Transcript for:
Cambridge AS Level Biology Overview

hi everyone and welcome to miss estc biology and in this video I'm going through all of year 12 or as Cambridge International biology so this is going to be a mega video get yourself comfy you might even want to watch it at times 2 speed if you're a bit short of time but this is all the theory straight from the spec that you need to help you to get the grades that you're aiming for for your a Lev and if you do need any more help then don't forget to check out the link in the description which has got the link to my AEV notes which covers all of the theories so you don't need to make your own notes and it includes the key marking points key terms and special examiners tips for every single topic but for now let's get into this entire year 12 as video so let's jump into then all the information you need to know for Cambridge International a level for topics 1 to 4 and we're going to be going through one to four which is cell structure biological molecules enzymes and cell membranes and transport start with cell structure which is split into these two subsections the microscope in the cell studies and cells are the basic units of living organisms so we're starting with microscopes and there are three types of microscopes that you need to be aware of light microscopes and then there are two electron microscopes light microscopes have a poor resolution or at least it's poorer in comparison to an electron microscope and that is because the the resolution is determined by the wavelength of the light and wavelength of visible light is longer than the wavelength of an electron an advantage of light microscopes compared to the electron microscopes though is you can view living samples which isn't possible with electron microscopes and also you do get color images without having to artificially adding color to a photo afterwards so then if we have a look at the first type of electron microscope electron microscopes do have higher magnification and higher resolution and that's because the electrons which are used to create the image have a shorter wavelength compared to visible light the way the image is created is the electrons pass through the specimen that's why it's called transmission the electrons are transmitting through the specimen and they'll absorb different amounts of electrons and that's how you get the different shades of gray to create the image image so a transmission electron microscope will enable you to see the internal structures of organel scanning electron microscopes also have a higher magnification and resolution because they are creating these images with electrons which have a shorter wavelength compared to visible light but this time you get a 3D image which shows you the Contours on the outside and that's because the electrons will bounce off the surface and the way that they are reflecting is what creates that 3 3D image so we've talked about resolution and magnification a little bit but we haven't actually defined what they mean yet so resolution is the minimum distance between two objects in which they can still be viewed as separate so that is your key definition to learn you could turn that into a flash card and with Optical microscopes that resolution is determined by the length of the wavelength of light and as we said electron microscopes is determined by the wavelength of an electron which is short than for visible light which is why electron microscopes have a higher resolution the term magnification refers to how many times larger the image that you're viewing is compared to the actual object and that's a formula that we'll be going through shortly as well so to work out the magnification you would do the size of the image that you're looking at divided by the size of the real object so for example if you wanted to know the magnification of this image You' need to use a ruler to measure the length of a cell and then you would have to know the length of that actual cell as well so in an exam question they would have to tell you the actual length you would then have to use your ruler to measure the image size but it's key that you have them in the same units because cells are often measured in micrometers whereas you'll be measuring in millimeters so here's a little conversion which again you might found helpful to put onto a flash card CU it's letting you know if you wanted to convert millimeters into micrometers you would need to Times by a th and if you wanted to convert micrometers back into millimeters you'd need to divide by a th000 so make sure you have these in the same units and then that would give you your magnification sometimes you might have to work out the size of the real object and in which case you'd rearrange this formula and that would then be size of image divided by magnification you might also have to do scientific drawings this is one of the skills and this is when you are taking observation of structures from under the microscope and representing it as a scientific drawing and there's a few key features that you need to know about scientific drawings I do actually have an entire video on scientific drawings which I'll link up here that you can watch but this is in summary what you would need to make sure you are following in terms of the rules it should be drawn in pencil you should have a title uh for the diagram and indicate what the specimen is within that title if the magnification is known which hopefully it is you're doing it on a microscope then you should State the magnification you should always annotate the cell components the cell sections any tissues visible just to show what you are visualizing there shouldn't be any sketches and what that means is um you should only use solid Lines no overlapping lines it's not an artistic drawing it's a very f factual drawing to showing shape proportion location and there shouldn't be any color or shading in either so that's the whole aim of a scientific drawing showing the size location and proportion now you might have to use an eyepiece graticule as well to be able to measure the actual size of the object that you're viewing under the microscope and to do this you need to calibrate your IP graticule using a stage micrometer so inside the light microscope there is a scale on a glass disc which is inside of the microscope and that is called the eyepiece graticule so it's within the eyepiece which is the long part that you look down and you use this to measure the size of objects you're viewing under the microscope but as I said you need to calibrate it each time because as you're looking at this scale in the eyepiece you need to know what each one of these division is worth at each magnification so you'd place a micrometer a stage micrometer within your view to calibrate it so let's go through how you'd actually calibrate it then so step one is you need to line up your stage micrometer which is the ruler that you would put on the stage of the microscope line that up with the ruler which is the eyepiece graticule which is already within the microscope so that means when you look through your eyepiece you should now see two rulers and they are lined up so we've got our eyepiece graticule lined up with the stage micrometer and what you then need to do is count how many divisions on the eyepiece graticule fit into one division on the stage micrometer and the divisions on the micrometer are known distances so each division on the micrometer is 10 micrometers so this can then be used to calculate One Division on the ipce graticule is worth at that current magnification so for example here one division on the micrometer is 10 micrometers and we can see here that two divisions fit into one of those stage micrometers so this top one is the eyepiece graticule the bottom one is the stage micrometer we know that one division is worth 10 micrometers two IP graticule divisions fit into that so we' do 10 / 2 which gives 5 micromet so that means at this magnification One Division on the IP graticule is worth five micrometers and you would then take away the stage micrometer ruler and then you'd put in your slide and you can then measure cells using your ipce graticule when you now know what each division is worth and measure the actual size of the images that you are viewing then we go on to the electron microscopes in a bit more detail so a beam of electrons is what is creating the image and they have a very short wavelength and that is why you have a high resolution and because the resolution is so high that means small organal and internal structures can be viewed the image is created by condensing that beam of electrons into a really fine beam and that is using an electromagnet that is what focuses the beam of those negatively charged electrons now electrons are absorbed by air and this is why when you're using an electron microscope it has to be a vacuum so there's no air present youve just got your specimen there and for that reason you can't view living specimens because if it's a vacuum that's going to cause the specimen to die so you can't use living specimens which is a downside um and also you only get black and white images and you have to the sample now we did talk about some differences between the transmission and the electron microscope we're going to go into it a bit more detail for a transmission electron microscope because the electrons are transmitting or passing through the specimen that means the specimen has to be sliced extremely thin and you need to stain it as well then you put it in a vacuum the electron gun will then be fired at the specimen to produce a beam of electrons that is then going to be focused using the electromagnet and some parts of the specimen absorb the electrons and that is why they appear darker on your image so you end up with a 2D image like this one where you can see the internal structures of an organel and this here is showing you the internal structure of a mitochondria the scanning electron microscopes don't need to be as thin because the electrons aren't passing through they are instead reflecting and Scatter in off the surface and because there're scattering off the surface that's how you get these different Contours and therefore this 3D image of the surface of your specimen so that's what you need to know about microscopes the next part of cell structure is knowing this part 1.2 cells are the basic units of living organisms so here is an extensive list of all of the organel you need to know about in eukaryotic cells and you need to know structure and the function of these and I've split it into the top part is what you'll find in animals and plants the bottom ones that are highlighted in green you would only find in plant cells so let's go through the structure and function of each of these one thing you could be asked to do as well is to identify the organel within a cell so here we have an image which is showing us an animal cell the cell membrane is that outer layer we do have a vacu labeled here but animal cells don't have permanent vacuoles they can have temporary vacuoles so for example a faite which is the white blood cells that engulf pathogens they trap the pathogen after it's been engulfed inside of a fagia Zone which is a temporary vacu we then can see here are rough endoplasmic reticulums we can see those folded Cate with the ribosomes on the outside the goldi apparatus does look very similar to the smooth and endoplasmic reticulum but the key difference is the goldia apparatus curves so it looks more like um often people tell me looks like a Wi-Fi symbol so you can see it curves a bit more and often you'll see vesicles budding off the edges as well that's how to tell apart the smooth endoplasmic reticulum and the goia apparatus ribosomes are very very small so you're looking for a very small spheres lomes are larger than the ribosomes mitochondria you have these inner foldings which helps those to be identified as well then if we have a look at the plant cell so all of the same organal plus some extra so we've got the chloroplasts which do look similar to mitochondria they've got these inner foldings as well we've got a permanent vacu and the membrane on the outside of that it's called the tonoplast and then in the cell wall that's an extra layer on the outside and the pores in the cell wall are the plasma desata but let's go through each of those structures looking at the structure and function in more detail starting with the cell surface membrane cell surface membranes are found in all cells and it's made up of this phospholipid by layer meaning you've got two layers of phospholipid where you have the hydrophilic heads on the outside and the hydrophobic Tails pointing inwards you have molecules embedded within that as well which are typically proteins and cholesterol ol the proteins could be these protein channels which enable molecules to pass through or protein carriers which also allow molecules to pass through you also get glycoproteins which is where you have a protein embedded within it and a carbohydrate attached or you can get as well other molecules such as a glyco lipid which is where you have a carbohydrate attached to the phospholipid and those roles for those two molecules are often things like receptors so the function of the plasma membrane we'll learn more about in the topic which is looking at membranes and controlling what can enter and exit but that is what the role is it can control what can pass through the membrane meaning what can enter and exit a cell next then we look at the structure and function of the nucleus so the nucleus is a membrane bound organel and that membrane is the nuclear envelope which we can see here there are pores which are tiny holes Within that nuclear envelope and that's how mRNA which is created inside of the nucleus is able to leave the nucleus to go to the cytoplasm inside of the nucleus there is nucleoplasm which is a granular jelly like material it's also where you find the chromosomes and in eukariotic organisms chromosomes are protein bound so they're attached to histone proteins and we describe the shape as linear you have inside of the nucleus as well a nucleolus which is the smaller sphere inside and that is where RNA specifically R RNA is made and R RNA is used to make ribosomes so the function then it is the site of DNA replication it's also the S of transcription which is the first stage in protein synthesis which results in the creation of mRNA it's also the site of our RNA production and ribosome synthesis and it contains the genetic code for each cell fella is the ne structure and this is a whip-like structure we can see here and this will spin around at the base using a motor and as it spins it enables movement now you don't have this on every single cell but one example of cell that would have it is a sperm cell for example cyia again aren't on all cells but some cells do have cyia and these are hairlike projections coming out of the cell now these cyia can be mobile or stationary mobile cyia help move substances in a sweeping motion so the cells Lin in your trachea which is part of your breathing system connecting to your lungs have cilat and they are mobile cyia to sweep and move mucus up and out of the trachea so it's to prevent lung infection basically stationary cyia are important in sensory organs as well so for example in the nose microvilli again aren't on every single cell but some cells do have microvilli and these are folding in the cell surface membrane to create these finger-like projections and the function of this is it increases the surface area for transport across the membrane so for example the epithelial cells lining the ilium have microvilli and that increases the surface area to maximize the absorption of molecules like glucose and amino acids after digestion also within the proximal convoluted tubal in the nefron of the kidney there are microvilli to increase the surface area to maximize the reabsorption of glucose cental and microtubules are the next organal we're going to have a look at and centrioles are made up of microt tubules and they occur in these pairs to form what is known as a centrosome the function is to produce or they're involved in the production of spindle fibers which are released to organize the chromosomes into particular positions during cell division the microt tubules in particular also Aid with the movement of CIA and fella the cytoskeleton is the next one and this is a network of fibers found within the cytoplasm all over a cell and it consists of microfilaments microtubules and intermediate fibers which we can see here the function is it provides mechanical strength to cells it helps to maintain the shape and stability of a cell and many organel are bound to the cytoskeleton also so we can see that here that organel are actually attached to this cytoskeleton the microfilaments within it are responsible for cell movement the microt tubules are responsible for creating a scaffold like structure and then the intermediate fibers provide some mechanical strength next then we have a look at the endoplasmic reticulum and you have rough and smooth endoplasmic reticulum both have folded membranes which are known as cyanate and we can see those here the difference then is the rough have ribosomes attached on the outside and therefore the function of the rough endoplasmic reticulum is protein synthesis because it's got these ribosomes on the outside and the smooth end plasmic reticulum their function is to synthesize and store lipids and carbohydrates the goldi apparatus which is shown here in this peachy orange color again it's made up of folded membranes which are known as syy but it's more of a curved shape and you also get these secretory vesicles that pinch off and that is because anything that's been processed and packaged within the GOI apparatus is then secreted out in these vesicles So within that GGI apparatus the functions are you'll have carbohydrates being added to proteins to form glycoproteins they might produce secretory enzymes they're going to secrete carbohydrates transport modify and store lipids they might form lomes molecules are labeled for their destination here as well and they get sent off in those secretory vesicles and that's how the finished products are transported in these vesicles which then fuse with the cell surface membrane which then means they relas from the cell lomes are our next organel lomes are the next organel and these are bags of digestive enzymes and they can contain 50 different digestive enzymes so they will hydrolize fastic cells that's one example of a liome that you learn about in fages sites they can completely break down dead cells which is known as autois you also get exocytosis which is where they can release enzymes to the outside of the the cell to destroy material and they can digest worn out organel for reuse of materials as well next time we have a look at the mitochondria and this is a double membrane bound organel the inner membrane is highly folded and we call it the Christi inside of that we have a fluid Center called the mitochondrial Matrix and that contains ribosomes the smaller ones which are 70s and it also contains Loops of DNA so that it can create its own enzymes so this is the site of aerobic respiration therefore the site of lots of ATP being produced and as I already said it has DNA so it can code for its own enzymes required for respiration ribosomes are our next organel and these are made up of two subunits we have a large and a small subunit a ribosomes made up of protein and R RNA and there are two types of ribosomes at s are the larger ribosomes found in eukaryotic organisms 70s ribosomes are the smaller ones that procaryotic cells have but it's also the ribosomes that you find in the mitochondria and chloroplasts of eukaryotic organisms and the function is it's the site of protein synthesis we then move on to the organel that are just found in plants so chloroplasts this is another double membrane bound organel and then inside we have these folded membranes so this is your thilo covid membrane which is highly folded to create these Stacks that look a bit like stacked up coins and those Stacks are known as the Grana and they are embedded those membranes are embedded with lots of pigments and proteins which are needed for the light dependent reactions in photosynthesis in peach color here that is a fluid Center which is known as a stroma which contains lots of enzymes that are needed for the light independent reactions of photosynthesis so that's the function of this organel it's the site of photosynthesis the cell wall is found in plant cells but also fungi fungi are also eukaryotic organisms you do have cell walls in procaryotic organisms as well but we're just going to focus on cell walls of the eukaryotic organisms for now so plants have a cell wall made up of cellulose whereas fungi have a cell wall made up of kiten which is a nitrogen containing polysaccharide and the function of the cell wall is to provide structural strength plant cells also have a large permanent vacu and this is a single membrane bound Sac for example we've got the ftic vacu in animals but those are temporary and we're just focusing on the permanent vacuoles in plants and those have a tonoplast that's the name of the membrane that surrounds them the plant vac's function is to regulate osmosis and also it contains the pigments which give flowers their color so it's going to attract pollinators the plasma Des Mata is the next structure and these are pore-like channnels within the cell wall which we can see here and that provides a channel between cells to enable the movement of water and dissolved mineral ions between cells so we then go on to photo micrographs which is how you can identify these different organel from images taken under the microscope and a photo micrograph is an image that's been captured by a light microscope they offer a lower resolution because of everything we said about the microscopes so the light microscope the image is created using light which has a longer wavelength of light but what you can work out from this is in plant cells you might be able to identify features such as the cell membrane chloroplasts and the vacu in animal cells you'll be able to see key structures like the cell membrane nucleus and cytoplasm but to be able to see other smaller organel and the internal structure of organel that's when you'd need to use your electron micrograph or an electron microscope to create an electron micrograph that's the name of the image that is created using an electron microscope and because those microscopes have a higher resolution that's why you're able to see all of these extra organ nails and also the internal structure structures of those organel so if we move on to procaryotic cells next then and look at the key differences between the procaryotic cells and eukariotic cells so first of all procaryotic cells are much smaller so typically they're 1 to 5 micrometers in diameter they don't contain any membrane bound organel they do have ribosomes but it's the 70s smaller ones they contain DNA but not within the nucleus they do have a cell wall but it's made of a molecule called murine some procaryotic cells also contain plasmids a slime capsule around the outside and fella but they don't all contain those so let's have a look then at those differences they don't contain any membrane bound organel so that means they don't have any mitochondria chloroplast endoplasmic reticulum Gia apparatus lomes but they will have circular DNA loose Within the cytool which is the name of the cytoplasm they do have ribosomes as we said but it's the smaller 70s ribosomes they don't have a nucleus instead their DNA is circular and is loose within that cytoplasm we did say some of them contain plasmids and plasmids are small Loops of DNA which only carry a few genes and you can get varying numbers of these in your procaryotic cells which are typically bacteria the cell wall we said they do have but it's made of a glycoprotein called murine and that slime capsule the capsule on the outside of the cell wall that is only sometimes there it's made up of a protein and the function is it prevents the bacteria from drying out or desiccating and it also helps to protect the bacteria against the host immune system it help to partially cover the antigens the fella again that's only sometimes present on bacteria that can rotate and it helps to make the bacteria move so this would be a good table to copy down to have in your revision to compare the structures that you'd find in a procaryotic organism and eukaryotic organisms but also split into the plants and animals lastly then is known about viruses and viruses are non-living and non cellular so we often describe them as virus particles so they are even smaller than bacteria and they only contain a nucleic acid core which could be DNA or RNA a capsid and make sure you do not confuse this with the capsule that's found on some procaryotic organisms because the capsid is this part here that surrounds the nucleic acid core this protein layer on the outside there are attachment proteins which are used to attach to receptors on the host cell and then some of them have an outer envelope made up of lipids which would be phospholipids viral replication occurs inside of host cells and involves the injection of that nucleic acid into the cell and bacteria phage are an example of a virus that can infect bacteria next then we move on to the topic biological molecules which is split into these four components and we're going to start with testing for biological molecules so the first biological molecule that we're going to look at for testing is starch and this one's quite straightforward you would add the chemical iodine which is an orangey brown color and if starch is present it goes blue black the next turn is to test for reducing sugars and there's a bit more to it for this one first of all you need to add Benedicts re agent which is this blue color but for this one if you don't heat it up the reaction won't happen so the mark schemes will be really specific that you have to say add Benedict's reagent and heat after heating a positive test result will mean that that blue color will change to one of these colors and the more red it is the higher the concentration of sugar present so here we can see this orangey color so that' be a medium high concentration of reducing sugar present you can also use reagent test strips and those can be used to test for the presence and concentration of reducing sugars then the test for a non-reducing sugar so for example suit Crose you would still have to do your Benedicts test to start with and if your sample remained blue then you move on to the next stages but there's still a mark for saying following a negative Benedicts test you would then add acid and boil and it does have to be boiling hot so that you can hydr sucrose into fructose and glucose so you'd have to say boil you then need to cool the solution and add an Alkali to neutralize and then you would add Benedict's reagent in heat and then you should get a color change if a non-reducing sugar was present and it will go it says here blue to green yellow orange or brick red but typically actually goes orange or brick red because if you're testing and you do have a reducing sugar because you've hydrolized that disaccharide into monosaccharides you've doubled the concentration of sugars present so it should go brick red then we've got the semiquantitative Benedicts test so you'd prepare your Benedicts reagent and you would then add this to a known concentration of glucose and note down the time it takes for that color change to occur so to prepare the sample you could dilute the reducing sugar solution to a known volume of distilled water so you can link this to the skill of Serial dilutions to create a series of different concentrations known concentrations of glucose and for each one You' perform the Benedict's test time how long it takes for each of those concentrations to change color and then You' note that down and if you plotted that as a graph the time taken for each one to change color then it is semiquantitative the test for proteins then would be adding boret and the reason I split up into by Ur is to try and help you remember the spelling because often students get this confused with buet which is a piece of apparatus you use in chemistry for titrations and the spelling does matter byette and that is this pale blue color you would add that to your sample you do not need to heat and if there is protein present it turns this purple lilac color then we have the test for lipids the first step would be you need to dissolve your sample in ethanol and to do that you would add ethanol and shake once you've done that then you would add distilled water and if you have a lipid present you'd get this white emotion and you do have to State the color which is white and emotion is the description of the fact that you've got this thicker substance it's not a precipitate but it's what we call an emotion next then we move on to carbohydrates and lipids so you need to know the difference between a monomer and a polymer so monomers are smaller units which can bond together to create larger molecules and a polymer is made from lots of monomers bonded together and you need to know about the following monomers and polymers so we're going to go through those but you also need to know about macro molecules and those are giant molecules there are three that you need to know polysaccharides which are the top three listed here proteins and then the polynucleotides which form in DNA and RNA so if we have a look at the carbohydrates first of all carbohydrates are made up of carbon hydrogen and oxygen and they can be categorized into monosaccharides disaccharides and polysaccharides mono means one saccharide means sugar so a monosaccharide is the monomer that's when you just have one sugar Unit A disaccharide is a DI which means two units joined together and d means two saccharide means sugar so it's Two Sugars joined together polysaccharides are the polymers poly meaning many or in this case it literally means more than two and that's when you have many sugar units bonded together and here are some examples of each of those that you need to know so if we have a look at glucose alpha glucose to start with this is is the key monosaccharide that you will learn about glucose and the formula is C6 h126 and here we have alpha glucose the structure that you would need to know glucose has two isomers though which means two forms of glucose that have the same molecular formula but a different structure and we can see here we've got alpha glucose on the left and on the right we have beta glucose and the key difference is Al glucose I always think it's pretty much symmetrical you've got hydrogen on top and the hydroxy on the bottom that's the same on this side over here whereas for beta glucose you have the hydroxy on top and the hydrogen on the bottom and that slight change in the position of the hydrogen and hydroxy has a big impact on the location and the type of bonds that can form when creating the polysaccharides and therefore the final shape of the polysaccharides so monosaccharides these can be categorized according to how many carbon atoms they contain a hexo sugar hex means six and wherever you see o e at the end that means it is a sugar so hex o means it's a sugar that contains six carbons pent o means it's a sugar that contains five carbons for example ribos the disaccharides these are made of two monosaccharides bonded together with a glycosidic bond they're formed via a condensation reaction and the key ones that you need to know are these here moltos lactose and sucrose all three of them contain glucose as one of the monosaccharides but it's the second monosaccharide that differs so Mose contains two molecules of glucose lactose contains glucose and galactose and the way I always remember that is there's lactose within the name and then sucrose it's made of glucose and fructose so when you join those together because it's a condensation reaction you form a bond between those molecules and that also involves the removal of water which is why we've got plus water for all of those so we said it's a condensation reaction that forms them a condensation reaction is when you join two molecules together by removing water and that forms a chemical bond hydrolysis is the opposite reaction it's when you split apart molecules through the addition of water which breaks a chemical bond and we see these two reactions creating all of the polymers and also hydroling the polymers back into their monomers so here it is in action we're just showing um glucose but without any of the hydrogen or hydroxy groups except for the ones involved in the condensation reaction so here we have two molecules of glucose and the water is going to be removed from these hydroxy groups it doesn't actually matter which way around the full hydroxy and then the single hydrogen is removed from the point is you're left with a single oxygen atom behind and that is what the glycosidic bond is the carbon to oxygen to carbon so that's the bond that is formed to join these two molecules together and it involved the removal of water and we'd call that a one to four glycosidic Bond because the bond is formed between carbon 1 and carbon 4 and we always number the carbons going clockwise from the oxygen in the ring so carbon 1 2 3 4 5 6 and again carbon 1 2 3 4 5 6 so the bond is formed between carbon 1 on this glucose molecule and carbon 4 on this glucose molecule hydrolysis action then would involve adding that water back in to break that glycidic Bond and then we'd get those two hydroxy groups back and we now have our monosaccharides again so the polysaccharides these are created by repeated condensation reactions between many glucose monomers starch is found in plants and its function is a store of glucose cellulose is also found in plants and that is a structural molecule so it provides structural strength to the cell wall and gly is found in animals it's also a store of glucose so glycogen and starch are very similar in structure because they have the same function it's just one is found in plants one is found in animals so here is the summary table this would be a good one to screenshot and print out or to write it out so you've got your summary of the structure and function of all three of those polysaccharides so the first one we've got is which isomer of glucose the monomer is in all three so starch and glycogen both have alpha glucose whereas cellulose has beta glucose and it's that key difference which explains why cellulose can only form one to four glycosidic bonds whereas alpha glucose enables the formation of 1 to six glycosidic bonds as well and when you have a 1 to six glycosidic bond that causes a branch to come off the structure and that is why starch and glycogen if we jump to the structure part they both are branched molecules now that is an advantage for starch and glycogen because the fact that they are branched means that there is a greater surface area to these molecules so therefore when enzymes attached to hydroly that store of glucose back into glucose they can more rapidly hydrolize that molecule and that's good because it means you get the glucose being released for respiration more rapidly all three molec ules are very large so they're insoluble which means they won't dissolve won't affect the water potential or osmosis in the cell cellulose is a very different structure this is the one that we said is made of beta glucose one to four glycosidic bonds join some together and that means you don't have any branches you just get these long straight chains of the polymer which can therefore lie really closely together in parallel and hydrogen bonds then form between these chains and the fact that so many hydrogen bonds form between them is what provides this structural strength to the molecule a single hydrogen bond is actually very weak but because there are so many holding together your chains of beta glucose which is then called a fibral or a microf fibral or a macr fibral that is what provides the structural strength the lipid was the other part of this subm module and these are macro molecules but they are not polymer you do not have repeated units bonded together so it is still large but it's not a polymer they're nonpolar molecules and for that reason they're insoluble in water and they will only dissolve in organic solvents such as ethanol they are hydrophobic which means they will repel or they won't interact with water and they're made up of three fatty acids for triglyceride and a glycerol molecule and for a phospholipid it's two fatty acids and a glycerol plus that phosphate group but what they all have in common is they're made up of glycerol and fatty acids so these are the two key lipids that you will need to know the structure of and the main difference is that a phospholipid has only two fatty acids so instead of that third fatty acid it's got a phosphate group attached to the glycerol and that completely changes the properties of the lipids so how a triglyceride is made is actually the same way that phospholipid is made your glycerol fatty acids join together through condensation reactions which we said was the joining together of molecules forming a chemical bond removing water and it's at this point here between the glycerol and the fatty acids that the water molecule would be removed and if it's a triglyceride you have three condensation reactions so three molecules of water are removed and we then get three bonds and those bonds are known as EST bonds and that is an R your R Group here is the fatty acid hydrocarbon chain and then we've got the C double bond o o um and the H is over here so that would be your Esther bond this is just showing you in more detail how that condensation reaction happens between the glycerol and those fatty acids so you'd have a molecule of water being removed and that then leaves you with the triglyceride and your Esther Bond and three molecules of water would be removed now the fatty acids can either be saturated or unsaturated and what we mean by that is whether they contain a single or double bond between the carbon atoms in the R Group which is that hydrocarbon chain so this top one we can see only single bonds between the carbon atoms so that would mean it's saturated because it's holding the maximum number of hydrogens possible that's why it's saturated and saturated fatty acid you have at least one double bond between the carbon atoms so it's not fully saturated it could have held two more hydrogen's here and where you do get that double bond between the carbons it causes a kink in the chain we can see here it's bending so the property s of triglycerides they can transfer energy and that's because of the large rtio of energy storing carbon to hydrogen bonds compared to the number of carbon atoms a lot of energy be transferred when it's broken down also due to the high ratio of hydrogen to oxygen atoms they can act as a metabolic water source and this is because triglycerides can release water if they are oxidized and That's essential for Animals such as camels in the desert also because lipids are large they're hydrophobic molecules which means they're insoluble so they're not going to affect the water potential or osmosis they also have a relatively low mass and that means compared to other molecules of their size such as a protein they do not have anywhere near as high a mass so you can actually store a lot of them in an animal without increasing the mass as much which would prevent movement phospho lipus on the other hand so we've talked about the fact that those are made of a glycerol molecule two fatty acid chains and a phosphate group that means that they would only require two condensation reactions to join those fatty acids on and you get two the bonds the properties are different though because of the phosphate group on what we describe as the head of the phospholipid so the head is the glycerol and the phosphate group and the phosphate group has got a negative charge to it and because it's got a negative charge that changes the properties and it makes it hydrophilic which means it can interact with water the tail is the hydrocarbon chains or those fatty acid chains and those don't have a charge so they are hydrophobic which means they will repel water but they can interact and mix with lipids or fats and for that reason you get this phospholipid bilayer structure forming with lots of phospholipids and that's because those hydrophilic heads can interact with water but the tails are repelled by water so if you were then to put large amounts of phosph in water you will get the heads on the outside interacting with the water and the Tails spin inwards repelling away so this behavior of the Tails moving away from water is what results in that phospholipid B layer which forms the plasma membrane around cells and some organel and the hydrophilic nature of the phosphate head enables that surface of the plasma membrane to stay in place and the phospholipid Bayer Arrangement enables carbohydrates also to attach and form important receptors on the membrane and that would be your glyco lipids so next time we're going to move on to the proteins so proteins are made up of one or more large polymers creating a Macro Molecule and the monomer that they're made up of are amino acids so here is your general structure of an amino acid you have nh2 which is the amine or amino group you have your caroal group which is co you have a central carbon and then we have an R Group which is a bit different on all 20 amino acids so R means it's variable and then you have a hydrogen so the way the I always remember how to draw it is remember you have this Central carbon in the Middle with four different groups coming off it then you have to try and remember the groups your aing group carboxy group R and hydrogen so proteins are polymers they're these macro molecules made up of the monomer amino acids and there are four levels of structural organization and we're going to describe each of these starting with the primary structure so straight after protein synthesis you have your primary structure which is just a sequence of amino acids in a polypeptide chain and you have to say either the sequence or the order because that exact order the amino acids is going to determine the bonding location that happens in the later stages so it is the order or the sequence of amino acids held together by peptide bonds that primary structure then folds or coils to make either a beta ple sheet or an alpha Helix and those are held in place by hydrogen bonds so describing the structure of the secondary structure of a protein would be a two mark question the first mark would be for saying that you get these alpha helixes or beta plet sheets second Mark is saying they held in place by hydrogen bonds the location of those hydrogen bonds then is between different amino acids and it's always between a hydrogen atom and an oxygen atom next up we have the tertiary structure and this is the further folding and it's held in place by a range of different bonds you have hydrop very Bic and hydrophilic interactions which are quite weak you have even more hydrogen bonds which are also weak but then you'll have ionic bonds which are slightly stronger and the ionic and dulfi bonds the dulfi bonds being the strongest of them the Cove valent bonds those are going to form between the r groups of different amino acids within the polypeptide chain now you actually only sometimes get disulfide bonds cuz D sulfide means it's a bond between two sulfur atoms and that means you're only going to get this Bond if you have the R Group which contains sulfur because sulfur is not in the rest of the general structure so that tertiary structure then it's the further folding to create a unique 3D shape held in place by those bonds so it' be a three Mark definition the further folding is one Mark unique 3D shape is a second and naming the bonds is the third and the location that those bonds form is determined by the sequence of amino acids in the primary structure and where those bonds form is what determines the final unique 3D shape so that's why the primary structure is so important that sequence of amino acids determines the location of these tertiary structure bonds and that determines how it folds and the 3D Shape it makes the last level of organization is a quary structure so some proteins not all are made up of more than one polypeptide chain so you still get that 3D unique shape of the tertiary structure it's just you have multiple polypeptide chains bonded together so for example hemoglobin is made up of four polypeptide chains and hemoglobin has four polypeptide chains each chain has a prothetic group attached which means a nonprotein group attached to the polypeptide chain and that prothetic group contains ion so the group is called a heem group and it contains ion so we then have a look at fibrous versus globular proteins so we've talked about the fact that the tertiary structure is this 3D unique shape because of that um further folding but the way it folds you can either get spherical shapes which would result in globular proteins or more ROP likee shapes which would be your fibrous proteins so the fibrous proteins that is when it folds to create these long Twisted strands and because of that it creates a really stable structure which is insoluble in water and the function would be to give structural strength so collagen for example in bones or keratin in your hair in contrast the globular proteins they fold up into these sphere like shapes which means they're relatively unstable they are soluble and they are involved in physiological functions so for example all the enzymes antibodies and some hormones in hemoglobin but because they're relatively unstable these are all very temperature and pH sensitive so let's have a look at hemoglobin in a bit more detail we said it's a globular protein it also has a quary structure it's got four polypeptide chains two that are called Alpha chains and two that are called beta chains it has a prothetic group attached to it and that is the heem group which we can see here um it's describes a conjugated protein conjugated means it has a prosthetic group added to it and that prosthetic group is the heem group which contains ion and it's the ion that the oxygen is going to be able to bind to collagen was our example of a fibrous protein so collagen molecules are triple huses composed of three polypeptide chains wound around each other like we can see in this diagram here and these chains are held together by hydrogen bonds and some coent bonds the fibral formation then is that the collagen molecules interact with the adjacent molecules next to them and that's going to form these cross links between their R groups and they can then align in parallel we get these staggered ends which prevent weak spots in the fibral so overall it creates a tensile strength so collagen's unique structure provides both flexibility but also tensile strength so tissues like your Achilles tendon in your ankle is rich in collagen fibers so it can withstand significant pulling Force without stretching or breaking and the collagen fibers can align differently based on the forces they encounter in tendons they form parallel bundles along the direction of the tension in SK in layers of collagen fibers run in various directions to resist the pulling force from multiple angles so the final biological molecule is water so water is a polar molecule due to the uneven distribution of charge so you have two hydrogen atoms and oxygen the oxygen has a slight negative charge the hydrogen atoms have a slight positive charge so that's what this Delta negative and Delta positive symb are representing and that is going to enable hydrogen bonds to form between different water molecules and that's what we're shown here we've got hydrogen bond forming between the oxygen and the hydrogen of different water molecules and it's the formation of those hydrogen bonds that provide the properties that we're going to be talking about of water so the Key properties that you need to know is that it's an important solvent in reactions it has a high specific heat capacity and a large latent heat or vaporization so if we start with the fact that it's a solvent this is due to the polar nature of the molecule because the hydrogen atoms have a slight positive charge and the oxygen have a slight negative charge that means that it can attract positive and negative ions when they're placed within the water and that is what causes the dissolving because the water can surround those ions so this could be sodium chloride for example in this example and um the sodium would be the positive the chloride would be the negative so the oxygen which is a slight negative would be attractive to the positive sodium that can then separate that lattice and surround the sodium ions and the hydrogen can do the same thing to chloride ion and as it separates all of those that is what dissolving means so it's Poss POS because of that polar nature but it can't dissolve nonpolar molecules and instead non-polar molecules would actually repel the water the cytool and eukariotic and procaryotic cells is mainly water though so this is really beneficial because it means many solutes can dissolve within the cytoplasm of the cell and therefore reactions are going to happen more rapidly but also it means molecules can be easily transported dissolved in the solution so that links this idea of Transport mediums as well because water is a good solvent plants for example they will have mineral arms dissolved in the water which is then transported up through the xylm and not only that because of the hydrogen bonds that form between water molecules the water molecules stick together creating cohesion and that means water can move up the xylm in the transpiration Street as a continuous column of water and that makes it much easier to draw the water up the xylm with all of those dissolved mineral ions within it so that the cells further up can gain access to both water and mineral ions it's actually the same idea in blood not that there is this cohesion but blood is made up of plasma which is mainly water and that means you can dissolve ions in it and glucose and that can be easily transported around the blood in animals next then is the high specific heat capacity and water has a high specific heat capacity because of the large number of hydrogen bonds that form between water molecules and therefore it's going to require energy to break those hydron bonds to split apart the water molecules and for that reason a lot of energy is required to raise the temperature of water so water acts as a temperature buffer and this is an advantage as internal temperatures of plants and animals should therefore remain relatively constant even if the external temperature is fluctuating and that should prevent enzymes from denaturing it's also particularly important for any organism that is aquatic meaning it lives within bodies of water because that should mean that the temperature of the body of water that they live in should remain relatively constant as well then we move on to the large latent heat of vaporization this means that a lot of energy is required to convert water from its liquid state to its gaseous state so in other words for evaporation and again that's because of the energy required to break the hydrogen bonds between the water molecules and because a lot of energy is required to evaporate water that means that it can provide a significant cooling effect so when you sweat water is being released onto the surface of your skin the heat energy that's radiating from your skin skin is used to evaporate the water and in doing that large amounts of heat energy are being removed from your skin and it provides a cooling effect next then we move on to module three which is enzymes split into these two three topics and we're going to be starting with mode of action of enzymes so enzymes are an example of globular proteins and they are biological cists the active site is specific and unique in shape due to the specific folding in that ter ter structure which is determined by the primary structure and the location of the bonds in the tertiary structure due to this specific shape they get an active site that is unique which will be complementary in shape to only one substrate so that means enzymes are specific they'll only catalyze one particular reaction and that could be intracellular or extracellular reactions so for example catalase is an intracellular enzyme inside of liver cells that breaks down hydrogen proct oxide into oxygen and water whereas triin is an extracellular enzyme in the small intestines that hydes proteins so if we think about how they are speeding up these chemical reactions it's because all reactions require a certain amount of energy before they occur and that is known as activation energy which you'll be familiar with from chemistry at GCSE when enzymes attach to the substrates they lower the activation energy needed for the reaction to occur and therefore they speed up the reaction so there's two models that hypothesize how they lower the activation energy the lock and key model is the one that suggests that the enzyme is like a lock with a fixed shape and that the substrate is like a key which is perfectly complementary in shape to that lock so they fit together and you create an enzyme substrate complex um and that will then result in the Distortion of the substrate lowering the activation energy now they'll only bind together because of random collisions the difference between this and the induced fit model is in this instance it's more like the analogy that the enzyme is like a glove and the substrate is like your hand so that means that they're not perfectly complimentary to start with but as soon as they bind together like your hand going into the glove they then become perfectly complementary so what this means is the substrate is almost complimentary in shape to the active site when it collides induces the enzyme to mold around that substrate and in doing that it puts tension and strain on the bonds in the substrate and therefore less energy is needed to break those bonds and that is how it lowers the activation energy now this is the current accepted model because of research been done they've realized that enzymes proteins are slightly flexible so this would make sense that that is the case and also it better explains how the activation is lowered the activation energy is lowered you need to know a little bit about certain reactions so investigating enzyme catalyze reactions starting with let's have a look at the catala reaction monitoring so catalase we already said that's the enzyme that catalyzes the breakdown of hydrogen peroxide in the liver into water and oxygen so you could be asked to investigate the progress of this reaction where you can measure the rate of formation of oxygen over time so you could do this by collecting the oxygen produced in a measuring cylinder or maybe a gas syringe and at set intervals record the volume of oxygen being produced alternatively you could use a Data Logger that's going to be a more accurate way to measure the oxygen being produced but what you would then do is plot the volume or the pressure of oxygen produced Against Time and the graph can be generated to then visualize the rate of the reaction because rate is the amount of product produced over a set period of time the amalay reaction monitoring is the alternative option so amas is an enzyme that catalyzes the hydrolysis of starch that's the substrate into simpler sugars such as moltos and then eventually molas would hydrolize that into glucose to monitor the progress of this reaction we can measure the rate of The Disappearance of starch over time and we'd need to use iodine for this so You' need to take samples of the reaction mixture at regular intervals and test for the presence of starch using iodine as amalaye would be hydroling starch into moltos once the starch is hydrolized the iodine would no longer change blue black and instead it remain orangey Brown so you could time how long it takes for the reaction to occur by seeing how long it takes for the starch to be broken down and therefore you don't get a blue black color anymore and you could always use a Colorimeter as a way to quantify this so a Colorimeter then is an instrument used to measure the absorbance or the transmittance of Light by a solution but it's normally the absorbance it works on the principle that certain substances absorb light at specific wavelengths and that results in a change in the intensity of the light that can be transmitted through the solution enzyme catalyzed reactions often involve color changes due to the formation of reaction products or the loss of a substrate so you could measure this within a Colorimeter so You' place your sample in a cuvette which is the name of the plastic holder put it into your Colorimeter you then press the test button and that will cause a beam of light to shine Through Your solution and then you can see how much was absorbed by the solution versus gets transmitted and picked up by the detector and that will then give you a numerical value so you get a quantitative result next up we have a look at the factors that affect enzyme action and the key factors that you need to know about are temperature pH enzyme concentration and substrate concentration now the first two link back to what we were saying in the proteins part of this lesson where whereby enzymes are globular proteins and globular proteins are less stable and therefore they're sensitive to certain conditions meaning that they are more at risk of having tertiary structured bonds being broken and therefore they lose their unique 3D shape and that is what temperature and pH cause to happen if there isn't a high enough temperature enzymes don't Den nature but at lower temperatures there's insufficient kinetic energy for the success ful collision between the enzyme and the substrate and therefore you get fewer enzyme substrate complexes and the rate of reaction is lower if you go above the optimum temperature though there will now be so much kinetic energy that it causes the bonds such as the hydrogen bonds to break and that results in the protein unraveling and losing its unique 3D shape that means that active site changes shape and therefore enzyme substrate complexes can't form and we say that the enzyme has denatured it's a similar idea with ph because if you have too high or too low a pH it will interfere with the charges in the amino acids in the active site and if you're changing the charges that can cause the ionic and hydrogen bonds to break that changes the tertiary structure and therefore changes the active site and therefore the enzyme has dened so you won't get those enzyme substrate complexes and therefore the rate of reaction is going to be lower now each enzyme will have a different optimal pH based on the location that they are functioning in so most of them will be around neutral but some are slightly more alkaline and some for example different proteas enzymes that work in the stomach have an Optimum significantly lower maybe around pH 1 or two so very acidic conditions next time we have a look at the substrate and enzyme concentration this is nothing to do with denaturing now it's all to do with successful collisions whether there is an aite available or not so if there is a low concentration of substrate the reaction will be lower as there will be fewer collisions between the enzyme and substrates because they're less available if you increase the substrate concentration you'll therefore get an increase in the rate of reaction because at that point here on the graph substrate is the limiting factor but at High substrate concentrations the rate of reaction platter because all of the enzyme active sites will already be in use so even if you had more substrate there are no empty active sites them to collide with so the reaction is already going at its maximum rate with the enzyme concentration similar idea at low enzyme concentrations there's going to be a lower rate of reaction because there'll be fewer collisions between the enzyme and the substrate so fewer enzyme substrate complexes so as you increase the enzyme concentration there'll be an increase in the rate of reaction but at high enzyme concentrations unless you also have unlimited substrate being added the rate of reaction is going to Plateau as there'll be insufficient substrates to bind with all of those enzymes so you'll ends up with some empty enzyme active sites the next concept is inh Inhibitors which can prevent enzymes from working a competive inhibitor is one example and these are the same or very similar in shape to the substrate and therefore they're complementary to the active site and they can actually bind to the active site blocking it and therefore preventing the substrate from binding and if you have an enzyme inhibitor complex that prevents an enzyme substrate complex and therefore lowers the rate of reaction now most competitive Inhibitors are reversible and what that means is if a high enough substrate concentration is present then the substrate can actually knock the Inhibitors out and therefore you can get the enzyme substrate complex is forming and the rate of reaction will increase again so reversible means the inhibitor can be removed non-reversible means the inhibitor cannot be removed non-competitive inhibitors are Inhibitors that do not bind to the active site they bind to a different binding site on the enzyme which is known as the allosteric S now this doesn't block the active site but instead when it does attach to the protein it binds it causes the protein to change shape and therefore the active site changes shape and the substrate will no longer be able to bind so no matter how much extra substrate you add you will not get any more enzyme substrate complexes because the acti site changed and that's why you get these shaped graphs with Inhibitors the solid line is showing you without any inhibitor this is the curve that we just talked about showing the effect of adding the substrate um eventually it plate because all of the enzyme active sites are in use competitive Inhibitors the curve is shifted to the right indicating a lower rate of reaction but at high enough substrate concentrations that would knock out the inhibitor so you do end up at the same Vmax which is the maximum rate of reaction for that enzyme reaction non-competitive Inhibitors though there's a lower rate of reaction and it Plate at a lower rate as well and that's because it doesn't matter how much extra substrate you add the rate won't increase because the active site has changed shape now enzyme Inhibitors often what people think is what is the point of an enzyme inhibitor now sometimes they are just harmful they are poisons things like cyanide for example but some of them are actually very beneficial and naturally occur in our bodies and it's this concept of end product inhibition and what this means is the products of some reactions are actually reversible competitive Inhibitors and in that way it controls when reactions are occurring to make sure cells don't overheat and that you're not wasting resources because if there's a lot of product present that product acts as an inhibitor so it will inhibit the enzyme at the start of a reaction and therefore it means the reaction isn't going to occur while you have lots of product present because you don't need that reaction to occur but when that product gets used up that means there'll be no more inhibitor present and the reaction will start again so it's a way to control when reactions do and do not curve so we saw on that graph this idea of Vmax and Vmax refers to the maximum rate at which an enzyme catalyzes a reaction when the active sites of all enzyme molecules are fully saturated with the substrate and at Vmax the enzyme is functioning at its maximum capacity and further increases in substrate concentration won't increase the rate of reaction so V-Max is a key measure used to characterize enzyme kinetics and is determined experimentally by by plotting reaction rate against substrate concentration until you see that Plateau being reached you then got Michaela's menum constant or km and km is a measure of the Affinity of an enzyme for its substrate it represents the substrate concentration at which the reaction rate is equal to half of the V Max so km can be thought of as the substrate concentration required to achieve half maximum velocity ID with lower km values have a higher affinity for their substrates as they reach half maximal velocity at lower substrate concentrations so km is derived from the madus mum equation which describes the relationship between reaction rate and substrate concentration lastly then we have a look at this comparison of enzyme Affinity km values can be used to compare the Affinity of different enzymes for their substrates enzy with lower km values exhibit greater substrate affinity and are more efficient at converting substrate to product even at low substrate concentrations and conversely enzymes with higher km values have lower substrate affinity and require higher substrate concentrations to achieve maximal velocity you also need to be aware of immobilized enzymes compared to enzymes free in solution and enzymes can be immobilized meaning fixed within a matrix such as algate or they could be just free to move around within a solution when investigating the difference in activity between immobilizing alate or freeing solution experiments can be conducted comparing reaction rates under controlled conditions so for example the activity of an immobilized enzyme can be compared to that of the same enzyme in a solution by measuring the rate of substrate being used up or product being produced over time now the advantages of using a mobilized enzymes are it makes them more stable immobilized enzymes are less sensitive to temperature and pH changes and that makes them very useful to use in industrial reactions because you can use a slightly higher temperature to speed up the reaction without dening the enzyme it also makes it much easier to separate the product from the enzyme because here we have the enzyme immobilized and alate Beads you could easily just SI those out and then you have the product remaining in the liquid you can have the continuous use of enzymes as well mobilized enzymes can be used continuously in bioreactors and Industry as they're packed into columns or membranes and you just have a flow of your substrate going over them continuously that means they're also easy to reuse use making it much quicker and also cheaper and we've got here improved reactive performance immobilized enzymes can improve enzyme activity as well by providing a higher local concentration of substrate near the active site so it increases the rate of reaction also next time we're going to have a look at cell membranes and transports starting by looking at the fluid mosaic model of membranes so all cells and organel membranes are composed of a phospholipid Bayer and this provides a partially permeable membrane so that you can control what can enter and exit the cell it can also be the site of chemical reactions and have a role in cell communication so the fluid mosaic model then is this concept that you've got the mixture and movement of the phospholipids proteins embedded within it glycoproteins glycolipids and also that cholesterol so it's a mosaic because it's made up of different molecules and it's fluid because there is some movement in this molecule so left to right movement the phospholipids Align as a Bayer and we talked about earlier in this video that that's due to the hydrophilic heads being attracted and interacting with water on the outside and the hydrophobic tails are repelled so they spin inwards proteins within the cell membrane can be intrinsic meaning they or and they're called intrinsic or integral and that means means they go all the way through the membrane or they can be called extrinsic or peripheral which means they're just on the outside of the membrane the extrinsic proteins provide mechanical support or they can make glycoproteins um they wouldn't be a glyco lipid because that's not got a protein in it the glycol liid would actually be these green Parts which are separate but the function of all of those is cell recognition as receptors as well intrinsic or integral proteins are protein carriers and channel proteins involved in the transport of molecules across membranes protein channels form these tubes that fill with water to enable water soluble ions to dissolve and then diffuse through the channel whereas the carrier proteins will bind with the ions and larger molecules such as glucose and amino acids and change shape to transport them to the other side of the membrane cholesterol is shown here in yellow and that is present in some membranes and this restricts that lateral meaning the side to side movement of other molecules in the membrane and this is useful as it makes the membrane less fluid at high temperatures and therefore prevents water and dissolved ions from leaking out of the cell so cell signaling refers to the transmission of messages or signals from one part of an organism to another and it ensures coordinated responses to internal and external stimuli this process is vital for the proper functioning and survival of organisms and the cell membrane plays a role in this so the purpose of the cell signaling all the cells and organisms must respond to their environments to and be able to survive changes in the environment and signaling Pathways coordinate cellular activities those Pathways could be electrical for example in the nervous system or chemical for example in the hormone system and they involve various molecules such as neurotransmitters and hormones so the state in the chemical signaling pathway and this is where we'll see it link back to the role of the membrane you have secretion of a specific chemical or a ligant and cells secrete specific chemical messages and that's what the ligans are in response to a stimuli and that could be molecules like hormones for example glucagon which is then going to be released into an extracellular space that will then be transported through the bloodstream in the case of hormones to the Target cell and once again to the cell the LI will bind to receptors on the cell surface membrane of those target cells and this is where we see the role of the cell membrane in the chemical signaling Pathways because they have those receptors on the cell surface membrane that's what the hormone or ligan can bind to and that will initiate a signaling Cascade so the cell surface repors are protein molecules located on the cell surface membranes the Lian receptor binding triggers the confirmational changes in that protein receptor allowing the message to be transmitted into the cell and that process is known as transduction it often involves G proteins and the production of a second messenger so another chemical that's going to amplify the effect second messengers um will relay the message by activating enzymes and once an enzyme is activated it's going to cause a chemical reaction to happen inside of the cell so that sequence of events triggered by The Binding to the receptor is known as a signaling Cascade as we just went through and The receptors can alter cell activity by opening ion channels or acting as membrane bound enzymes or serving as intracellular enzymes as well and hydrophobic signaling molecules like steroid hormones can diffuse directly across the cell membrane and bind to receptors in the cytoplasm instead or even in the nucleus you also have other mechanisms of signaling so you could have direct cellto cell contact using receptors on the cell surface membrane so that's what we can see here for example antigens embedded on the cell surface membrane you're going to have a cellto cell contact through the antibody or an antigen presenting cell and maybe a t- helper cell next time we move on to the movement into and out of cells which is controlled by the cell surface membrane and there are six key modes of Transport that you need to know simple diffusion facilitated diffusion osmosis active transport and then endo and exocytosis so simple diffusion is the net movement of molecules from an area of higher concentration to an area of lower concentration until equilibrium is reached this process does not require ATP it doesn't require a membrane either even though we can see that here it doesn't always happen across a membrane um but we can see we've got a concent gradient and as long as the molecule is small and lipid soluble it can then dissolve and diffuse across that membrane until equilibrium is reached facilitated diffusion is also a passive process meaning it doesn't require energy from ATP and that's because it's still going down the concentration gradient but this would be used for molecules that are either not lipid soluble or they are large and therefore they have to go through a protein instead because they can't dissolve through the phosph lipid by layer now this could be either using a protein Channel or protein carrier so protein channels for example you would have a channel which is a tube filled with water which would mean ions or polar molecules can dissolve in that water instead of the phospholipid by layer and then move through that channel by diffusion carrier proteins is when you'd have the molecule complimentary in shape to that particular protein bind when when it binds it causes a confirmational change which results in the molecule being released on the other side of the membrane water moves across the membrane by osmosis so your definition of osmosis is the movement of water from an area of higher water potential to an area of lower water potential or more negative across a partially permeable membrane so there's different types of solution when we think about water potential isotonic is when the water potential which is a measure of how concentrated a solution is is the same outside of the cell as it is inside of the cell so ISO means equal hypotonic is when the water potential of the solution surrounding a cell is more positive which means it's closer to zero which in other words means it's less concentrated so you don't have as much solute dissolved in the solution compared to the cell hypertonic is when the water potential of the solution surrounding a cell is more negative than the cell so a hyperonic solution means that you have more solute dissolved in the water and we can see here when you place animal cells which don't have a cell wool into these three different types of solution the effect it has on the cell so if you were to put red blood cells are example of an animal cell into a hypertonic solution because the solution has a more negative water potential the water is going to move from the cell to the surrounding Solution by osmosis and that causes the cell to shrivel up or crenate plasm is a term we use if it's happening in a plant cell if it's an isotonic solution because you've got an equal water potential inside and out there's not going to be any net movement of water so some water will move in some will move out but the cell will stay the same size and shape hypotonic solution is when the inside of the cell is more negative compared to the solution in terms of water potential so water is going to move into the cell bi osmosis which can cause the cell to swell and if enough water moves in it causes the cell to burst because there's no cell wool to provide that structural strength active transport is the movement of molecules and ions against the concentration gradient so going from an area of lower concentration to higher concentration and because it's going against the concentration gradient energy is required from ATP and also you need a carrier protein and it is always carrier proteins not channel proteins now this is a selective process because it's still linked to the idea of a particular molecule has to be complementary in shape to a specific carrier protein so ATP is involved and it will bind to the protein on the inside of the membrane and as it is hydrolized into ADP and Pi is going to release energy and it causes that energy causes a change in shape to the protein to cause it to open out to the other side of the membrane and as it opens up to the other side of the membrane it releases the molecule to the other side of that membrane the pi which is the inorganic phosphate is then released from the protein and that causes that carrier protein to revert to its original shape and as long as it's the ATP that process can continue next time we have a look at endocytosis and this is a type of active transport and it is the bulk transport of molecules into a cell so Endo means in the cell surface membrane will bend inwards around the molecule surrounding it to form a vacle the vesicle will then pinch off and moves within the cytoplasm um endocytosis can be classed as either phagocytosis which is what we can see here in the left or it could be pinocytosis when it is a liquid being taken in so that's the difference phagocytosis is when it's surrounding and pinching inwards with a solid particle the pinocytosis is when it is a liquid this requires energy from ATP for the cell to engulf and chain shape around the material exocytosis is our last type and this is the bulk transport of molecules out of the cell so vesicles within the cell will move towards and fuse with the cell membrane and as it fuses it releases its contents outside of the cell this process requires energy because ATP is needed to move the vesicle along the cytoskeleton up to that cell surface membrane where it fuses now the surface area to volume ratio is key in considering how fast these types of transport can happen across the cell surface membrane so exchange surfaces in organisms have very similar adaptations to increase this rate of transport and surface area to volume ratio is one adaptation that we see the relationship between the size of an organism or structure so for example an organel and its surface area to volume ratio plays a significant role in the adaptations so if we think about first of all what surface area to volume ratio means just looking at cubes if we were to work out the surface area of this Cube it'd be the area of one side so 1 * 1 is 1 but there are six sides so we times it by six that's why the surface area is 6 cm cubed the volume is length time height * width which would be 1 * 1 * 1 so the volume is 1 so our surface area to volume ratio you would do the surface area divided by the volume so 6 ID 1 gives you a surface area to volume ratio of six you could do the same thing for these cells here as well so on this one we've now got a 2 cm in dimension the picture actually doesn't show the full cube I've realized because you've just got um the first layer where it should be two across it is two up but it's not going two back the same here we've got three across three up but it's not showing you three back but it' be the same idea you'd work out the surface area of one side um and then times it by six for a cube and then the volume is 2 * 2 * 2 you then do your surface area divided by your volume and the pattern that we can see is the larger the object in this case a cube the smaller the surface area to volume ratio and that would mean transport would happen slower because you have a lower surface area compared to the volume so the smaller a structure is the larger the surface area to volume ratio and therefore the more rapid the transport across the membrane so that's why small organisms such as amoeba they have a very large surface area to volume ratio and that means they don't have any special exchange surfaces like lungs because they can just do simple diffusion across their surface to meet their respiratory needs but larger organisms they will have a larger surface area to volume ratio and therefore they will need adaptations to make sure they are getting enough oxygen in and enough carbon dioxide out as well as it could be other structures within the body and that's why we then start to see these adaptations not only that the larger an organism they will have more cells and therefore a higher metabolic rate and they'll have a higher demand for oxygen but also they'll be producing more waste products that need to be removed so some of those key adaptations will come up in later topics but it's ideas such as having micro Villi on cells or having millions of alveoli in the lungs as well so topic five then is mitotic cell cycle and it's split into two parts and we're beginning with replication and division of nuclei and the cells so let's have a look at chromosomes to begin with in eukaryotic organisms the DNA is stored as chromosomes and humans have 23 pairs of chromosomes which means there's 46 in total and you have two copies of every chromosome and those matching pairs or the two copies are known as homologous Pairs and what we mean by homologous whereever you see homo in biology that means the same so a homologous pair of chromosomes are two chromosomes that are the same size and key is they have exactly the same genes but they might have different alals and that's what we can see here on this diagram we've got the gene for hair color but they've got different alals this chromosome has straight this one has curly and then you've got a selection of other genes so this is one chromosome this is another chromosome because you count chromosomes by how many Centrum there are so we do have two romes in this image and they are a homologous pair of chromosomes because they're the same size and they contain the same genes a bit more than about chromosomes in UK cartic organisms we said they're stored in the nucleus and in order for that vast amount of DNA to fit in the nucleus in this linear shape that's how we describe the shape of the chromosome it has to be tightly coiled up to fit and to assist with that the DNA wraps around proteins called histones and I always say to think of this like if you were to try and pack away your hair dryer if you wrap the cord around the hair dryer handle it tightly compacts really neatly and that's the same idea with DNA wrapping around histone proteins it helps to really tightly Compact and coil it up in a neat way so you're not going to damage the DNA chromones also have a centromere which we can see here and that is the pinching part in the middle of a chromosome and after DNA replication this is what a chromosome looks like it's made up of two sister chromatids before DNA replication it looks like a single stick like structure and it would still have a centromere in it but at this point the role of the centromere is to hold together those two sister chromatids at the end of the chromosomes you have what's known as a tiir and that's a protective cap and essentially it's a DNA sequence and it's proteins that are right at the end to protect the DNA during cell division so it's these repetitive short sequences that make the DNA longer but those sections aren't coding it is just to protect the coding regions of the DNA and tase is an enzyme that adds bases to the tmis to help maintain their length so if you then go on to cell division in ukar cells they enter the cell cycle and they can divide by either mitosis or meiosis procaryotic cells divide by binary vision and viruses do not undergo cell division as they are non-living so we're going to focus on just mitosis in this video the cell cycle is all of the stages involved in creating new cells and it's split into three stages you have interphase which is the longest stage P by a long way and it's shown here in Gray so you can see the majority of the cell cycle is interface and that is split into G1 S phase and G2 and we'll go through what those are in a minute you then have M or the nuclear division which can either be mitosis or meiosis we're just focusing on mitosis in this video and then the last stage of the cell cycle is cytokinesis so these are the three steps let's let's go through each of those in a bit more detail so interphase as I said is the longest stage G1 is when protein synthesis occurs to make proteins involved in synthesizing organel and then all the organel can replicate because if you're going to split the cell in half you need to make sure both of those new cells that are created have the correct number of organel so that's why we have to replicate all the organal first the cell is also checked that it's the correct size has the correct nutrients growth factors and that there's no damage to the DNA and if a cell doesn't pass those checks then interphase will not continue S phase is next and that is the stage where DNA replication occurs and then the last part of interface of G2 and this is when the cell continues to grow so that when it does split the two cells are the same size as the original cell it also has energy stores that are increased and the newly replic at DNA is checked for any copying errors and if any errors are found those are either corrected or the cell is destroyed to make sure that these mutations aren't going to be replicated in multiple cells stem cells is the next part of this topic and the definition of a stem cell is that it is an undifferentiated cell that can self renew which means to continually divide and it can become specialized and there are different levels of potency which means their ability to divide into a number of different types of cells so toy potent is the most potent meaning it can differentiate to any type of cell then as we go down the list it becomes less potent so Pur poent multi potent and uni potent so let's take a look at those terms in a bit more detail so toy potent stem cells are the cells that can divide and produce any type of cell in the body and during development T potent cells translate only part of the DNA resulting in cell specialization tent cells occur only for a limited time in the early mamalian embryos plur poent cells those are also found in the embryos and can become almost any type of cell they just can't become the placenta for this reason these are the ones are used for research with the prospect of using them to treat human diseases because you could could potentially use these to create any type of cell or tissue except for the placenta there are issues with this though as sometimes the treatment doesn't work or because stem cells continually divide they can result in the formation of tumors additionally there is the ethical debate on whether it's right to first of all make a therapeutic clone of yourself cuz to use these types of stem cells in treating a patient there would have to be identical DNA to the patient so they don't get rejected and the only way to do that would be to make a therapeutic clone of themselves you would also have to create an embryo and the embryo then gets destroyed and that can be seen as playing God or murder now in reality they have actually got advances on this now and they used something called induced Pur poent stem cells and but that isn't part of the specification next then we go on to multi poent and unipotent stem cells and these are found in mature mammals and they can only divide into a limited number of different types so multi- poent stem cells is for example the stem cells that you get in bone marrow and those can only specialize into or differentiate into the types of blood cells so it's a limited type of different cells I can differentiate into uni poent means that it can only differentiate into the same type of cell so for example skin cells can replicate and differentiate into more skin cells so some potential uses of stem cells then could be in research and also in medicine so for example they could be used to repair damaged tissues or the treatment of neurological conditions such as Alzheimer or Parkinson's where there's damage to the neurons in the brain or it could be to look and use these stem cells in developmental biology so for research purposes now we did mention that stem cells in theory they could be amazing for treating different diseases but because they self-renew they could lead to the formation of tumers and that takes us onto this concept here of what is a Tuma and what is cancer so mitosis which we're going to be going on to is a gene controlled process and there are genes that produce proteins that help to initiate and to control when my Tois stops to make sure that new cells are only being replicated when the body needs those new cells but mutations can occur in these genes that control mitosis and if a mutation occurs in those genes the proteins that are produced that are meant to control when mitosis starts and stops may not function and as a result you have uncontrolled mitosis and if mitosis is happening uncontrollably that means you're going to be making new cells when when the body didn't need those new cells and that is what a tumor is now not all tumors are cancerous if it's cancerous we call it a malignant tumor and some properties of malignant tumors compared to the non-cancerous which are known as benign tumors is that a malignant tumor has the ability for some of those cells to break off and then spread in the blood or it could be in the lymphatic system and then Lodge into new tissues in the body and create a secondary tumor and we call that metastasis they also can develop their own blood supply and if they've got their own blood supply that means they'll have lots of oxygen and glucose being supplied to these cells so they can respire aerobically more rapidly produce more ATP and that will mean mitosis can happen even faster so many cancer treatments for example chemotherapy work by preventing these rapidly dividing cells from entering mitosis and therefore that means their tumor can't get any bigger and the way this works is some of those drugs using chemotherapy will Target spindle fiber formation in metaphase and this prevents mitosis from happening and we'll have a look at how when we get to the actual stages of mitosis later on in this video but ultimately that prevents the cancer cells from dividing further the downside is though it doesn't just affect cancer cells it affects any fast dividing cells so that is cells in your body such as hair cells skin cells the cells line in your intestine those are all fast dividing cells and this chemotherapy will therefore affect all of those and that is why chemotherapy has so many really unpleasant and nasty side effects the next part of topic five then is looking at the chromosomes behave in mitosis or in other words we're going to be going through the stages of mitosis so mitosis is one of the types of nuclear division that occurs in the cell cycle and it creates two identical diploid cells and diploid means you have two copies of every chromosome it's used for growth tissue repair and it's also used in asexual reproduction in plants and animals and fungi there are four key stages you have prophase metapas phase anaphase and tease so you still have the cell cycle occurring so you start with interphase but then when you enter mitosis you go through these four stages and then at the end of the cell cycle we have cytokinesis so the way that people often remember this is just thinking about pmat as an abbreviation or is it an acronym I don't know Pats that's the way to remember it um prephase metaphase anaphase and taase so I'm going to talk you through what happens at each stage and going back to what we said here how the chromosomes are behaving at each stage that's the phrase that is used to describe the position of the chromosomes so prophase is the first step and this is when chromosomes condense meaning they coil up really really tightly and that means they become visible as individual chromosomes and in animal cells the cental which are going to be responsible for releasing the spindle fiber those are normally together at one pole of the cell and instead they'll start to move apart to the opposite ends or the opposite poles of the cell the centrioles that create the spindle fibers are released from both poles to start to create this spindle apparatus and these will then attach to the Centere and the chromatids in the later stages plants also have a spin apparatus but they lack those cental the next stage is metaphase and in metaphase the Chrome behavior is that they will line up in single file at the equator of the cell and the equator is the term we use for the middle of the cell because it's a sphere we use the term equator a bit like we do for the Earth so they align in the center which is the equator of the cell and at this point those spindle fibers that have been released from the cental will attach to the Centro mirr and some of the chromatids on those chromosomes and this again again helps them to align at the equator of the cell the spindle assembly checkpoint also occurs at this stage and this is where there's a check to ensure that every chromosome has attached to a spindle fiber before mitosis can proceed into the next stage which is anaphase so in anaphase this is when those spindle fibers start to shorten and move back towards the centrioles and as they do that it pulls the Centon chromatids and it splits that centromere in half and that is what results in the chromatids so cister chromatids being separated and being pulled towards the opposite poles of the cell so that's what we've got written just here now this stage does require energy in the form of ATP which is provided by Arabic respiration in the mitochondria so this links back to what we were saying in terms of cancer the fact that malignant humans have their own blood supply therefore they get more oxygen and more glucose for aerobic respiration to happen at a faster rate therefore there's more ATP and that is going to be helping in this stage here anaphase but when we talked about the drugs chemotherapy affecting that spindle fiber formation if spinal fibers aren't forming you're not going to be separating the chromatids the opposite poles and therefore you don't end up with two new cells that have the correct number of chromosomes and those cells would therefore be destroyed now lastly we've got til phase and this is when the chromosomes are now at each pole of the cell and the chromosomes start to become uncondensed so they get longer and thinner again and therefore they are starting to become no longer visible as individual chromosomes the spindle fiber will also start to disintegrate at this point and we can see that nuclear membrane starts to reform the final step is the cell cycle this doesn't count as mitosis but cyesis is the last part of the cell cycle and this is when the cytoplasm splits into two genetically identical cells so in animals you get this cleavage Furrow forming in the middle of the cell and the cytoskeleton causes the cell membrane to draw inwards and that is then what causes the cell to split into two eventually in plant cells the cell membrane splits into two new cells due to the fusing of vesicles from the GGI apparatus and then the cell W forms new sections around the membrane to complete the division into two cells now you could be asked to observe mitosis under a microscope and often this is done with root tips of plants such as onion and garlic and that is because at very tip of those roots and that's because that is where lots of mitosis is occurring and therefore you're more likely to be able to observe OB erve mitosis at those points so a thin slice of those root tip is placed on a microscope slide broken down with the needle you'd also often add acid and heat so that you are breaking down the connections between the cell walls so you get this thin layer when you squash down on that sample you also add a stain and the heat helps that stain to really stain the chromosomes so they become visible so that's what we've got here a is added to make the Chrome Zone visible and the cover slip is then pushed down on the pushing down is going to squash that tip so you get a single layer of cells so the light can pass through and therefore you can observe what is going on in those cells and you might get something that looks a bit like this now all of these ones here where it just looks like a pinky purple circle you can't see individual chromosomes in those and that would mean those cells are in interphase of the cell cycle and most cells will look like that because interphase is the longest stage of the cell cycle and therefore most cells will be in interface but in these two we can see the chromosomes are visible and it looks like at this point they are lining up along the Equator so those two cells would be in metaphase and you can work out what's known as the mitotic index and this is by counting how many cells are visible in your field of view and how many cells are visible that are in the stage mitosis and you would then use the formula the number of cells in mitosis divided by the total number of cells to give you a mitotic index which is essentially an index to give you an idea of the rate or how much mitosis is occurring so you could do a comparison between different tissues so here is topic six and in this topic we're going to be looking at nucleic acids and protein synthesis starting with 6.1 which is the structure nucleic acids and replication of DNA DNA and RNA both occur in the monomer form and as the polymer form and the monomers of DNA and RNA are known as nucleotides and the nucleotide consists of a nitrogenous base which for DNA can be either cytosine thyine adenine or guine and for RNA it could be uracil instead of thyine cytosine adenine and guanine both them then have a pentos sugar and for DNA that is deoxy ribos and for RNA it's ribos that's why there's the D and the r difference and then they both have one phosphate group now with these bases the nitrogenous bases you can categorize them according to their structure adenine and guanine are classified as purines and that means that the nitrogenous base is made up of two rings which we can see one ring here and a second here and that's the case for both Adine and guine then we have thyine if it's DNA uracil if it's RNA those three nitrogenous bases are peridin which means that they only have one ring structure so these bases have a complementary base which means when you have the two DNA strands the bases will align opposite a particular base which is complementary to them and thyine and adenine are complimentary or if it's RNA it would be uracil and adenine are complementary so they'll always align opposite each other and guanine and Cy are complimentary to each other so they always a line opposite and what that means is you always have a purine and a perimidine base facing each other and this complimentary base pairing is really important because when the DNA replicates it ensures that you get identical copies being made both DNA and RNA nucleotides as I said earlier can form a polymer and the way that you go from having a monomer to having a polymer is a condensation reaction and that is when water is removed joining together two molecules and a bond is formed and the bond that forms is a phosphodiester bond the polymer of the nucleotides is known as a poly nucleotide and that phosphodiester bond that forms is a really strong Cove valent Bond end up getting what is known as a sugar phosphate backbone which is where you have the sugar which is here the sugar the phosphate the sugar the phosphate the sugar the phosphate all attaching to each other although that's actually showing ATP here um pointing out that you need energy for this reaction so I'll do it on this one we've got the sugar the phosphate the sugar the pH phosphate that's your sugar phosphate backbone and it's all connected by these strong calic bonds the phosphodiester bonds so you end up with a really strong polymer which is important because you do not want that genetic code to be changed such as mutations um because that is your hard copy of all of your genetic material next up we have a look at ATP this is a nucleotide derivative so it's very similar in structure the key difference is it contains three phosphate groups so these three phosphate you still have a sugar and a nitrogenous base but it is always adenine and it is ribos so you have adenine ribos and three phosphate groups and ATP is essential for metabolism it is an immediate source of energy when you break these bonds between the phosphate groups it releases energy and that can be used for all the different chemical reactions which is what metabolism is all the chemical reactions in the cells and also some processes so the way this happens then is first of all ATP is made during respiration via condensation reaction and it uses the enzyme ATP synthes so we have ADP which is diphosphate which is when you have two phosphate groups and you need to add on that inorganic phosphate that's what pi is so that inorganic phosphate group gets added on Via condensation reaction and that's how you make ATP and because it was a condensation reaction water is removed now to release the energy from ATP that's stored in those chemical bonds you have to hydrolyze ATP and that is done using the enzyme ATP hydrase so this time it' be a hydrolysis reaction which is when you are bond to separate two molecules through the addition of water so we're going to break the bond between the phosphate groups that releases energy and that then means we have ADP and Pi so breaking one of those bonds between the phosphate groups releases a small amount of energy that means you don't have wastage energy so if you need more energy you just break the bond between more ATP molecules and that can then be used in chemical reactions that inorganic phosphate group can also be added onto other molecules and that's known as phosphorilation when you add a phosphate group onto another molecule and when you do that it makes the new molecule more reactive and it gains energy and that's actually what you see happening in the first stage of respiration in glycolysis so if we have a look at DNA in a bit more detail DNA or deoxy ribonucleic acid that codes for the sequence of amino acids in the primary structure of a protein which in turn is what determines that 3D structure and function of a protein because it determines where the bonds can occur and therefore how it folds in that 3D shape it's essential that the cells contain a copy of this genetic code and it's really essential it gets passed onto new cells without being damaged because if it does get damaged you will change your DNA base sequence therefore code for a different primary structure potentially and you end up with a non-functioning protein DNA as we said earlier is a polymer and the polymer is made up of two chains which will then form a double helix the nucleotide we talked about previously you've got your phosphate group deoxy ribos and one of those four nitrogenous bases so the polynucleotides we also briefly talked about so that is the polymer created by those condensation reactions you get those phosphodiester bonds which are the strong calent bonds B the sugar phosphate backbone you can see a little bit clearer now cuz it's shown in blue around the outside of this double helix and the DNA polymer occurs in pairs joined together by hydrogen bonds so these colored Parts sticking out here representing the complimentary bases and at every point that would be either two or three hydrogen bonds holding together those two chains the hydrogen bonds can only form between the complimentary base pairs so you'll have those hydrogen bonds between guine and cytosine and adenine and thyine and as I said you either have two or three adenine and thyine can form two hydrogen bonds whereas cytosine and guanine form three hydrogen bonds so why are these complimentary bases really important then the two strands of the DNA molecules first of all are antiparallel and what we mean by that is they run in opposite directions so on this this side you would have this is the sugar phosphate backbone so that would be your phosphate and the sugar at the bottom whereas this side it's upside down you have the sugar and the phosphate on the top you can't quite see it very clearly in this picture but that is the concept of anti- parallel and instead of saying top and bottom you have it described as five Prime and three prime end which is referring to which carbon within the sugar ring is most exposed so you'd have a three prime end and a five Prime end and then in anti- parallel be the opposite way around so you'd have three prime and five Prime now the complimentary base pairing is important because it ensures the specificity of DNA replication and transcription processes the five to three prime orientation of one strand will align with the three to five of the other one and it allows the accurate copying and therefore the accurate expression of genetic information which means that you have your correct DNA base sequence which will then code for the correct amino acid sequence now we talked about RNA as a nucleotide and as a polymer and one of the polymers that RNA can form is messenger RNA or mRNA for shorts and mRNA is a copy of one gene mRNA is made in the nucleus so because it's a copy of one gene it has to be copied in the nucleus because that is where the DNA is located you get one copy of it which we'll be looking at later on in this lesson in transcription cuz that's how you make mRNA it then leaves via the nuclear pore to the cytoplasm where it'll find a ribosome to attach to so this is really important because DNA cannot leave the nucleus because it is so large whereas mRNA is much shorter because it's only a copy of one gene but this is actually a good thing we don't want DNA to leave the nucleus because that is your hard copy of your genetic material and if you got into the cytoplasm there are enzymes in the cytoplasm that could break down that DNA so instead when the genetic code is required to make a protein we make an mRNA copy of one gene that can leave the nucleus CU it's shorter that can be used to create the protein and if the MRNA breaks down which it will do that doesn't matter you just make another copy of it from your DNA so it is shortlived because it is going from the nucleus into the cytoplasm where it will get broken down after it's been used in protein synthesis and it is single stranded it forms a straight line and every three bases on your mRNA sequence is known as a codon so three bases three consecutive bases on mRNA which codes for one amino acids a specific amino acid is known as a codon next time we're going to have a look at how DNA replicates and it replicates through semiconservative replication and what we mean by that is each time the DNA replicates one strand is conserved and one strand is newly synthesized so it's semiconserved semiconservative but it's really important you say one strand not half because half could imply it all breaks apart and mixes up and half is new half is old so you have to specify one strand is new one strand is old or conserved it's in this stage that mutations could occur because sometimes copying errors do happen in DNA replication and they are random spontaneous and that would result in a change to DNA Bas sequence and therefore code for a different amino acid potentially but we're going to come on to that right at the end of the video so this happens in S phase of interphase of the cell cycle and this concept of the three prime and five Prime end are useful in describing the stages of DNA replication because instead of saying the start or the end you can talk about the three prime or five Prime end and this is relevant because we're going to look at the enzymes involved in DNA replication and the enzyme that catalyzes one of the stages of DNA replication is complimentary in shape so the active site is complimentary in shape to the shape of DNA only at the three prime end and that means that that enzyme can only attach at the three prime end of the DNA so describing the stages of DNA replication could be a potential long answer the question there's four key Steps step one is the DNA first of all has to be separated apart from that double stranded double helix and that's done by the enzyme DNA helicase DNA helicase breaks the hydrogen bonds between the complimentary base pairs and that is what causes the double strands to unzip unwind and you get these replication forks which is what we can see here it's actually labeled slightly differently on the diagram and but there's our DNA helay breaking those hydrogen bonds and you get one strand over this way one strand over that and that is known as a replication fork step two then those two separated DNA strands will now both act as a template for new DNA strands in DNA replication free floating DNA nucleotides that are always within the nucleus will align opposite their complimentary bases and they'll form hydrogen bonds between those complimentary bases but at this point the nucle Nu Tides aren't joined together with that phosphodiester Bond and that is where the enzyme DNA polymerase comes in DNA polymerase is able to join together those adjacent DNA nucleotides through the catalyzation of the condensation reaction and it forms the phospho diester bonds and that then results in two daughter DNA molecules each consisting of one of the original parental strands and one new synthesized strand so one key focus is knowing the process of DNA replication but you also need to know the roles of different enzymes involved and we've talked about DNA polymerase we said that DNA polymerase catalyzes the formation of the phospho bond between those adjacent nucleotides on the newly synthesized chain and this is the enzyme where I saying it is complementary in shape to the three prime end so DNA polymer will always bind to the original template strand at the three prime end that means the newly synthesized strand which is anti-parallel will have new nucleotides being added in the five to three prime Direction and that leads to differences between the leading Strand and the lagging strand in DNA replication which if I just go back to this diagram here we can start to see that concept of leading strand versus in strand so the leading strand is where you do have this continuous addition of the bases being catalyzed that condensation reaction the lagging strand you get it in separated sections which we call okazaki fragments and that's where we see the role of DNA ligase so DNA ligase is involved on the lagging strand during DNA replication so DNA polymerase synthesizes short DNA fragments called okazaki fragments in in that opposite direction of the replication fork movement and as a result those sections those okazaki fragments have to be joined together and that is what DNA liase does it joins those okazaki fragments by catalyzing the formation of phosphodiester bonds completing the synthesis of that lagging strand on the DNA molecule next time we have a look at protein synthesis so for protein synthesis the first concept is you need to have an understanding of the genetic code and there's three special features the genetic code is degenerate it's Universal and it's nonoverlapping what we mean by degenerate is amino acids there are 20 amino acids but there's actually 64 Triplets of bases so amino acids can be coded for by more than one triplet of bases Universal is that the same triplet of bases codes for the same amino acid in all organisms and lastly non-overlapping this is when each base in a gene is only a part of one trip of bases or you could describe as a discrete unit so each one each codon is its own separate discrete units there's no overlapping of the bases in multiple triplets so the advantage of this is the fact that the genetic code is degenerate means even if a mutation occurred changing one of the bases in a triplet that new new triplet due to the mutation might still code for the same amino acid so it reduces the impact that mutations might have the fact that it's Universal has been really helpful in genetic engineering because it means that we can take a human gene and insert into the DNA of bacteria and that bacteria will then produce the human protein non-overlapping is also linked to the concept of mutations so it's really useful that each base is only part of one triplet because if a mutation did Ur in a triplet then at least it's only one codon which is affected and therefore only one amino acid so protein synthesis occurs on the ribosomes or the rough endoplasmic reticulum because they're rough because they have ribosomes transcription actually happens in the nucleus and that is the first stage and that is where the DNA is copied into an mRNA sequence and that's just for one gene translation is the part that happens on the ribosome and this is where the polypeptide chain is created so we're going to go through those two processes but just a few other key things that you need to know number one is what introns and exons are so introns are sequences of bases on the DNA so in a gene in particular that do not code for amino acids and therefore the polypeptide chain so these introns have to be cut out or removed or spliced as a technical term out of the MRNA once the copy of the gene has been made so mRNA is made and then the introns are spliced out that then just leaves the exons behind and exons are sequences of bases in the gene that code for sequences of amino acids so that's the coding section that's needed to code for the polypeptide chain there's also start and stop codons so at the start of every Gene there is a start codon which is three bases which will code for a particular amino acid which will initiate translation the stop codeon is the final three bases at the end of every Gene and these will not actually code for any amino acid and as a result it causes the ribosome to detach and therefore it stops or ends translation so let's go through the two stages then transcription is the first step and this is the process that's happening within the nucleus where we get an mRNA copy of one gene on the DNA being created so the steps are very very similar to DNA replication first of all DNA helicase breaks the hydrogen bonds between the bases in the two DNA strands to unwind that double helix and to separate the two strands here's the first difference though only one of those strands will act as a template whereas in DNA replication both of those strands of DNA will act as a template next then we have three mRNA nucleotides lining opposite the exposed complimentary base basis on the DNA same concept but this time it's mRNA nucleotides instead of DNA and then the next bit again is very similar it's just a slightly different enzyme this time it's RNA polymerase that will join together the adjacent nucleotides forming a phoso dier bond through that condensation reaction and that is how you then get an mRNA pmer and once that one gene is copied then you would have the introns spliced out and then the mRNA can leave the nucleus via the nuclear pores and go and attach to a ribosome in the cytoplasm and that then takes us on to the next step which is translation so once that modified mRNA has left the nucleus via the nuclear pore it attaches to the small subunit of the ribosome at the start codon tRNA molecules which are a different type of mRNA that carry specific amino acids they have anti codons on them which are three bases complementary to a codon on mRNA so the TRNA molecule with the complementary anti-codon to a codon will align opposites and the ribosome is able to hold two tRNA molecules at a time the two amino acids that will be at the top of the TRNA molecule are therefore delivered and is specific bason the anticodon and the codon and they are then able to join via a pep peptide bond and this requires an enzyme and it also requires ATP energy released from ATP to form that peptide bond the TRNA is then released and the ribosome will move along the MRNA molecule to the next codon and that process happens again so the next TRNA molecule can then align opposite his complimentary um codon compar to its anticodon bringing a specific amino acid and this process continues until the r reaches the stop codon at the end of the MRNA molecule and that is what causes the ribosome to detach and therefore ends translation that then results in your finished polypeptide chain which has been created which can then enter the goldi body for further folding or modification such as maybe adding a carbohydrate to it so the last Concept in this module is gene mutations and a g mutation is a change in the base sequence of DNA that might result in a different polypeptide they occur randomly and spontaneously during S phase of interphase which is when DNA replication happens but these mutations are more likely to occur if you're exposed to certain chemicals or high energy radiation so for example UV lights gamma rays X-rays and the chemicals we call carcinogens so mustard gas for example a g mutation could result in either a base being deleted or substituted so for example we've got our original DNA base sequence here and we can see that base cytosine has been substituted so changed for the base adenine so that is a substitution gene mutation the next one we've got is a base has been added or inserted it's exactly the same sequence except thyine has been added at this point so that means we've now changed all of the subsequent triplets after that mutation and we've also got an extra base is just not a part of any triplet we call that a frame shift when it shifts along like that deletion has a similar effect if you delete one of the bases all of the triplets after the point of the mutation change and that means it's a frame shift this time though it's all of the triplets move back one position so this one we don't even have a triplet anymore so that wouldn't even code for an amino acid so you're coding for different amino acids and you'd have one fewer so some sometimes a substitution can be described as silent meaning that the new codon still codes for the same amino acid and that's because of that feature of the genetic code we talked about it being degenerate meaning that multiple triplet bases can still code for the same amuno acid however those deletions or insertions those can result in frame shifts where after the point of mutation all of the subsequent codons are changed and therefore we'll probably code for different amino acids and you'll get get a very different primary structure or sequence of amino acids therefore the protein will fold into a very different shape and it will be nonfunctioning or it might have a completely different function in terms of enzymes that would mean the active site would be completely changed and the enzyme would no longer catalyze the reaction it's meant to so that is far more harmful topic seven then we're going to be looking at transporting plants starting with the structure of Transport tissues so this table here summarizes the distribution of xylm and flum across the different parts of the plant so looking at the distribution in stems roots and leaves so within the stem the xylm tissue is located towards the center of the stem and it forms a central vascular bundle is surrounded by the flam tissue and the zylin vessels are arranged in a characteristic pattern often forming a ring or several Rings within the stem whereas the flm is found between the xylm and as we said just here on the outside and it's the OU most layer of the stem and it forms a ring around those xylm in The Roots the xylm tissue is typically located in the center again forming that vascular bundle and the xylm vessels radiate outwards with the youngest xylm tissues towards the center and the oldest towards the outside or the periphery the flm is arranged in a ring surrounding that xylm and this Arrangement allows for the efficient transport of sugars and other organic compounds producing the leaves to the roots for storage finally then in the leaves the xylm are found in the mid rib and the veins and extend the leaf lamina and it provides structural support and it facilitates the transport of those water and mineral ions that have been absorbed by the root hair cells to the leaves the flm are located adjacent to the xylm in the veins and it transports organic compounds such as sugars produce Dre pH synthesis from the leaves to other parts of the plant so if we have a look at the structure a flum and xylm here we can see the flm tissue and it's made up of two key types of cells we have the Civ tube element cells which are shown here in the middle and the companion cells which are on the outside or either side of the CFT chbe element the sift chbe elements were initially living with all the organel and they are still classed as living cells but as they start to develop they then contain very few organel and no nucleus and you also have these perforated end walls which make like a Civ hence the name Civ chbe elements and this enables the sugars the organic substances to move up and down through the Civ tube element with Little Resistance from those organel now because it doesn't have organel though it is reliant on the companion cells to provide ATP for the active transport of organic substances so companion cells do have all their organel and they have lots of mitochondria for aerobic respiration to be able to provide lots of ATP next then if we have a look at the xylem tissue zyon vessels are composed of elongated Hollow cells called vessel elements this is actually looking through a cross-section going into one of those and in red here this is showing you one of those Hollow xylin vessels now these cells are dead when they're mature and they have lignified cell walls so there's lots of ligin in them which makes some water proof and really tough as you go through the tube as well there are perforations called pits or pores the structure of the zon vessel elements allows for the efficient of unidirectional flow of water and mineral from the roots to the shoots through capillary action and cohesion tension mechanisms because it essentially makes one continuous Long Hollow tube so water can flow through it as one continuous column of water next next then we have a look at the transport mechanisms so we're going to be looking at the transport of water through a plant first of all and water enters the plants at the root hair cells and that is bi osmosis and root hair cells are adapted to maximize osmosis by having thin walls so there's that short diffusion distance because osmosis is a type of diffusion and also they have that long protruding parts that creates a large surface area to maximize the absorption of Water by osmosis as well once the water is then inside of the root hair cell it's then going to travel to the xylm either through what we call the sast pathway or the apoplast pathway which we can see here in the diagram the simp plast is shown in blue and the apoplastic pathway is shown in Orange so the apoplast pathway is through the cell walls which we can see here the water moves through those cell walls the water can enter the cell wall and move cohesive forces meaning the water sticks together with hydrogen bonds and it forms this continuous stream of water which moves through the cell walls towards the syum this pathway transports the water really quickly as there's little resistance to the water in the cell WM so it can move through quickly however when it gets to the endodermis there are a specialized layer surrounding the vascular tissue which is known as the casparian strip and that's composed of hydro phobic or waterproof subing and that forms this waterproof Imperial barrier in the cell walls and at that point it forces the water and all the dissolved solutes within it to enter the S plast pathway then if we have a look at the sylas pathway this is when the water and the solutes cross the endodermis through the plasmo desmat which is a gap here in the cell walls the simplus pathway is moving through or it's when the water is moving through the cytoplasm of the cell so the water moves through the cytoplasm and when it gets to a cell wall it has to pass through a plasmo mat which is one of these gaps each successive cell cytoplasm has a lower water potential then the next and that's how the water is moving so it moves through the cytoplasm bi osmosis and this is a slower process compared to the apoplast pathway you need to know some adaptations that plants have linked the idea of transpiration or reducing transpiration and reducing the water that can be lost from a plant so plants have stamata and stamata we're going to be looking at in more detail later on in this video they're the tiny pores on leaves that can open and close to reduce water loss but open to enable gases to exchange so zarapes are plants that have adaptations to reduce water loss because these plants are found in environments with very very little water or it could be water but the high salt concentration or it could be very very hot as well but traditionally we mean there's limited water Maring grass is an example of aerides and it's found at the sand genes which despite it being next to the ocean which is water there is a limited water supply due to the fact that sand is so porous so the water runs away and here we can see a microscope image looking at the cross-section through a leaf of a zeraph so we can see some of the adaptations that they have to reduce water loss first of all we can see the leaf is curled up and that curling up means that any water that does evaporate out gets trapped in this area which increases the local humidity and therefore it reduces the water potential gradient from the inside of the cells to the outside and therefore there's less transpiration there are also these hairs which have the same advantage in that they trap the moisture in the air and that increases the local humidity therefore decreasing the water potential gradient so there's less transpiration the sunk andata is yet again creating that increased local humidity because it's lower down in the cell so as the water evaporates again you get this trapped humid air on the outside here there's a thicker cuticle which helps to reduce the water loss by evaporation of the surface and also not shown in this image but there are longer root networks so that more water can be reached to absorb more water into the plant in the first place so that then leads us on to what is transpiration and how does the plant transport water through the xylm so we've looked at how the water gets into the roots how it gets from the roots to the xylm now we need to see how it transports through the xylm through the rest of the plants and how it can actually leave the plant so transpiration is the evaporation of water from the internal surfaces of the leaves and it's followed by the diffusion of water vapor through the stat and the stomato as we said is these holes in the leaves which are created by guard cells and plants can control water loss using these guard cells the guard cells will swell and bend when the plant has a lot of water in them and when they swell and bend that ends up in creating this opening which is known as the smarter now that enables carbon dioxide to diffuse into the leaf but at the same time water vapor is able to evaporate out so the smarter open when it is light and the plant cells are turgid you can actually measure the rate of transpiration with a piece of apparatus called a Pomer as well so thinking about how this water moves up the xylm then we've just said that transpiration is evaporation through those Stato on the leaves and as evaporation is the conversion of liquid water to water vapor there are certain factors that are going to increase the rate of that temperature is one of them because as you increase the temperature the water molecules gain more kinetic energy and therefore they're moving more rapidly and you're going to have more evaporation if the surrounding area is less humid or there's a lot of wind to carry away evaporated water molecules then you have a steeper water potential gradient and therefore more water is going to evaporate out we've partly touched on this concept here as well already but it's just pointed out the starting place of this water so water is absorbed by osmosis VI the root hair cells um and there's a big root Network to increase the surface area to maximize osmosis once that water then reaches the xylm we're going to be looking at how it transports through those hollow tubes we talked about that make up the structure of those xylon vessels so the water can move in One Direction only through the xylm which is typically Against Gravity so going upwards and that's due to the transpiring water from the leaves which creates this pulling force from where the water's being lost this is often known as transpirational pull or transpiration pull water is absorbed by the root hair cells by osmosis and that water then moves up the xylm within the stem or in this picture it's up a trunk and you get this continuous water column and the reason for that is water molecules Stick Together by cohesion so water is a polar molecule which means you've got a slight positive charge on the hydrogen atoms and a slight negative charge on the oxygen atoms for that reason hydrogen bonds can form between different water molecules and those hydrogen bonds between them all creates this cohesion they sticking together of water molecules create this continuous column of water now those water molecules can also adhere to so stick to the walls of the xylm which is what this gray here is representing the walls of the xylm so you would also get hydrogen bonds sticking this water molecule to the walls now this cohesion as we said results in that continuous column of water also know as a transpiration stream in the plant stem tension is is put on that transpiration stream or in other words a pulling Force when water evaporates out of the stamata and that's because you get this negative pressure as the water evaporates out there's a negative pressure and that creates this tension or pulling on that continuous column of water this movement of water out of the stamato results in the water column being pulled up the xylm towards a stata and that is known as the transpiration pool this pool will draw up the water and it also puts tension on the xylm because the water is stuck to or adhering to the xylm walls so this pulls the xylem inwards making the hollow tubes narrower and longer and this change in diameter of the xylem is measurable for example the diameter of a tree trunk will change according to its transpiration rates and when it is a narrower tube it makes it even easier to pull that column of water up the xylm next time we're going to have a look at the mass transport of organic substances in plants so these are for example sugar such as glucose or sucrose that are made from the photosynthesis of a plant and those sugars are needed for respiration so it's important that although the sugars organic substances will be made in the leaves they can be transported up and down the flm to any respiring cells in the plant this takes us back back to what we were talking about in terms of the flum tissue which we mentioned earlier those CBE elements and the companion cells which are involved in this MH transport of the organic substances translocation is the term that we use to explain how organic substances are transported in a plant and this is an active process meaning it requires energy so we're going to go through this mass flow or translocation from what we describe as the source which is where these organic substances are produced which is the leaves and photosynthesis to the sink which is what we call the cells which are going to be using the sugar now although it says a root here in Brackets is any respiring cell so we're going to look at how those organic substances are transported from the source which is where they made to the sink which is where they're used first of all we're going to have a look at it with this model here this source to syn explanation so we've got the flm shown in Gray the xylm shown in green we did talk about the structure that you have the xylm typically in the middle and the FL on the outside and we've got a tank of water here as well just to represent this model so we've got the source cell is the photosynthesizing cell and we've got our SN cell is the respiring cell the photosynthesizing cell because it's going to be creating lots of sugars that lowers the water potential of that cell and as a result water can enter bi osmosis at the respiring cell you're using up lots of organic substances and sugars so that means there going to be a more positive water potential or less negative and therefore water will leave those sink cells by osmosis now this difference in whether the water is moving in or out by osmosis is going to affect the hydrostatic pressure as water moves in at the sore cell there's an increased hydrostatic pressure pressure and as water is leaving at the sink cell you have a decreased hydrostatic pressure that then creates this pressure gradient and as a result the sugary solution in the source cell is going to be forced up and through the flow towards the sink cell due to that high hydrostatic pressure in the sore cell in comparison to the sink cell so that's the concept of mass flow in terms of the pressure changes but you also need to know how does the sucrose which we're using as our example of the organic substance get from the sore cell into the CBE element in the first place and this is where we see the role of active transport and the need for energy so Step One is we've got the photosynthesizing cell such as your leaf cell is going to be creating that organic substance sucrose and that creates a high concentration of sucrose at the site of its production and therefore it can diffuse down its concentration gradient that would be via facilitated diffusion though because it's too large to move through the plasma membrane and it goes into the companion cell at this point there'll be active transport of protons or hydrogen ions from the companion cell into spaces within the cell wall and because it's act to transport that requires energy that creates a concentration gradient and therefore the protons move down their concentration gradient via protein into the Civ tube elements and that is how we get the soup grow into the Civ tube element Co transport of sucrose with hydrogen IRS occurs VI protein co-transporters to transport it into those C tube elements this is now where it links to that model we were talking about because we've got that sucrose inside of the C tube element it lowers the water potential that means water is going to enter bi osmosis that increases the high ostatic pressure and it forces the liquid to be moved towards the sink cells at those sink cells sucrose is going to be converted into glucose and used in respiration or it might be stored as insoluble starch more sucros is actively transported into the sink cell which causes the water potential to decrease this results in osmosis of water from those Civ tube elements to the sink cell so some water also returns to the xylm as well the removal of that water decreases the volume in the Civ tube element and therefore the hydrostatic pressure decreases and there we have that pressure gradient then so you've got a high hydrostatic pressure at the source compared to the sink end of the Civ tube element and therefore the solution moves on mass so topic 8 for Cambridge International then we're going to be looking at the circulatory system transport of oxygen carb dioxide and then finally the heart so starting with the circulatory system large animals require circulatory systems because they have high metabolic rates which means they're doing lots of chemical reactions at very fast rates but they have a lower surface area to volume ratio so they need to have these Transport Systems to ensure that they are getting the resources that they require for the chemical reactions was also removing the waste products so each animal has a circulatory system adapted to its particular needs and all circulatory systems will transport gases for example carbon dioxide and oxygen as well as nutrients like glucose around the body within liquid such as the blood and the liquid is transported around in vessels and there's always a pump to help move the liquid and one type we're going to look at is the double clay circulatory system so in a double closed circulatory system the double is referring to the fact that you've got two loops and the closed means the blood always remains inside of a blood vessel now for birds and most mammals this is what they have a double closed circulatory system and one of the circuits is taking the blood from the heart to the lungs to become oxygenated and to remove the carbon dioxide and the other circuit is delivering oxygenated blood to respiring cells around the rest of the body there's quite a lot of details that you need to know about the different blood vessels but because this is one of the summary videos I've got it all summarized here in one table so you can screenshot or pause and draw this down as your own version so you've got it in your notes or you can make it as flash cards but the key thing you need to know is about the arteries arterials capillaries Ven and veins those are the five types of blood vessels you need to know the structures and properties of so we've got information here on the smooth muscle and the elastic layer the collagen layer the overall thickness of the wall and whether they contain valves or not and then I've got it linked to how that structural feature links to its function as well so we can see that the arteries they've got thicker muscular layer than the veins that enables this constriction and dilation of the blood vessel so the Lumen gets larger and wider and in that way it can control the volume of blood arterials they've got a thicker muscular layer than in the arteries and that's so that you can contract with even more Force to help restrict the blood flow into the capillaries you don't have a muscular layer in the capillaries you do in the venal and veins relatively thin so it can't actually control the blood flow the elastic layer is a similar concept here in terms of the differences so you've got a thicker layer in the arteries and veins and it helps to maintain the blood pressure it's what enables that stretch and recoil in response to the heartbeat you've got a thinner layer in the arterials as the pressure is getting lower the further away you are from the heart no elastic layer in the capillaries or in the venules and there's a very thin layer in the veins then we get to the collagen collagen is that outer layer to provide support and you've got a thinner layer in the arterials compared to the arteries none in the capillaries none in the venules but you have a lot in the veins it needs that structural support lastly then if you consider all of those you get the overall thickness of the walls so the walls are thicker in the arteries and the veins and that's one thing you can really notice on electromicrographs they're thinner in the arterials because the pressure is slightly lower the capillaries the reason they don't have muscle elastic layer of collagen is they're only one layer thick so you've only got one layer of cells making that epithelium of the capillaries and that's to provide a really short diffusion distance because it's the capillaries where we have gas exchange happening and also tissue fluid formation in the veins it's very thin and you can see that again in any microscope images you can see just how thin the wall of a venal and then also the veins are compared to the arterials and the arteries and then lastly valves you only have these in the venal and veins and that's to prevent the back flow of blood there's lower pressure in the venules and veins and that's why they need these valves to prevent the back flow so here we can see the capillary in more detail that single layer of cells making that endothelium and they form capillary beds so networks of capillaries where you have many of them branching and that would be exchange surfaces so for example surrounding the Villi in the small intestines and surrounding the Alvi in the lungs they have a narrow diameter and the advantage of this is it slows down the blood flow because they're just wide enough for red blood cells to fit through and because that then slows down the blood flow that means there's more time for exchange such as diffusion to occur so here we can then see some of those differences that we were talking about and this is one skill that you need to know how to do and that is identify an artery vein and capillary on either a photo micrograph or an electron micrograph and that's what we can see here so a photo micrograph is an image taken using a light microscope or from a light microscope an electron micrograph is an image from an electron microscope so with the arteries we can see an artery here and vein there the way that you can tell the difference is the artery wall is much much thicker and the Lumen is smaller compared to the veins you'll also typically see that the artery remains more circular whereas the vein the Lumen can be distorted and you can actually squash the vein and you get this nonuniform or asymmetrical shaped Lumen the capillaries which is what we're looking at here is the electro micrograph have much much thinner walls and we can also see here this is a red blood cell within the capillary and it only just fits in which we were talking about on the slide before you have such narrow diameters of the Lumin in capillaries so that red blood cells can only just fit through in addition to being able to identify the blood vessels under the microscope you also need to be able to identify the different components of the blood so the different components of the blood that you need to be able to identify are blood cells monocytes neutrophils and lymphocytes and what we've got here is a diagram of each of those and the red blood cells which we can see down here on the bottom left you can recognize these because they have that b concave shape and that dip in the middle is where we can see this darker image or it's where it's dipping in it's almost like a shadow then we've got the photo micrograph of a lymphocyte you don't have gran cytoplasm so it looks slightly smoother and there's a very large and pretty spherical nucleus so that's how you can identify a lymphocyte this one here is showing you a monoy and these are non-granular cytoplasm but the nucleus looks a bit like a kidney bean which we can see here it's LED and it's almost like a kidney bean shape the one at the top then is a photo micrograph of a neutrophil and this time it is granular cytoplasm so you can see it looks a little bit Dotty and you also have a nucleus which is LED and it looks more like a string of beads so we've got multiple sections or loes to that nucleus so the tissue fluid then we said this is one of the things that is occurring at the capillary beds and this is where you have water and small molecules forced out of the capillaries and they then surround the cells or the tissues and it's all due to high hydrostatic pressure and oncotic pressure so hydrostatic pressure is the pressure exerted by a liquid oncotic pressure is the tendency of water to move into the blood via osmosis and it's the interaction of these two that first of all results in the formation of tissue fluid and then results in the reabsorption so let's have a look at the formation first of all as the blood enters the capillaries which we can see here from the arterial there's a smaller diameter of the capillaries compared to the arterials we have the same volume of liquid and this results in a higher hydrostatic pressure forming that high hydrostatic pressure forces water and small molecules such as glucose amino acids fatty acids ions and gases Like Oxygen out of the gaps between the cells that make up that endothelium layer of the capillaries now that liquid small molecules has forced out is they're known as tissue fluid because it surrounds the tissues and this is essential because those small molecules that we talked about the glucose amino acids oxygen those can now enter the cells by diffusion or it could be actually transport and be used by the cell simultaneously any waste products within the cell will be diffusing or moving out back to transport into the tissue fluid and that waste can then be reabsorbed with the rest of the liquid from the tissue fluid back into the capillaries to be removed from the body so at this point the hydrostatic pressure is higher than the oncotic pressure and we're talking about the arterial end here and that's why the net movement of water is out of the capillaries to form the tissue fluid when we get to the other end though the venal end of your capillary you will have reabsorption happening and this is because first of all large molecules so for example plasma proteins those don't get forced out of the gaps between the cells and the capillaries and that's because they're too big to fit through so they remain in the capillaries and this lowers the water potential of the blood which remains in the capillaries so this lowered water potential will result in higher oncotic pressure towards the venal end of the capillaries and simultaneously you have a lower hydrostatic pressure because water has been forced out so you have a lower volume of liquid within the capillary and that's why the hydrostatic pressure is lower in comparison as well to the oncotic pressure so that results in a net movement of the water moving back into the capillaries by osmosis now once equilibrium of the water potential has been reached so you have the same water potential in the capillaries and the tissue fluid no more water can enter or re-enter the capillaries and that final amount of tissue fluid then that can't be reabsorbed by the capillaries or into the capillaries is instead absorbed into the lymphatic system and once it has been absorbed into the lymphatic system it does eventually drain back into the bloodstream through a blood vessel near the heart once the liquid is in the lymphatic system it's called lymph and lymph has a very similar composition to plasma except it doesn't contain those large plasma proteins or red blood cells and it has less oxygen within it next then we're going on to the transport of oxygen and carbon dioxide so the transport of oxygen is done through the protein hemoglobin and hemoglobins are groups of globular proteins found in different organisms and each organism has a slight different protein hemoglobin has a quary structure and hemoglobin is found in the red blood cells and it's responsible for transporting oxygen so here's hemoglobin and we can see it's made up of four polypeptide chains and that's why it's a quary structure because it contains more than one polypeptide chain myoglobin isn't hemoglobin but it is a protein that also has a heem group and it can transport oxygen but there's only one polypeptide chain and it's in the muscle tissue invertebrates and some organisms also have mlob lobin it has a very very high affinity for oxygen even at very low partial pressures and we're going to come back to that concept so oxyhemoglobin dissociation curves is the way that we can have a look at the Affinity that hemoglobin has for oxygen so on these graphs we get the percentage saturation of hemoglobin with oxygen at different partial pressures and you always get this s-shaped curve or sigmoid shaped curve and we can see that oxygen is loading in regions with a high partial pressure and it's unloaded in regions with a lower partial pressure so this is your oxy globin dissociation curve and the way we can actually tell that this loading and unloading happens is at these higher partial pressures we can see that the hemoglobin is 100% saturated so that means it must have the hemoglobin must have a higher affinity for oxygen at high partial pressures of oxygen therefore it loads the oxygen more readily and it's binding to the hemoglobin and that's why it's fully saturated at lower partial pressures we can see that the saturation has dropped so the oxygen must be unloaded from the hemoglobin now this typically would be occurring in the respiring tissues because in respiring tissues Oxygen's being used up for aerobic respiration so there is a lower partial pressure of oxygen now that's an advantage because if the Affinity that hemoglobin has four oxygen is lower at respiring tissues that means it will unload that oxygen and be available for aerobic respiration the alv have high partial pressures of oxygen because that is where gas exchange is happening so this is useful then that there's a higher Affinity because that means the hemoglobin will then be able to load up with all of that oxygen and become fully saturated to transport it to the respiring tissues these graphs also demonstrate cooperative binding and this Cooperative nature of oxygen binding to hemoglobin is due to the hemoglobin changing shape when the first oxygen binds so the reason there is a lower Affinity at these lower partial pressures is The Binding sites aren't as exposed when you don't have any Oxygen bound to it but as soon as the first oxygen binds to hemoglobin it slightly changes the shape of the protein to reveal those binding sites and that then makes it more light ly for the subsequent oxygens to be able to collide and bind with hemoglobin and that's what explains that sigmoid shape graph carbon dioxide also has an effect on hemoglobin's affinity for oxygen and this is known as the bore effect the bore effect is when a high carbon dioxide concentration causes the oxyhemoglobin curve to shift to the right and what this means is even at the same partial pressure say for example at 20 when the curve is shifted to the right you have a lower saturation than you would if the curve was shifted to the left so even at the same partial pressure of oxygen you have a lower Affinity which means that it's going to be unloading the oxygen more readily the advantage of this is if you have a high concentration or partial pressure of carbon dioxide the fact that hemoglobin has a lower affinity for oxygen is good because that would indicate that there must be respiration occurring because carbon dioxide is made in respiration that's an acidic gas and it's changing the shape of the hemoglobin so it unloads the oxygen more readily so that means oxygen is being delivered to the site of respiring tissues so that aerobic respiration can continue for longer and more ATP will be created there are also differences between the Affinity of hemoglobin depending on the organism itself and how it's adapted to its environment and that's what we're going to have a little look through so a human fetus we're going to have a little look at here so here we have the fetal hemoglobin compared to adult hemoglobin and we can see it's shifted to the left now if a curve shifts to the left that indicates a higher affinity for oxygen and the way we can tell that is even at the same partial pressure so let's say 25 we can see that that when the curve shifts to the left there is a higher saturation of the hemoglobin with oxygen and that's an advantage because the fetus gets this oxygen from the mother's hemoglobin as it transports round in the blood in the red blood cells through the placenta so it needs to have the fetal hemoglobin needs to have a higher Affinity than the hemoglobin of the adult so that it can essentially take that oxygen from the adult hemoglobin another example is animals that live at high altitude so for for example a llama lives at a high altitude where there are lower partial pressures in that particular environment so there's lower partial pressures of oxygen so for a llama they also have hemoglobin with a higher Affinity so they even at very low partial pressures which is what their environment is like their hemoglobin can still become loaded saturated and they're able to get that oxygen for aerobic respiration another example is a dove or any other smaller organism which has a high metabolic rate because they have a faster metabolism they require more oxygen for continual aerobic respiration or faster rates of continual aerobic respiration and that is so that they can release the energy or create ATP for Contracting muscles so they actually have a curve that shifts to the right indicating a lower Affinity the hemoglobin has a lower affinity for oxygen because even at the same partial pressure we can see it's got a lower saturation and and that means it's going to be unloading oxygen more readily which means the oxygen is being delivered and unloaded to respiring tissues so that aerobic respiration can continue earthworms and other organisms that might borrow and live underground or it could be deep diving animals they are at lower partial pressures of oxygen in their environment so they need to have a higher Affinity so the curve is shifted to the left so that even in those low partial pressure environments the hemoglobin can still become saturated with oxygen next then we have a look at the transport of carbon dioxide and there are four ways that carbon dioxide can be transported one is dissolved in the blood plasma next we have as hemoglobin acid and carbon dioxide can react reversibly with amino acids in hemoglobin to form hemog globonics be in the cytoplasm of red blood cells in the form of hydrogen carbonate ions and also it could be the formation of carbo Amino hemoglobin now almost 85% of the carbon dioxide is transported as hydrogen carbonate ions in the red blood cells which is what we can see here with this reaction water and carbon dioxide react in a reversible reaction and that forms hydrogen ions and hydrogen carbonate ions Carbonic and hydras is an enzyme in the cytoplasm of the red blood cells and that catalyzes that reaction the carbonic acid can move out of the red blood cells by diffusion and it exchange chloride ions diffuse into the red blood cells both of these ions are negative so these exchanges maintain the electrical balance of the red blood cells and this is known as the chloride shift carbon Amino hemoglobin is formed when carbon dioxide binds to the amino groups of globin proteins in the hemoglobin and this reversible process occurs in tissues where carbon dioxide levels are higher facilitating the transport of carbon dioxide from tissues to the lungs The Binding of carbon dioxide to hemoglobin helps to remove carbon dioxide from tissues and transports it back to the lungs for exhalation and therefore to be removed by gas exchange from the body finally then we're going to have a look at the heart in particular we're looking at the mamalian hearts so the heart is an organ It's Made up of cardiac muscle which is a specific type of muscle only found in the heart and it's myogenic which means it automatically contracts and relaxes it doesn't require an input from the nerve system to make it contract and relax it does require the nerve system to control the heart rate but we're going to come to that later in this video it also never fatigues unlike sceletal muscle which can fatigue cardiac muscle as long as as a constant supply of oxygen and and glucose it will always contract and relax and that's the role of the coronary arteries they Supply the cardiac muscle with oxinate blood and glucose so that they can respire aerobically produce ATP and therefore the muscle can continually contract and relax the heart is also surrounded by a pericardial membrane and these are inelastic membranes which prevent the heart from filling and swelling with blood so then if we have a look at the inside of the hearts there are are four chambers you've got the two ventricles the left and the right and then the two atria the left and the right and you might notice that literally this would be your right side if we're looking at the picture but we've labeled it as the left and that's because you've always got to imagine it as if it was on you so if you were to pick up that picture and hold it against your chest the big colors in red would actually be on your left side so that's how we label the heart as if you were holding up against your chest and that would be on the left and the left ventricle which we can see here has a much thicker cardiac muscular wall and that means it can contract with more force and pump the blood out of the heart at higher pressure and the blood leaves the left ventricle through the aorta to go to the rest of the body so that's an advantage because we need the blood to be forced out at higher pressure so that will then be able to reach all of the respiring tissues in the body the right ventricle is only pumping blood out of the heart of the lungs which is much closer and also you don't want a really high blood pressure in the lungs because it could cause damage to the capillaries so for that reason the cardiac muscle in the walls of the right ventricle are much thinner because they don't need to contract with as much force and the blood is not pumped out as at as higher pressure both of the Atria the right and the left have much thinner muscular walls and that's because they don't need to contract with much force at all cuz they're only pumping blood from the Atria down with gravity into The ventricle next time we can have a look at the cardiac cycle and this links together the contraction of these different muscles in the walls and also the valves the Atri ventricular valves which are between the Atria and the ventricles and the semilunar valves which are between the two ventricles and the arteries carrying blood away from the heart and it split into three key stages we have diol or diast people pronounce this differently atrial cyly or cyol and ventricular cyly or cyol so as I said everyone pronounces this slightly differently depending on where you're from I tend to say both just to be uh user friendly for anyone that happens to be listening so here we have our cardiac cycle and first of all we can see both the Atria and the ventricles are in diast which means the cardiac muscle is relaxed that's what diast or diol means that is when the muscles in the heart are relaxed and when they are relaxed that means that all of the chambers are slightly larger in volume therefore the pressure inside of them is lower and that is what causes the blood to enter the two atria at this point as the Blood starts to enter the Atria that increases the pressure in those Atria and it will get to the point where it increases them to a point where the pressure in the Atria is higher than the pressure in those empty relaxed ventricles and that forces open those atrio ventricular valves we then get to the point where we have atrial syy and this is when the muscles in the atrial walls will start to contract which increases the pressure further and will force the blood from the Atria into the ventricles then the Atria will relax and we go into ventricular syy which is when the muscles in the walls of the ventricles contract and at this point because the muscles are Contracting that would then result in a higher pressure in the ventricles compared to the Atria and that causes the Atri ventricular valves to shut and when the muscles are Contracting even more it increases the pressure further so the pressure is higher in the ventricles compared to those two arteries the palmary artery and the aorta forcing open the semi lunar valves so the blood now carries on flowing in one direction from the ventricles up and out of those two arteries can't go back into the Atria because those Atria ventricular valves are shut and that is the role of these valves that ensures that the blood flows in one direction through the heart and that's all controlled by the pressure changes between the different chambers and the arteries so here then we've got that information that I was just talking you through so if you do want to pause make notes or flash cards you can do that diast or diol the Atria and ventricular muscles are relaxed this is when blood will enter the Atria by the venina Carver and pulmonary vein and the blood flowing into the Atria increases the pressure with the Atria atrial Sicily that is when the Atria muscular walls contract increasing the pressure further which causes the Atria ventricular valves to open and blood will then flow into the ventricles but at that point the ventricles are relaxed or in dial and then last we get that ventricular syy when after a short delay the ventricular muscle walls then contract that increases the pressure beyond that of the Atria causing the atrio ventricular valves to close and the semilunar valves open and the blood is pushed from the ventricles into the arteries which either the pulmonary artery or the aorta now you could be asked to do this particular math skill which is calculating the cardiac output and that is your heart rate times the stroke volume and the heart rate is the number of times your heart beats per minute and the stroke volume is the volume of blood that leaves the heart after each heartbeat so essentially your cardiac output is the volume of blood which leaves one ventricle in one minute and that is how you'd go about calculating it or you could be asked to rearrange the equation to work out heart rate or strike volume as well so what is controlling the speed at which the heart is Contracting and relaxing and therefore pumping the blood and that's what we're going to go on to so we'd already said that cardiac muscle is myogenic so it doesn't require input from the nervous system to make it contract and relax but the rate at which it contracts is controlled by electrical activity and the nervous system and the key structures are the Sino atrial node which is located in the right atrium and it's also known as the pacemaker you then have an Atri ventricular node the AVN which is located near the border of the right and left ventricle but it's still within the Atria now within this picture it's here um but really is quite a bit closer to the septum the bundle of His runs down the septum and up the walls of The ventricle and then the perine fibers are also going up the walls all the way around um so it's going to reach all of that cardiac muscle and all of these structures can conduct electrical activity so the S releases the wave of deodorization which is the electrical activity the AVN can then transport that wave further and then it transports down the bundle of His and the perine fibers and when this electrical activity or depolarization touches cardiac muscle it causes it to contract so let's have a look at this process the first thing that happens is the S the pacemaker releases a wave of depolarization across the two atria and that causes the Atria to relax so that is our atrial syy now you do have have across the division between the Atria and the ventricles a layer of non-conductive tissue so that means that that wave of depolarization can't go directly down into the ventricles and instead when it hits the AVN the AVN then releases another wave of deodorization and that causes a slight delay between when the Atria contract and when the ventricles will then be able to contract and that's an advantage because it means that there is a time delay between when the blood is pumped from the Atria and then when the ventricles contract so essentially there's time for the ventricles to fill up with all that blood before they contract and that's what we can see here instead of that wave of depolarization going directly down into the ventricles it will be picked up by the AVN the AVN releases the wave which then goes down the bundle of His up the perine fibers and then it will cause that ventricular muscle to contract and the contraction happens at the apex of the heart first which is the very bottom and that then means it will contract from the bottom all the way up the walls of the ventricles and it should force out all of the blood from the ventricles then we get to this Dias stage and that is when repolarization happens and that is when you don't have that electrical activity anymore causing the muscles to contract so instead all of the cardiac muscle relaxes cie topic nine and in this one we're going through gas exchange so the mamalian gas exchange system then you need to know the key structures the tracha or trocha Brony bronchial and the Alvi and the root that air takes during ventilation is it will be inhaled through the nasal cavity or mouth then it passes down the trachea which is the wind pipe it then is split between these two tubes which are the Brony it then branches into multiple smaller tubes which are the bronchioles and then we get these air sacks at the end which are the Alvi so let's have a look at these structures in more detail now you could be asked to identify these structures on a photo micrograph or electrom micrograph so we're going to go through these structures what their function is but first i'm just going to talk you through what to look for to be able to identify them so for the trachea you're looking for a large tubular structure which is lined with ciliated epithelium which you might be able to see on an electron micrograph so those hairlike structures coming out of the cells you may also see goblet cells which are interspersed amongst epithelial cells which would be this big almost like um indent into the cell where you have mucus being cruced the traal wall should contain cartilage as well and you get these c-shaped rings of cartilage the Brony are similar to the trachea but smaller diameter so the Brony are also lined with Cil epithelium they contain these cartilagenous plates instead of complete rings and the plates may appear as irregular shaped segment along the Broncho wall the bronchioles are smaller less structured Airways compared to the tracha and Brony the bronchial is aligned with simple ciliated epithelium without the presence of cartilage you have smooth muscle fibers which may be visible in the bronchol wall appearing as irregular bands or layers now the alvioli there's lots of round structures with an airs space in the middle and they've got very very thin walls they only one cell thick so if we go through these structures in more detail than just what they would look like on a microscope so we're starting with the tra which is the air pipe or windpipe and you have these c-shaped rings of cartilage which is what you can see here in this beige color and that cartilage provide structural support so the airway is constantly open and it doesn't get flattened or stuck together and it's c-shaped rather than the whole way round because your esophagus would be here and you don't want that hard cartilage against the esophagus because as the esophagus is Contracting and relaxing with peristalsis that could be interfered by that cartilage you also have ciliated epithelium with goblet cells this cyia those hairlike structures are there to sweep mucus up and out of the lungs to prevent infection of the lungs and then it's the goblet cells that produce that mucus so goblet cell's upper section swells with mucin droplets mucus comprises mucin and it's this viscous solution of glycoproteins with multiple carbohydrate chains making it really sticky and capable of trapping inhaled particles which could be dust it could be pathogens mucus glands beneath the epithelium produce the mucus certain chemical pollutants like sulfur dioxide and nitrogen dioxide can dissolve a mucus creating an acidic solution that irritates the airway lining so that's not a good thing smooth muscles is within the water the traa so smooth muscles are within the walls of the trachea the muscle contracts if there are harmful substances detected in the airway and this results in the Lumin of the traa constricting and reducing air flow to the lungs as a way to try and protect the lungs when the smooth muscle relaxes the Lumin dilates this stretch and recoil of the Lumin as possible due to the elastic fibers within the tracheal wall next in the bronch and the bronchol the trachea splits into two tubes the Brony so you have a left and a right one and that leads to the left lung and the right lung and those Bronies split into the bronchioles which are these smaller tubes and both the Brony and the bronchioles have cartilage within their walls for structural supports to keep the tubes open now you will have noticed in that previous slide we said the Bron don't have cartilage they will have cartilage at the very top Parts but as they Branch further and further those smaller tubules in the bronchioles don't have cartilage then the bronchioles end at the alvioli which are these air sacs and they're located at the end it's the site of gas exchange oxygen diffuses from the alvioli where you have a high concentration of oxygen or partial pressure into the blood where there is this lower partial pressure of oxygen and carbon dioxide does the opposite it's also moving down its concentration gradients the blood that is entering the capillaries at this point is a high concentration of carbon dioxide so it diffuses from the blood into the alveoli where it'll be exhaled so in terms of adaptations then first of all the fact that there are so many Alvi in both lungs is what provides a large surface area one individual Alvi doesn't produce a large surface area it's the fact that there are millions in both lungs the short diffusion distance though that is created by the fact that the alvioli wall is made up of just one thin layer of cells and those thin layer are called squamous epithelial cells which I love that word squamous is such a cool word basic is like the idea is squashed it's a squashed flat cell and that reduces the diffusion distance also the endothelium of the capillary is just one layer of cells as well so you've got a very short diffusion distance the gas is only have to diffuse through two cells which are both flat the maintaining of the concentration gradient that's done through ventilation but also the fact that the blood is constantly being transported away so as soon as the oxygen diffuses into the blood it's being transported away so a bit more then about this gas exchange in the alvioli we've said that oxygen is inhaled into the Alvi and diffuses across the layers of those two um structures but we haven't said yet that the fact that the moist lining of the alvioli is there so you have this moist layer on that layer of cells and that's so the gases can dissolve in that liquid and then they diffuse across that way we did talk about that single layer of cells which is squamous epithelial cells they're flat they've got that really short diffusion distance the oxygen then diffuses through the endothelial cells lining the capillaries simultaneously calm down oxide which is the waste product of respiration or aerobic respiration diffuses from the blood in the pulmonary capillaries into the alvioli and carbon dioxide diffuses in the opposite direction of the oxygen moving in the efficiency of gas exchange is due to those three factors that we talked about the large surface area because there's so many Alvi the short diffusion distance because of these squamous epithelial cells and the fact that both the Alvi wall and the capillary endothelia is only made up of one single layer of cells and the concentration gradient is maintained by ventilation and that blood flow in the capillaries next then you need to know about the distribution of tissue and cells in the gas exchange system we've talked about this throughout but we've got a summary here for you so you can just create a summary sheet of information so the cartilage is distributed in the walls of the trachea and those larger Brony providing structural support so that it doesn't collapse those tubes don't flatten and collapse the ciliated epithelium that's in your nasal cavity trachea and Brony and it's to move the mucus to sweep that mucus up and out of the lungs goblet cells you have lots of them in the respiratory epithelium secret a mucus to trap and remove inhaled particles the walls of the alvioli we said consist of a single layer of squamous epithelial cells and that allows for the efficient gas exchange between the alvioli and the capillaries smooth muscle is found in the bronchioles that helps to regulate air flow by controlling the diameter of the Airways and the capillaries form a dense Network surrounding the alvioli and the lungs which helps to facilitate rapid gas exchange because it maintains that concentration gradient topic 10 we're going to be looking at infectious disease looking at infectious diseases first and then antibiotics so within the infectious diseases topic you need know that bacteria viruses protoy and fungi are able to cause these infectious diseases but you actually focus on these three in particular for your exam board so pathogens can cause harm through directly damaging tissue or through the release of toxins and the three particular diseases you need to know caused by these pathogens are tuberculosis and chera for bacteria HIV which can develop into AIDS and then malaria as a protoctista disease so we're going to go through each of these starting with the bacterial diseases and tuberculosis so this is caused by two different strains microbacterium tuberculosis and myobacterium bis it can infect humans deer cows pigs Badges and it causes harm the bacteria causes harm by damaging the lung tissue and suppressing the immune system it can be cured though using antibiotics because it's caused by bacteria and it can be prevented in the first place if you have a vaccine so you develop artificial immunity to it so let's have a look at it in a bit more detail tuberculosis spreads mainly through the air when infected individuals cough sneeze or speak releasing the microbacterium tuberculosis bacteria in tiny droplets transmission usually requires close and prolonged contact particularly in cled or poorly ventilated settings and factors like having a weakened immune system increases your risk of developing the symptoms and therefore you're able to transmit the disease as well so TB tuberculosis can also remain latent in the body without causing symptoms next then the micob bacterian bovis which is the other strain this is the one that is found in animals such as cat and badges and it poses a risk to humans through Direct contact or consumption of contaminated food now control measures include testing vaccination and other biocurity practices um such as trying to prevent the spread through having more space and this is crucial to prevent that spread among animals and reduce human infection so a bit more on the prevention and control so biological factors then the microt tuberculosis bacteria is primarily transmitted as we said through air droplets and understanding that TB transmission can help then to reduce the risk factors and infection because you can do simple things such as cofin into your hands washing your hands you could also do quarantining people who are infected if we have a look at social factors social economic factors such as poverty overcrowding malnutrition because that lowers or weakens your immune system and limited access to health care so maybe you aren't vaccinated could contribute to the transmission so TB control efforts should address social factors as well so trying to alleviate poverty maybe providing vaccines for free improving living conditions and that should help prevent and control the transmission of TB next on the economic factors you need to have adequate funding of TB control program so for example diagnosis treatment with the antibiotics and preventing with the vaccines are all essential to try and reduce the incidence of people getting the disease and dying from it so strengthening Health Care Systems including laboratory infrastructure the ability to diagnose all of these will be crucial to help prevent and control TB the next bacterial disease is cholera and this is caused by vibrio choler and it's highly contagious pathogen that thrives in contaminated water and food sources it spreads p primarily through the consumption of contaminated water or food particularly in areas where there's poor sanitation and hygiene it infects the small intestines where it produces toxins that leads to severe diarrhea and vomiting and without treatment chera can rapidly lead to dehydration and even death making it a significant Public Health concern especially in regions lacking access to clean water and proper sanitation facilities so there are efforts to prevent col outbreaks and this often focuses on improving sanitation promoting hygiene practices and providing access to Safe Drinking Water and this slide here just goes through a bit more detail on those broken down into biological social and economic factors so one way that's helped to prevent and control the transmission was understanding the biology of it because now we know that it's transmitted through contaminated food and water and that it's a bacteria we know that you have to make sure you're drinking water that has been completely cleaned and food is Thoroughly cooked and you can treat it with antibiotics social factors as well knowing that drinking or having access to clean water is essential improving hygiene practices such as washing hands can also have a huge huge role in trying to prevent these spreads as well as education and having communities aware of how it is transmitted lastly then we've got the economic factors so again it's linking to the idea of poverty core infrastructure um if you can improve all of those it's going to help reduce the spread and contraction of Chala next one we have a look at viruses and viruses are non-living they a cellular which we talked about in earlier topics and videos they're smaller than bacteria and they just consist of genetic material which could be DNA or RNA a capsid and an attachment protein the viral replication happens inside of host cells and the virus has to inject its nucleic acid into the cell of the host to be able to replicate and bacteria fade are actually an example of viruses that infect bacteria now the key example that you need to know is the virus HIV and it consists of the following structural features a capsid which we can see here as these blue the dark blue circles and that is an outer protein coat surrounding the genetic material that is what is in the core which is the genetic material which is RNA for HIV and the enzyme reverse transcriptase is also within that which is needed for the viral replication there is an envelope layer which is an extra outer layer made out of lipids which have been taken from the host's cell membrane and then we have the protein attachments and these are on the exterior of the envelope to enable the virus to attach to the host's helper tea cells so if we have a look there at how HIV is transported and how infection occurs it's transported in the blood and it attaches to CD4 proteins which are these receptors on the outside of Hela tea cells which are part of the immune response the HIV protein capsule can then fuse with the help of t- cell membrane and that enables the RNA and the reverse transcriptase that will within that capsid to enter and it's entering the host cell the HIV enzyme reverse transcriptase which has been entered along with that RNA into the host cell are then copied into DNA and that DNA copy can move into the nucleus of the helper te cell and once is in the nucleus of the helper T cell that hosts DNA as well as the viral DNA will be transcribed translated and so the viral proteins are going to be made along with the other proteins that would typically be made in the helper T cell and in that way it can then reassemble all of those proteins and a new viral particle has been created so someone is described as HIV positive when they're infected with HIV but it's only described as AIDS when the replicating HIV viruses in the helper te cells have interfered with the normal function of the immune system so if I just go into a bit more detail on this the point above here where we talked about how HIV replicates inside of the host cell once all of those viral proteins have been assimilated to make a new virus particle when you have enough new virus particles in that helper T cell the helper T cell gets destroyed and if you have lots of helper te- cells being destroyed that then means that your immune system is compromised and it won't function normally and that is when someone has AIDS so with the help of T cells being destroyed that means you are unable to have this immune response and defend yourself against other infections and even cancer and that's why HIV when it's destroyed enough helper tea cells to result in AIDS can cause death so the HIV itself doesn't cause death but when you've developed AIDS because the he tea cells have been destroyed you can then die from other infections because you can't defend yourself so here then we have prevention and control methods for HIV so first of all it was understanding HIV so we know now that it's transmitted through sexual contact blood to blood contact so for example sharing needles and perinatal transmission so that means through the placenta from mother to child and understanding this means that we can then put in place preventative meth methods to try and stop that transmission so for example having barrier methods is contraception so condoms for example Bloods blood contacts and not sharing dirty needles as well social factors then we've got stigma discrimination social marginalization of key populations including it has been in the past sex workers men who have sex with men people who inject drugs has happened um but it's best to actually think about these biological factors of how you can protect people without having this discrimination um economic factors as well so again poverty always plays a role that links to the lack of Education that people might have of how they can protect themselves but also it might link to lack of access to drugs so anti-retroviral therapies or art which an infected mother can take while they're pregnant to prevent it being transmitted to their child then we look at the protoctists so the protoctista or protist are UK carot they're single cell organisms or cells grouped into colonies very few are actually pathogenic but the few that are are incredibly dangerous so the pathogen prootics are parasites and are usually transmitted through a vector so we're going to be looking at malaria which is transmitted by mosquitoes so this is the example you need to know malaria and it's caused by the protoctista plasmodium and it's spread to humans through the vector's mosquitoes plasmodium reproduced both sexually and asexually within mosquitoes and within the the human host so it's passed from mosquitoes to humans when mosquitoes bite and take blood from humans in humans the plasmodium infects the red blood cells the liver and the Brain there are some preventative medicines but no vaccine and no cure and we can see here a range of the different symptoms that this plasmodium causes once it's infected a human so how it can be prevented and controlled the main way it's prevented is through preventing the vectors which are the mosquitoes so having that understanding of the life cycle enabled us to realize that the transmission through the vectors could be a key way to prevent humans getting infected so this again links the social factors economic factors to prevent that transmission you can have medicines in advance so antimalarial drugs to try and prevent you guessing the disease but having things like insecticide treatments to kill those um vectors the mosquitoes or having bug spray to try and prevent yourself being bitten having mosquito Nets to prevent them being able to get to you when you're asleep at night in countries that have lots of mosquitoes as well next let we go on to antibiotics so an antibiotic is a substance produced by a microorganism and it inhibits the growth of other microorganisms since the discovery of penicillin which was the first antibiotic discovered in the mid 20th centur antibiotics have been used widely to treat bacterial infections and save many lives so the way that antibiotics kill bacteria because they do only kill bacteria are by preventing cell synthesis and this could be that it inhibits the enzymes responsible for making molecules in the cell walls and the bacteria then die from the leakage of the contents or lice from too much water entering or it could be through disrupting cell membrane so it could be that it binds to the phospholipids in the bacterial cell membrane to distort the structure and it makes the membrane too permeable so it bursts and therefore the bacteria would die and the final way is they can interfere protein synthesis so it can attach onto bacterial ribosomes which prevents the protein synthesis and therefore if the bacteria doesn't have the proteins it requires it will end up dying so antibiotics only work against bacteria and not viruses because viruses don't have cell walls so those mechanisms that we just described of how that antibiotic can kill bacteria wouldn't work and unlike bacteria viruses lack cellular machinery for metabolism growth or reproduction and again that's why it doesn't affect them since viruses lack those metabolic pathways that is why the antibiotics won't cause the destruction of them as well as the fact that viruses are within the host cell themselves so you'd have to destroy the host cell as well as the virus to be able to treat them now antibiotics is not a perfect medicine CU antibiotic resistance has developed in bacteria and this has happened through random mutations that happen in the DNA of bacteria and by chance a mutation would have occurred which results in the production of a new protein that provides a selective Advantage meaning it creates some protein which now means that antibiotic cannot kill that particular bacteria and as a result that bacteria Will Survive reproduce pass on that mutated version of the gene which creates a protein that enables them to survive until eventually you have this WID spread population that all have the antibiotic resistance Gene now this was really sped up by the widespread use and misuse of antibiotics because the antibiotic was the selection pressure in this example of natural selection and the more you were taking the antibiotics the more that meant the non-resistant bacteria died the resistant ones survived and then they had no competition so then they could really Thrive um so they weren't competing for resources water and that's why the non-resistant ones were able to thrive inside of the host and as a result you had even more production and passing on of that resistance Gene so that resistant bacteria reproduces rapidly until you have an entire strain of bacteria that are now resistant to that antibiotic now the two most common resistant bacterial strains are clostridium defil and MRSA now MRSA is actually a strain of bacteria resistant to multiple antibiotics because once this process happened once another random mutation happened in one of those bacteria and this whole process happened again and again and again until you had this strain of bacteria resistant to multiple antibiotics so the consequences of antibiotic resistance and prevention then antibiotic resistance poses a significant consequence for public health and Health Care Systems and economies worldwide resistant infections are harder to treat because you don't have the antibiotics to kill the bacteria and that can lead to increase illness deaths and health care costs limited treatment options exacerbate the problem as health care providers may result to broadspectrum antibiotic use and that further increases the resistance because you're now adding an even more or adding another selection pressure moreover the antibiotic resistance also under undermines infection control efforts increases the risk of outbreaks and compromises the effectiveness of medical procedures like surgery and chemotherapy so to reduce the impact of antibiotic resistance you have different things that are occurring so for example doctors are now less inclined to prescribe antibiotics unless you really really need them so maybe you have a weakened immune system so your immune system won't be able to fight the pathogen by itself there's lots of awareness campaigns as well to educate people on the importance of not taking antibiotics unless they've been prescribed not taking them for viral infections because they'll have no effect and making sure you take the entire course of antibiotics that you have been prescribed to take as well so let's have a look at topic 11 and topic 11 covers the immune system antibodies and vaccination and we're starting with the immune system looking at phagocytosis now fagio sites so for example the macras and neutrophils which are two types of blood cells traveling the blood and squeeze out the capillaries to engulf and digest pathogens and that's what phagocytosis is it's a non-specific response whereby any foreign material that's detected will get destroyed by the fyes and here we see the process of phytosis damaged cells and pathogens release cell signaling chemicals which are the cyto kindes and they attract the fites to the site of infection opsonin protein can attach to pathogens to to mark them and make it easier for neutrophils and macrophages to then engulf them fages sites have receptors which can attach to chemicals on the surface of the pathogen and the pathogen then surrounds and engulfes the pathogen into vesicles to create a phagosome within the phyes there are lomes which contain hydratic enzymes and those lomes will then fuse with the phagosome to make a fagia lome and it exposes is the pathogen to that enzyme the lioy which hydes the pathogen and any soluble useful molecules are absorbed into the cytoplasm of the fagite the fites will present the antigen of the digestive pathogen on the surface and they then become antigen presenting cells the second line of defense involves lymphocytes and this time it is specific and the lymphocytes respond specifically to particular shaped antigens there's two types of lymphocytes the B and the T lymphocytes both are created in the bone marrow but the B cells mature in the bone marrow which is why they're called B lymphocytes whereas the te- cells mature in the thymus which is why they're called T lymphocytes so we're can to have a look at the cell mediated response which is the response which involves te- cells it's called the cell mediated response because it involves these T lymphocytes binding to to anen presenting cells so it's binding to cells themselves which happen to have the antigen on their surface and when you have the receptors on the te- cells binding to anen percenting cells it causes the te- cells to divide rapidly by mitosis which is this clonal expansion because mitosis results in identical copies of cells so you get this large number of t- cells being created which are all identical and they're ident IAL in that they contain exactly the same receptor on their surface complementary to this particular antigen anen presenting cells are cells that present a non-self anen on their surface and that could be infected body cells presenting FAL antigens on their surface a maccrage which is engulfed and destroyed a pathogen presenting the antigens on their surface cells of a transplanted organ will have different shaped antigens on their surface compared to your self cell antigens and lastly cancer cells will also act as antigen presenting cells because they have abnormal shaped self antigens on their surface so let's have a look then at this whole cell mediated response once a pathogen has been engulfed and destroyed by fyes the antigens are positioned on the cell surface membrane which we saw and we now call in antigen presenting cell t- helper cells have receptors on their surface and those can attach to complementary shaped antigens on the surface of these antigen presenting cells once those attach inter lucans are produced which activates the t- helper cells to start to divide by mitosis and that's when they'll then replicate and make large numbers of clones so lots of these tail te- hel cells with that particular shaped receptor those clone T help cells then differentiate into different types of tea cells you'll have some which will differentiate into even more tea helper cells to produce more interlukin to keep this process going and also to activate B lymphocytes some produce inter lucans to stimulate macras to perform more phytosis you also get t- memory cells which will store a memory of that particular shaped antigen and then teiller cells or cytotoxic tea cells and those ones we'll have a look at in a bit more detail detail T reggulator cells will suppress the immune response to ensure the cell mediated response will stop and therefore it's only occurring when the pathogen is present because you don't want this response happening all the time you only want it to happen when you are infected with a particular pathogen so the C killer cells or those cytotoxic T cells these are the tea cells that destroy abnormal or infected body body cells and they do this by releasing a protein called perin which embeds into the cell surface membrane and it makes a hole a pore so that any substances can enter or leave the cell and that is what causes cell death because either you have too much liquid and substances leaving the cell causing it to dehydrate and die or you have too much liquid entering and that causes it to burst so most this is most common in viral infections because of virus infects the body cells and by destroying the body cell and sacrificing your body cells it prevents the virus being able to replicate further next let's have a look at the B cells and those are part of the humoral response so B cells are activated by t- helper cells and this is done by the t- helper cells binding to B cells with complimentary antibodies to antigens and this is clonal selection because the C cells will only bind to B cells which do have a complimentary shaped antibody on their surface so is selecting the correct shape that complimentary shape B cell and then they get cloned in mitosis and that's what we're going to have a look at here so that B cell is activated by the release of inter lucans from that t- helper cell once they're bound that causes the B cells to divide by mitosis to make large numbers of clones which have that exact act shape antibody on their surface so that is your clonal expansion the B cells then differentiate into either memory B cells or plasma cells the plasma cells are the ones that can produce antibodies and the antibodies attached to the antigens on the pathogen to help destroy them by glutation and that's coming up later in this video they also Mark them so that fade sites can locate them and Destroy them this is a primary immune response which means it's the first time that you are encountering that pathogen and you store these memory B cells which remain in the blood for a long time after infection so if you are then reinfected with the same pathogen with that sha same shaped antigen the B cells can rapidly differentiate into plasma cells and produce large numbers of antibodies rapidly so that you can then destroy the pathogen before it causes any symptoms so that's your primary and secondary immune response the primary response is the first time you're ever exposed to that pathogen and antigen and because it's the first time it can take a few days for the lymphocytes to create enough of the correct complementary shaped antibodies to help to destroy the pathogen and therefore the time that that takes the pathogen is dividing causing damage and therefore you have symptoms of the disease before the pathogen's destroyed in a secondary immune response because of being reinfected with the same pathogen the memory B cells can produce large amounts of antibodies rapidly so that the pathogen is destroyed before it can cause any symptoms and that is what active immunity is you're immune because you've been actively infected with this pathogen next then we have a look at antibodies and vaccination carrying on from this idea of immunity so antibodies are proteins and it's those t- helper cells that we saw stimulate the B cells to produce inter lucans initiating the humoral response which results in the production of plasma cells which produce antibodies so antibodies are globular proteins they're called tary structures and we actually have four polypeptide chains we have two lighter chains which are shorter and two heavy chains which are longer The Binding SES are up here and that is where you have this unique shape which will be complementary to the shape of a particular antigen and that's where a particular antigen can bind to a particular antibody the rest of the antibody is constant so it'll be exactly the same shape in all antibodies and when an antigen binds to an antibody we call that an antigen antibody complex and this is where it links to utenation so antibodies can work in three ways utenation or through marking pathogens and also acting as antitoxins a glutin is what we can see in this image it's the clumping together of pathogens to make it easier for fages sites to locate and then engulf the pathogen Allin one go antibodies also act as an opsonin when an antibody antigen complex has been formed the antibodies are marking the antigen making them more susceptible and more easy to locate for phytosis then also antibodies can bind to toxins prevent venting them from entering the cells and causing harm and in this way they're acting as antitoxins now monoclonal antibodies is a technology that has been used based on your knowledge or our knowledge and science of antibodies and the hbom method is a widely used technique for producing monoclonal antibodies which are identical antibodies produced of a single type of immune cell so here's how they are created Step One is mice or other small suitable animals are immunized with an antigen of interest and the antigen is typically a protein or other molecule that triggers the immune response step two after a suitable period the B lymphocytes from that animal are collected and these cells can produce the antibodies for that particular antigen step three is you fuse them with these Myoma cells which are a type of tumor cell that can rapidly divide so that means by fusing them together and creating these hybridoma cells we have cells that can rapidly divide but also produce the antibody of Interest so the F cells are then cultured in a selective medium that that supports the growth of those hypas and the medium usually contains substances that prevents the growth of unfused Myoma cells the hyoma cells are screened to identify those producing antibodies specific to the antigen and this this can be done using the Eliza test which we're going to look at in the next slide finally those positive homas which means the ones that are producing the antibodies of Interest are isolated and cloned and then lastly you let them produce lots of those antibodies which are harvested and can be used in different types of medicines and treatments so the different things that they can be used for are medical treatment medical diagnosis pregnancy test and other drug tests as well so for example direct monoclonal antibody therapy some cancers can be treated using monoclonal antibodies which are designed with a binding site complimentary in shape to the antigens and the outside of the cancer cells the antibodies are given to cancer patients and attached to the cancer cells while the antibodies are bound to the cancer cells this prevents chemicals from binding to the cancer cells which enables uncontrolled cell division therefore the monoclonal antibodies prevent the cancer cells from growing and as they are designed to only attached to cancer cells they won't affect other normal healthy body cells indirect monocl antibody therapy um is this example here so cancer cells can also be treated with monoclonal antibodies complimentary in shape to antigens on the outside of cancer cells which have drugs attached to them these cancer drugs are therefore delivered directly to the cancer cells and will kill them and this reduces the harmful side effects that traditional chemotherapy and radiotherapy can produce this is often referred to as bullet drugs and that is because it delivers the medicine directly to the site that they're needed so the other things that we talked about were it could be used in pregnancy tests and for diagnosis so it has been used to diagnose influenza hepatitis chlamidia prostate cancer and even more recently in those covid-19 tests as well and this is all working via an Eliza test so this is how we do our Eliza test the enzymelinked amino absorbent assay that's what it stands for you could use two antibodies so first you'd have a mobile antibody complimentary to an antigen being tested for and this has a color die attached to it you then have a second antibody complimentary in shape to the antigen is is a mob in the test and then a third antibody is immobilized and is complimentary in shape to the first one so what you would then do is add the test sample from a patient who you want to diagnose to see if they have a particular condition to the base of a beaker you'd wash to remove any Unbound test sample you then add the antibody complimentary in shape to the antigen you are testing the presence of in the test sample wash remove any Unbound an body and then add a second antibody the that is complimentary in shape to the first antibody and will bind to the first one the second antibody has the enzyme attached to it and the substrate for the enzyme which is colorless is then added and this substrate produces colored products only in the presence of that enzyme so the presence of the color indicates the presence of the antigen because you'll only have that enzyme present to cause that color change if you had the antigen in the test sample in the first place then we have a look at types of immunity and we have passive and active we've mentioned active already so it involves the exposure to a particular pathogen or antigen so you make the blood cells yourself your own memory B cells and you're making your own antibodies passive immunity is when you aren't making any of these cells or antibodies yourself you're being directly injected with the antibody so the pathogen has not entered your body it doesn't provide any long-term immunity but you do have some temporary immunity because you directly receive a source of antibodies so for example antibodies can be passed to a fetus through the placenta or through breast milk to a baby that's an example of passive immunity there's two types of um active immunity natural which is when you become immune because you've been EXP exposed to the pathogen or artificial immunity which is when you become immune because you've received a vaccine which either had a weaken version of the pathogen or the antigens vaccines play a key role in immunization and disease prevention so they can induce passive or active immunity depending on whether you're injecting in the antibodies or the antigen passive immunities we said is you're just directly injecting in the antibodies but artificial Act of immunity is when you're being injected with small amounts of weakened or attenuated pathogen and that will trigger a primary immune response but with very very limited symptoms compared to what the actual pathogen would cause you if you were infected so therefore if you do get reinfected with the same pathogen you will rapidly produce antibodies and in large quantities because you would then be experiencing a secondary immune response and this is how vaccines provide this active artificial immunity so let's just have a look at that and we've got your primary and your secondary immune response now they're not always effective in the long term and that is because pathogen's DNA can mutate or RNA if they have RNA and if the genetic material mutates it could result in a mutation that now has a bacteria or virus has a different shaped antigen on its surface and if that's the case the memory cells that you have circulating in your blood after your primary immune response to that vaccine will now be producing plasma cells and antibodies are incorrect In Shape for this newly shaped antigen and this is known as antigen variability so the last little bit then linked to vaccines is how they can protect an entire population so an epidemic is when a disease spreads rapidly on a national level So within one country whereas a pandemic is when a disease spreads rapidly on a global level like covid-19 Mass vaccination programs prevent the further spread of the pathogen causing the disease so these vaccines are frequently updated resulting in booster vaccines to account for antigen variability again much like covid-19 there wasn't just one vaccine there are multiple vaccines and you're encouraged to take booster vaccines especially if you're someone with a weakened immune response and if a large enough proportion of a population are vaccinated then herd immunity arises and this is the concept where if most of the population are immune that means they can't get the symptoms of the disease and they're not able to transmit the disease or transmit the pathogen which causes the disease so if enough of the population are vaccinated and immune then that means transmission should be so low that people that are too vulnerable to have the vaccine are protected and you might be vulnerable cuz you're pregnant you're elderly you're very very young or you have a weakened immune system so herd immunity is really important to protect the individuals who are too vulnerable to have the vaccine themselves [Music] a [Music]