hi every everyone welcome to the atan notes bio 34 lecture for July we're going to be talking about all things sort of related to unit four particularly the first area of study so a lot about immunity today uh my name is LZ I'll be running through the lecture with you before we do get into it though I would like to firstly acknowledge the traditional owners of the land from which I'm presenting from today so the warry and the bong people of the cooler Nations and I'd like to pay my respect to their Elders past present and emerging so a few of you may be familiar with some of the lectures you may have attended some earlier this week or you know in previous years or earlier this year as well um essentially a notes runs these lectures for you know vce and a couple of other states and across Australia um we do have a lot of other resources that essentially are made for high school students by past students um so that include the lectures it includes a lot of other things as well so some of the stuff you see here you may be pretty familiar with our study notes also the discussion forums um you know especially if you guys are in the year 12 you may be using things like atar calculators obviously a lot of um you know revision stuff coming up into this next term but yeah if you do find yourself you know being interested feel free to head to the at notes website just to have a look at anything that might um be useful to you bio is a really really popular subject um and a lot of people take it obviously so there's a lot of resources available there's a lot of input from past students and um lots of resources kind of AA available especially due to the new study design change um you guys are the second cohort to use the study design so I think there's a lot of useful information on there maybe from past students who have done it last year as well um if you do find yourself being more interested in some of our other resources we do have a couple more so too smart is the Tutoring company run by Aton not so I tutor bio there for example um and there's a lot of other subjects available that you guys may be taking again if you're in year 11 or year 12 I don't know maybe year 10 even um there you know maybe something there available for you otherwise if you are interested in the study guides that I was mentioning um you can get hard copies you can also get copies of you know course notes topic tests some Nee past exams as well all available on Ed unlimited it's sort of like um like a little Netflix but for our 800 study resources so you can access ACC on your laptop and your iPad all that all that sort of stuff um and then yeah you just have access to every atar notes publication so if you do think that is something that might interest you feel free to head to a notes and you can register an account and have a look at all of these things all of these things as well okay so for our lecture today we're essentially going through three major sort of blocks um again it's all to do with this first area of study of unit 4 um is quite a bulky area of study and you know some of your schools may have started with immunity already some of you may be going into it you know in this upcoming term um it is a big area of study there's a lot of stuff and it can get complex at times I feel like sometimes it's regarded as um you know the most tricky subject again it depends on what people say but I feel like sometimes it's a little bit notorious um I don't think it needs to be I think it is relatively complex but once you break it down it can be easier to understand um I think for me it was probably the era study that I enjoyed the most I would say maybe that were like er study 1 um of unit 3 but I yeah I really liked it and I think it was definitely hard to understand particularly the adaptive immunity stuff but once you sort of break it down and hopefully once we explain some of the common pitfalls today in some of the I guess common misconceptions that students might have um hopefully it be a little bit easier to grasp already in these past 6 months you would have probably picked up on some study strategies that help you for this area of study I really highly suggest um like a lot of videos of sort of visual stuff again I know people have different learning types but just because of the nature of immunity and the fact that it's on such a molecular level and there's lots of um you know processes and sort of steps involved um sometimes watching a visual kind of explanation of that can be helpful I know I found it really helpful um so like a lot of videos even drawing diagrams you know you can use others but drawing your own diagrams can really help explain processes as well going along with a lot of flowcharts that sort of thing I feel like in BIO in general it's pretty helpful but particularly for this area of study or at least this first block in particular kind of explaining your first second and third lines of Defense it can be really really helpful um in terms of the experimental design again schools may do experimental design in terms of your actual sack at different times however it's so so so so so so important to keep on revising this for your exam um in saying that while you're at this point of the year you know you've just finished unit three it's quite important to be revising all of this information as you go into unit 4 because the last thing you want is to sort of get to you know September October and you haven't looked at anything to do with transcription translation C respiration in a couple of months um cuz then you're going to have to sort of waste time going back and almost like learning it again when you could have been just revising it sort of infrequently throughout this term um just to sort of maintain that knowledge I feel like it'll help you in the long run um yeah those are kind of the main things we'll talk about some exam tips at the end if you have any questions please pop it in the live chat I'll help you you know answer them and all that sort of stuff um again there is quite a bit of content but I think we're going we'll be able to go through it in hopefully a good amount of depth today but if there anything that you don't get obviously feel free to ask a question um but also these slides will be available to you and you can also email me as well um it's just lordes tmart.com is my email so if after this I'll remind you guys at the end um if there's anything that you feel like you missed or you'd rather email me about um feel more than free to send me anything but yeah those are probably the main um things but we'll obviously explain more as we go through it okay so the first part of the of study is looking at um kind of immunity as a whole um so we have our little study design dot points that will appear in the corner so just refer to them as I mention this the study design is really really really important I've already discussed how you guys are ultimately the second cohort to use this new study design um I guess it is I mean I feel like being at the end of study design is definitely a bit better than being at the start just because you've got Plus prce practice exams and things like that um but there was I would say more stuff taken out of this study design than was put in so I think that's a good thing that you guys can sort of work with and use to your advantage um in terms of immunity not a lot of stuff was changed um I think most of the stuff that's in the study design at the moment was in the study design previously but again just some things have been cut out a little bit um but yeah use the study design to your advantage I would try not memorize it word for word but definitely have an idea of all the dot points that are in each area of study because this can be really helpful when you get to your short answer questions um especially when you don't know what the question is sort of asking of you sometimes you just get to a question and you read it and you just you just don't know honestly um and you don't know you know what it's trying to ask you you don't know what it could be referring to and at that point um speaking from kind of my experience when I get to a question like that I always just try to think I almost like run through the study design in my head and I think what dot Point could this possibly be referring to What DOT Point are these you know V car examiners what are they trying to kind of nudge me towards if that sort of makes sense I feel like having a good grasp of the study design can be really helpful for that but I'll talk about that I guess a little bit later on um okay to start with our actual stuff we're discussing pathogens so it's important to understand the distinction between different types um you know how antigens kind of appear on pathogens and that sort of thing um definitions so this is sort of the definition in terms of um biological agents that can cause disease basically um so they impair the normal functioning of the host organism obviously they replicate and that's how they can kind of spread their disease and how a disease progresses essentially um and this idea of separating our pathogens between cellular and noncellular also very important because via will you know include questions about this um in terms of definitions sorry I feel like I'm putting a lot of tips in before I'm getting into the actual content but um definitions are super important in BIO um more so than other subjects I would say I remember my teacher always going on about keeping a glossery um and I think it is something that's really important because a lot of the questions in BIO are definition based so particularly I mean it can happen in multiple choices well um but particularly a lot of short answer they can use um basically like a lot of marks are associated with using a definition um and I I feel like I didn't really like making a glossery particularly early on um so I used to kind of like ignore my teacher and be like oh whatever like a glossery like cuz I hadn't used a glossery in the past and I feel like I was very sort of stuck in my ways when I was um entering year 10 um I realized it didn't really say much about how I experienced bio but um I did bio when I was in year 12 so I did one and two in year 11 I did three four in year 12 um I got a 45 in BIO and I did enjoy it I would say I think I enjoyed 3 four I would say a lot more than one two um yeah and I think I was able to do well in it because I sort of was able to figure out and I think this is a really important Point um how to answer bio questions I always say to my bio students um it's a complete different thing knowing the bio content and being able to score well or not even score well but being able to answer bio questions properly and getting the full Mark for the question um again talking about how I was always stuck in my ways I never really did you know practice questions and glossies and that sort of thing I was very much um uh you know do your chapter summaries and then you know write your notes and then you answer the question you get it right um but in BIO I found that that wasn't exactly true um I would do my chapter summaries but then you know because I think I would get a pretty good grasp of the content but then initially I basically wasn't answering the questions properly I think bio is very specific in the way that examiners want you to answer questions in a particular way and there's definitely a very particular marking scheme again I would say more so I found it to be different to some of the other Sciences where maybe that technique my old technique that I used to use would work fine but I think for that reason you know having a a glossery doing your practice questions it's all really important because um you can know the content like the back of your hand but if you don't understand what the question is asking of you and you don't know how to phrase all the knowledge in your head properly it's not going to work out and you're not going to get full marks um so that is something really really important to be aware of okay I think I've got enough tips Shar now we'll talk about um other things later but in terms of the actual pathogens that you have to know bacteria are a really important one they're probably the most common one that pops up on your exams um so unicellular procariotas compared to your sort of UK carots and your more complex ones um so procars basically they're just very very simple organisms reproducing independently so bya binary fishing that is a big problem for them I mean I guess for us because of them because of that idea that they can reproduce really really really quickly um so obviously we think about pathogens and bacteria in this context of spreading disease but bacteria are really helpful we obviously you know talk about our normal flora and stuff and how that can form a bit of a defense system um but yeah you've got bacteria all over you your skin your gut everywhere um mostly everywhere but um in that certain case they're not pathogenic because they're not causing disease in fact they're doing the opposite they're being helpful um so when we talk about pathogens it's in that context of causing disease sometimes you might call them opportunistic pathogens so that's when bacteria that perhaps exist on your body that don't usually cause disease um suddenly they get the opportunity to and then they do so um so that's just a bit of an example there um in terms of the cell wall this idea of Pep glycan it's not something vital to know but it's um something that is important for certain bacteria and it can be a good Target for a lot of antibiotics um and we classify them based on their shape so you can see you've got eye you've got rods spes all these different um types it's not vital for you to know you know what's what and you don't need to know specific examples of bacteria but just understand that they come in different shapes typically the ones used on a lot of V diagrams and stuff like that are your rods um but yeah there are different types so just be aware of that be aware of some of the common um sort of like characteristics so you've got your you can have like fella so you know this thing that almost like a little bit of a tail you can have your py which sort of stick out um again you've got your cell wall you've got like a capsule sometimes and so all of these things can be sources of antigens so we'll get into antigens in a second um but basically just these things that can almost be like little tags on bacteria that are immun cells can recognize so it's important to be able to recognize you know these things like fella and P so you can see it on a diagram and know that you're looking at a bacterium but also so that you understand that you know the flagellum may be part of an antigen that an antibody specific form for example um but yeah just get very comfortable with knowing key things about bacteria and knowing what they look like on a diagram as well um okay so ways that they sort of work producing toxins invading tissues consuming nutrients so you know you've got your exotoxins your endotoxins um not a vital distinction to be aware of but just the idea of exotoxins being secreted while the bacteria are alive and obviously the toxins can be harmful to ourselves um or you know the host organism cells and then your endotoxins are basically when the bacteria bursts when it dies the toxins that are inside as an endo they leak out and they can obviously cause a lot of damage as well um so invading tissue so we kind of think of bacteria as extracellular pathogens so they exist sort of outside the cell and then they can come in and um invade tissues they can release these enzymes release these other toxins that ultimately break down that tissue and break down the cells in that tissue and that's obviously going to lead to you know consequences symptoms um and ultimately sometimes death of those cells and those tissues consuming nutrients is a big thing because basically they just out compete everything else so you've got um your bacteria and the consuming nutrients that your cells need your cells are losing they're going to die ultimately um so that's often why in bacterial infections you can get um changes in the level of glucose because of this idea that bacteria are consuming the resources that your cells need um and that's kind of pretty General inhibiting Normal cell functioning as well okay hopefully that all makes sense viruses are your kind of second like main pathogen um that often use so definition here obligate intracellular pathogens so obligate um is the way that they because viruses are noncellular very important to understand that as well non cellular please remember that um they can't reproduce by themselves which is why they are an obligate intracellular pathogen they rely on being inside a cell and having a host and having something that transcribes and translates in order to replicate so that's why they're an obligate they can't like sometimes invade a hostel and then sometimes they can just reproduce by themselves they have to basically hijack um the yeah Machinery or um the replication system um in order to replicate and then spread those virus particles to other cells um okay so then as we've mentioned yeah so they will basically infect a cell transcribe translate the genetic information that sits inside of their little capsid um and then produce more varians or viral particles those will then leave the cell infect another cell and that's how the infection spreads um and at the same time they can go around killing those cells as well so there are heaps of different viruses um you can be based on their genetic information so they may have DNA they may have RNA bacteria fases are they look like little spiders um you've probably seen it when you looked at crisper um but they are very specific to bacterium um bacteria sorry they aren't really you know they don't really infect human cells so we don't see them as often in our examples or like in VR questions um but it might be good to recognize especially in that context of crisper um then yeah there's other different types of viruses again no virus that you need to know specifically some viruses will come up more than others you know you probably get a couple questions on covid HIV those sorts of things but um there will never be a really specific question about a certain virus that because it's not on the study design you know what I mean like you have to know viruses generally but they'll never ask like what is the exact specific mechanism of an RNA virus or HIV or um you know describe all of the different antigens of covid and stuff like that um this is another common thing a little tip with bio as well you'll often see things that are unfamiliar don't let it psych you out so you kind of get lost and think oh my gosh no I haven't revise this like I didn't look at this specific example of HIV or I didn't look at this specific example of Co um because V often will try to distract you especially in multiple choice questions they'll give you this whole chunk of information they'll talk you know all about Co and this and that and blah blah blah blah blah all this random information and you read it and you go oh my gosh no like I haven't looked at this before I've never heard of this before I'm not going to be able to answer the question um and then basically the question the hidden question will be like are viruses you know cellular or non but they'll sort of hide it amongst all that information so then students who aren't aware of what they need to know and what they don't need to know might get frazzled um so again why the study design is important because in questions like that you don't need to worry and go oh my gosh I've missed something um because you'll be able to read the question and understand that oh it's they're just providing some extra context and almost trying to distract you a little bit um okay so prons are another type of pathogen that we can see down the bottom there they are also non cellular they are ultimately misformed proteins um so prons basically they're like um yeah misformed proteins you see them often the disease May spread from animals so if you have these really harmful misformed proteins um and let's say you get infected with one so say you may eat meat um that's infected with a pron right so you'll eat this and you'll obviously eat the protein and because it's a misformed protein protein it will come into contact with the sort of normal version of the protein in your body and then it will like convert it it will change that normal protein to this misfolded protein um and it's really harmful it gives it's um kind of affects the nervous system so you get some the neurological disorders um so you had like mad cows disease and stuff like that um that's the kind of sort of things you're thinking about with um prons so they are cellular so important to remember that viruses are non cellular and preons are non cellular um but your viruses are you know your little hijacking genetic information sort of thing um and your preons are just misfolded proteins basically and so prons are thinking more neurological disorders prons I would say they honestly don't come up very often um in exams whereas viruses you'll be talking about them every second immunity question um okay so here's a nice diagram that sort of summarizes this you don't need to know the cycle of a virus but it just may help you visualize it so you've got your Veron which is just a virus particle that enters the cell you can see it's genetic information held sort of within that um the center of that particle and you can see it's like little proteins Spike proteins on the outside this is a very typical diagram like as in this of what um a virus will look like you can expect it to look like that in your V exams um but it basically yeah Will insert it genetic information into the nucleus we've got transcription going and then we'll have translation going those proteins um that that genetic information codes for which is obviously just to create more virus particles as you can see here we've got our Spike oh my gosh Spike proteins and stuff like that um those will be translated and then you get this new virus particle forming It ultimately exits the cell and then this will go on and infect another cell so that's the idea of how fire is work super important thing just to remember that it's non cellular okay so some of our eukariotic pathogen so these are cells that are a little bit more similar to our cells um so a little bit more complex so we've got our fungi so they um you know you think of like your fungal infections ultimately so you know like your ten your athletes foot that sort of thing um their salal is made of chitten so you can think again just like peptidoglycan with your bacteria um the chitten is sort of another Target that you could use um but yeah those are your sort of fungal infections and then your protozoa so these are eukariotic pathogens but they're single celled so I feel like often we tend to think like ukar UK carots are multicellular and procars a single cellular remember that that's not always the case such as these um protozoa that are UK carots but they're a little bit more simpler they're so unicellular um so these can sort of be quite parasitic so like plasmodium um is the cause of malaria so often we think mosquitoes are the cause of malaria they're the um Vector so just like you know in unit 3 when you discuss plasmids and all that stuff and how your plasmid is the vector for sort of carrying your target gene into your bacterium um your mosquito is basically the vector of carrying this protoo this plasmodium into the human let's say um so yeah that's the pathogen we're thinking about and then worms so what we've got depicted here um you know your tapeworms your lip flukes that's pretty self-explanatory in terms of what they are they just look like real worms as well um but they can be obviously a lot bigger and yeah that sort of parasitic um nature and where they can just take up the nutrients and absorb all of that at the expense of the host okay so those the pathogens you need to know really important again bacteria and viruses the main ones you sort of think of um Okay so terms of our actual sort of Immunology stuff here so an antigen very important again definition to know so it is a molecule that is capable of inducing an immune response so we've got our self and our non-self antigens so on our pathogens they will have their own little antigens you know if we're thinking of a bacteria um maybe just a little protein on the capsule or if we're thinking about the virus like Spike protein that is the antigen it's just like a little I like to think of antigens as name tags it's just like a little name tag basically identifying um what that pathogen is and if you think of a self antigen so like your MHC markers um these are again little name tags that say Hey like I belong to the body basically um so your MHC markers are your your mhc1 in particular are basically your self antigens um so they are found on all nucleated cells so be aware that they aren't on you know certain cells like um red blood cells and things like that but they have their own little like they've got their system so there's still ways of identifying cells there um but your mhc1 are essentially yeah your little name tags and the way that they work is and I think this is important to know I remember I didn't know this um this sort of second dot Point here I didn't know it until we were kind of further into the area of study and I think to me it helped everything click a little bit more especially when you think about the difference between um cytotoxic tea cells and natural killer cells knowing what mhc1 actually does as opposed to just being a self antigen for me was really helpful so just bear that in mind as we talk through them um so with the mhc1 I like to think of mhc1 as basically little windows I think I might elaborate on this when we get to natural killer cells and stuff like that but they basically um show immune cell so I think of I like to think of um yeah so cells as houses your mhc1 is Windows and your immune cells is police so your immune cells go around and they just basically double check everyone's antigens and make sure that there's no foreign antigens hanging around that they need to be a little bit wary of so the way that they do that is through these mhc1 markers so that's why I like to think of them as little Windows cuz basically the police so the immune cells they run around and they look in everybody's window so they look at this mhc1 and mhc1 shows what proteins are being made in the cell so they present peptides derived from cytosolic protein so your cytool proteins that are hanging around in your cytool they take like little bits of that and they put them on their mhc1 and then that shows the immune cells this is what I'm up to inside of my cell so that's why I think of them as a little window um so then if something is going a bit dodgy in there in your mhc1 then the police can realize and then they can sort it out um yes that's what I like to think of it as so obviously if you're making the proteins that you're meant to be making that's how mhc1 works is basically a self antigen a self marker it tells the immune cells um you know I am a cell from this body I'm meant to be here I'm not doing anything wrong your class two are a little bit different they are associated with antigen presenting cells um so not every single cell has mhc2 only specific immune cells haveit um and these will be used I was going to say window again but not really window um these will be used basically just to show when you've got a foreign pathogen um hanging around the body okay so we'll show a little picture so here is this idea of self antigens and non-self antigens um so your tea cell which we'll get into in a little second is a really important immune cell um so they go around and they you know can check what's going on and it's this idea that you um they have different receptors if there's a theme for immunity it's receptors this idea of things being complimentary um you know matching up detection all that sort of thing a very very important sort of theme of immunity um so your mhc1 markers as we mentioned are your self antigens um and then your you know stuff that might be on a pathogen is your non-self antigen so t are able to basically detect what belongs in the body and what doesn't um yeah hopefully that makes sense okay so to get us sort of thinking so when a virus attacks or infects a human cell what occurs within the cell so again think about your um viral particles think about what our definition was so an obligate intracellular par oblate intracellular pathogen oh I thinking parasite yeah oblate the pathogen so we're going in a cell and we're basically hijacking that Machinery um so we are undergoing transcription we're undergoing translation and that cell so our human cell will begin to become basically a virus making factory um so mhc1 Mark is what they present on the outside of cells so hopefully you guys are all thinking of the little analogy of a window okay I don't know if it's helpful it was helpful for me if you think it's stupid don't use it think of something else but um yeah I just like to think of them as a little window so they present your little proteins that your cell is making um again just a way of showing the immune cells that you're sort of doing the right thing if you think about it um with a virus if you're infected with a virus um what you would be making if you're making viral proteins um you're going to be essentially displaying that on your mhc1 so that's this idea of how the immune system detects cells infected by viruses your mhc1 so your windows they'll be displaying your viral particles so you've got um I don't know a home invasion right the virus is a home Invader I guess they come in they start invading and your windows are still open and the police come around your immunes come around and they can see through the window that there is someone invading leing your home and then they sort it out from there so that's the idea of how immune cells detect when cells are infected by viruses um via their mhc1 markers okay so looking at our first line of defense um so basically we okay first line of defense I think it should be used kind of colloquially um according to the study design it's better to say you know you're innate and your adaptive immune response as opposed to first second I think that's something my teacher used to tell me as well um so just be aware of that sometimes it's easier to sort of comprehend your first your second and your third but um technically like in when you're writing like I in short answers I would never really write first second or third I'm sure depends how lenient your examiner is and all that sort of stuff but it's always best to use terminology that's listed on the study design um okay so you've got your non-specific or your innate immunity and your adaptive or your specific immunity so your non-specific immunity and it's important to know differences between these um your nonspecific immunity is basically your one size fits all works really quickly sort of like instant like putting a Band-Aid ultimately um so whatever the pathogen is if it's a virus if it's a bacteria if it's a pron if it's a whatever the innate immune system is going to act in the same way again one size fits all um there is no memory of Prior pathogen so this idea of memory will make more sense when we talk about adaptive immunity but it's this idea that it's one siiz fit all and the cells that are involved with this um you could be infected with the same bacteria over and over again but they won't recognize it is the idea whereas in adaptive you do recognize it um and then the level of response being the same for each pathogen of the same organism again that idea if you're infected by the same bacteria over and over again um when an eight immunity kicks in it'll just kick in it's one size fits all exactly the same copy and paste whereas with adaptive immunity because you have that memory of past infections if the same organism comes along that memory kicks in really well and you get a bigger response and you get a bigger response and you get a bigger response every time something you know the same organism tries to infect ultimately um okay so in terms of the first line of defense so this is preventing pathogens from entering um the individual really a big one is intact skin you can see it's underlined intact if you just say skin you will not get the mark because the skin could be open the skin could be damaged um intact skin it has to be closed so that's obviously a pretty clear physical barrier um and that's why when it's open that you know skin is sort of useless if there's a big gaping hole in it because then the bacteria can just jump right in um so mucus and your cyia in the Airways it's also important to know what is a sort of physical and what's a chemical I believe um I think it's in the other dot point but your yeah your physical your chemical and your sort of microbiota it's important distinctions to make um so your intact skin would be more physical your mucus and your Celia can ultimately be both a little bit um basically because the mucus I prefer to think about it in a physical sort of sense because I think it's easier to explain in a short answer um your mucus can ultimately trap those pathogens and then the CIA just pushes it so it gets um chucked you know back out or like swallowed and stuff like that um but you there are chemicals within the mucus as well that can help to sort of degrade that pathogen so if you're going to describe it in you know a chemical aspect just make sure that you're being specific and be mindful that vcar may ask you you know what are some examples of physical barriers what are some examples of chemical barriers and you need to know different ones um so a low PH in the stomach so this is chemical stomach acid is very acidic um so it can kill certain pathogens but of course there are some bacteria that hang around in the stomach as well um so lysm so these enzymes in your tears and in your saliva they can help to degrade certain pathogens as well um so your good bacteria this should be referred to as your sort of your microbiome your microbiota so they're found um in other places on your body um it says a few exceptions those are just sterile areas but it's this idea that this microbiome helps because they compete with your bad bacteria it's like a little bit of a good vers bad um so when you let's say you have a poor microbiome so I was talking about opportunistic pathogens before if you take um an if you take some antibiotics let's say um they may be pretty General and what they might do is they may end up killing um some of the good Flora or like the good bacteria in your body and what that means um is there's sort of less competition and so sometimes you can get other opportunistic infections often like um thrush can be an example so sometimes you have a um fungus that sort of sits um around your mouth for example and sometimes if you take antibiotics or even if you take um like uh like venine like if you take steroids um then you basically yeah kill some of the bacteria around and then those pathogens that are left they can become opportunistic and kind of grow so that's why it's really important to keep a nice um balance of the bacteria in your microbiome um for that reason because the competition is really helpful in making sure that they don't get too crazy but then also that you know your actual foreign pathogens don't invade as well okay so in terms of your second line so let's think you know we've gotten something's gone wrong with our first line maybe we have a big cut now we've got pathogens that are entering um our internal environment so this is when the second line kicks in this is your innate immunity um so these are your sort of General lucaites again this is your sort of one siiz fits all um so this is a nice little map of your lucites the one that are blocked out are part of the third line so your adaptive immunity so we'll look at those a little bit later um but these are the really important cells for you to be aware of be aware cuz I feel like sometimes I say it and it might not be captured as well so this is a good diagram but you'll often see this thing like a monoy um and they'll often link it to macres so monocytes are just like an earlier version of macres um I think it can be confusing sometimes students think it's two different things but you've got your maccrage which is a really big like main character in The innate immune system um and then your monite is just like a like the baby version of that basically okay so this is a really really important table or just an important thing to be aware of um flash cards can be good for this diagrams can be good for this whatever it is just know the main features of these key innate immune cells so your macres um basically we're thinking about them being really good at phagocytosis we'll discuss fagocitosis in a second um but it's basically just engulfing pathogens um yeah engulfing pathogens um as in like phagocytosis like you know like exocytosis and endocytosis phagocytosis like they're just like eating the pathogen basically and they degrade it um and chop it up your dendritic cells I should mention as well they aren antigen presenting cells so an APC so that's why they've got MHC class too um your dendritic cells are apcs as well and they're like the best of the best so your macrophages are very well known for phagocytosis your dendritic cells are very well known for antigen presenting um so that's something to be aware of nutrifil these are not antigen presented so they do not have MHC Class 2 they're the most common type of um Lucy that you see sort of in infections um so there's really really high numbers of neutrophils um and then they ultimately um do this like little kamakazi thing so they undergo apoptosis after phagocytosis so with macres when they fure cyose something they eat it up cool they move to the next one eat it up move to the next one eat it up move to the next one nutrifil is kind of like when a bee stings someone and then they die that's sort of the idea with neutrophils they will engulf a pathogen and the way they kill it is that they release all of these um like really harmful enzymes and toxins or whatever so it kills the pathogen but it ends up killing them in the process um so that's kind of a little characteristic about them M cells really key you always associate them with histamine um and they're very involved in your sort of allergic and inflammatory responses um something to be aware of is that they reside in the connective tissue so they're not kind of floating throughout the bloodstream they just sort of sit um and release the histamine natural killer cells also quite important um these work similarly not the same but similarly to cytotoxic tea cells so it's important not to get them confused um and they release these two things you have to know perin and granzymes which you can see here and those basically induce death in um certain cells so they will detect changes in your MHC class one so the way that they do this remember that innate cells are a one- siiz fitall um so what certain um pathogens might do so some viruses and especially some cancerous cells as well they know that you know the police are coming around looking through windows so what they do is they shut the window so they the MHC class one they downregulate it so they just don't have an MHC class one um this is what the natural killer cell will pick up on so the natural killer cell again one size fits all it's not checking you it is this chickenpox is this Co is this salmonella it doesn't care what it is it just goes around from house to house and anybody that has their window closed as in any cell that doesn't have an MHC class one they will release these perin and granzymes and that will induce a potos so cell death and that will kill the cell ultimately the cytotoxic tea cell is a little bit different because it's part of the Adaptive so the specific immune system so we'll talk about that when we get there but just remember that natural killer cell just like all of these cells they don't care what they're killing they just know that it's a pathogen um whereas the Adaptive system is a little bit different and more specific okay and then lastly your ear cils these are kind of like the random like like nobody really cares about it but um important in your parasitic infections and they can undergo phagocytosis as well um yes okay so we have a lot of like little Sidekicks that kind of support these immune cells so your complement proteins these are um really important so they basically just help these immune cells so they can enhance phagocytosis they can bring immune cells closer to the site of infection um they can actually lies some bacteria themselves so they form this thing called a membrane attack complex and they just kind of like sit on the like plasma membrane or the membrane of the pathogen and they form a little hole and then it causes all of the contents to sort of leak out of the pathogen and then they burst and they die um and then they can help sort of work with antibodies as well which we'll discuss soon so cyto are also quite important they're signaling molecules and they're basically just um methods of communication so if a cell wants to talk to another cell they'll release the cyto so cyto cyto really important interferons are also very important they're a sort of subset of the cyto Kines and they're released by cells that are infected with viruses and what they do is they basically warn the other cells nearby and they tell them um I'm infected by a virus watch out um what they also do is they will release if I'm a that's infected by a virus I'll release this interferon and I'll send it to my friends right telling them be careful but what I'll also do is I'll send it back to myself so I'll release it and it'll bind to a receptor on my membrane and it'll tell me like slow down with your protein synthesis like you're infected by a virus um relax a little bit so that's um white interference are really quite import important in viral um infections okay this is also extremely important your inflammatory response this ties in as well with allergies which we'll get too um so your inflammatory response is part of your innate immune system so again it's a sort of one size bits all idea so we've got damage occurring to the S side so this is our intact skin we've now got a hole that first line is breached um so these damaged cells release chemical signals so the damaged cells around here will detect that they've been you know like the cells in the tissue here will detect that they've been damaged and that will sort of call your innate immune system into play remembering that your immune system is very quick um so your macres are you know ready they're going okay I'm coming to the side of infection time to help out your M cells which are these ones here remember that they sit in the tissue unlike these other cells they're not running through the bloodstream these ones don't move they sit in the tissue um and they'll they'll kind of recognize like oh you know something's going on here and they will release these molecules here the histamine and the histamine really gets everything going in this inflammatory response um so we have our main sort of symptoms so redness heat swelling pain and loss of function it's like a thing they're like your five like cornerstones like major things of your inflammation um and they all kind of come as a result of this sort of histamine and this idea of getting your immune cells into this location um so the redness is because you dilate your blood vessels so your blood vessels become leakier they become more permeable they become wider so Vaso dilation and that just increases the blood flow and allows more immune cells to get to the site quicker the heat is because of that as well cuz your blood is warm um the swelling is because your blood vessels become as I mentioned like leakier and more permeable and this allows immune cells to squeeze through the gaps a little bit more easily um so that idea of them becoming more per permeable sorry means that your immune cells can come through and so again this causes a lot more cells in this area a lot more liquid you know fluid in this area and that's why you get this swelling um pain you get just because of the damage to the area and again all of these cells in this one spot and loss of function is kind of similar to that as well in terms of all this activity going on here um but yeah that's what you've got so your blood cells are leum or permeable so all of these you know neutrals macrophages your dritic cells they're all kind of coming in to help out um and a lot of Phagocytosis will go on um and then basically they will we'll talk about fosis they'll engulf these pathogens um and then this will Ely link us to the third line of defense so adaptive immunity but in general that's what we want to think about so we can see that the blood is licking out here because of all our immune cells coming in um so these are our fago sites you can see here it's just engulfing this little pathogen and it'll absorb it and just chop it up and kill it basically um okay so we'll work through a little practice question so which of the following matches a cell correctly with its role in an immune response so uh basically working through a process of elimination here so maccrage stimulates inflammation by secreting into Furon no because cells that secrete interferon it's your virally infected cells um dendritic cell presents fragments of antigens to tea helper cells that sounds about right because remember that dendritic cells are a really good um APC so an antigen presenting cell Mast Cell engulfs bacteria and debris no that would be more so a maccrage sort of thing a Marell it's really key with the releasing histamine remember that Mar cells don't move so they wouldn't make very good um you know things to engulf bacteria and your nutrifil secretes antibodies I know we haven't talked about antibodies but they're associated with the Adaptive immune system um and your nutrifil is part of the innate so that's why B is correct okay so this process of Phagocytosis can be seen in this diagram here so you've got your bacteria your pathogen it comes in it gets absorbed into this little vesicle called a phagosome so your phagosome then fuses with this other vesicle called a lome and in that lome you've got all of these um Lymes these enzymes that are involved with degrading things um and yeah chopping them up basically so your fome you've got your little vesicle with your pathogen you've got your little vesicle with your degrading enzymes um or like digestive enzyme kind of and then you fuse them into one which is your fago liome and then the enzymes basically get to work and you can see that they degrade this um bacteria this pathogen and then this is kind of just expelled so it's quite a neat process um so this is what we can see here fome your lome step four you just combine them together so that's the process of fosis in general um if you are an antigen presenting cell what will happen is you you're um you know degrading you're sort of like digesting this bacterium you will get part of that so it's antigens and what you will do is you will go and present it on your mhc2 so your mhc2 cells just like your mhc1 will sit on the plasma membrane so we'll take a little fragment of this you know showing your antigen and we're going to put it on our mhc2 markers which will just sit around here we will then go and find our you know cell or whatever and we will show them this antigen basically um so that's the idea there and then the Adaptive immune system will kick in so you can see that antigen presentation is the link between your innate immune system and your adaptive immune system um perfect okay so looking at our lymphatic system so this is where we're getting into our sort of adaptive stuff here um so the lymphatic system basically it trans supports lymph around the body and lymph is sort of like a filter filters your blood and all that sort of stuff um and gets rid of like fluid and all that sort of thing there um so it is like kind of closely linked with the circulatory system but it's not blood so it's not pumped by the heart it just moves um based on sort of like Valves and your muscles moving and kind of shooting the liquid up um so that's your lymphatic system in general your lymphatic organs are important to because they're where our cells can sort of reside um or grow so lymphocytes will lymphocytes sorry will sit in your lymph noes so with this process here of your tigen presentation when you present it to a lymy you're going to be moving to a lymph node um so in terms of their names tea cells mature in the thymus B cells mature in the bone marrow so all of your lymphocytes start in the bone marrow your tea cells will move to the thymus and that's where they'll mature your B cells will stay in the bone marrow that's when they mature hence tea cells for thymus B celles for bone marrow um and your spleen is kind of involved in this as well okay so um now we're getting into this real link here so you've got your APC say you've got a dendritic cell you know we've had this inflammatory response we've got an antigen we're putting it on our mhc2 and we're now going to go all the way to a lymph node so might might be in like your um neck maybe in your armpit wherever um but we go to a lymph note and this is where we're going to interact with a lot of our lymphocytes so our te- cells our B cells all that stuff hanging around there so once we've got our tea cells again we're get we're getting higher up here in our hierarchy of immune cells um we need basically a more effective system to kick in so what your adaptive tea cells or sorry your adaptive cells in general would do is they are very specific so that's why we've got an antigen um before we had you know our little one siiz fits all we don't care if it's a bacteria if it's a virus whatever now we've phagocytosed this um pathogen and we are finding its specific antigen remember an antigen is like a name tag so now we're saying okay this is the salmonella um bacteria you know this is eoli this is you know strep whatever it is and we're giving this name tag and we're showing this name tag to the te helper cell and the you know maccrage or the dendritic cell is saying you know the innate cells we've tried our best but we need something more targeted here that's the sort of idea that we're going with um so you can see that here you don't need to worry about the co stimulatory Lian this is what you're really thinking about so we've fager cytos this we've taken some of this antigen put it on our MHC Class 2 and now we're presenting it to the te helper cell and this tea helper cell is specific specific to this antigen so this is another thing as well we're not presenting this to any random tea helper cell that we bump into we're presenting let's say this is for like E coli or something like that we're presenting this to a t helper cell that is specific Fe coli so this maccrage will be in a lymph node and it'll take it to a billion different tea cells it'll take it to the co tea cell it'll take it to the chickenpox tea cell it'll take it to the I don't know like tetus te cell like whatever it'll take it to all these different tea cells but remember the whole theme of Bio complimentary we're thinking of receptors so we're finding a t- cell that has a receptor that is complementary to this specific antigen that is a really really important thing to understand okay so these are all our main players in our adaptive immunity so don't really worry about like naive and stuff like that but um you've got your B cell so again B cell will have sort of a similar receptor like this it's to a specific antigen if it's naive it means like it hasn't come across it yet so in our bodies like in 2018 we had our little BS oh maybe bile is a bad one for Co but like let's let's just say for example right may not be accurate um but we've got our little B cell that's hanging around that specific to co or whatever other infection um that would be naive because it hasn't come across its antigen yet then Co came into our body and this B was saying woohoo I found my complimentary sort of antigen so that's the idea of when they become like a mature B cell or an activated B cell um plasma cells and memory B cells fall under this division of B cells um I think I'll probably explain in a diagram but this is a good table to refer to plasma cells associate with your antibodies memory B cell you just associate it with being your memory so they're just kind of hang around and they're good for next infections um help a te cell like super important basically your coordinator of the whole adaptive immune response they activate B cells they activate other helper T cells and they activate your cytotoxic t- cells your cytotoxic tea cells remember I said were a little bit similar to your natural killer cells they also use perins and granzymes to induce apoptosis in infected cells but instead of detecting when the windows are down remember that this is part of the specific immune system so they detect when the specific end is being presented on the mhc1 so they're looking in the window and they're not only looking in the window and saying O there's an Invader they're looking in the window and saying this is the invader's first name their last name their date of birth all that stuff they're being really specific um okay so this is a nice diagram and sort of encapsulates this so this is our link from our innate immunity so we've got our antigen presenting cell here um we've got our antigen B cells can also be antigen presenting cells we just don't really like like vaa doesn't really use it in this context very much but they can't be um so whatever the case is often it's an APC they present our antigen this T helper cell will now be activated and what it will do is it'll make more tea helper cells it'll um what we call clonal expansion is an important thing to understand for all of these so remember that all of these have a really specific um receptor right so there's not a lot of them like let's think about the co one right before Co came along it's not really being used that much um so it would be useless for you to have like a thousand of these cells right so you may have a couple but once it's been activated once this tea helper cell specific to covid you know in 2019 or 2020 came into contact with this virus it obviously needs a bit more help right so it will go through this thing called clonal expansion it will basically just replicate and replicate and replicate so now we have a lot of tea helper cells specific to this Co antigen that will then activate your cytotoxic tea cells which is what we've got here this will also activate your B cells um and the same thing will happen clonal expansion you'll get heaps and heaps and heaps of these cells so B cells will go into your plasma cells and your memory B cells so the role of your plasma cells is just to make antibodies and again you've guessed it your antibodies have those specific receptors to that specific antigen um so these are really good for like bacteria and targeting sort oft extracellular pathogens your cytotoxic tea cells you know we've talked about like the windows they're really good for um intracellular pathogens and like your cancers and stuff like that so that's the idea there um okay so summarizing this so we've got a lymph node our tea helper cell is activated this is going to say okay let me find a B cell that has the exact same receptor I found it now you're activated now this B cell it's been switched on it's going to divide and it's going to create so many more B cells and they're going to be both memory B cells and your plasma cells so remember your plasma cells work to produce your antibodies and those will help kill your bacteria your memory B cells they just their role is basically just to hang around um and then once this infection is over the next time that we get infected with covid let's say we've got a lot of memory B cells hanging around it's their job to divide into more be cells basically um okay so yeah plasma B cells antibodies that's the idea there um so this is ultimately what we can see in terms of our sort of initial infection and this is your um your like antigen presenting cells you've got your T cells and your B cells being activated you've got your plasma cells and your B cells and then your plasma cells producing your antibodies which look like these little yse okay I am mindful of time so I'll keep kind of going through it um so te- cell responses um are targeted towards our intracellular pathogen so again think of our viruses out cancer stuff like that so you've got your you're at a lymph node your apcs come along te helper cell is activated that activates itself really and it divides and it creates your memory tea cells and your tea helper cells memory tea cells exactly the same I will say vard always talks about memory B cells they never really talk about memory T cells um but it's just they have the same job um and then your cytotoxic tea cells will obviously proliferate as well so here is how cytotoxic tea cells work again instead of um your natural killer cells detecting when mhc1 is not there what they do is cytotoxic te- cells go and they zoom in on your mhc1 and they will see that if there are any basically non-self antigens being presented on the mhc1 and then they will release per and granzymes and kill it so if you've got a virus your window is open you're showing your viral particles um or peptides on your mhc1 your cytotoxic t- Cil is going to come along and remember I can't emphasize it enough it's all about being complementary having the same receptor so this cytotoxic te- cell comes along and its receptor whatever the shape is fits really well over this um viral antigen so this is sitting in your mhc1 this is your cytotoxic te cells receptor it's going to come along and go aha this is the co um you know Co 2 like whatever this is the exact specific antigen that I'm looking for I'm now going to release perin and granzymes and I'm going to like destroy this house basically I'm going to kill this cell and kill the virus in it so that is the idea there um okay so allergens are similar to pathogens in an allergic response but obviously it's this idea of people with allergies and our response to allergens um it's a hyp sensitivity so you know you've got things like pollen dust peanuts compared to you know if you think about a virus or bacteria they can cause a lot of damage they can kill you right so it's valid that the immune system wants to mount a response against them with allergens our immune system is basically very hyperactive and it sees these pollen these dust this peanut which doesn't cause it isn't a source of a threat for us but for some reason it sees it as a threat and then it basically initiates an immune response so a lot of this stuff is quite similar but a a thing that you have to realize with um the allergic response is that you have this sort of priming so what happens is if we've got someone that's allergic to pollen so the first time pollen is going to enter their body um and we've got our immune system kicking in so you know the same thing that happened with our clonal expansion all that sort of stuff will be spefic specific to pollen and we're going to make antibodies to the pollen right because we think it's dangerous but something that we do is that with these antibodies we don't really use it to like kill it I suppose um what we do is we take these antibodies so there are specific form of antibodies IG g e and we sit them on M cells so that's obviously a bit different to what you do like if it's a bacteria um so you again this is your so the first time your body ever come into contact with pollen we mount an immune response specific antibodies are formed these antibodies go and sit on our M cells and that's that the person doesn't get sick nothing happens the second time pollen comes in that's when we get this full-blown response so the second time your pollen comes in and this is this idea of like sort of priming your IG so your antibodies are sitting on your M cells and they're they're just waiting and so as that pollen comes in what it does is it binds to that IG and that causes a really huge response in your mast cells and histamine is released and then you have this big inflammatory response and that's why people with allergies you know have inflammation they've got their like they get red um you know throat closes up snotty that sort of thing um so hopefully that makes sense and that's kind of what I was talking about in terms of hypers sensitivity but yeah the main thing to realize is that we've got our our first exposure like nothing happens to the outside you don't have that allergic response um but your M cells are just covered in this IG and then the second time it binds to the IG and then it causes that response um okay I'm going to probably race through this question um so cells are the immune system of different kinds of structures on the surfaces so you've got self antigens receptors for self antigens and then receptors for foreign an so hopefully that makes sense so you've got a self antigen so you can see that they've all got three things so you've got a self antigen you've got a receptor for self antigens and you've got a receptor for foreign antigens so from the information what are we able to conclude um again if you want you can take like a screenshot of it and have time to think about it yourself and stuff like that but I will move through it if you want to go back to it on the slides then I recommend that you do um the way that you can look at this is if you realize that you've got a self antigen a receptor for the self antigen um and for and a receptor for a foreign antigen you can basically figure out which one is which on each of these CU two of them will be complementary because you have a self antigen and a receptor for a self antigen so they must be complementary right and then the third one should be a random receptor for foreign antigens so what the question is asking you is what is a self antigen for each of these cells so if we go to cell P this fits into that so this must be the receptor and the self antigen so this will be the foreign one so therefore a can't be right B so cell R so this fits into this so this must be your self antigen and your receptor this is your foreign one oh yep that's looking pretty right let's check the others uh cell Q so this fits into this this must be your self anen this must be your ccept this is your foreign one um which is not right here and lastly this fits into this so this must be the receptor and the self antigen this must be the foreign one which again is incorrect so the only one that's right is B I hope that makes sense feel free to leave a comment in the chat if that didn't work I know I went through that quite quickly um but again take time to go back to it using the slides if you want sorry I just know we have a lot to get through um okay so now looking at some disease challenges so that is basically the simple oh it's not that simple the process the basic process um of your first line your second line and your third line so that's how immunity Works in general now we look at you know what are the types of immunity looking at vaccination stuff when immunity might you know be going wrong all that sort of thing um okay this is probably the easiest part of immunity I would say maybe so you've got your natural and fish immunity that you have to distinguish between and your active and your passive immunity immunity that you have to distinguish as well um so your natural immunity this is when you have um ultimately antibodies that you've made yourself basically um so with your natural immunity you have basically been infected by something and then you are expressing antibodies um in your artificial immunity this is when the antibodies are basically not your own ultimately um so with your active immunity this is when your antibodies are produced due to the exposure of a pathogen so again this sort of um again might not be a natural process of infection but this idea that your body is making its antibodies itself um and then with your passive immunity this is when you are not making your antibodies yourself so it's all about antibodies so natural immunity the antibodies have occurred due to a natural process artificial immunity the antibodies have occurred due to an artificial process active immunity the antibodies have occurred due to your body sort of making them passive immunity they've ultimately been made by something or someone else so a really common example that they use is um in terms of your natural immunity you think about um your natural active is like your typ typical thing that we looked at so you're infected by a pathogen and you mount a response you have antibodies as a result that's your natural active immunity your natural passive immunity is when you um basically are given antibodies through breastfeeding or through your mother that way um because it's natural because it happened without medical intervention but it's passive because the antibodies have been made by your mother and not by yourself in terms of artificial so artificial active is your vaccination so again very simp ilar to artificial sorry a natural active the body is mounting its own immune response you're making your own antibodies but it's just the source natural is I bumped into someone on the street who had covid artificial is I got the vaccine um and then lastly your artificial passive so you are getting someone else's or something else's antibodies via medical intervention so if you are bitten by um yeah a snake or something then you will get this antivenom which contains the sort of like pre-made antibodies so that's why it's passive cuz you're not making the antibodies yourself and it's artificial because they're being you know it's not coming naturally through your mom it's coming from wherever else okay hopefully that made sense um so in terms of our vaccin sorry in terms of our vaccinations um so the process with this is kind of what I've just described in the previous slide so we um work to kind of get immunity by injecting a little part of a pathogen into ourselves so we saw this whole process of when you know you've got your APC and you get your clonal expansion all of that so we want the end results of antibodies but we don't want the initial result of getting sick right so that's why we use an inactivated form of the virus or an attenuated or a weakened form so um yeah so basically like the pathogen is still alive but it's just very weak or inactivated in terms of like it just it can't cause disease at all um so that's why when you get a vaccine you don't usually get super sick um so that's why you yeah insert part of that pathogen and the idea is that you have inserted the antigens basically so on this inactivated or attenuated form of the virus let's say you've got a um pathogen no sorry antigen you've got an antigen from that pathogen and then your body is going to mount a response against that so then again the same thing's going to happen your t- cell is going to be activated with that specific receptor your B cells PL cells so on and so forth and so you get the really important thing is you get those memory cells the memory cells are really really important because that means say like I've never gotten um I don't know chickenpox or something like that so I've never gotten chicken yeah there's a Chickenpox vaccine sorry I say I've never gotten chickenpox um so I get this Chickenpox vaccine and now I've got this whole system going on and now I've got memory cells to chickenpox um what happens is when I encounter chickenpox in my day-to-day life instead of getting sick because my body you know hasn't seen chicken poox for the first time and it takes a long time because I've got these memory cells hanging around from my vaccination my body will recognize that chickenpox antigen and it'll mount a really huge response and it means that I won't get sick because it's going to work so fast and that's kind of the basic of vaccinations um so the really important aspect of that is having those memory cells okay hopefully that makes sense so this is a nice diagram to represent that so sorry so this is your initial exposure so I'm getting the vaccine for Chickenpox um so my antibodies oops my antibodies are being made my memory style are hanging around all that sort of stuff um and I'm getting this sort of primary immune response so I've gotten a nice amount of anti bodies you can see that this takes a long time so let's say that if I I'm not V like it's not through a vaccination it's through actually being exposed to chickenpox um this is a long time to be sick until your body actually gets to work anyway so I've got my antibodies they hanging around the numbers dwindle a little bit right um and then you know chickenpox is gone the antibody number is pretty low but I've got these memory cells still hanging around suddenly someone else is infected by chickenpox I bump into them those memory cells are going to say I remember you I'm going to go through my little clonal expansion thing again and I'm going to make all of these new plasma cells and all this sort of stuff and you can see that the amount of antibody skyrockets um and that's because remember at your initial exposure maybe you only had one or two cells that had this specific receptor to this chickenpox antigen but now I've got a bunch of memory hanging around after this you know vaccination or after this exposure so now I've got heaps of cells that are specific to this so once this Chicken Box virus enters my body for the second time the chance of it bumping into something that has a specific receptor is much higher which is why I get this really quick response and because there are so many other chickenpox you know memory cells hanging about once I'm activated I activate all of them and then you get heaps and heaps um more more cells and that's why you get a much larger response the second time as opposed to the first time and then it just goes on and goes on and goes on and this is the process of well when you get a booster um so if you had your covid vaccine you get this initial response and then if you get your second vaccine you get a nice bigger response and then a booster and so on and so forth um so you have a nice high level of immunity hanging around with Co obviously it's a bit different because it is a virus that mutates pretty frequently um if it is is a bacterial infection or a viral infection that doesn't mutate that much um then again it's like pretty fine you can have one vaccine or two vaccines in a or one vaccine in a booster but that's why you know influenza you have to get that every single year because it mutates um and so the immunity that you've you know this is the immunity that I've got for the 20 202 influenza um but and that's great so like if that comes through you know hope they won't get sick um but the 2023 one is completely different the antigen looks different so then that's why you have to get another vaccine every year okay please let me know if that did make sense just pop any questions into the chat um the main principle with your vaccinations and for them to work is this idea of herd immunity um so her immunity is when you basically have enough protection from everyone being vaccinated that your vulnerable m members of the community aren't going to get sick um so the idea here is you generally need a pretty high number so about like 95% um and then that's when you've got this sort of scenario going on so initially nobody's immunized sorry these people in red are sick everybody around them is susceptible they get the more sick everyone gets sick um so we've got a couple members of the population who are immunized again these people are sick um the people who are immunized they're not going to be sick right because they're immune to the um disease but again we've still got quite a lot of people getting sick just based on proximity and contact if we've got most of the population immunized we can see that this you know metaphorically creates a nice barrier that prevents these people from not getting sick and so these people may be people like the elderly or The immunosuppressed Who can't get vaccines or who would you know be sick if they were to get a vaccine um and that's what this idea of her immunity is it's very much in the name um it's the protection that the rest of the population gives to those who aren't able to be vaccinated due to the rest of the population being vaccinated so hopefully that um makes sense and it's obviously very helpful in containing um and almost like eradicating diseases as well okay so moving on to immunotherapy um so this is when we basically influence the immune system or manipulate the immune system in order to cure certain diseases um so monoclinal antibodies are a specific example you need to know you need to know them in the context of cancer and autoimmune diseases so with our monoclonal antibodies we have um you know just like any other ant antibodies and they are specific to for example let's say cancer um so what we do is we get basically a cancer cell and we figure out an antigen that a cancer cell may have and we put this into um like a mouse for example these are monoclinic antibodies that are made by mice so we put them into a mouse and then what we do is we um yeah put them in the mouse the mouse will mount an immune response against this specific antigen so you know again think about that little diagram with everything and they'll all have this specific receptor to this antibody so we're going to create plasma cells and they're going to create antibodies that have specific receptors and will Target this cancerous antigen um so the idea of epitopes here so we have um antibodies and then they obviously specific to antigens antigens themselves have little parts of them so maybe I'll see if I can draw this out um okay so let's say that this is a bacteria and we'll say that this is an antigen um now there are specific parts of the antigen that antibodies will bind to so you might have this sort of sitting on here obviously this is a very um you know they molecules and whatnot um okay I don't even know but yeah right so we've got three different things so these are what we would call epitopes so you can see that things can be specific for an antigen but then they can be even more specific to certain epitopes on that antigen um so that's why you can have for example here you can have three different antibodies for one antigen um so that's the idea there so some antibodies will be more effective for the epitopes than others and so when we figure out what antibod is the most effective that's the one that we'll Harvest from that Mouse and we'll clone it and then we'll use that in that individual because we know that that's a really good antibody so that's why it's called like monoclonal because it's specific to one particular epitope um so if that makes sense so you just put it in the mouse the mouse creates these plasma cells you take the plasma cells you make lots of them monal antibodies um okay so this is a nice little diagram of that here um so this idea of we pop it in a mouse it does its thing and we get this antibod so we fuse it with these tumor cells um and that means that the plasma cell will just keep on going and going and going and going and going because they basically um we choose these specific cells that don't have like an an end date basically and that means we can produce even more and more and more cuz the goal is just we want to create as much um as many antibodies as we can um so obviously this is quite useful it is a developing area of research you know there's lots of other um diseases that it's being used for again you have to know what in the context of autoimmune diseases so um like rheumatoid arthritis for example there's um a monoclinal antib that's really popular it slips my mind now it's like ruim or something like that I don't know you can have a look into it um but yeah that's being used you know in um the context of autoimmune diseases so you can use that if you've got an autoimmune disease so sometimes your you know your tea cells they may be targeting your self cells um because there's something a bit dodgy with the te- cells going on right so you can use these antibodies to actually Target those tea cells um as opposed to you know your cancerous antigens so that's another way of using monoclonal antibodies um but they're really helpful because they're very specific as you guys know I've been using the word specific about a billion times again use it in all your short answers um it comes up a lot in BIO but yeah it's very specific and compared to you know chemotherapy and radiation which just target fast um replicating cells in general it can result in less severe side effects because they're more targeted to cancerous cells as opposed to you know like hair cells or skin cells or stomach cells stuff like that um yeah that's basically the idea there okay so in terms of pathogens needing to understand um it's just kind of this context of Co really this idea of when known pathogens which you sort of eradicate can come back um so it's just this idea of especially it says there in the study design do point in a globally connected World you've got people moving about to different locations and we move very rapidly now um so it's very easy to be you know like in Australia where we've got a lot of diseases that are eradicated and you may go to another area um and then you know pick up a disease that's endemic there and then bring it back and that idea of again coming into contact with other people who travel and that can spread and so that's this idea of reemergence of pathogens that we know and are aware of but that we've kind of eliminated um so that idea of them kind of reemerging that's why sometimes you get like measles outbreaks um or you know like osis outbreaks and all those sorts of things um and yeah it may be from areas where tuberculosis or malaria is more emic and then that idea of kind of bringing them back the other thing you need to be aware of is emergence of new pathogen so this is obviously linking quite closely to co um it's this idea that nobody has ever seen it before and it's this emergence of a new pathogen um and it's this idea that these pathogens are more likely to cause pandemics so things like you know malaria tuberculosis they're endemic in certain areas of the world but they're probably less likely to cause pandemics because we are very aware of them whereas as we've seen with Co if you've got something that's quite new and particularly something like Co that's quite fastly mutating um it's very hard to get a grip on it early um and then that idea of nobody having prior immunity you know nobody has your little memory cells hanging around um so then that's when you get these kind of pandemics and um new pathogens can do a lot more damage is the idea there um okay so thinking about the effects of European settlement in Australia and the effect on the original t Islander population um the idea here is kind of what I was mentioning before in not having any immunity not having any prior exposure so it's this idea that in um Britain like before they came to Australia we bringing a lot of um communicable diseases with us on the boat right um and it's things that are endemic to this area of Britain for example um and that these people have been exposed to so they're bringing that with them and we then bringing it into a community into a community that has not been exposed to these viruses before so we can see you know small poox measles influenza this sort of thing that again would be um prevalent in um like the UK or in Britain and then it's this idea of bringing it to an area where um Aboriginal and torist Islander people hadn't been exposed to before so they don't have any prior immunity um and they're extremely susceptible to these diseases and it can wreak a lot of Havoc um and so that's what we saw at small pox this idea that there was an epidemic there's lots of um areas where you had really large outbreaks because ultimately nobody had immunity to it whereas you know some of the other people um like other people in Britain and obviously those that colonized Australia they would have certain levels of immunity to it having probably being exposed to it in childhood and things like that um so that's just one of you know the many obviously netive effects um and this idea of you know globally connected worlds and things like that and this spread of travel um and how that can bring diseases and we see that in lots of other examples of colonization as well and how that can really wipe out and ravage um a lot of communities so hopefully that makes sense it's just this idea of being exposed to something that you haven't been exposed to before and being extremely vulnerable to it okay so in terms of the transmission of infection um so we're looking at this idea of um this Chain of Infection so it's this idea that when you have a pathogen it kind of follows all these little steps so you've got um an infectious pathogen um you have a susceptible host really and this pathogen obviously infects this host via this portal of entry um in terms of these reservoirs it's where the Infectious pathogen basically kind of grow rows and just sits and it then exits that it's then transmitted into um somebody else so the reservoir may be another person really so the reservoir may be um yeah another person and then they're able to exit that individual and then it's transmitted into somebody else by that portal of entry hopefully that's making sense and then you've got the host who's infected and now they're creating more pathogens um so hopefully that makes sense you guys should be really on top of this by now with Co in terms of ways of controlling transmission particularly of our communicable diseases so hand washing physical distancing face masks all the stuff that I'm sure you guys are really really aware of um so there's a lot of modes of transmission so respiratory transmission droplet transmission um respiratory transmission is basically via the respiratory system so you kind of hack it out via respiratory system and then it goes into somebody else's respiratory system droplet transmission is kind of similar but a little bit different in that the pathogen can basically travel in the air via droplet so when you sneeze on something and you then like touch it and then touch your face or whatever that idea of being transmitted via droplets um contact transmission so via direct contact so for example the fecal oral rout um so yeah if you know the pathogen is excreted in the feces and somehow that kind of gets um you may not wash your hands properly after you know um going to the bathroom and then you may touch your mouth or you know you may eat something and then that gets in by the oral root so that idea of feal oral um Vector transmission so we talked about malaria at the start this idea of um the pathogen often being like a little parasite in that vector and that gets transmitted as well so if you think about malaria for example that idea of avoiding the vector preventing um areas you know so like preventing being bitten by a mosquito um getting rid of like mosquito breeding grounds that sort of thing um and then sexual transmission so kind of bodily fluids that sort of thing pathogen spreading bya there so like your STDs and all that sort of stuff okay so here is a bit of a question um we'll try and read it really fast um so BC is a preon disease of cattle so again how we were talking about how preons often commonly spread from animals to humans um so it's sometimes called mad cow disease caused by feeding cattle food that contains prons from other infected animals so you've got prons from other animals and then you feed that to cows and then basically like the humans eat the cows um blah blah blah blah blah the time between infection and symptoms appearing can be up to 5 years so you can have a Pon in you you can eat infected meat and then 5 years later you get the disease um if you think about it that's an extremely long incubation period um um and you can imagine the kind of trouble with that there are concerns that um vcjd in humans could be caused by eating infected cattle meat so this is kind of a variant from that so mad cow disease is in your cattle like the diseases in the cow hence mad cow and then when this kind of spreads to humans it's um your crit jaob disease so yellow fevers of viral disease that affects humans so here we're talking about something different so this is a pron this is a virus yellow fever is a viral disease that affects humans the yellow fever virus can cause symptoms 3 to 6 days after infection the virus is carried by a mosquito Vector which combination of approaches would be most effective at controlling the risk of outbreaks of both vcjd and yellow fever so you can see how they look so much information and obviously it's helpful for context but if you break it down again you're not expected to know what vcjd is you're not expected to know what yellow fever is Whittle this question down it's asking how can we prevent the infection of this pron how can we affect an infection um of a viral disease via a vector that's the idea they could have swapped the word vcjd and yellow F out for anything in the world um again you're just having to apply knowledge that you have already so prevent all cattle that show symptoms of mad cow disease from reproducing remove breeding grounds for mosquitoes um test or cattle for the presence of prons ensure that all Healthcare professionals wear gloves when working with infected patients um in terms of yellow fever so it's a viral disease that affects humans virus is carried by a mosquito Vector so you're going to want to look for something that is particularly targeting mosquitoes so removing breeding grounds from mosquitoes sounds pretty good ensure that all Healthcare professionals wear gloves when working with infected patients probably not the best thing um ensure that people take measures to reduce their chances of being bidden by mosquitoes yep that's pretty good instruct people who are infected with yellow fever to wear masks in public places not the best thing because this would be effective for maybe respiratory transmission or droplet transmission but not really for something that's caused by a mosquito um so you're kind of down to ument so you've got prevent or cattle that show symptoms of mad cow disease from reproducing destroy or cattle that have been fed infected food containing the prons um so again we're thinking of A and D that they could both be quite helpful so again what this comes down to is what is the best answer um so if you read you know a or C sort of by itself you may be choose sorry you may be inclined to choose them which is important oh my gosh which is why it's therefore important to read all of the answers so that you can get the best um option so prevent all that show symptoms of mad cow disease from reproducing so that same that sounds um you know relatively good but think about the method of transmission so prons from other infected animals um so basically the cow's got the pre-own in it right and then it becomes vcjd because somebody eats that cow so if you prevent or cattle that show symptoms of mad cow disease from from reproducing okay that might be good but does that stop that cow from having mad cow disease no does that stop that cow from being uh like cut up and then given his food no so that's why C is the better option destroy or cattle that have been fed infected food containing the prons um because of that idea that you're preventing at all costs um that from becoming meat that someone will eat whereas a prevent or cattle that shows symptoms of mad cow disease from reproducing that doesn't that cow can still be become meat and someone can eat it and they can get BC JD hopefully that makes sense okay I know we kind of raced through that one but hopefully that's all making sense um so we'll finish off with you know experimental design in our exam study again the study design is really helpful um with this you just kind of have to fish through it and see what's actually useful what's not most of the important terms are in here um when we get to it I will talk about reproducibility and repeatability because that's something that's been introduced with this study design um but super super super super super important if you haven't done your area of study of three area of study 3 sack yet um do all of this stuff as soon as you can because it's really important for that sack but also for your exam there are always questions on it um particularly towards the end of the exam I want to say towards the end of the exam is when your questions get longer so that's when you start to get big paragraphs when you start to get lots of multi-part questions and it's sort of where they try not where they try but where they do tend to bring in a lot of area study 3 stuff um I remember when I did bio I hated it I hated it with a passion um yeah that's basically it but you just have to study it and eventually you know you might find a liking for it somewhere I personally didn't really but um it's really important and I think because I hated it I never wanted to study it but I had to otherwise I would have lost a billion marks um so just be mindful and I think something as well I used to tell myself like oh you know I've done this for lots of years like I know it really well it's fine but you have to work like doing practice questions with it um so that you have ideas in your head of how via will ask questions relating to photosynthesis relating to cell respiration relating to transcription translation DNA manipulation Immunology all that sort of stuff um and how they will apply it in that context you can't just say like oh it's an application question so I'm just going to apply it when I get there it's an application question so I need to practice applying it in as many different scenarios as I can is what your thinking should sort of be um Okay so your variable so your IV is the thing that you manipulate your DV is the thing that is being um measured the whole point of your experiment is to figure out what the effect is of the IV on the DV um your controlled variables are basically any variables that could affect the DV that you obviously don't want to um they need to be kept controlled if you do not control these there is no way of saying the IV has caused this change in the DV because it could be this other variable that you haven't left controlled and then your experiment is useless basically um so your experimental group and your control group very important to distinguish controlled variables from your control group controlled variables are the things that could be the IV just the little variables control group is the whole like setting um so your experimental group is what is exposed to the IV so if you are observing light intensity and its effect on photosynthesis your experimental groups will be um you know I don't know dim light average light right light your control group will be something in the dark um it's something that is not exposed to the independent variable and it acts as a baseline comparison and it also makes sure that you don't have any confounding variables so you are checking yet light intensity on photosynthesis you've got your dim light your midl and then your bright light um and then you know your dim light doesn't grow that much midl grows a little bit more your bright light grows amazingly if your plant that is in the dark if that grows amazingly you're kind of thinking something's going wrong here right because we're not exposing this to the independent variable so it should serve as a baseline it should be like a zero really um or it should you know if it grows 3 cm then you'd expect everything else to grow above 3 cm um it's that idea of that Baseline comparison so that is why the control group is really really important and whenever you write about um a an experimental design you need to make sure you identify that you have a control group um okay so your validity and your reliability validity is basically um is this measuring what it's meant to measure so you can think about that in terms of equipment or in terms of your experiment it's is this experiment have I designed it in a way that it actually tests the IV and the DV so I want to check the effect of light intensity on the rate of photosynthesis is my experiment actually set up in a valid way that I am able to like answer the question basically um it's similar to accuracy but accuracy is basically um is this correct like um my plant has grown by 3 cm is this sort of like actually how much you know it's grown by um has it grown by 30 cm and I'm using the world's West ruler that sort of idea um reliability is if I repeated the experiment is the result going to be the same Precision is are all my results within a narrow range um in terms of your repeatability and your reproducibility repeatability is same time same place reproducibility is different time different person different place so your repeatability again think of the name of it as well repeat versus reproduce if I'm thinking about repeatability it's if I perform these measurements again in the exact same context the same person the same equipment am I getting the right results if it's reproducibility is it if I'm a different person on a different day in a different environment using different equipment am I getting similar results so that's what you should think about as well um so having a large sample size repeating the experiment is really important for your reliability and getting rid of your um oh my gosh your error your it'll come up yeah your random errors that's the way I was I was going to say standard errors your random errors um having a large sample size and repeating is really important for that so Random errors are just that really random errors um you know sort of like fluctuations in atmospheric pressure temperature that sort of thing um it's completely random and it will affect like one random result whereas your systematic errors affect every single result consistently so it's often to do with equipment so if you've got a measuring thing like I said like the worldwest ruler if you've got a ruler and it measures it's got your 1 cm 2 cm 3 cm but in actuality each of those cm are 1.2 CM apart it's going to create a systematic error because you're using it to measure everything and it's going to be out every single time whereas your random error um would be yeah the temperature in the room changed so then I don't know the plant wilted or something like that um so that's what you're thinking of there so um be really aware of errors and ways to improve errors and things like that um very very important qualitative and quantitative data I'm sure you've been bought to death of this sort of thing qualitative quality descriptive words subjective quantitative more objective more numerical quantitative data is what you sort of aim for qualitative is still very helpful but quantitative is just a little bit more robust um okay [Music] so um in terms of answering an experimental design question very different to answer an experimental design question in an exam versus you would for your like area study 3 sack um so there are a couple things just to kind of note um so it depends how many marks generally there might be about four marks is maybe less um so you just need to be really concise you're not writing out when you're writing out a method as well you're not writing out um a method as you would in your area of study 3 sack where it's like a billion step long you're just being really concise and giving a nice overview about your method um so your treatment and your control groups your you know your experimental your control groups remember that control group it's really really important students always forget it remember to include a large sample size um remember to be as specific as you can dependent and independent variables your controlled variables again listing about three a sentence or two a sentence or two nothing more nothing less um about your method but but again you don't have to go step by step by step by step this is a four mark question not a 40 mark question so really be mindful of that um but at the same time don't be too brief you need to give a proper explanation of what you're doing and lastly repeating the experiment um talk about this idea of you know your reliability or your repeatability repeatability that sort of thing um and talk about how you're minimizing your random errors through that hopefully you all said that at the same time um but yeah random errors are what you're thinking about in terms of repeating that experiment because if you think about it if you have um like four measurements and one of them is affected by a random error that can screw your results based on if you've got 40 measurements um you know one in four things being dodgy that's going to create a bigger effect than one in 40 things um so just be really mindful of that okay we will we go through this a little bit um so two researchers have discovered that they did not properly label a bottle containing the enzyme amalay which catalyzes the breakdown of starch the amalay could either be amalay from a human or from thermos aquaticus found in 80° Hot Springs so devisor test they could conduct on the amas to determine its source and includeing your answer which characteristic of enzymes makes this possible so we're thinking about um the optimal conditions of enzymes here in terms of temperature so optimal in a human would be about 37 in De optimal in this Theros aquaticus is 80° so you're going to try and figure out um what works in what environment so you'll have about four groups here you'll actually have two different control groups um because you will have your control groups at different temperatures so you're going to do one in your human sort of thing so you'll have um your amalay with your starch in your 37° um temperature and obviously if that works you know and you get glucose from that um that will tell you that it's a human you will also have your amalay by itself at 37° that acts as a control because you don't want any glucose to come from that your thermos aquaticus the same thing you'll have your starch and your amalay at your 80° again if that works you get glucose from there you're thinking of your thermos aquaticus being from there um you're also going to have another control group you're going to have your starch at your 80° so you can see what I mean by two control groups there um so your independent variable is essentially the temperature your um dependent variable will be the breakdown of starch so that kind of indication of the level of glucose there um your controlled varibles so you'd think about um the amount of amalay that you're using the amount of starch that you're using that sort of thing um in terms of control variables in terms of your method you just kind of talk about what we talked about in terms of that setup so maybe you leave it for um 10 minutes and you check the glucose reading every 2 minutes perhaps um and you would repeat the experiment that's a sort of idea there I don't know if I've missed anything but you just follow this little step um okay maybe I'll leave you to have a go at this just based on the time but um a molecular biologist suggests that The Binding of a specific hormone to muscle cells causes them to produce a much greater amount of a specific protein design an experiment that the biologist could undertake to determine if his hypothesis is supported so your independent variable here would be the presence of the hormone so basically you'd have specific hor to muscle cells so you'd have um muscle cells and you would have some exposed to the hormone some not and you're measuring how much protein is produced so dependent variable is the amount of protein X that's produced your independent variable is basically the presence of this endon and your control group is the muscle cells without endon um you might use varying levels of endon perhaps um but yeah your control group would be sorry your controll variables would be um you know maybe the amount of muscle cells that you've got the um you know presence of other hormones you would want to minimize that um perhaps yeah that's kind of what you're thinking of there um in terms of your method kind of what we've talked about in terms again of that setup you would just leave it for a couple of minutes measure the protein level think about how you might pressure the measure the protein level um perhaps with a little protein X detector I guess that's the most um specific thing to be using um and yeah it would repeat the experiment as well okay but again feel free to write that out and elaborate a little bit more on that um okay so these are some of the ethical principles in this study design bioethics are um emphasized a lot more than they have been in previous years um so Integrity basically just being honest communicating all of the results even if they're bad Justice ensuring that everyone is treated fairly ensuring that you know whatever you're researching like say it's a drug or something um it'll be accessible to like all people and you're not going to create this sort of unfair Market really beneficent so beneficent and non-maleficence are sometimes confused beneficent means doing the most good and non-maleficence means doing the least bad basically um so beneficent you're always thinking about yeah promoting benefits always doing good um and then non-maleficence you're just wanting to avoid um harm you're wanting to not yeah cause any um negative consequences along the way basically and respect I'm sure you guys are all familiar with respect um okay so approaches to certain bioethical issues so they can be consequences based Duty based or virtues based um so consequences based basically means that the um emphasis is placed on the outcome so it doesn't matter what you did along the way as long as the outcome is ethical um you know that is what you did along the way but as long as the outcome is ethical that's where the most importance is placed um Duty based or rule based is basically this idea that whatever the outcome is you have to be moral along your journey or you know be ethical along your journey so that's the kind of they're almost a little bit opposite Duty based and consequences based um and then virtues based is this idea of if you acted sort of morally vir space is kind of a bit like like a bit random but um yeah consequences based as long as your outcome is ethical that's your main focus Duty based as long as along the way everyone's being treated ethically that's the most important and virtues based is as long as you acted really morally that's where the most importance is again this is very application based um you likely get like some sort of scenario and then um if you were to act in a virtues based use a virtues based approach what would this involve in that specific you know scenario or context um okay so a new drug to treat malaria is being Tri by scientists to apply the concept of non-maleficence to their research the scientists should ensure that what so non-maleficence um so any harm to the participant resulting from The Trial is not disproportionate to the benefits obtained from using the new drug yep that sounds pretty good data that shows the new drug is ineffective is not published that would be um to do with integrity and that would be breaching Integrity consent is obtained from all of the participants in the trial that's just um I guess like respect informed consent really um the participants experience only the benefits of the trial also sort of beneficent in that way um so Precision medicine can be used to develop anti-cancer drugs that Target and silence the gene or genes that cause a particular cancer the government does not provide funding for many of these drugs and patients may need to spend upwards of 100,000 for one course when many courses of the treatment are likely to be needed to prolong life this leads to unequal access to these life-saving drugs in society situation shows a lack of hopefully you all said Justice um again you had like seven sentences there or just less than um you could literally just use the last sentence this leads to unequal access to these life-saving drugs in society you can answer the question just based off that so again be mindful of not getting too caught up um in unnecessary or irrelevant information okay um so we'll finish off with just kind of going over some exam study tips my biggest one practice questions I used to hate practice questions my teacher told me to do a lot of them and I used to think it was silly until I like literally as I mentioned like didn't know how to answer or realized I didn't know how to answer bu questions um I would recommend practice questions for all of your subjects for me buo was the most important subject that I had to do practice questions for just because they're so picky like you can think that you're getting all the points and like ly you are getting all the points but if you don't write it in a specific way they'll Mark you down um so use practice questions again I know you guys are using a new study design so some of old exams may not be as helpful but you can still go through them and you can still sort of recognize what is on your study design and what's not um focusing on your weaknesses is a big thing I um I okay I don't want to lie I didn't really do it for um my VC subjects that much but I did it for the ukat when I was studying for that and it was really really helpful um and I think I kind of take that with me and uni now this idea of making a little log of everything that you get wrong and the types of questions that you typically get things wrong on you should do those over and over until you get them right really um so this idea you know I kind of mentioned like oh I would love to do questions or even subjects I'd like to do stuff that I knew I was good at um but then that doesn't help you in the long run because then I would stay bad at questions that I was terrible at basically um and then so the more you practice and do those questions and the better at them you'll get and then you'll want to do more of them um asking questions so obviously your teachers your friends um your tutors you know on the internet you can find resources for Bio everywhere cuz like everybody studies bio um as in like you know it's done in uni it's done in like every school overseas that idea of Bio being a very very very popular subject um so there's no shortage of resources so please use them to your advantage um and also as we get to this time of year going into term three again a lot of you may be in year 11 a lot of you may be in year 12 um particularly those for in year 12 but of course if you're in year 11 as well um you can get really stressed at this time of year so it's really important to kind of check in with yourself make sure you're not burning yourself out especially not now term three is often the one where you lose a lot of motivation I know I did and I think I got slightly Little Burn out um burn out yeah just like I got really demotivated by the middle of term 3 um and so it's important I think not to go too hard too fast and always be checking in on yourself and something I always did was I always gave myself breaks um I knew that if I just pushed a little bit more sure like maybe I would have gotten an extra Mark in a bit of a higher grade but it would have come at the expense of my like mental health really um and I knew that it wouldn't have been produc for me anyway again of course everyone's got different learning styles but I think it's really really important not to ignore when your body and your mind just really need a bit of a break um okay so in terms of your exam I know this is only coming up in a while we're talking about exams at this time but don't get too psyched out you've got a lot of time um and that's kind of what this point is relating to as well everything that's gone on in the past 6 months with your saxs and all that you don't need to worry about them too much like obviously SE are important try your best but your exam is where most of the money is um and there's no reason why you can't improve on this semester sex and do well in your exam and then that can take your grade up a lot as well um my teacher used to always say that sex are a draft so they make up you know a smaller percentage um of a bigger score so it's important not to focus and dwell on sex scores too much especially when you've still got a whole half of a year to focus on um it's really important and don't think and don't get into yeah the sort of head space that oh you know I've done badly in my sack so I can't do well um even if you do better than all of your sacks which I'm sure none of you will um but you know moving closer to the exam still try in your exam you can still do well it's a lot more um a bigger proportion of your grade so just always you know keep doing your best and don't ever think that um a bad sack will mean a bad study score because that's not the case at all I think in BIO I had a that was um really quite low um and I remember I thought the same thing like oh okay I've already flunked it um but then I didn't so the same could happen to you um learn from your sex I know my teachers are a bit funny in like giving sex out but sometimes they'll let you like look at it you know in there like they might not let you take it home but hopefully they'll let you read over it um and just learn it's just the one thing like learn from all of your mistakes like when you get into your practice exams as well note your mistakes down note especially ones that keep on recurring and why you made the mistake I always say marking your exam is almost more important than actually doing it because there's no point in doing an exam and not marking it because then you're going to make those same mistakes you know a billion times um really really really try to learn from things that you get wrong and also things that you get right even when you get things right think did I get this right like particularly for multiple choice did I get this right because I you know came to the right conclus clusion via the right pathway or did I just kind of like guess a little bit or did I think something completely wrong and I just happened to get this one right by chance um so yeah just be aware of that um unit three I feel like I mentioned this before but keep on revising your stuff for unit 3 do not let it slip to the back of your head now is a really good time to think of all the stuff from area study 1 I know most of you would have just finished like your um you know if you haven't started immunity already before the term ended um but matter have finished you know your cellular respiration your photosynthesis don't forget your transcription translation stuff your protein stuff super important with antibodies and Immunology antibodies are an example of proteins so all of the protein stuff from AA study 1 that's all relevant still in immunity anything that you talk about with proteins can still apply um in terms of antibodies so um yeah always continue to revise your unit three stuff and it just saves you time because otherwise you're going to get to September October you're going to have to go back and relearn everything and it's just going to be a lot harder than if you just did like a couple questions on the weekend um or the week or you know whenever you want but just like slowly revising stuff and keeping it in the back of your head rather than losing all of it um and then having to yeah catch up again a little bit later um okay practice exams emphasis on maybe time I personally started practice exams a little bit later I would say like um maybe like six weeks out I want to say take what I say with the graen of salt it's been it's been a long time but um yeah I would say like six weeks out I know some you know of the other tutors and some other students some of my other friends even tend to start practice exams a lot earlier it just depends on where your confidence levels are at just depends on how you feel you wish to prepare for me I didn't like the idea of doing practice exams before I was really confident with everything practice questions are different um but practice exams I yeah prefer to be a little bit more on top of the content so I would actually be sort of like mimicking how I would feel you know on the day um and I feel like if I did practice exams earlier like practice exams before I finish the content a lot of my friend did that a lot of my friends did that I just never really like that idea but again it's whatever works for you um but yeah with bio past exams so many of them are accessible again there's heaps of vard ones unfortunately for you you're just going to have to like Shi um sift through what is still relevant on this study design um or but yeah a lot of schools do those like exam booklets and so those are quite helpful as well and they tend to give them out pretty early um but yeah use your reading time think about how you're going to approach it are you going to do short answer first are you going to do um multiple choice first figure out that sort of stuff um and yeah try to build up your stamina as well so do it under timed conditions obviously doing it closed book um and Mark your exams of course don't waste your practice exams is kind of what I think cuz otherwise you could just be doing practice questions um we kind of talked about this in terms of keeping track of your mistakes but yeah be really helpful to observe them um okay I think this is the yeah the last slide um so we've talked about complimentary this idea of being specific just comes up and bio all the time like I'm almost sick of saying it so much um all the time so just be aware of it and make sure you are explaining things especially with immunity like on an in enough depth but also concise I know that's so annoying to hear that like use a lot of words but don't any um but being concise in BIO was really important especially cuz it's just so much stuff like I tend to be a waffler when I write and I remember like this one I was thinking about this one question in my exam that I did in 2020 um and I remember I like waffled on and as I was writing it I remember like I used extra line space I was writing in the corners and I was like oh as I wrote it I like knew like okay like I've done what I'm always like thinking I shouldn't be doing um so you know even if you have to plan questions um do that but yeah once you sort of get into that habit of waffling it's hard to get out of um and so just practice practice practice for those like practice questions really help because it's it's technique um as opposed to like knowing content um I'm just trying to think about yeah the other stuff are just kind of General things um I I'm just thinking about if I have any other study tips that I haven't mentioned again visual things always worked really well for me um you know hopefully I've answered most of your questions in the live chat but um yeah they always worked for me and I think that they helped consolidate information a lot and sometimes I wouldn't understand things until I saw it visually again you may be a different type of learner but it might work for you um yeah flashcards mind maps all those sorts of things structure your notes around the study design I don't know if I said that um but that's really really important again knowing the study design like the back of your hand but structuring your notes around the study design can be really helpful because it can show you what is relevant and what's not um creating mind maps linking the areas of study together as well which kind of comes into that last dot Point um don't get too in the zone with one area of study like you don't be on immunity and think like okay I'm only talking about immunity I'm only talking about immunity and then vco trying to weasle in this little question about proteins to do with antibodies but you're like immunity immunity immunity and you don't realize that you're having to bring stuff in from other areas of study um I think I remember there was a question like that I can't remember if it was on my exam um but it was about like photosynthesis and something to do with enzymes and then linking that to proteins and I think via wrote like you know a lot of students weren't able to make that correlation um so it's really important to not get too like to not like um almost like segregate the areas of study okay hopefully that all makes sense um again hopefully all your questions have been answered in the chat but otherwise do feel free to email me again lordes tmart.com um hopefully that has all helped again immunity is a big topic but once you break it down once you get through the processes um and once you just revise them constantly constantly constantly I know this would sound like but it just clicks um and I know it's easier like said than done just to wait for something to click but um if you keep on revisiting them the process makes sense and that's why I find like if you like I read about it I drew it I watched videos I Tred to get as much information from it as possible and kind of absorb the information in different ways so that it painted a bit of a bigger picture in my head I think with stuff like this where it's very process um that can kind of help and yes don't let experimental design fall to the back of your mind always keep that up to date same with the rest of unit three okay I will not keep you any longer I hope that all makes sense thank you guys so much for tuning into the lecture hopefully it's been a bit helpful and good luck with all of your exams good luck with bio 34 um any other 34s that you're doing as well I'm sure you do really great thanks guys bye