 So, did you know that sepsis account for 20% of all causes of death worldwide? Well, sepsis or blood poisoning is caused by a systemic infection. And you might wonder, since we do have antibiotics, why can't we treat these patients? Well, it is actually not the infection that kills these patients, but it is an uncontrolled activation of the immune response that does. So, I would like to have a better understanding of what is happening during sepsis, which potentially could give us new treatment targets. So, what I did during my PhD, I induced sepsis by injection of an E. coli that has the ability to produce lyre. And lyre is a protein that can penetrate the membrane of other cells. This causes release of ATP, which can then activate other cells. It can do it by activating of the receptors, one of which is the P2Y2 receptor. So, since we know that lyre has the ability to activate the P2Y2 receptor, we did wonder, could this receptor have anything to do with deceptic symptoms? And I have also shown in a previous study that the ability to produce lyre correlates with the amount of septic symptoms and mortality rates. So, I did this setup again, but this time I'm doing it in two types of mice. One having this receptor and one lacking it. And one that did see was that mice that lack this receptor has a higher survival probability compared to mice having it. It means that they live longer. I did this setup again, but this time I draw a plot from these mice. I assessed parameters which we also are able to look into in septic patients. And this time I saw when I counted the platelets that the mice that lack this receptor has a less pronounced drop in platelets. Meaning, when I'm comparing healthy mice to septic mice, there was a smaller difference in these two compared to the mice having this receptor. So, based on that, we conclude that the septic symptoms and mortality rates depend on the P2Y2 receptor. So now, I want to have an even better understanding of what is happening during septic. I want to know where are the platelets going and can we take any advantages of this. And that would probably be what I'm trying to do for the rest of my PhD. Thank you.