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amazing. So, um, thanks for that rubber anti, everyone. My name's Sri and, um, today we're basically just going to be a continuing on from Justin's session from last time. So the main things I'll be covering today, or muscle contraction, chemistry of life and all the other things listed I think the main bulk of my session today would be muscle contraction, microanatomy and respiration. Chemistry of life and buy a biological market. Molecular structure is more of a review of concepts from a level, but I'll still go over them. So let's just get started right away on muscle contraction. Amazing. So, um, these are the learning outcomes I'll be covering in the muscle contraction section. So I think first, what's important is to actually be able to about line the structure of the sarcomere. So what I've done on this slide is I'm going to, like, label each part of the sarcomere and sort of give a way to actually remember, um, what the label is. So the first one is the M line or the middle lines. The way I like to remember this is M for middle. So the M line comes in the middle of the sarcomere. The next one is the Z line, so the Z line represents the end of the Sarcomere. Z is also the last letter of the alphabet. So that's how I like remember it. So Z Line is the end of the sarcomere. Next is are thin acting filament, so this portion only represents the thin filaments and it's alternatives. I bend. So the way like remember, it is I is a thin letter, so it only represents the same active filaments. The next one is just the thick mice and portion to the thick filaments, and that's represented by the age zone or the H band, Um on. And this H is a thick letter, so it's sort of only representative. Think filaments on. Then Finally, the sections that overlap the steak and that then filaments about the acting and mice and filaments is represented by the A band on the way. Like remember is that letter is kind of like a hybrid of the letter I and aged so they contain both the think on the thin filaments Before I move on. I also need to think we need to be able to go outline the difference between troponin and tropomyosin because sometimes they're used interchangeably. But they're two completely different molecules. So what happens is, during the muscle contraction, your calcium is actually gonna buy into your troponin on. That's going to move the trouble mice and out of the mice and binding site, thus exposing the mice and head so the calcium doesn't buy into the trouble. Mice in the calcium only binds to the troponin, and the troponin will basically move their trouble. Mice and out of the mice and binding site. Well, I'm going to cover that more in depth in the next few few slides, so don't worry if you didn't quite get that great. So, um, again, if you have any questions or if you need me to go faster or slower, let me know. Someone's asked. How long will this session be? The session should be around 1 to 1.5 hours, including breaks and questions. Great. So now moving on to excitation contraction. Couple things. So first, let's start off with school it'll and cardiac muscle because it's slightly different in the's than in the smooth muscle. So what happens is your action potential is going to arrive at your Axon terminal on that's going to trigger your synaptic because of physicals to buying to the synaptic membrane on what's contained in your synaptic musicals is acetylcholine. So once it binds to the membrane, it's basically going to release Theus. It'll Colon, which will then bind to the acetylcholine receptors on the Teach you bill on once advice to the receptors on the Teach you bill. It's going to signal your sarcoplasm ridiculous to release calcium ions. Now your calcium islands, like I mentioned in the previous slide, will bind your troponin, and that's gonna move tropomyosin out of the mice and binding site on. That's basically gonna couple cause a crossbridge to form in muscle contraction. So again, just to reiterate that what happens is your action potential is gonna arrive at your Axon terminal. That's going to cause your synaptic physicals to release the seat. So, Colin, this will bind here acetylcholine receptors, and that's going to trigger your teeth. You built to trigger the sarcoplasm ridiculous to release calcium. So that's basically how excitation contraction coupling, Uh, since little on cardiac muscle. Now for smooth muscle, it's slightly different. So, um, what happens is, you actually have a more He'll notice calmodulin. So the first difference is your calcium. I owns a rowing to be supplied both from a sarcoplasm in particular on your extracellular fluid from outside. So once the calcium enters a cell, it's going to bind to Calmodulin to form the calcium Kalamata Lynn complex. What that's going to do is it's going to activate this molecule known as mice and light Chain kind is on your kind a XYZ or you're kind of enzymes are always responsible for force. Follow phosphorylation a molecule, whereas your phosphatase is arguably responsible for defense for for dephosphorylation your molecules. So what happens is, once you're mice and light chain kind is is activated. That's going to phospholine phosphorylase your mice and light chain. And that's going to cause the muscle contraction to occur. So now once it's occurred, um, you calcium is going to be released from her calmodulin. And once it's released from the calmodulin, your phosphatase is a runner be released, so Phosphatase is a basically gonna dephosphorylation your mice and light chain and thus cause the relaxation. So again, I just put these steps on the slide so that If you want to review them again, it'll sort of refresh your mind. But basically what happens is, um, accounting the calcium kalamata and complexes Going to activate mice and light chain kind is which will phosphorylase the mice and light chain. And that's what's going to cause the contraction. So I hope that makes sense. Um, great. So, um okay, someone's asked me to go slower. If you want me to repeat anything as well, feel free to put that in the chart. Great. So I'll go slower now, um, so moving on to a sliding filament theory. So this is actually where the muscle contraction occurs, so there are basically four main steps to be aware of. First we start off with detachment. So, um, this is when your ATP molecule is going to bind to the mice and head on. That's gonna cause your mice and had to detach from the acting filament. So, like the Bagram represents, the ATP is going to bind to the mice and head, and that's going to cause it to detach from the acting filament. Your next step is hydrolysis is so the basically the ATP is going to be hydrolysized into a D. P and an inorganic prostate. So what that's going to do is, once the ATP is hard realized, it's going to expose the mice and head, which means the mice and head is ready to bind to other things. So that's what's gonna happen in your third steps or third step is gonna be crossbridge formation. So since you're mice and head is exposed, it's gonna form across bridge between the act and filaments on. Then finally in your power stroke. What's gonna happen is your ATP and inorganic prostate molecules are gonna be released on. That's going to cause the angle of the mice and had to change. So it's gonna caulk back the mice and head on. That's basically gonna cause the thinking, then filaments from relative to one another or shorten the sarcomere, which is actually what causes muscle contraction. So again, just to reiterate, I've put the steps on the slide. So first we have detachment where the ATP binds to the mice and head on down. That's going to cause the mice and had to release itself from the acting Filmon. Then we have hydrolysis of the ATP molecule, so that's going to form ATP, an inorganic phosphate, and that's going to expose the mice and head. Next, we'll have crossbridge formations. And now that the mice and head is exposed, it's going to former crossbridge between the active and filaments on. Then finally, we have the power stroke and the power struggle is basically caused by the release of ATP and an inorganic phosphate. And that's gonna cause the mice and had angle to change. It's gonna caulk it back on. That's gonna cause a thin and think filaments to move relative to one another. So I hope that make sense. Uh, let me know if you want me to repeat that or anything. So finally, the link tension first. So I think this is one of the learning outcomes that I mentioned previously, and this is only something I actually understood when I was making these slides. But it is actually a very easy concept, so let's just go through it first before I start. Um, I just need you guys to know that the think filaments represent the mice and heads, and the center line here actually has no mice and heads the red. The red color is represented in acting filaments and the if you want the most amount of tension to be generated. That's when there's going to be the most amount of overlap between the mice and heads on the act in filaments. So again, if you want the most amount of tension generated from your muscle contraction, you want the most amount of overlap between the red Act and filaments and the blue mice and heads. So 1.1, you can see that the acting filaments overlap the mice and heads, but they also overlap the center, which has no mice and heads, and in this case, the acting filaments overlap each other, so it's sort of wasting its potential. It's not. It's not perfectly overlapping the mice and heads, which is why the force generated is not at its maximum capacity, whereas if we move on to 0.2, you can see that the acting filaments perfectly overlap the mice and heads, Which is why here is, um, the optimal resting length, or the highest amount of attention that could be generated by the Sarcomere. Then, if we move on to, um, Stage three, you can kind of see that the acting filament um is not is not overlapping some of the mice and head some of the mice and heads or just exposed. So again, the amount of tension that's gonna be generated it's dropped is there's not enough overlap on finding the fourth step. You can see the active filaments are barely if it's all overlapping the mice and head. So that's going to cause thie attention generated to drop to zero. So I hope that makes sense again. If you'd like me to repeat any of the concepts, let me know. Um, so, yeah, that completes the, um, muscle contraction section of it. So here's just one ST a, um, Justine, could you launch the pole for this, please? So the question is, um, regarding crossbridge cycling in smooth muscles. What is the job of the calcium call model and complex in the Siris of reactions for contraction? I'll give you guys around 30 seconds down to this. Yeah, so I can see one really clear answer. Um, I'll give you guys a few more seconds on this. Yeah. You guys already smashing this? Yeah. Amazing. So end it there. Um, So the answer was be, um and the reason for that is because the, um pulling. Yeah, so it activates in my son like chain kind of ease. And, um, if you remember, what happens is this happens instant muscle contractions. So the calcium is going to buy into the calmodulin to form the calcium kalamata and complex on that's going to trigger your, um that's going to trigger the mice and light chain kind azo phosphorylase the mice and light chain. And that's what that's what's gonna cause the contraction. So yeah, great. Well done, guys. Um, so moving on to chemistry of life. So this section is quite short just cause it's a recap of some a level concept. So these are the main things that I'm gonna be covering. So first we'll start off with cattle belisa, um, versus an embolism. So, um, in capitalism, it's basically when you're breaking down molecules and the way like to remember this is it cuts down the molecules of possible is, um, when you're breaking down these molecules, it's going to release energy. So it's an energy yielding reaction on an example of a cattle. A PR reaction would be like now a supposed to capitalism in animal is um, you're actually building up the molecules. So in this case, you would require energy in order to build up the molecules on. An example of this reaction would be gluconeogenesis. So you need enough energy to produce these glucose molecules. I've also included the gives free energy reaction in this slide. But the main thing you really need to know about this formula is that if the gives value is negative, then the reaction of spontaneous So, for instance, the breakdown of ATP yields minus 30 30.5 pill a jewels for mole on. Since it's a negative value, that means the reaction of spontaneous. So that's like the main things you need to know about. You need to pick up from the slide. Um, this next light is really worthy, and, um, I'm not really going to go through it just because it's something you kind of need to learn. But I've put it on here just in case you want to recap the slides later, and you can put this down in your notes. The main thing you need to know in the slide is just those six recurring reactions we have and the enzymes involved and what these reactions actually do. So, unfortunately, unfortunately, it's just a case of actually learning these things. So, um, we went to the next slide, um, which is patent regulation. So, um, the first thing we'll start off with is Alice. Trick and ambition and non competitive inhibition. So in both types of inhibition, you have an inhibitor that binds to a site that is not the active side. So one thing I struggled to get my head around is how is allosteric modification actually different a non competitive inhibition because both of them buying two a sight that's not the active side and causes inhibition. Well, the main difference is that in Alice start inhibition, what happens is when the inhibitor binds to a site that is not the active side, it actually changes the confirmation of shape of the active side. Whereas a non competitive inhibition when the inhibitor binds it, basically, it doesn't cause a change in the shape of the active site. It just basically causes the enzyme to become dysfunctional. So the main difference is that in allosteric inhibition, you're going to have a change in the shape of the active site. But that doesn't happen in our competitive inhibition next moment onto Covalin modification. This is basically when two molecules in tract in a violent fashion, so they have coagulant bonds that are binding them together and ago. An example of this would be phosphorylation, where a phosphate phosphate group is attached to an enzymatic of in fashion on. Then finally, you have your rate limiting steps so your rate limiting step is basically the slow step of the reaction. And that is what determines a great so an example of this would be fossil for your kindness and glycolysis moving on to biological American molecular structure. So these are the main learning outcomes that I'll cover, right? So first we start off with our protein structures. So this table, I think, is very important to get your head around. But it is quite simple. So first we start off with our primary structure of the protein. So the primary structure is basically determined by the order of the amino acids that occur in the chain. Um, and the main bones involved in this would be your peptide bones. So it's basically determined by the suit that sequence of the amino acids in the chain and as we go down the table, so as we go from primary to secondary gets a little more complex. So now this primary sequence of amino acids are basically going to be folded up a little more on, but they can be folded up into alpha helix seas or be depleted chiefs. So you're gonna have another type of bond known as hydrogen bombs that are involved in this folding next one. We move on toward grocery again, it gets a little more complicated. So secondary structure is folded in up into a three D shape to form a sort of active site, Um, for things like substrates to buying, too. So, um, enzymes and stuff would actually have a tertiary protein structure on again. It has a few more bonds involved. And then finally, we have our quarter nitty structure. So this is the most complex protein structure, and this is when two or more polypeptide chains are bound together on an example of this and medicine would be hemoglobin, which is the structure I've put in here. So we move on to our amino acid. So the amino acids, unfortunately you do need to know um, the names of the essential, non essential and conditional amino acids. So I've sort of put in you Monica here that I used to use PVT. Tim Hall and just the amino acids, if you need to be aware of. So for your essential amino acids, it's basically the ones that can be made from the body. So you have to have pain it from the diet as opposed to a non essential amino acids, which can be produced from our body, so you don't have to get it from your diet, but you still can on then find the are conditional. Amino acids are basically the ones that are used in times of illness or in stress. So, um, they're not really made by your body, but you only need it in very specific times. So if we move on to our fatty acids, it's the same. The same kind of thing we have are essential, non essential and conditional, so again are essential. Fatty acids are the ones that cannot be made by the body, so you have to get it from food, your diet or any sort of supplements. Examples of this would be omega three and Omega six. Now the number like three and six, basically determines where the double bond in the fatty acid change occurs. So the reason these are essential is because your body can only naturally place the's double bonds past omega nine. So anything that has double bonds past omega nine are non essential, which means they can be come from or they can come from our diet, and they can be made by our body. Whereas omega three and omega six. Since the double bonds cannot be placed before omega nine, they have to be. They have to come from our diets because I can't be made by the body. Naturally, so are non essential. Fatty acids can be produced. Sorry, um, are non essential. Fatty acids can be produced by the body, even if we don't get it from our diet. And finally, the conditional ones are the ones that we need in times of illness and in stress. Great. So, uh, now moving on to the lipids and carbohydrates. So the main thing you really need to pick up from this is the sort of structure of the differences between saturated unsaturated lipids. So the main thing is that in saturated lipids you won't have a double bond in the fatty acid chain where, as an unsaturated you will have a double bond and this will cut kind of cause a kink in the chain. Um, you also need to know the difference is between assists and trans fatty acids. So insist back you acids. Basically, your chemically similar groups are gonna be on the same side of the fatty acid chain on the way. I like to remember this insist it is kind of like sisters. So the sisters stay on the same side of the fatty acid chain, whereas in your trans fatty acids, your chemically similar groups are gonna be on opposite sides of the of the double bone. And then finally, for your carbohydrates, you basically need to know the monosaccharide that form the different disaccharide. So glucose and glucose make maltose glucose and galactose Michael Actos. So lactose is in the word galactose. So that's how I remember it. And finally, Glucose and Throat does make Soopers. Um, the reason I'm kind of going through these quite fast is because I'm aware that this is a recap of, um, concepts that you've learned previously, and I kind of want to get onto microanatomy and respiration, which will be the both of this presentation. Ah, finally we come onto our scientists a little filaments. So I think the main thing you need to know is how they sort of work according to the cells shape. So you're microtubule usually provide the cellular shape and they also provide cell motility because they have motor proteins such a dying and Tennessean, they also form this spindle fibers at the polls of the cells for sell my Tosis. So if you guys remember the spindle fibers or what pulls the primitives apart to the opposing bowls of the cell, so you're microtubule are in charge of forming the spindles and then we move on to your act in. So if you remember, acting plays a curable in muscle contraction. With your thin act and filaments, they also cause the shape of the cell to change. So with your microtubulin, it actually provides a cell shape, whereas for your act, and it causes the cell shape to change, and it also acts as a sort of a support network for the cell. Finally, you're intermediate filaments provide mechanical support on this is mainly when the cells come into contact with one another. So it's basically important to know which one's provide shape. Which ones causes the the cells shape to change and which one provides that mechanical support? Great. So, um, that was the end of the biochemistry section. So here is just another SBA Justin. If he could launch the pool, please. So Adam is taking supplements for his Oh, just released the answer. The Adam is taking supplements for his diet, as he has recently become vegan. The doctor explains Teo Adam that these supplements are given to him since his body is unable to make it and he can no longer receive it from his diet. As he's become vegan, what is the most likely supplement he has been taking? So I think, um, the main thing you need to be able to understand is which one is the essential amino acid? Which one is a non essential? So this one is slightly harder, but hopefully you guys can get it. Amazing. So, um, just a few more responses. Yeah, I think most of you have got it. Probably cause I release the answer by mistake, but yeah, the answer is he, um And that's because that is the essential amino acid. So, like I mentioned, I think you just need to be aware of the essential nonessential. You kind of just need to learn it with the new Monica I gave you guys. So PB teach him. Hold this for the essential amino acids. Great. So before we start off this section, I think we should take a little break because microanatomy and respiration are gonna be the both care ones. So, um, if you guys want to come back on it 7 40 we'll just have a three minute break. Okay. Um, I hope that break was long enough, so let's just power through my car anatomy. So, um, the main thing I want you guys to take from this part is, um, the interpreting micro Gosh, because that is very high yield. And that's tested a lot. So, um, before we go on to actually interpreting my progress, let's just look at the different types of epithelial we have. So first, let's start off with our, um, simple epithelia. So the simple ones are basically just made up of one cell layer. Um, they're only one seller thick. So if we start off with our simple squamous, you can already see they're quite flattened. And they have these dish a pin nuclei. Um, and the reason for that is there quite flat because they usually act as diffusion barriers. And if you guys remember, you want a very short diffusion distance in order to increase the efficiency of diffusion. So these basically allow passage of material by a diffusion, and you're gonna find them in places that partake in diffusion A. Lots of things like the albuterol I kidney and the lining of the heart. Next, if we move on to simple cuboidal, you can already see these cells are very cute black, and they have a large central nuclei. So that's the main way of sort of distinguishing them between the simple squamous ones, um, your cuboidal cells, whether they're simple or start. If I did there, they're usually in charge of secrete. A refund is and absorption as well, but more often than than not, they usually partake in secretions, so they're found places like the kidney to builds over the surfaces and pancreas. Next, we move on to our simple kilometers, so you can already see These cells are a lot taller than the keyboard and squamous ones, and they also have these over the new player as if they've kind of been like, stretched up or pulled up. Um, and so sometimes it can also have got bit cells incorporated in them to secrete things like mucus. So their main function is absorption and secretion of mucus and enzymes. Sometimes they can even have cilia on top to sort of walked any mucus or dust particles away. So those are the main simple ones. Next, we'll move on to the stratified. So the difference between simple and stratified is that stratified actually has multiple layers of cells where, as simple as I mentioned before, it's just made up of one seller. So, um, are stratified squamous epithelium. They. They also have a similar function to the previous one. It's just made up of more cell layers, so they have a very protective function because since they're more of these sellers, they can sort of, um, protect against any damage or wear and tear so they protect against abrasion and their friend and places like the esophagus mouth and vagina. The skin is also a card, and I started fried squamous. So what that means is if you have keratinized epithelial. What that means is it's basically water in soluble, so it provides this waterproofing layer. So as you can imagine, our skin does provide a waterproof layer doesn't absorb any water as opposed to your non current Master Padilla. So non current messed up epithelia are soluble in water, which means they can't absorb order. Well, they can't absorb order. So that's the main difference. Then we have our started five cuboidal epithelia. So these ones are cube like cells again, like we previously mention, that they have that large central nuclear. Except they have their like stacked up on top of each other on day also serve a protective function on. Like I mentioned, cuboidal cells are very secretive, so you're gonna find them in glands which secrete a lot. So things like sweat glands which secretes sweat, salary go glands which secrete saliva and memory glands. And then finally we have are stratified columnar. So these are again. You're tall cells with the oval shaped nuclei, except they're multiple sub layers on their main functions. are protection and secretion. Now, um, a question in the chat. So now we have our pseudostratified and transitional epithelia. So these ones are slightly different from the general pattern, so they don't really follow the pattern. So our pseudostratified epithelia they usually have gall but cells incorporated in them to secrete things like mucus there also found in the respiratory tract so they can also secured things like surfactant, um, in the lungs. What happens is they are only one cell layer thick, but they have nuclei had different heights. So this is also known a staggered nuclei so that make that makes it seem like they're multiple sub layers. But it's just once a layer with nuclear different heights. And then finally we have are transitional epithelia. So your transition epithelia you can already see the cell shapes, and the sizes are very different, and it's arranging a very random pattern as opposed to the previous ones on. The reason for that is because of transitional. Epithelia can alter their shape according to their function. So you're gonna find it in places like the bladder, which is, um, constantly contracting and relaxing just to, like, expel urine and also relax. So you're whenever you see bladder in like what type of what type of epithelial is found in the bladder? Always think transitional empathy. No, this is another high yield question that comes up a lot. Amazing. So, like I said, um, it's a very important skill to be able to, um, interpret all these types of epithelial on actual micrograph. So So the first one. I've sort of given you guys the answer, but for the next ones, I'm going to try and ask you guys to put it in the chat. What you think of what type of epithelial you think it might be. So as you can see here, um, it's only the pink one set of the epididymis. You can see the cells are quite flatten. And if you look closely the nuclear kind of disc shape So this is very characteristic of your simple famous epithelia. If we move on, um, can you guys in the chart maybe just put what type of epithelial epithelia you think this is? I will sort of give hints a swell as we go along. So they're they're like, cube like shape, and they have these large central nuclei. Don't be. Don't be shy to put it in the chart. It's okay to get it wrong. Um, so, yeah, if you have any guesses, just put it in the chat. Yeah, amazing. So someone said simple cuboidal which it is on this one's actually found in the Bowman's capsule of the NEPHRON. So, like I mentioned, um, your simple, cute little cells or cube like and they have this large central nuclei. The reason they're simple rather than trying to fire it is because there's only one cell layer of them. It's just kind of, um, surrounding it. It's it's forming a circular shape, but it's only one seller. Think, which is why it's a simple type of media. Next, we move on to, uh, this one. So again you can put your guess is in the chat as to what this might be, um, their toll. And they have these oval nuclear. Um, so, yeah, if you have any guesses, you can put it in the chart. Yeah. Come on, guys. It's okay if you if you if you get it wrong, it's completely fine. Um, there these toll, uh, tall shape and they had the oval, Nuclear like I mentioned. So the over nuclear, kind of like they've been stretched out. Yes. Oh, someone said simple columnar, which that's that's correct. And the reason for that is again, it's simple because it's once a layer thick, and it has these over nuclei. This particular one was actually in the small intestine. Next, um, can you guys guess what this one might be? So here we have multiple sub layers. Um, on as you can see, they're quite flattened. And they have these Deschamps nuclei. Um, so you have multiple layers of them. So just for the sake of time, I'll just put the answers So this one would be start if I'd squamous, um, and you'd actually find this one in the esophagus, the gastroesophageal junction. I think I can, uh, rise. That now is all because that one is quite important. Your gastroesophageal junction is basically squamocolumnar junction. So, like I mentioned, your esophagus is made up of squamous epithelium. Um, and this changes in your stomach where your stomach becomes simple kilometer epithelia. So that's basically the distinction of the gastroesophageal junction. You guys will come up. This will come up more in your future cases, so yeah, it's just something I wanted to point out. Amazing. So here's the next micrograph. So we have multiple layers of these Cuba like cells with again the large central nuclear. So this one would actually be your stratified cuboidal cells on. Like I mentioned, your cuboidal epithelia is usually found in secreted resells, So this one would be finding a salivary glands which secrete saliva. Um, and then your next one, which is your You have a bunch of these told shape with oval nuclei epithelia, and they're multiple layers. So this one would be your stratified Columbia EPITHELIA on this particular one is found in the male urethra. So this one, I've given a few hints here again. So this is actually just one cell layer thick, but it has the staggered nuclear to make it seem like they're multiple cell layers. They also have the cilia on top. So this one would actually be your pseudostratified Columbia patella, and you'd find this in the lining of the trachea. Um, the reason for the cilia is because this area will actually watched any mucus or any dust particles away. Because, as you can imagine, the trickier will face a lot of mucus and dust particles that it interacts with. So the cilia basically act walked any of this away. And then finally, I think the easiest type is your transitional epithelia. So this is when you have, um, like different shapes and different sizes of the cell, and it's completely around them. It has. It's like mosaic pattern on. The reason for that is because the cells can actually alter their shape according to the function. And like I mentioned before, whenever you see transitional epithelial, just think bladder. So, yeah, this one is seen in your bladder. Amazing. So that was just a brief overview of epithelia. I hope that was helpful. And then we'll move on to the elements of connective tissue. So before we actually look at the different types of connective tissue, let's see what they're comprised of. So first we have our college and fibers. So we have four main types of collagen fibers here. I've kind of just put the way I like to remember them so you'd find your type on collagen in your bone. So the word one is in bones, so you try and type one and bone your time to holiday and fibers would be present in your cartilage. So the way I like to remember this is cartilage, so you have type two college and fiber in your cartilage. Type three is found it. Maintain bone healing for card. If you never see students, when you get to case one, you see one healing a lot, so you're knocking room. You're not going to forget Type three College in, but there's no real way to remember. It is just type three is found in wound healing on. Then finally, type four is found in the floor or basement membrane, so four sounds like floor, so you're type for collagen is found in your basement membrane. Now, if you look at the Micrographia, concede that the appearance of the college and fibers are very thick and they're on branch. There. Also parallel e aligned on it. It's very important that, um, that you recognized that when your fibers are probably aligned, that means they're able to withstand a lot of compressive force is making them stronger, Um, as a poster, if they're just randomly orientated. So our next one is a lasting. So, um last in, basically provides elasticity. It provides flexibility. And the reason for that is you can see the fibers are a lot more jumbled and a lot more randomly packed so they don't have that parallel alignment. So instead of providing rigidity, there be a lot more flexible. So you're going to find this in places where, um, where the organs are actually very multilayered. Move a lot. So things like your vocal cords, aorta and pulmonary arteries They obviously have to be very flexible. Um, on Daz, you can see the fibers are actually thin and their branch, and they're very randomly scattered around. Next, we have a reticular fibers. So these ones, they basically act to protect capillaries, nerves and muscles fibers. Um, and then next we have her fiberglass. So you're five oppressed, fibroblast produce extracellular matrix on. You'll find ECM in college in a last in particular fibers and ground substance. On the next light, I'm basically going to pull through what extracellular Matrix is because it plays a very important role in connective tissue. On finally, you're a dip aside. So you're a dip aside, so basically they are your fat cells or your adipose tissue cells and they act exactly the way fats do. So they act as a food store. They insulate, they support that provide energy, and they also provide protection. Um, it's very important also. And this is very high yield is well, that, um, when you see a micrograph for the nuclear is sort of look like they've been squash the side, you should immediate immediately think this is an adipocyte, um, cell micrograph. Because what happens is your factor up. That sort of takes up the whole space in the cell, the squishing the nuclear to the site. Which is why this nuclear has a squished appearance. Great. So now that we've looked at the elements of connective tissue, let's look at the different types of connective tissue we have. First, we start off with a loose connective tissue, which basically wraps and cushions and protect any organs on they contain. Oldest. The fibers that I mentioned in the previous slides a collagen last in an articular fibers on. The reason they're very good at rapping around is because they have a lot of flexibility because of the way the fibers of impact. So they're not Palaly aligned. They're very scattered and randomly arranged, which is why they can sort of. They have a lot of this flexibility and elasticity to wrap around the organ. Next we have are dense, irregular connected tissues, so a Z conceal it. The fibers are kind of jumbled, but they're very tightly packed, which makes some more dense on. But, um, they can resist. The's compressive force is so they're a little thicker than your connective tissue. Um, and its main function is protection. So example of this would be your skin, and then finally we have are dense, regular connected tissues. So here you can see that the college and fibers have been arranged parallel e, which is why they can sort of. They're protected against these resistant forces on. They're protected against wear and tear, so their friend and pendants and ligaments where where interest very frequently observed. They also contain many fiberglass. So you're fibroblast, if you remember, are responsible for secreted extracellular matrix. So what exactly is Extracellular Matrix? And what does it do? So it's basically made up of things like Agricole's water college and fibers, hyaluron IQ acid glycosaminoglycans or your bags. And what they do is they provide the cell shape and Anchorage for the cell, and they also cause cell motility. Um, they also allow the cell to migrate and they cost salad Asian. So they're basically all in all their responsible for a lot of cellular functions. The main thing you need to know is that your exercise your matrix is important for providing cell shape and sell motility. Um, so now we'll move on to our cartilage. So we need to be aware of three types of cartilage first less fertile for their highland cartilage, which is the most abundant type on their made up of type two collagen with elastic fibers. So, um, if you guys remember type two cartilage Sorry, type two collagen cartilage. So that's why you're type two. Collagen is found in your cartilage. Your highland cartilage also act as a precursor for bones. So before your bone actually forms, you may have highland cartilage in place until the bone actually forms so that your highland cartilage you're gonna find a lot of that in your body. That's the most abundant type. Next we move on to our elastic cartilage. So as you can see, the fibers are very randomly packed, which provides the flexibility and ella elasticity of the elastic cartilage there made up of collagen and elastic fibers on you can find them in places like your external ear on your epiglottis is, um, your external years also refer to as your Pinna, And then finally, we move on to our fiber cartilage. So the fibers here are parlay aligned as opposed your elastic cartilage, where they're jumbled about so as they're probably aligned, they're able to resist. Any compressive force is, and they can be a lot more protective, so you're going to find them in places like your tendons and ligaments, which are very susceptible to wear and tear. These are your strongest type of cartilage. On their made up of highland matrix and parallel, we arrange layers of college and privates. I've also put a diagram here on it's very high yield to sort of know which type of cartilage occurs where. So this is a very helpful diagram to make a note of that. So as you can see, your highland cartilage, which is marked as purple is found a lot over here. So it's so it's the most abundant type your elastic cartilage here you can kind of see in your pin or you're here, and then your fiber cartilage. You can see in things like your interview tibial disks, your pubic symphysis is and basically your main pendants and ligaments because they're the strongest type of cardio. A judge. Amazing. So, um, now briefly move on to the bone. So before we go on to bone formation, let's talk about the main terminology that we use when we describe bones. So first we have our osteoclasts, which are in charge of cutting bone, bone cutting or bone resorption and and easy way. Remember of remembering that is osteoclasts or for cutting? So they both have the letter C in it. Then we have our osteoblasts, which are in charge in charge of bone formation or building up the bone. So again, osteoblasts build bone. And then finally we have are osteo science which are basically matured osteoblasts, and they cause, um, matrix turn over or they basically maintained the bone tissue from, um, sort of dying out. Finally, we have two different types of bones, are trabecular A and are compact bones or Trebek trabecula or counselors. Bone are basically porous bones, and they're less dense than your compact bone. Um, your compact bone is basically just a stronger type of that bone. So in about bone information, we have five main stages. First, what happens is your osteoblasts will aggregate together. One they aggregate, they start to secrete something known as osteo, which is basically just bony matrix on. Then what happens is, um, this or osteo secretion will start in trapped. Some of the osteoblasts that have aggregated on calcium will start to bind to the Matrix. And that's going to, um, that's going to hard in the Matrix, and it's going to contract some of your osteoblasts now. The osteoblasts that have been trapped in the Matrix are then going to differentiate into osteo sites, which is what causes the matrix turn over, or which is what maintains the bone tissue. So that's basically how bone formation occurs. I can repeat that again if you'd like. If you guys would want me to, um, and blood vessel appearance base basically means that the osteoblasts secrete osteo around the blood vessels rather than on top, just so that your bone consistent get circulation from the blood. Um, and now this one is finally your muscle. So this table, I'm not really gonna go through because I'm sure you guys have seen this before. Um, it's just a matter of learning it. I've just put this in your slides just so that you can rise this over. I think these are the main things you kind of need to know which ones are nuclear did like which ones are multiple you created. And which ones have single nuclei, the different functions and where exactly you'll find these types of muscles. So, yeah, that concludes my microanatomy portion. I'm sorry. That may have been a little fast, but, um, I just want to make sure that we're still with time. So here is our next question for the microanatomy portion. One guy's I can't see. The answer is no one can see the answer, So don't be afraid of getting it wrong. Just put down um, and answer. Great. So we've got a variety of answers, and I understand because interpreting micrograph is quite a hard skill. Um, I still struggle with it to this day, so I think I will end the pull here. Um, so the answer for this one was actually, he tried to fight Cuboidal, and it's found in the parotid glands on. The reason for that is because there are multiple cell layers of the cuboidal cell. So you can see a lot of these Cuba like cells with the large central nuclear on Daz I mentioned before. Cubital cells are associated with secreted. He functions so purported blank gland is a very secretive gland, which is why you'll find started like your bottle epithelia here. Great. So finally, the dreaded respiration portion. Um, for this one, I'm basically gonna go over the TC a cycle the electron transport chain and the different types of shuttled you see in the electron transport change. So let's just get right into it. Great. So here is the TC a cycle. I know it looks a little complicated, but, um, I've sort of given any ammonic your to remember the different steps. So citrate is crab starting substrate for making oxaloacetic on. That's basically the order in which the substrates occur. Um, if I were you, I would not really memorize all the enzymes because we weren't really test on the enzymes. But it is important to be aware of citrate sent days isocitrate dehydrogenase and alpha ketoglutarate dehydrogenase. And the reason for that is because they are three regulatory steps or they up regulate on down, regulate the cycles. So what do you mean, before I go on to, like, why ATP Up regulates this enzyme? Or why these molecules down regulate this enzyme? Let's talk about what up regulation and down regulation actually means. So upper regulation is basically anything that sort of motivates this cycle to occur and to increase ATP production on down regulation basically does the opposite of that, so it's going to discourage the cycle from happening. And that's usually because their mail did he be too much ATP in circulation. So it's kind of peeling the cycle to stop ATP production. So that's what down regulation is. So if we start off with, um oh, it's also important to make a note of the carbon number. So if we start with um, acetylcholine, which is a to carbon molecule, it's going to bind Talk. Saddle acid stayed on, but that's a carbon four molecule, so two plus four is six, so that's gonna form a carbon six molecule citrate. Now that reaction is gonna be catalyzed by an enzyme known a citrate sent days, which is upregulated by ATP on down, regulated by ATP citrate, NADH and succinylcholine. Now the reason this enzyme is down regulated by ATP is because, um, if there's already too much a tiki in the circulation, there needs to be a mechanism to stop this cycle from occurring so that there's not a surplus of 80 beeping being produced. So the way that it signals the cycle is basically, um, if there's too much ATP in circulation, that ATP will bind the citrate's and this just sort of stop the cycle from occurring, too, prevent more production of ATP. Um, this is similar for citrate and 88 sectional Coetzee's so citrate in Sex It'll co way are both substrates that come up future in the cycle. So if there's already too much ATP, you kind of on. If there's already two more sexual Kuwait, you kind of wanted to say, Hey, we already have enough in circulation. So let's sort of hold the cycle for now. So that's why these sort of down regulate the, um down regulate citrate. Seven days now, ATP upregulated citrates and days because if there's not enough ATP in the circulation, there's gonna be a ATP and ATP is basically going to sing. Signal the enzyme to say, Hey, we don't have enough ATP in circulation. So can you Can you motivate the cycle toe happen and can you cause a cheap production to increase? So that's basically why I ATP is gonna up regulate the enzyme. Great. So, um, now that we have citrate, it's basically going to, um, go through a connotation, which is another enzyme in for my sister trait on an Isis citrate is going to form. It's going to be converted to have alpha ketoglutarate by an enzyme known as isocitrate dehydrogenase. Now, another key thing to remember is that whenever you see a dehydrogenase enzyme, just immediately think that Oh yeah, and 88 is going to be is going to be formed in this reaction says he can see Isocitrate Dehydrogenase is here, and there's a nadie age formed. I'll forget it Glutamate Dehydrogenase is here, and another NEDA, it is formed and find. Finally, Malate Dehydrogenize is here, and that's going to form another NADH. So whenever you see a dehydrogenase ends I'm just think Oh yeah. And NADH is going to be formed in this step. So if we talk about isocitrate dehydrogenase, it's going to be upregulated by ATP and calcium and down regulated by 80 and NADH again. It's for the similar reasons is the previous one ATP NADH, you're going to down regulate the cycle just to prevent a surplus of ATP from being produced on ATP is going to up regulate the cycle just in case if there's not enough 80 If there's not enough ATP in circulation, it's going to say, Hey, can you make more ATP? So that, um, we have more in circulation now The interesting one here is calcium. So well, why does calcium actually up regulate the cycle? Well, if you remember from my muscle contraction talk, um, calcium. Calcium actually is a very important role in muscle contraction on, So a muscle contraction requires ATP in order for it so curb. So if there is less ATP, what what's gonna happen is your calcium is going to bind to your isocitrate dehydrogenase and say, Hey, we don't have enough ATP for muscle contraction, Parker. So can you up regulate the cycle can you make more ATP so that the muscle contraction can occur? So that's the main reason why calcium is going to up regulate your T C A cycle. Um, so once we had the Alpha keep the glutamate, it's going to be converted to Sectional Coe and that reactions be catalyzed by alpha ketoglutarate dehydrogenate. It's the same reasons is the previous one. So it's gonna be upregulated by calcium. If there's not enough ATP for a muscle contraction to occur on, it's gonna be down regulated by any DHA and succinylcholine. The reason it's down regulated by sectional Coetzee's because that's going to be the next step of the reaction. And if there's already too much sexual Coetzee, um, that's not being used up. It's going to sort of prevent a surplus of sexual copay from being produced. Great. So now the next few steps a Z concede, we, uh, there was also a decarboxylase shinin isocitrate. So when your carbon number decreases, you shall immediately think, Oh, there there was a carbon dioxide molecule that's been released. That's why our carbon molecule has produced by one. So from isis citrate, the alpha ketoglutarate we have a cow we have. Ah, carbon dioxide molecule being released. So it's gonna go from C six to see five on again from Alpha Ketoglutarate to subtitle Kuwait. We have another carbon dioxide molecule release. It's gonna go from C five c four and then it's going to stay at C four for the rest of reactions because no other decarboxylase reactions are going to occur. So when we go from sectional Kuwait to start today, we're gonna have it Molecular, ATP, GTP and coenzyme A being produced, uh, and go from substances fumarate. We're gonna have a molecule of fad. It's pretty Houston on then, from humor, it's a mallet. And then finally mallet toe oxaloacetic because there is Molly Dehydrogenase catalyzing this enzyme we're gonna have in any DHA being released. So the main outputs of this reaction is gonna be two molecules of carbon dioxide, two molecules of NADH, three hydrogen ion, one molecule of fad eight and one more one more acute GTP. Now, if you guys remember in black Colaces one glucose molecule, actually a yields to pirate molecules and this one rotation of the cycle is only for one pirate molecule. So that means that for one Cooper's molecule. This reaction is actually gonna happen, Price. So you're gonna have twice the amount of out but that I've mentioned here, So you're actually gonna have four molecules of carbon dioxide, six molecules of NEDA, etcetera. You're just gonna have to multiply that by two. Um, for um, for the breakdown of glucose. I think it's also important to mention here that your NEDA shin fad itches Going to enter your electron transport change, which I'm going to discuss in the next slide on down your NADH will yield 2.5 80 p. Where is your effort? The age only use 1.5 ATP molecule. This reaction also occurs in the microcontroller matrix. So that's also another key thing to note. Amazing. So now that we've gone to the PCA cycle, let's finally go through the electron transport change. So this one is just basically a sequence of complex is one after the other. Um, what happens is your any D h from your Krebs cycle is going to enter the electron concert chain at Complex One on. What's gonna happen is it's going to donate. It's electrons too complex one, and that's going to give it enough energy to pump hydrogen ion is into the intramembrane space. So before I go on, I think it's just important to mention that there are more hydrogen ion in the microcontroller matrix done in the intramembrane space, which is why you need energy to pump it against his concentration. Grady in. So now that, um, the hydrogen ion have been pumped into the intramembrane space, the electrons air, then going to sit at coenzyme Q next year, Fad age is going to enter the electron transport chain and company at complex to rather than complex one, and it's going to donate it. Select combines two now complex to Doesn't. Actually, it doesn't actually take part in the movement of hydrogen ion. So what it's going to do is it's immediately going to donate. It's electrons to coenzyme Q. Great, so not coenzyme. Q. Has theologians from both complex one and complex to so. What it's going to do is it's going to donate those electrons too complex three to give it enough energy to pump the protons into the intermittent brain space once that happened, once that has happened, it's going to pass the electrons on to side of prompt See which passes it on Too complex for finally on. That's going to supercharge complex for giving it enough energy to pump the hydrogen ion is into the into Remember in space. So now, once this is all up it happened. All these electrons will then be accepted by oxygen, which is the terminal or final, except er of the electrons on what happens just before this is your oxygen is going to split into two, um, and hydrogen ion Zerg going to be added to these oxygen molecules, dust forming to water molecules. So once your oxygen is accepted, the electrons, um, you're you're going to have a lot of hydrogen ion see the intramembrane space rather than the mitochondrial matrix. So there's going to be a concentration Grady in. So what's gonna happen is you're hydrogen ion Zerg going to move via 80 Pecent days, um, down its concentration, Grady in. And that's going to drive the synthesis of ATP into ATP. So that's basically how your ATP is, how your ATP is produced. Now this reaction can continue to occur as long as any DHA and fad it's on oxygen are all present. The reason this this reaction doesn't occur in an in an aerobic conditions is because you won't have oxygen in anaerobic conditions. And oxygen is the final accepting of electrons. So if you don't have oxygen than you have nothing to accept the electrons, it can actually across the mitochondrial member and without the assistance of a shuttle. So what these do is they basically assist the movement of any th into the micro chondral matrix and into the intramembrane space. So we have two main shuttles. Um, you have two main settles that you have to be aware of. First, you have your mallet aspartate shuttles. So this one is, um, slower. But it is more efficient. And the reason for that is because your any DHA is going to be recycled now. What I mean by that is, firstly, you don't need to know the steps of the shuttle. I've just put this here to sort of age my explanation. What happens is you get your ADH from your T c a cycle and that's going to move across all these different steps and then finally your NADH is going to form any D plus on that any plus is going to be recycled. And it's going to go back into the PCA cycle to be reduced again to form an ADH, and that any day age is going to power the shuttle again. So so the mileage aspartate shuttle is more efficient because it basically reuses the NADH molecule. But it is slower because it has to wait for the any th perform any D plus. Where is. On the other hand, we have our glycerol to be phosphate shuttle, which is less efficient because it doesn't have this recycling, reckon is, um, But it's a lot faster because, as you can see, it has a lot fewer steps than the mallet aspartate shuttle on it. Also, um, it doesn't have to wait for the NADH molecule to be recycled, which is why it's a lot faster. Finally, I think this is a question that comes up that comes up a lot in the exams, which is why is the actual yield of ATP lower than the theoretical healed off 38 now, the reason for that is I'm just gonna go back to the slide. What happens is your intramembrane space is actually quite leaky. So what happens is before they hide. So as soon as your hydrogen ion Zerhouni Iran concentration in the intramembrane space, we have that concentration. Radiant. Right. But some of these hydrogen ion is don't actually go to the 80 Pecent days. They sort of just leak through into the mitochondrial matrix. And that's going to reduce the concentration radiant. Which is why it's going to reduce the amount of ATP that's actually produced. Um, it ultimate counts for things like energy losses and losses of other molecules. And I'll, which is why the actual yield of ATP is not always 38. So I hope that's made sense for you guys. Um, and this is our final s p S o adjusting. If you could just launched the pool, please, someone's ask me to repeat the part of the ATP. I'll repeat that right after the question is been answered. Yeah, so let's get as many people answering. This is possible. We can't see who's answering what so we can see if you've answered it right or wrong. So don't be. Don't be worried about that. Amazing. So I think the majority of you guys have got the right answer. I think I'll end the pole there, So yeah, the right at once there there would be see Lewisville three phosphate. And the reason for that is because she used to be sprinting. So she needs thief ass test shuttle to sort of prettiest 18, the fastest way possible. And if you remember from the previous slide, your cholesterol, the phosphate shuttle is faster than your um then you're married aspartate shuttle. So that's the reason why I GTP or glycerol to fall. So it would be the right answer here. Amazing. So just been where I end. I think someone asked me to go over the CT p um, the Y The actual yield is lower than the theoretical yield. Um, and the reason for that is because basically, what happens is sorry. Wrong slide. I'll just go back to the previous slide. Um, so what happens is the one actually drives the conversion of 80 pizza. ATP is the movement of hydrogen ion is through the ATP Sendai's molecule Sorry through the eighties. And there's transporter. So the thing is, your membrane is actually quite leaky. So something started and I don't don't even flow through the eighties and things. They'll just flow around it and they'll just move down its concentration radiant on. Since not a lot of them are flowing through the ATP. Sendai's not a lot of ATP is gonna be converted. The ATP, Which is why your actual yield of ATP is lower than the theoretical yield. I hope that made sense. Um, I think the feedback link has been released. I'll just release it again. Um, yes. So that is the end of my talk. I'm sorry if it was a little fast paced. I kind of just wanted to get through because I understand PCs is so busy, your day is gonna be so busy. So you kind of just want to go home. And you just want to, like, relax. So I hope this has been really useful for you guys. Um, please do fill in the feedback form so we can know what to improve on. And you can get access to the slides on the recording, So yeah. Thank you, guys. So much for attending