |
|
|
55:30 | in terms of keeping away from pathogens slow their growth down. So we |
|
|
55:34 | things like transforms uh human level, don't bind iron is present. |
|
|
55:40 | But in actuality, pathogens also have kind of iron binding protein. That's |
|
|
55:46 | sara for. They bind specifically binding . Um the s uh antimicrobial |
|
|
55:55 | these are widespread uh various cells in bodies can produce these. OK. |
|
|
56:01 | kind of act like a uh uh me rock, they form a tunnel |
|
|
56:06 | in the uh the assembler form of in the some membrane causing lysis. |
|
|
56:10 | kind of like a membrane attack We just talked about uh this will |
|
|
56:14 | the type of the same kind of . It's really widespread what, what |
|
|
56:19 | can um attack, right? Not bacteria but different types of pathogens. |
|
|
56:25 | and sounding like macrophages, uh computer , other, other, other cell |
|
|
56:31 | in here, tissues in the So there's something like 50 or 60 |
|
|
56:36 | more than that. There's like hundreds different varieties of these things um that |
|
|
56:40 | this antimicrobial activity that um so is so we're gonna recap this section and |
|
|
56:51 | a little bit about adaptive system. are there any questions about, we'll |
|
|
56:56 | about that response amps? What have ? OK. So let's look at |
|
|
57:04 | question here. Just kind of talked . I think all these things |
|
|
57:09 | OK. So which choice is Yeah. For transfers? Remember an |
|
|
57:17 | complex s interfere on type one C you. What? Try it |
|
|
58:06 | OK. All right. Counting down 15, 321. All right. |
|
|
58:41 | it is, choice is true is A is true. OK. That's |
|
|
58:50 | true one. Um Remember the tech is, that's comp a comp forms |
|
|
58:58 | um so complement can't figure size It's a, it's a protein. |
|
|
59:04 | . Um Interfer on type one. the antiviral amps or these antimicrobial |
|
|
59:12 | uh transference or iron binding uh Um OK. So there are a |
|
|
59:21 | in your book. Uh I think question electrolytes have kind of a summary |
|
|
59:27 | , here's the physical and chemical factors you like to use that. Uh |
|
|
59:32 | also a summary of the second line . Um You know, the uh |
|
|
59:39 | , you know, a lot of quiz this week, we give a |
|
|
59:42 | uh sampling the kind of questions you'll the same ones you've been seeing in |
|
|
59:47 | clip of questions. So, um let's talk a little bit. This |
|
|
59:54 | an overview about the immune system. get more into the details about it |
|
|
59:59 | time, but just for now, of setting it up. So this |
|
|
60:03 | third line defense is typically termed and T cells B cells and J. |
|
|
60:09 | also remember that macrophages interact. macrophages aren't technically part of this this |
|
|
60:18 | , but they interact with these cell , um dendritic cells, OK. |
|
|
60:30 | uh interact with T cells, Um So, um there's kind of |
|
|
60:38 | overview, so we call, we distinguish these two systems by human |
|
|
60:43 | system, which is your B cells antibodies and your cell mediated community. |
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60:49 | . Um And each have their roles so uh there of course, are |
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60:54 | types of li science BB type of type and T type lymphocytes. Um |
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61:02 | cells kind of matured in the, both made in bone, but they |
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61:05 | traveled to the thus where the T tr the thymus really developed uh and |
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61:10 | T cells in the PAC system. but in terms of their, what |
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61:17 | do, right? So B cells , they differentiate into what's called a |
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61:22 | cell. And plasma cell is what the ABI OK. Memory cells. |
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61:27 | remember there's memory, there's actually memory both. Your book doesn't really go |
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61:31 | it. But and I'm not gonna you to know it, but there's |
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61:37 | memory cells that are also part of T cells. So both sides have |
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61:40 | memory component. OK? I'm most with the B cells that have the |
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61:45 | component, uh vaccination, you get and if that if you get affected |
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61:51 | the same antigen again, you'll produce . That's the memory memory component. |
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61:58 | ? But there are special B cells that's what they become right? So |
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62:02 | cells don't produce antibodies, the plasma do. OK? And the um |
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62:08 | the end, the role B cells with extra c of attack. |
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62:14 | So an antibody cannot go inside of cell and attack the antibodies only combined |
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62:21 | pathogens that are outside of cells. . So um the T types T |
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62:29 | types, they're what are called defector . And these deal with intracellular pa |
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62:35 | . So uh they recognize cells are and they deal with them, |
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62:39 | That's your cytotoxic T cells. Um these to be called, there's |
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62:45 | type called inflator T cells, they typically become T helper cells. Uh |
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62:51 | , um the uh other cell types T helper cells of other types, |
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62:57 | like two types of T helper Basically one type activates um B |
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63:05 | OK. Another type um activates macrophages dendritic cells. OK. So you |
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63:14 | a differentiation between the two. Um Dendritic cells. OK. So |
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63:23 | we'll see how A B cell works being activated. Typically, not |
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63:27 | but usually activated by a certain type T cell T helper cell to produce |
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63:31 | . And the macrophages and uh cells with other T helper cells to activate |
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63:37 | . OK? Um And so the uh so antigens are antibodies. |
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63:46 | So an antigen is typically gonna be it's of course, what, what |
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63:52 | to an antibody? OK. And these are gonna be various types of |
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63:56 | protein in nature, but they can lots of different chemical components, protein |
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64:03 | can't be antigens. Um You think of what's on the periphery of |
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64:07 | cell, right? It could be , it can be like lipids, |
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64:11 | cetera, all can potentially be OK. So uh that's the thing |
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64:17 | the adaptive immune system. It is stimulated by the presence of man. |
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64:23 | it must be recognized, seen and bound to it and then stuff |
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64:29 | OK. So uh so in terms the antibody, there's kind of two |
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64:36 | to look at it. One is epitope. So the epitope is the |
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64:42 | part of the energy that is OK. So we can see example |
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64:47 | , this would be the gray, big gray block is the answer. |
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64:53 | . That's what's recognized within that. antigen is the actual epitope shown in |
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65:00 | , right? That's where the actual occurs, in fact. So antibody |
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65:06 | antigen within it is an epitope where binding actually occurs. OK. And |
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65:13 | , and there's a, there's as we'll see, although we don't |
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65:17 | into the details of it because it's the immune response involving the death of |
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65:21 | system is very complicated. OK? there's memory to it, there's actually |
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65:27 | learning curve to it. So individual that are formed initially in response to |
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65:32 | antigen uh actually get better at binning antigen as long as they keep getting |
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65:39 | to it. OK. So the cells formed aren't, isn't as strong |
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65:44 | terms of their immune response but gets . So there's also a learning curve |
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65:48 | goes with it. So, um course, it all involves the chemicals |
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65:53 | activated and things like that. But we're not gonna go into complex nature |
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65:58 | it but kind of more overview. uh I guess the point I'm saying |
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66:03 | that it's more complicated when I'm presenting you here. But you know, |
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66:08 | this is this, this level is fine, right? This, |
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66:11 | this will deal with what you need know. OK. Um But proteins |
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66:16 | to be the best Ams in terms their, there's a lot of variety |
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66:19 | protein, significant number of combinations that to be a type that energy is |
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66:26 | tightly to, OK, less. with um carbohydrates and fat, just |
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66:32 | the same variety of those types that are proteins. OK? Um And |
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66:40 | antigenic determines, so ops, antigenic means the same thing. OK. |
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66:45 | , um let's see. Any, stop, any questions, then we'll |
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66:50 | ahead and stop there and we'll pick with finishing up couple 17 next |
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66:56 | |
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