 Okay. This is a picture of a normal human brain. When blood flow gets cut off because of a blood clot or a tear in a blood vessel, then brain cells die within hours, and that's what we call a stroke. And you can think of a stroke as something like an earthquake. It happens unexpectedly, and the devastation that it causes is really dependent not just on its size, but also its location and what it's destroying. And stroke is unfortunately very devastating. It's actually the number two cause of death in the world today, and it's the number one cause of serious long-term disability, and the number two cause of dementia. And as you can see from the darker colors on this map, there's an even greater burden in less developed countries. And unfortunately, although we have hundreds of clinical trials, they all failed, and we have no treatments that are proven to help people after they've been disabled by a stroke. This contributing to this black hole has been relative underfunding of stroke research and poor communication between scientists at the bench and clinicians at the bedside. And this together has engendered a sense of hopelessness on the part of scientists, funding agencies, and pharmaceutical companies. However, we at Stanford feel like this is too important of a problem to give up on. There's an urgent need to take people who are in wheelchairs or in bed or unable to speak and get them to a point where they can function again, enjoy life, and contribute to society. So what are we doing about it? Well, first of all, we're concentrating instead of bringing dead things back to life, we are concentrating on how the brain rebuilds itself, how does it build new circuits, and why and when does it fail or stop doing that. Second, as if you would need, if you were going to build a new bridge after an earthquake, we've assembled people with a wide range of expertise. As part of our team, we have 34 Stanford faculty from basic science, clinical science, engineering, and social sciences. And we're doing many things, I'm going to tell you about some of them. One of our primary goals is to replace the old yardstick measures that we use now with newer sophisticated techniques that we can use not just to look at recovery, but see how does it work and manipulate it later. So one is Dr. Etkin's tool he was just talking to you about. We stimulate the brain and map the circuits, and so we can look and see how they change as people recover or fail to recover from stroke and make inferences about how it works. In parallel, our engineers are making new devices that can really precisely measure movement and sensation as people are recovering, and they do this in the laboratory. But we're also making novel Bluetooth-enabled devices to study how people recover at home or in a rehab hospital, wherever they happen to be. And then finally, our engineers are helping us to improve translation from animal models to human models. This is a wirelessly powered microimplant that we are developing to put in mice to measure how, when they recover from a stroke, it's different or similar to how a person recovers from a stroke. And we're also testing therapies in mice. This is a picture of something called a composite polymer, and it is engineered by our bioengineers to have two in the two different areas to have two different substances it releases at different time points. The idea is to mimic the beneficial effects of stem cells, but in a very reproducible and hopefully eventually cheaper fashion. Then finally, we've been studying how the brain clears away dead tissue. So we've learned that this may actually explain why stroke causes so much dementia later in life. We've discovered that sometimes when the immune system comes in to clear away dead tissue, it can stay too long and be too active. And this is a picture of a stroke in a mouse brain seven weeks after the stroke, the little brown dots are each immune cells that have come in as part of the response to clear away dead tissue. But when they stay too long, the mouse develops memory problems. And we know that these cells are actually the cause, because when we treat mice with a drug five days after stroke that prevents the large majority of the cells from getting in the brain, then the mice, when the cells don't come in, they don't develop memory problems. So this is fairly new information, and we're just starting to look in people to see if a similar phenomenon happens in people. And this is actually a picture of the brain of somebody who died, who had stroke and dementia, and you can see the same type of immune cells, the brown dots, are present in this person's brain as well. So we're very hopeful that the mouse therapy we've developed will translate to people and that it will join a list of therapies that we as a group hope to produce to fill that black hole in our list of stroke therapies. Thank you.