 So there are a couple of really interesting applications here. First of all, again, everybody's cool. If we form too much clot, it's going to be a sad story. And there are situations where people, for whatever health reason, their blood is more likely to clot. Maybe they don't have good circulation, and so their blood tends to pool. Maybe they have varicose veins, so they have a greater volume of space in their, like veins in their lower limbs or whatever. And if there is a greater space, the blood flows through their slower. Blood flow, if blood flow stops, that can stimulate clot formation. That's one of the triggers that the blood goes, oh dude, this isn't good, let's clot. It's not exactly an ideal situation, but that is what happens. So there are a couple of situations where you might want to take an anticoagulant or a blood thinner. So there are a couple of strategies here. One common blood thinner is cumudin. C-O-U-M, I have no idea, D-I-N. Cumudin is a chemical that decreases vitamin K in your blood. So heck in what? How is that related to blood clotting? Look, do you remember? Vitamin K was necessary to build prothrombin. If you have prothrombin in your blood, then you can't make thrombin to activate fibrinogen into fibrin, you're not going to form a clot. Obviously, there are situations where this would be really bad, like you want to be able to clot. And in fact, people who are on cumudin, you have to be careful, you bruise super easy. If you break a blood vessel, it's going to take a while to form a blood clot. That's because you've decreased vitamin K, which has decreased the amount of prothrombin in your plasma. So cumudin is one way. There's another one that's really interesting, this connection, aspirin, aspirin. Aspirin plays a role in blocking an enzyme called cox. In fact, it's known as a cox inhibitor. That's an enzyme named cox. And aspirin comes in and says, sorry, dude, you're not going to do your job. So you probably are thinking, so what? Who cares about this cox enzyme? Why would we even care about that? Well, let me tell you why you care, because the cox enzyme is one of the substances that helps produce thromboxane. And remember this guy, thromboxane A2. And remember what thromboxane A2 did. Number one, it caused vasoconstriction. If you don't have vasoconstriction, you're less likely to have a clot that blocks a blood vessel. Number two, thromboxane A2 activated the platelets. The platelets that are activated play a role in dealing with this pro-coagulant balance and increasing the number of pro-coagulants in the blood and encouraging clot formation. So by blocking platelet activation, aspirin can decrease the likelihood of your blood clotting. So those are a couple of interesting places. Anticoagulants, medical anticoagulants, that you could look at the mechanism for those. You know, anytime you have lots of chemicals involved, you can find a medicine that either blocks one stage in the process or simulates one stage in the process and manipulate the whole thing. The last chunk that we're going to do in this lecture is we're going to do this, hopefully, is reviewed to you from General Biology. But we're going to do a little review of blood typing. So we're going to move away from the whole hemostasis phenomenon and the process of blood clotting. And we're going to look instead at kind of an introduction to the immune system and an introduction through something that hopefully is kind of familiar to you already and that's blood typing. We're going to start out by talking about ABO blood types and look at RH blood types. And I think to do that, we need to talk about antibodies. Antibodies, immune system. So now we're doing our immune system transition. Did you understand that? Oh, that wasn't my off button. That was my blood clot button. This is my off button.