We're a lab that does volume EM, structural work, to say how do platelets activate, how do they aggregate? How do they form a thrombus that causes bleeding cessation and how in the case of over stimulation, they bring about occlusive clotting. In doing this, the premise is that if we know the structure, we can then better target drugs and bring about better outcomes.
We use mouse models in our research, as many researchers do, and we all have the challenge of establishing how our findings in mice and in our case in the arteries and veins in mice, carry over to the mechanisms in the much larger arteries and veins in humans. We all hope that the principles are the same in mice and humans. If you take our work and using volume EM approaches, the big things that we've contributed are one, to say that platelets are not just suicide bombers.
They retain granules. They do things in response to signaling. They have stable states, and these stable states are part of a normal thrombus and they're also part of an inclusive clot.
Two, we've brought the sense that there is really structure to the thrombus that forms, it's not just simply a pile of bricks, but rather it's an ordered structure in which platelets are ordered with respect to their activation, et cetera. And three, we've brought the sense that one should be able to apply and understand from structure what needs to be either stimulated to get a good outcome or what needs to be suppressed to give a outcome that will protect people from bad outcomes. We collect sequential images at near nanometer scale of a near millimeter distances.
We assemble those into the single montaged image. Hence, we can observe any given spot within the image at a scale of near nanometers to near millimeter, which is sufficient to place individual features inside of the whole thrombus. Researchers now have a powerful tool, and they can ask the new question, how do coagulation cascades and cellular signals or drugs act spatially at local to global levels in thrombi?