Hey everyone and welcome to Miss Estri Biology. And in this video, I'm covering all of topic 2 for AQA Alevel biology. And if you didn't know, you can download for free by clicking the link in the description the workbook that I created that goes alongside this entire video. So save yourself time having to make extensive notes and do this instead to get a general overview. But if you want even more detail and a better idea about key terms, examiner's tips and topic summaries, then check out my readym made aable notes or my flashcards. But that is it for now. Enjoy the video. AQA topic, the entire topic. Let's get into all of this information then starting with 3.2.1 which is cell structure for the ukarotic cells. These are the 10 organels that you need to know both the structure and how that structure links to the function. So, we're going to go through all of these. Here's just showing you an overview though of what they look like inside of the cell. So, we have our cell membrane on the outside. Now, although it does say vacule here, and it's an animal cell. Animal cells don't have permanent vacuoles, but they can have temporary vacules. Things like your fagosome that you get in fagicites, but we can kind of ignore that for the sake of this slide. Roughen plasmic reticulum. So you've got these folded membranes with the ribosomes on the outside. They look rough or bumpy. Gi apparatus, the one that looks like a Wi-Fi symbol. the cytoplasm, losomes, ribosomes which are the smallest and then smooth endopplasmic reticulum and the mitochondria. So centrosome is not on the AQA spec. In plant cells, they have all of those structures plus three additional ones. They do have a permanent vacule which is surrounded by a membrane called a tonoplast. They have the chloroplasts which is a cytosynthesis and then they also have the cellulose cell walls. So if we have a look at the nucleus first of all the structures and the functions the nucleus has got an envelope which is this membrane around the outside this double membrane and there are holes within that called nuclear pores. The liquid in the middle or the jellyike material is the nucleoplasm. You have the chromosomes within the nucleus which are protein bound and described as being linear DNA. And then we've got the nucleololis which is this additional small sphere inside of it which in terms of the function really that should be on that side but the function is the site of RNA production and it makes the ribosomes. So if you were asked to describe the functions of the nucleus one of them we've already said down here RNA production and it makes ribosomes. It also contains all the genetic code for each of the cells and it's the site of DNA replication and transcription which is the making of mRNA. Endopplasmic reticulum can be rough or smooth and both of them are made up of folded membranes called the cyine but the rough has ribosomes attached to the outside which is what makes them rough. So here it is under the microscope and all those tiny black dots are the ribosomes giving that rough feel or rough look. The function of the rough endopplasmic reticulum is for protein synthesis and the smooth endopplasmic reticulum is the synthesis of the lipids and carbohydrates. The GGI apparatus and then the GGI vicles that pinch off. First of all, the structure though it's folded membranes making these sistony again and it creates this wif-fi symbol is what I hear most people describe it as because you've got these curved folded membranes and then the vicles bubbling off. So those secretary vicles pinch off from the cyine. There's a whole range of functions for the ggi apparatus and the vicles. So you could have carbohydrates being added to proteins to form glyoproteins. You also get secretary enzymes being made, secrete carbohydrates. They transport, modify, and store the lipids. They form losomes. Molecules are also labeled with their destination here, meaning you might add on some sort of chemical tag. So, they can only bind to a target cell. And also, we've got the finished products are transported to the cell surface through these gold vicles. They move up and fuse with the cell surface membrane and that then releases the contents of the vicle. The lossomes are these bags of digestive enzymes. We can see one here. So just like sacks filled with digestive enzymes. So all of their functions are going to be to do with hydraying and digesting. So they could be hydraying pathogens inside of the fagosome. So in your fagosytes in topic two which we'll get into later on in this video you've got your fagosome that has got a pathogen engulfed within it the loone contains digestive enzymes that fuses with the fagosome and that digests the pathogens. It could be to completely break down dead cells within the body that you don't need anymore. You could have exocytosis meaning the release of those digestive enzymes to outside of the cell to destroy material and also it might be to digest worn out organels so you can reuse those materials. The mitochondria is a double membrane bound organel. We've got the outer membrane here and the inner membrane is folded. It's shown as this bright yellow structure here folded so that you've got a really large surface area for some of the stages of respiration. So that folded inner membrane is called the christi. Inside of that you have a fluid fil center which is known as the matrix. You learn more about this in topic five when you learn aerobic respiration. You also have loops of DNA and 70s ribosomes which are the smaller ribosomes you typically get in proarotic cells. And you need both of these structures so that within the mitochondria you can have the creation of proteins for example enzymes that are needed for aerobic respiration. So the function then is it's the site of aerobic respiration not anorobic just aerobic which means you have lots of ATP being produced here and also we get enzymes being created for respiration. Ribosomes. These are small. They're the smallest of the organels made up of two subunits of protein and RNA. Those are the two molecules that a ribosome is made up of. You have two different sizes. ATS which are the larger ones which are found in ukareotic cells and 70s are smaller in size which are found in proarotic cells but also inside of the mitochondria and chloroplast in ukareotic cells. And the function is for protein synthesis, meaning making proteins. Then if we have a look at a vacule, so we're thinking about a permanent vacule that you get in plants here. This structure is filled with fluid and it's surrounded by a single membrane which we can see here is this darker layer which is known as a tonoplast. The function is by having liquid in the center. It pushes everything outwards and that makes the cell turgid and therefore it provides support. It can also be a temporary store of sugars and amino acids and the pigments that may color petals to attract pollinators can be found there as well. Next then chloroplast which again are found in plants. This is very similar in structure to a mitochondria. It's also double membrane bound, but this time we have the outer membrane and the inner membrane directly next to each other, both creating a sort of oval shape. Instead, these folded stacks are additional membranes called philyloids. So, we've got these folded philyloid membranes that fold up to create almost like pound coin or discshaped stacks. And those stacks are known as granum for singular or grana for plural. You learn more about that when you get on to topic five for photosynthesis. You also have a fluid fil section here which is known as the stroma and the function is photosynthesis. cell walls which are found in plants and fungi but also in bacteria but we'll come back to bacteria in the proarotic cell section. So the cell wall in plants is made of cellulose. The cell wall in fungi which are actually also ukarotic cells is made of kitin and whatever it's made of the function is the same. It provides structural strength to the cell. plasma membranes. This is found in animals and plants actually found in all living cells. So we've got it's the phospholipid billayer which we can see here. We've got one layer of phosphoipids. A second we've got the hydrophilic heads on the outside hydrophobic tails pointing inwards. And within the plasma membrane we also have proteins embedded. We have some carbohydrates on the outside as well. And you also have a lipid called cholesterol embedded within. And the function of the plasma membrane is to control what can enter and exit the cell. And this comes up again later in this video when we look at transport across membranes. So that's the ukareotic cells and their organels. Next, let's have a look at proarotic cells. For example, bacteria. And we can see a range of the organels here. Some on here you don't need to know, but you do need to know that it has a plasma membrane, a cell wall. Sometimes it has a capsule. You don't need to know the pilli for AQA. We've got a fleellum here, which some of them have, and some of them may have one or more plasmid. You do need to know that they have cytoplasm ribosomes and then the DNA is as a loop of DNA in the cytoplasm. So, let's have a look at that information. The key differences then are between a proarotic cell and a ukareotic cell. Proarotic cells are much smaller. In exams they insist that you say much smaller, not just smaller. They don't have any of the organels that have membranes and we describe that as membrane bound organels. They do have ribosomes just like ukarotic cells except they're smaller in size. They're 70s. They do not have a nucleus. Instead, their DNA is found as a single circular DNA molecule in the cytoplasm. They do have a cell wall, but it's made up of a glyoprotein, not cellulose, not kitin. And that glyoprotein is called mureine. Some of them might also contain any of these three extra structures. They might have one or more plasmids, which are small loops of DNA that only have a few genes on them. often the genes for antibiotic resistance. Some of them have a capsule around the cell wall as well. This prevents the cell from desiccating meaning drying out and also it helps to cover the antigens to evade the white blood cells. And they might have one or more fugella which is for movement or locomotion. Viruses these are not classed as living. So they're non-living and they are asellular. This has come up as an exam question before to define what those two terms mean. So non-living, it's classed as not being alive because it doesn't do any metabolic reactions within the structure or within that particle. It cannot move. It cannot respire. It cannot replicate without using a host. And it has no means of getting nutrition. It's called ascellular, meaning it's not a cell basically. and it's not classed as a cell because it doesn't have a cell membrane. Viruses are even smaller than bacteria and they only contain three structures. They contain the genetic material, capsid and attachment protein. The genetic material is this here in the middle and that can be DNA and it can be RNA. It'll be one or the other. That genetic material is surrounded by a protein shell called the capsid, not to be confused with the capsule that some bacteria have. So capsid is the protein shell that protects the genetic material. And then the only other structure that all the viruses have are these attachment proteins on the outside and that's what they use to attach to receptors on host cells. Now we can see additional structures in this picture. We've also got an envelope and some viruses do gain a lipid envelope by taking it from the host cell that they infect. They aren't able to produce their own one. So that is the three things that all virus particles contain and that's what we call them a virus particle because it's not a cell. So next then is looking at how you can study cells and how this has evolved so that we've been able to understand these organels that different cells have and you can use a microscope cell fractionation and ultraentrification. These are things we're about to go through the types of microscope magnification calculation calibration calculations linked to this idea of the eyepiece graticule and then self fractionation and ultra centrifugation. Starting with these two key definitions, knowing what's meant by magnification and resolution. Magnification of a microscope refers to how many times larger the image sizes compared to the actual size of the object you are viewing. Resolution of a microscope is the minimum distance between two objects in which they can still be viewed as separate and therefore you get a clear crisp image. Still the resolution of any microscope is determined by the wavelength of the energy source. So for an optical microscope, light visible light is the energy source. So the wavelength of visible light is what determines the resolution. For an electron microscope, beams of electrons energy source. So the wavelength of electrons is what determines the resolution. So if we have a look then at some of these differences between optical which are the light microscopes and electron microscopes which can be scanning or transmission. First then is what it is that creates the image. So for light or optical it's a beam of light which is condensed to a fine point using a glass lens. An electron microscope it's a beam of electrons which is condensed to a fine point using an electromagnet. Optical microscopes have a much poorer resolution and that's because the wavelength of light is longer. Electron microscopes have a much much higher resolution or resolving power and that's because electrons have a shorter wavelength. Optical microscopes have a lower magnification and electron microscopes have a higher magnification. Optical you can get color images whereas you can only get black and white images with an electron microscope. You can then artificially add color to that image using different Photoshop kind of programs, but with the actual microscope, you only get black and white. And then optical microscopes, you can view living samples, but you can't in an electron microscope. And that's because when you're preparing the sample, it all has to be inside of a vacuum, meaning there is no air. And that's because the air would absorb the electrons and then you wouldn't get in the image. So, it has to be a vacuum, but because it's in a vacuum with no air, that means you can't create samples with living things because they would die. So, just um to see an image here, we've got what we can see with an optical microscope. Because they have a much poorer resolution, that means that we can't see the small organels in a cell. We can see the cell membrane, not in detail, but we can see it's there. cytoplasm and the nucleus and the chromosomes when they condense but we can't see all of the organels and we cannot see inside the organels but we do get a color image and we can look at living cells with an electron microscope the electrons as we said can be absorbed by air so it has to be prepared in a vacuum which is why we can't have living samples and it's why it's black and white a transmission electron microscope these are the ones where the electron electrons transmit meaning pass through the specimen and that is why we have to have extremely thin slices of the specimen. They are stained and placed in the vacuum and an electron gum produces a beam of electrons that passes through the specimen. Some parts of the specimen absorb the electrons and appear darker. So that's how we get these different grayscale black and white parts of the image. So you end up with a 2D image but you can see inside of the organels. So this here is a chloroplast and we can see the membrane, we can see the philyloids, we can see those stacks, the gran. So you can see details internally. A scanning electron microscope, the specimen does not need to be thin because the electrons are not passing through the specimen. Instead, the electrons are beamed onto the surface and the electrons scatter back. And because they scatter back in different places because of the contours, you end up with these 3D style images. You can't see the internal structures. The electrons bounce back or they scatter back, but you can get an idea of the contours creating a 3D image. The math skill linked to this then is magnification. and it's being able to calculate the magnification or you might have to rearrange the formula to work out the actual size. So the key thing is knowing the formula. I always remember as I am so image equals actual size time magnification and then I'd rearrange it if I needed to work out magnification. And you usually have to do unit conversions with this because most organels the actual size will be measured in micrometers because they're very very small structures. But when you're measuring your image size that is usually going to be in millimeters. So that means when you do your calculation let's say we're working out the magnification and we're doing image size divided by actual. They both need to be in the same units. So you'd either need to convert your millimeter image size into micrometers and to convert millimeters into micrometers you would times by a th00and or you'd need to convert your actual size in which would be micrometers into millimeters and that would be divide by a th00and. Now you could also be asked to calculate the actual size and in which case we need to swap actual and magnification here. So actual size would equal image size divided by magnification. And if they want you to work out actual size, they'll probably state that they want the answer in micrometers. So again, you might need to do a conversion. Then we move on to what is the eyepiece graticle. So inside of the eyepiece, which is this part here, there is a scale on a glass disc which is called the eyepiece graticle. So when you look through the eyepiece, you will see what looks like a ruler. And this can be used to measure the size of objects that you are viewing underneath the microscope. But you need to know what each of these divisions on this graticule or ruler is worth. And that is going to vary depending on what magnification you are viewing the specimen at. So that's why we have to calibrate the eyepiece graticle every time we change the magnification. And when we say calibrate, what that means is work out what each of these divisions is worth in terms of a distance. So the way that we would do that is you have your eyepiece graticule in the eyepiece, but you also place a stage micrometer on the stage, which is this bit here. And a stage micrometer is typically 2 mm long and it has subdivisions 10 micrometers apart. So, it's a glass slide that already has known distances etched onto it. So, you line up your stage micrometer on the stage of the microscope. And you would maybe need to twist the eyepiece a little bit so that the eyepiece graticule is now completely lined up next to it. And we then need to look at how many divisions on the eyepiece graticule fit into one division on the stage micrometer. And we know that one division on the stage micrometer is worth 10 micrometers. And we can see that we've got two fit into one division. So that then means if that is worth 10 micrometers, we need to do 10 / 2 which is 5. And that tells us that each of these small divisions on the eyepiece graticule is worth five micrometers at that particular magnification. So anything you view, you can use your eyepiece graticle to measure the size. And then we know that the number of divisions times by five is the actual size. And then if you're going to go up and change the lens to a different magnification, you would do this process again to work out what one of these divisions is worth on the eyepiece gratule. Next is cell fractionation and this is used to isolate different organels so that those organels can then be studied and this has helped us to identify organal structures and functions. So there's two stages to this. We do homogenization and then ultra centrifugation. And homogenization this is when the cells are broken open to release the contents and the organels are then separated by ultraentrification. But throughout this process, the cells must be in a particular prepared solution. It has to be cold, isotonic, and buffered. And you need to be able to explain separately for all of these points why it has to be cold, then why it has to be isotonic, and then why it has to be buffered. So, because you're breaking open the cell, that means you're going to have some organels now exposed to enzymes that they might not usually be exposed to in the cell. We've broken it all open. And those enzymes might damage the organel before we can examine them. So, we make sure it's very cold. It's ice cold to reduce enzyme activity to prevent any enzymes potentially damaging the organels before we can view them. It has to be isotonic which means the water potential of the solution is the same as the water potential inside of the organels. And this is to make sure that there is no osmosis because we don't want any water moving into the organels cuz that could cause them to burst and we don't want water moving out cuz that could cause them to shrivel. And then it has to be buffered, meaning you use um something to maintain the pH because we don't want the pH to change because that could damage the organels. And the key thing I've underlined each time is organels. If you say damage to the cell, that is incorrect because we've already broken open the cell. The cell doesn't exist anymore. It's the organels that we need to now make sure they're undamaged so that we can go on to examine them. Okay, so a bit more about this homogenization process. Basically like a blender. And in fact, when I've done this in lessons, that is literally what we used, a blender. So homogenization is when you break open the cells. And we do that with a ice cold isotonic buffered solution. Then you have to filter your solution to remove large cell debris. And then that filtered solution can be spun in a centriuge at varying speeds starting at low speeds. And this is going to separate organels out from that solution according to their densities. So that's what we can see here. Here is our original solution that we've filtered. The centrifuged will spin and the centrifugal forces cause pellets to form at the bottom of the most dense organels. So the first time we spin it, we start at a low speed and then we increase the speed each time. But our lowest speed that is going to cause the nuclei to sink to the bottom in the first pellet because the nuclei are the most dense. You then remove the pellet and you then put the rest of that liquid or the supernent into another tube. Spin it at a slightly higher speed and this time you would get the chloroplast if you're using plants and also the mitochondria cuz they've got similar density. Again remove the pellets and the supernent can be spun again. Next then it would be lizoomes after that endopplasmic reticulum. After that the ribosomes and you do need to remember that order. They have done exam questions where they've asked how would you isolate mitochondria and for the mark you needed to know it'd be on the second spin. So chloroplast and mitochondria are both on the second. We then move on to 3.2.2. All cells arise from other cells or in other words we're looking at the cell cycle of mitosis. Now not all cells are able to continually divide in multisellular organisms but the ones that can go through the cell cycle and in ukareotic cells when they enter the cell cycle they will then divide by mitosis or meiosis. Proarotic cells replicate by binary fision and viruses do not undergo cell division because they are ascellular meaning they don't have a cell to divide and they are non-living. Viruses can still replicate though, but only once they are inside of a host cell which is the cell that they are infecting and they have to invade by injecting their nucleic acid into the cell to replicate the virus particle there and that comes up later in this topic in immunology. So binary fision then we said this is how proarotic cells or bacteria replicate and this involves first of all we have the circular DNA and the plasmids if they have plasmids will replicate and that's what we can see here we've got circular DNA and we've got plasmids that is going to replicate the cytoplasm splits to then create two daughter cells and each daughter cell has one copy of the circular DNA Okay. But the plasmids if they are present don't necessarily split equally. So they might get different numbers of plasmids. It's shown here they have the same but it could be different. So then let's have a look at the cell cycle. There are three key stages. Interphase, nuclear division and cytochinesis. Interphase is the longest stage and we can see that here. Interphase is shown here as G1, Sphase and G2. So we can see about 90% of the cell cycle is interphase and this is when the organels double they the whole cell grows and also DNA replication occurs. So G1 of interphase that is the growth phase. So that is when we're going to have the growth of the cell and also some of the organels doubling. Sphase is when the DNA replicates and G2 we have more growth. Also we have checks for any DNA replication copying errors and we have final preparations for mitosis or it could be meiosis. And then this stage is our nuclear division which can either be mitosis or meiosis. In this topic topic two we only look at mitosis and that is when you create identical diploloyid cells. Diploid die meaning two diploid cells are ones that have two copies of the chromosomes. Meiosis which you learn in topic four you end up with four genetically different daughter cells are hloid. Hloid meaning one copy of each chromosome. Mitosis creates cells with identical DNA and therefore it's useful for growth and repair. Whereas meiosis creates gameamtes which are all genetically different. The final stage which is just shown as this red line here. It's a very very short stage is cytochinis. And this is when we get the division of the cytoplasm and the cell membrane to create the new cells. So we're going to focus on mitosis which is just one of these stages in the cell cycle. And mitosis is split up into multiple steps as well. We have prophase, metaphase, anaphase and tilophase or pmat to remember the order. Key facts about mitosis. You only have one division occurring. So you go from having one parent cell to two daughter cells. You get identical genetically identical cells. They are diploloyid meaning two copies of each chromosome. We've only got one chromosome shown here, but we can see we've got the red copy and the blue copy. That's in the parent cell and it's the same in the two daughter cells and as we said the function growth and repair and we're going to see that later in this topic when we see clonal expansion in immunity. So prophase is our first stage. What you need to know throughout mitosis is what is happening to the chromosomes. In the spec they describe it along the lines of the behavior of the chromosomes. So that's what we're going to focus on. what's happening to the chromosomes and why. So in prophase the chromosomes condense and that makes them visible. So that is what is happening and in animal cells these centrialsles will also move to be at the opposite poles which means opposite ends. The centrialsles are responsible for creating the spindle fibers and because they move to both ends they start to releasing it from both poles and they'll start to attach to the centromeir on chromosomes and the chromatids on the chromosome in later stages as well. Plants have spinal apparatus but they don't actually have centrialsles metaphase. So in terms of what is happening to the chromosomes, the chromosomes will now line up in the middle of the cell which is known as the equator. Spindle fiber that is released from the centrialsles will now attach to the centromeir of these chromosomes and that's what causes them to go in this single file line at the equator. In anaphase, the behavior of the chromosomes is now that they'll be split apart at the centromeir and then each chromatid is pulled to the opposite poles of the cells. So those spindle fibers that were produced start to retract and that is what pulls and splits or divides the centromeir in two. So those individual chromatids are pulled to the opposite poles of the cells. So they're now separated and once they are separated we can now call those chromatids once they're at the opposite poles chromosomes again this stage does require energy in the form of ATP which is provided by respiration in the mitochondria tapase is our last stage the chromosomes are now at each pole of the cell and they're going to uncondense so they become longer thinner and no longer visible spindle fibers will start to disint integrates the nucleus starts to reform. And then the very last step which is not in mitosis but it is in the cell cycle is cytochinesis which is when the cytoplasm splits so does the cell membrane. So you end up with two genetically identical daughter cells. You could be asked to calculate the mitoic index and this is a way of looking at the proportion of cells that are currently undergoing mitosis compared to the number of cells present when you're looking at a sample underneath a microscope slide which links to required practical two. So in order to calculate the motic index in your field of view, which means the section that you can see when you look through a microscope, you need to count how many cells are currently in mitosis. The way that you can tell that is whether you can visibly see chromosomes, which is squiggly lines. If it just looks like gray, or in this case, it's stained purple. If it just looks like dots almost and you can't see any squiggly lines, that's an interphase. So that is not in mitosis. And most cells, if you remember, we said 90% of the cell cycle is interphase, which should mean about 90% of the cells will be in interphase and only about 10% will be currently going through mitosis. So it count how many cells are in mitosis. Divide that by the total number of cells present and that gives your motic index. You might get questions on how can you standardize this. So you could say you're only going to count cells in which you can see the entire cell in the field of view. Now uncontrolled cell division comes up again later when you learn more details about cans from topic eight. But mitosis is a highly regulated process, meaning it's very controlled to make sure that cell division is accurate and it's only happening when it's needed. But disruptions to this control do occur and that then results in uncontrolled cell division, which means you're going to get lots and lots of cells being made even if you might not need them. And that is how you get a tumor forming, which is just a mass of cells. And those tumors could be benign, which means they're not cancerous, or malignant, which means they are cancerous. And because these tumors are formed because of the uncontrolled cell division of mitosis, many cancer treatments will target mitosis to try and control the rate. Now, this mainly comes up as application questions for topic four. You learn more theory on this in topic 8 in year 13. 3.2.3 is the next part of topic two, transport across cell membranes. So this takes us back to the plasma membrane, the cell membrane, which could be a cell surface membrane, but also an organel membrane. So when we talked about the chloroplast being a double membrane bound organel, they have one of these membranes. Well, they have two of them cuz it's double membrane bound. So the membrane is described as a fluid mosaic model and that's due to the fact that it's a mixture of different molecules. That's why it's a mosaic. So it's made up of the phospholipid billayer. We've got proteins embedded within it but also just pinching in externally. We have glyoproteins and glyco lipids and it's described as fluid because there is some slight lateral movement of those phospholipids. All of these molecules are arranged within that phosphoipid billayer and that is what creates the partially permeable membrane which is that property that we talked about or the function it can select or control what can pass through the cell surface membrane. So let's just go through this in a bit more detail. The main component of the membrane is phospholipids. And this links back to topic one which if you haven't already seen my entire topic one video where I go through lipids or if you haven't seen my lipids video in detail then just search lipids or mastro phospholipid billayer misestric entire topic one you'll find it. So the phospholipids align as a bi layer by meaning two. So, two layers, that's what it means. And we have the hydrophilic heads on the outside, the hydrophobic tails are on the inside. This is actually zooming in on one phospholipid, and we've got these structures here that need labeling. So one is the phosphate group. Two is the glycerol. Three and four are both fatty acids but three is a saturated fatty acid. Four is an unsaturated fatty acid because of that double bond between the two carbons. A is the hydrophilic head. Hydrophilic because of this negative charge on the phosphate group. And then B is the hydrophobic tail. Those fatty acids are nonpolar. So they are hydrophobic meaning they will repel water. Whereas hydrophilic hydro meaning water hydrophilic heads will interact with water. So that's why phospholipids and aquous solution or aqueous environments will create this billayer. The heads can interact with any of that solution, the water-based solution on the outside, but it will repel the tail. So, they spin inwards and that's how you get this billayer. Now, this goes towards making this partially permeable membrane property because molecules can only move through the phospholipid blayer by simple diffusion if they can dissolve in lipids and if they're small enough. So it has to be a lipid soluble substance which means it has to be nonpolar. So it can't be charged and that's going to be some hormones like estrogen and also very small molecules like carbon dioxide and oxygen gas are able to molecules that can't pass through the membrane and why by that I mean dissolve through the phosphoipid billayer by simple diffusion is anything that is polar or water soluble so it has a charge because that will be repelled by those phospholipids. So things like sodium ions or any molecule that is too large to fit through the gap. So glucose for example. Now you do have other components in the cell membrane making that mosaic feature of the fluid mosaic model. So cholesterol is another type of lipid and that's present in some membranes in varying amounts and cholesterol restricts the lateral movement meaning the sideways movement of other molecules in the membrane. So that's going to be useful as it makes the membrane less fluid at high temperatures and we want that so that it can prevent water and dissolved ions from leaking out. You also have proteins in your membrane. And proteins can be embedded across the cell surface membrane or they could be just on the outside. So if it's embedded across, it's known as integral. If it's just on the outside, it's known as peripheral. Sometimes that's intrinsic and exttrinsic. So the peripheral proteins those can provide mechanical support or they can connect to carbohydrates to make glyoproteins and carbohydrates can bind to the lipids to make glyolippids and those are normally the function is for cell recognition as receptors. The integral proteins are going to be carrier proteins and channel proteins which are involved in active transport and facilitated diffusion which is coming up shortly. protein channels which we can see one here. These form tubes. We can see it's like a hollow-like tube and that fills with water that will enable any of our polar substances. So they're going to be water soluble to dissolve in that water and then they can move through the membrane in that way because they can't dissolve in the phosphoipid blayer. Whereas carrier proteins, these will have a molecule bind with them such as glucose or amino acids. And when that molecule binds to the carrier protein, it causes it to change shape and that then releases it on the other side of the membrane. Which leads us into the five key ways that molecules can transport across these plasma membranes. We have the top three which don't require energy. Simple diffusion, facilitated diffusion, and osmosis. And the bottom two are both active types of transport, meaning they require energy from ATP, from respiration, active transport and co-ansport. So let's go through all five of these. Now, one thing that they'll all have in common is there are certain adaptations to increase the rate at which those types of transport happen. So you could be asked to identify adaptations that cells have for rapid transport. And the sorts of things you need to look for are features that increase the surface area. So for example microvilli which is highly folded membranes increases the surface area or if it's a type of transport that goes through a protein channel or a carrier protein then there might be more of those proteins embedded in the membrane. So again you've got a larger surface area for that to happen. If it's a cell where there'll be a lot of active transport or co-ansport because those require ATP from respiration, you'll also have many mitochondria as an adaptation as well. So let's have a look at simple diffusion. This is the net movement of molecules from an area of higher concentration to an area of lower concentration. So it's going down the concentration gradient and that will occur until equilibrium is reached meaning same concentration in both sides. This process doesn't require any additional energy from ATP. The molecules do still have energy because they're moving but this is due to kinetic energy that they possess and that is what enables them to constantly move in fluids whether that's gas or liquid. For small molecules to diffuse across a membrane, they must be lipid soluble and small. So that is the criteria for simple diffusion across a membrane has to be lipid soluble. So that would be a nonpolar molecule, meaning it doesn't have a charge or a small molecule. Facilitated diffusion is still going down the concentration gradient. So it's still a passive process. No extra energy is added in the form of ATP. is going down the concentration gradient, but it's for any molecule that doesn't fit the criteria we said here, lipid soluble and small. So, it's going to be for molecules that are polar. So, that means they have a charge, they are not lipid soluble, they're water soluble, and they are too big or they might be too big. So, um this is going to happen through either protein channels or protein carriers. It can be through either of those types of membrane proteins for transport. If it's a protein channel, this is the ones where we have the tube like center filled with water that enables the ions or polar molecules, water soluble molecules to dissolve and then pass through the membrane through that tube filled with water, that protein channel. It is still selective though as the channel proteins will only open in the presence of certain ions when they bind to the protein. So it is still selective transport across the membrane. Facilitated diffusion can also happen with carrier proteins and in this case the molecule will bind to the carrier protein such as it could be glucose and that causes a change in shape to that carrier protein and that change in shape causes it to release the molecule to the other side of the membrane osmosis. So this is still passive meaning no extra ATP or energy is needed and it is going down a concentration gradient but we need to use the terminology water potential not concentration gradient for osmosis to get the marks. So for this water potential is the pressure created by water molecules and it's measured in kilopascals and represented by this symbol here. This means water pressure. Pure water has a water potential of zero. So zero is the highest water potential you can ever get and that's for pure distilled water. As soon as you dissolve any solutes in it, you get a more negative or you get a negative water potential. And the more negative a water potential is that indicates more solutes are dissolved in it. So that's what we mean by water potential. And osmosis is the net movement of water from an area of higher water potential, even though it will still be negative, unless it's pure water, but it's a higher water potential to a more negative or a lower water potential. And that's the direction that the water will move. And it's across a partially permeable membrane. So water is the thing that moves, not the solute. and it's always moving towards a more negative water potential which means more solutes are dissolved in the water at that location. Now you could get questions linked to this are mainly actually links to the required practical to do with plant tissue but the terms isotonic, hypotonic and hypertonic. Isotonic means the water potential of a solution is the same as the water potential in a cell. And because there's no difference in the water potential, you don't have any osmosis happening or there's no net movement of water. So the cell will stay exactly the same size and shape. A hypotonic solution is when the water potential of the solution is more positive, meaning closer to zero than the cell. And that means there's more water in the solution than the cell. So water is going to move into the cell by osmosis and in animal cells that can cause it to swell and even burst. Hypertonic solutions is when the water potential of the solution is more negative than the cell and that will cause water to leave the cell by osmosis and the cell will then shrivel up. Next and we move on to our active types of transport. So we have active transport first and this is the movement of a substance from a low concentration to a high concentration. So it's going against the concentration gradient. To do this it has to use metabolic energy. So that means ATP from respiration and also it always goes through a carrier protein. So you have to state it's a carrier protein for active transport. So the way that this happens then is step number one is the transport is going through or transport is occurring with a carrier protein and those are ones that are going to span the entire cell membrane. A molecule will bind to a receptor on that protein complimentary in shape. ATP will then also bind to the carrier protein from the inside of the cell. So we can see here in the cytoplasm on the inside it then binds and it's hydraized into ADP and PI that releases energy and that is what causes the carrier protein to change shape and release the molecule to the other side of the membrane. This inorganic phosphate arm was attached the whole time after ATP has been hydrayed and that then gets released and that causes the protein to return to its original shape. So in order for active transport to continue to occur need a constant supply of ATP from respiration. Next then is co-ansport and this is a type of active transport because one of the steps in the process is active transport. So to absorb glucose from the illium lumen in the gut which we'll see in topic three in digestion and absorption because there's a higher concentration of glucose in the cell than in the illium it's hard to get the glucose to move in because it's going against a concentration gradient. So that's why we need a type of active transport which is coransport. So the first thing that happens is actually here sodium ions from within a cell are actively transported out of the cell and into the blood in capillaries that then reduces the concentration of sodium ions in the cell and as a result we have now created a concentration gradient from the illium to the cell. So sodium ions are able to move from the illiam into the cell down a concentration gradient, but they are an ion. They're sodium ions. So they have to do this through a protein. And the protein that they do this through is a corransporter protein, which means it transports two molecules at the same time. And it transports a sodium ions plus glucose or it could be amino acid as well. That then gets the glucose into the cell. And then we have a higher concentration of glucose in the cell compared to in the blood. So glucose can now move down its concentration gradient from the epithelial cell into the blood in the capillary by facilitated diffusion through a protein and it has to be facilitated because glucose is too large to move by simple diffusion. Next then is 3.2.3 2.3 cell recognition and the immune system. So the first part is all about cell recognition and identifying what are self cells meaning part of your body and non-self cells which are not part of your body. And your immune system has cells to identify the presence of pathogens which are non-self cells and other non-self cells which are potentially harmful. And then your immune system will either destroy those or neutralize them to prevent harm. So those cells are the lymphosytes. And each type of cell has a specific molecule on its surface to identify it. And those molecules are usually proteins. And because they're proteins, they have a unique 3D shape. There's overlap here with biological molecules from topic one because common marking points linked to this are stating that it has a tertiary structure because it's a protein and that's what gives a unique 3D shape but tertiary structure would be the key marking point and that would be complmentary in shape to and that's actually going to link to some of the cells that we learn about later. Um, but it's the idea of tertiary structure, complimentary in shape. That's how you can work out if it's a self or non-self cell. And a bit more on that when we get to the T and B cells. But thinking now more about what counts as a nonsself. So if a non-self cell is detected, a response will be triggered to destroy that cell. And these are the four examples that you need to know that could trigger an immune response because they're detected or could be detected as non-self cells. So number one is a pathogen. So bacteria, fungi, they'll have antigens on their surface that can be used to identify them as non-self cells. It could be cells from another organism of the same species. So, for example, if you've had an organ transplant, that could be detected as nonself, and we don't want that to happen because then your immune system will start to attack and destroy the cells from that transplanted organ. It could be abnormal body cells. So, for example, cancer cells, their antigens on the surface will slightly change. They now don't get detected as self cells. They're now detected as non-self. or it could be toxins because some pathogens release toxins into the blood such as cholera. So I use this word antigen quite a bit but an antigen is a foreign protein that generates an immune response by the lymphosytes when it's detected and it's located on the surface of cells. That is quite a common two mark question. You need both of those points to define what an antigen is. Antigens can change though over time and this links to antigen variability. So a pathogen's DNA can mutate frequently and if the mutation occurs in the gene that codes for the shape of the antigen then that shape of the antigen will change and therefore any previous immunity that you might have had for that pathogen based on the recognition of the old shaped antigen. It will no longer be effective because the memory cells have a memory of the old antigen shape. So this is known as antigen variability and for example the influenza virus which is the virus that results in the flu that mutates and changes antigens very quickly and that's why you need a new flu vaccine every single year. So let's go on to the immune response then if you do have this nonself detected we said an immune response occurs. So if a pathogen gets past any chemical or physical barriers which you don't learn for AQA for A level but that's things like your skin barrier your stomach acid and it can then enter the blood then this is when the white blood cells are the second line of defense and you either get a specific response by the lymphosytes or a non-specific response and in fact you'd get both starting with the non-specific response of the fagocytes and then the lymphosytes. So the non-specific response by the fagocytes is fagocytosis and a fagocy is a type of white blood cell for example a macrofase is an example of a fagocytes and fagocytes are white blood cells that can do fagocytosis. They're found in the blood but also in the tissue and fagocytosis is a nonspecific immune response. What that means is any non-self cell that is detected and that means any of those four items that we listed a couple of slides ago if they are detected it will trigger fagocytosis to happen every single time. So fedocytosis then the first thing that happens is our fagocite for example a macrofase which is in the blood or in the tissues and any chemicals or debris that are released by the pathogen will attract the fagicite to move towards the pathogen. So that's how the fagicite is able to detect where the pathogen is. Now on the fagasite there are many receptors which are binding points on the surface of that fagocite that can then bind to the antigens or any chemicals on the pathogen. The fage site once it's then bound to it the fage site changes shape which is known as engulfing. So it completely surrounds and engulfves the pathogen and it then will put it inside of a vicle inside of the cell and that vicle is known as a fagosome. So we can see here the pathogen's been engulfed and it's now trapped inside of the fagosome. You then have the lysosomes within the federite will move towards. So the lysome shown here in blue. It will move towards and fuse with the federosome and it will then release its contents. And the contents of a lizoome is digestive enzymes. And in this case they're known as lizosyme enzymes. They're digestive which means they're litic or they're going to split. are going to break apart, hydrayzeed the pathogen. So that is how the pathogen is then destroyed. from the broken down hydrayzeed digested pathogen. Any soluble products that are going to be useful can be absorbed by the fagocytes and then the antigen is placed on the surface of the pathogen and that is going to be used later on as a way to signal to other white blood cells known as lymphosytes that a pathogen has been detected and destroyed. So that takes us on to the first type of lymphosy we're going to go through tlymphosytes or te- cells for short. These lymphosytes are involved in the specific immune response meaning they respond in a particular way based on the particular shaped antigens that are detected. Lymphosytes are made in the bone marrow and this is extra information. You don't need to know it, but they're called Tlymphosytes because TE-C cells then go to mature in the thymus, which is this structure here in the body. And they are involved in the cell mediated response. So this is where we look at how the antigen presenting cells are going to help trigger the cell mediated response. And the antigen presenting cells could be like we just said a fage site for example a macrofase which has engulfed and destroyed a pathogen and then it presents it on its surface. But it's actually any cell that has a nonselfigen on its surface. So that could be one of your own body cells that's become infected. It could be one of those fagocytes presenting the antigen on the surface. It could be cells of a transplanted organ. It could be cancer cells. And because they have antigens presented on their surface, that is going to enable lymphosytes to respond to those antigens in this cell mediated response. So let's carry on from this bit we were at. So once the pathogen has been engulfed and destroyed by the fage site, and are then presented on the cell surface. It's now called an androgen presenting cell. And we can see an example of that. Here we've got an androen presenting cell. One type of T- lymphosy is known as a helper T-C cell. And helper tea cells, they have these receptors on their surface and that can attach to complimentary shaped antigens on androgen presenting cells. Once it then attaches that activates the helper tea cells to divide by mitosis and that will then replicate and make large numbers of clones of that exact helper tea cell that had the receptor complmentary in shape to that exact antigen. That stage is known as clonal expansion. Clonal because you're making identical copies, expansion because you're making large numbers. And this is where there's that link back to mitosis. We said the role of mitosis is growth and repair. In this case, it's growth and making large numbers of identical T- helpper cells. Now we've got that large number of identical T- helpper cells. They actually differentiate into different types of Tlymphosytes. So some will actually just remain as helper tea cells because those are then going to go on to activate the belymphosytes which we're going to go on shortly. Some of them are able to stimulate macrofasages so that they will perform more fagocytosis and engulf and destroy more of those non-self cells and then some of them become cytotoxic tea cells sometimes called killer tea cells. AQA use the term cytotoxic tea cells. And a cytotoxic tea cell is able to destroy your own body cells that are infected with a pathogen, typically a virus. And the way that they do this is cytotoxic tea cells release a protein called perforin. And that protein can embed in the cell surface membrane to make a hole or a pore. And that means that either lots of water will move in and cause the cell to burst destroying the infected body cell or it will cause lots of water to move out causing the cell to shrivel and again it will cause cell death. So this is most common in viral infections because viruses can only replicate when they're inside of the body cell. So if you destroy the body cell, the virus can't replicate and that gives more time then for the fagocytes to locate and destroy the virus before it can replicate and cause more damage. And this is why you get a sore throat when you have a cold. The cytotoxic tea cells are destroying the infected body cells in your throat. You're sacrificing body cells to prevent the virus replicating and infecting even more cells and tissues. Now belmphosytes this is the humoral response again all lymphosytes are made in the bone marrow you don't need to know this but the B is because it matures in the bone marrow as well this is a humoral response meaning within liquids or within body fluids because in this instance the B cells will only respond to antigens that are floating within the blood within body fluids they don't respond to the androgen presenting cells in the same way as a cell mediated response with the T- cells. So let's have a look at the B cell activation. So you have approximately 10 million different B cells which have antibodies on their surface complmentary in shape to 10 million different antigens. And you have these circulating in your blood. And if you get an antigen in your blood, collide with the complimentary shaped antibbody on a B cell that is going to cause the B cell to take in that antigen by endocytosis which means basically surround and engulf it. So this is responding to the antigens in the blood, not the entire cell. When the B cell then collides with the helper tea cells that we talked about in the previous slide, that activates the B cell to go through clonal expansion and differentiation. Now, this can happen because when that B cell takes in the antigen, it's going to break it down, but it can then actually also present it on its surface. So, that means it's able to bind to helper tea cells that have that receptor complimentary in shape to the antigen. That is then going to trigger the B cell to be activated to do the same thing as the T- cells. It under goes mitosis. You get a large number of clones clones of that B cell that has that exact shape and antibbody on its surface complementary to that um foreign protein the antigen. But this time the cells differentiate into different molecules. They can either become plasma cells or memory B cells. The plasma cells, which you can see here, these are the ones that make antibodies. Memory B cells are the ones that remain in your blood for long periods of time, and they can divide rapidly into the plasma cells to release large quantities of antibodies so quickly if you get reinfected with the same pathogen. So, they're responsible for you being immune basically to particular pathogens and disease. So let's have a look at this. Memory B cells as I said they can live in your blood for a long time. They can be decades in your blood. Whereas plasma cells are very short-lived and those are the ones that make the antibodies. So that's why we need to store a memory of the antibodies. So if you are reinfected, you can then have the memory B cell rapidly differentiate into plasma cells which can then make lots of antibbody so quickly that it should help to destroy the pathogen before you get any symptoms which means you are immune or it might just mean you get very very minimal symptoms and this is known as active immunity. you are immune to that pathogen and it's active because you have memory B cells against that pathogen. So this links this concept of primary and secondary response. Primary immune response is the first time you are exposed to a pathogen. And because it's the first time you're exposed, it can take a longer period of time for the B cell to collide with that antigen causing it to engulf the antigen and then you get the clonal expansion differentiation. All of that process of the humoral response has to happen. So it takes a longer time to make antibodies and you don't get as high a concentration. The second time you're exposed to that same antigen because you now have the memory B cells present in your blood. Those can then collide with the pathogens antigen again and differentiate rapidly into plasma cells. So you end up with large quantities of antibbody much much quicker. And this is why the secondary response should mean that you get no symptoms or very few because you get the antibodies being produced so rapidly and in large concentrations. So let's have a look at what antibbody is. They are proteins that have a cortary structure meaning more than one polyeptide chain and they happen to have four polyeptide chains. The N bits here are the variable regions, meaning those are the parts that are going to be different in shape and combine to the different shaped antigens. The red part is constant, meaning it's the same in all antibodies. The heavy chain is this longer one. You have two heavy chains. The shorter chain is known as the light chain. Here are the binding sites. You can bind one here and here. And then you also have these bonds here which and the hinged section which makes the antibbody flexible. So it can easily bend and attach to one antigen over here, bend and attach to another over there which is how we get a glutination happening. And a glutenation is the idea that multiple antibodies combine together lots of different antigens at the same time. So they all clump together. that makes it easier for the fagocytes to first of all locate where all the pathogens are and then they can more efficiently engulf and destroy them. So antibodies they create these antigen antibbody complexes and we get a glutination happening but they don't directly kill the pathogen they just make it far more efficient for the fagocytes to then destroy the pathogen. So different types of immunity. First of all, passive immunity. Passive immunity is when the antibodies are introduced into the body and the pathogen doesn't enter itself. So you don't actually get any antigen or pathogen in you. So that means the plasma cells and memory cells are not made. You just get a direct source of antibbody. So you don't get any long-term immunity because there's no memory B cells. A natural example of this is in breast milk. So through breastfeeding, breast milk contains antibodies. That means babies will have passive immunity whilst they are breastfeeding. And when I say whilst, it's not literally just while they're breastfeeding. The antibodies can last for a short period of time. Active immunity is when you have been exposed to the pathogen or the antigen and therefore you do have memory B cells in the body. And that could be natural active immunity following infection or it could be artificial active immunity following a vaccination where you might have a weakened version of the pathogen or the androgens injected in. say vaccines that means a small amount of either weakened or dead pathogen or the antigens itself introduced to the body and that could be as a liquid through the nose or mouth or it could be an injection and exposure to those antigens activates the B cells to go through clonal expansion and differentiation just as we saw in the humoral response. So those B cells will then undergo mitosis, make large numbers of identical cells which then differentiates into plasma cells and memory B cells. Plasma cells will make antibodies which will then destroy any of that weakened or dead form of the pathogen. And the B memory cells will then remain in your body for decades. So if you are reinfected with the same pathogen, you can make large numbers of the antibodies so rapidly that you shouldn't get symptoms. Herd immunity is if enough of the population are vaccinated against a particular pathogen. That means that the pathogen cannot spread or transmit amongst the population. And that's because if you have most of the population immunized, that means that they can't transmit the pathogen onto someone else. And therefore, hardly anyone in the population is going to have the pathogen. And this provides protection for those who are not vaccinated. So maybe they are too ill to be able to be vaccinated or maybe they're pregnant or they have some lowered immunity that means they aren't able to. The next bit is then looking at HIV an example of a virus and it is a retrovirus. It has a lipid envelope around it but that is taken from the host cell membrane. The envelope has the attachment proteins which are glyoproteins which is how it attaches to the host cell. So here are the key structures that you have in the HIV particle. You have the core and that is the genetic material which is RNA and it has the enzyme reverse transcriptise as well which is needed for the virus to replicate. You have the capsid which is the outer protein coach protecting the genetic material. There is the envelope that is an extra outer layer but that is made out of lipids taken from the host's cell membrane and then you've got the protein attachments on the exterior of the envelope to enable the virus to attach to the host's helper T- cell. So let's have a look at how HIV replicates in helper tea cells because those are the host cells that it infects. HIV is transported around in the blood until it attaches to a CD4 protein on a helper tea cell. So here is a helper tea cell. Here is a CD4 protein which is a receptor. And we can see that the HIV with the attachment proteins binds to that receptor. The HIV protein then fuses with the help of T- cell membrane and that enables the RNA and the reverse transcripttoise enzyme to enter with the capsid and then it does get released from the capsid. The HIV enzyme reverse transcriptise copies the viral RNA into a DNA copy and moves into the help of T-C cell nucleus. And this is why it's called a retrovirus because it's doing the reverse of transcription. You've got an RNA copy being turned back into DNA. The DNA then moves into the nucleus. It combines with the host's DNA and that is where the mRNA is then transcribed along with the host cells mRNA to create the viral proteins. The viral proteins are then reassembled and they'll then move towards a cell surface membrane and they are released from the cell and that then goes on to make a new virus particle. Now the difference between HIV and AIDS is HIV is the virus and it specifically targets and it destroys helper tea cells because as it replicates inside of them it destroys the helper tea cells which activates B cells. So if we don't have those helper tea cells they're not there to activate B cells that means we have now significantly reduced the immune system. And if enough helper tea cells are destroyed then you end up with AIDS acquired immuno deficiency syndrome where you've become so vulnerable to opportunistic infections and cancers and you can't defend yourself. So symptoms of AIDS are chronic infections, weight loss, fever, night sweats and they can be followed by more serious illnesses like pneumonia, tuberculosis and certain cancers. a person is HIV positive if they're infected with HIV. AIDS is when the replicating virus in the help of tea cells interfere with the normal function of the immune system and it's normally classed by how many of the helper tea cells have been destroyed. The last bit of this topic is monoconal antibodies. Mono meaning one, clonal meaning identical. And a monoconal antibbody is a single type of antibbody that can be isolated and cloned. And antibodies are proteins which have binding sites complimentary in shaped certain antigens. Now this is what is created in the immune response. Monoconal antibodies lots of identical copies of the same antibbody. But this has been manipulated to create monoconal antibodies for medical treatments, medical diagnosis and even pregnancy tests and other chemical tests. Now targeted medication this can use direct monoconal antibbody therapy and this is when you have some cancers that can be treated using monoconal antibodies which are designed with a binding site complimentary in shape to the antigens on the outside of cancer cells. Those antibodies are then given to the cancer patients and they'll attach to the cancer cells. While the antibodies are bound to the cancer cell antigens, this prevents chemicals from binding to the cancer cells which enable the uncontrolled cell division. And therefore, the monoconal antibbody prevents the cancer cells growing anymore. And as they're designed to only attach to the cancer cells, they should only affect the cancer cells and not healthy body cells. Indirect monoconal antibbody therapy can also be used and this is when you would attach a drug to the monoconal antibbody. So in this instance you've still created the antibbody to be complimentary in shape to the ant and antigens on the cancer cells but the cancer drugs are then delivered directly to the cancer cell and it kills the cancer cell rather than lots of healthy body cells. So this should reduce the harmful side effects that affect traditional chemotherapy and radiotherapy can produce and this is known as a bullet drug. It's going straight to where it's needed. So if you have a look at medical diagnosis, monoconal antibodies can be used to test for things like pregnancy, influenza virus, hepatitis, chlamyia, prostate cancer, but also it's not on the spec because this happened after the spec was created. But COVID 19, all of those lateral flow tests that we used to have to do all the time use monoconal antibodies and this works via an ELISA test. So in a test the enzyme linked aminoabsorbent assay it uses two antibodies. We can see here in the pregnancy test we've got first of all a mobile antibbody and then we have a immobilized antibbody and we actually have a third one here. We've got an immobilized one as well. And in this instance what happens is you would dip your pregnancy test into the urine that you are testing to see if someone is pregnant or not. Because when you are pregnant you create this hormone hCG and it's can be secreted your urine. So this is absorbent paper. That means the urine with any hormones dissolved within it are going to move up through that absorbent paper. The hormone is complementaryary to the mobile antibbody which also has a colored dye attached to it. So that will then move up the pregnancy test and at point C you have a immobilized meaning it can't move antibbody that is also complimentary in shape to the hormone. So that will then cause the first antibbody that has the hormone attached to it to attach to the immobilized one and it also has that colored dye on it and that's why at that exact position you get a colored line. Any antibbody that didn't bind to the hormone will move past section C. But we do have antibodies also immobilized at point D that are complimentary in shape to the end of that antigen. So those will bind and you get a second line. And in this way whether you have that hormone or not you should always get the line at D. And that is to help prevent false negatives because it shows us that you don't have a colored line here if you don't. But the antibodies are definitely able to move. So the test is working. Whereas if you have a line here, that means you are pregnant because you do have that hormone present. And this line here confirms that the test was working. So antibodies did move through the test. Now you can also have different versions of this. So we've got one here where we would add the test sample from a patient to the base of a beaker or the base of a well and we then wash to remove any unbound test sample. Then you'd add an antibbody complimentary in shape to the antigen you are testing for and that will bind if it's present. Again wash to remove any that didn't bind. We then add a second antibbody that is complimentary in shape to the first one. So that's only going to bind if the androgen was present and therefore the first one bound. Again, wash to remove any that's unbound. Then you'd fill the wells with a liquid sub which is a substrate for this enzyme. And when those react together, you get a color change. So the presence of the color indicates that you do have that androgen present. And the intensity of the color indicates the quantity present. Now there are some ethical issues around monoconal antibodies because creating monoconal antibodies requires animals such as mice to produce those antibodies in tumor cells which leads to ethical debates as to whether this use of animals is justified to enable better treatment of cancers in humans and detect disease because in order to do this there will be suffering to the animal and then at the end they would be killed because they wouldn't be needed. So that takes us to the end of topic two. And if you did find this helpful, then don't forget you can check out my Alevel notes and flashcards for mark scheme specific points. But that is it for today's video. Hope you found it helpful and I'll see you in the next one very soon.