Hello, I'm Terence McNally, listening to Disruptive the Podcast from Harvard's Peace Institute for Biologically Inspired Engineering. The mission of the vase is to transform healthcare, industry, and the environment by emulating the way nature builds. Our bodies and all living systems accomplish tasks far more sophisticated and dynamic than any entity yet designed by humans by emulating nature's principles for self-organizing and self-regulating. These researchers develop innovative engineering solutions for healthcare, energy, architects, robotics, and manufacturing.
They focus on technology development and its translation into products and therapies that will have an impact on the world in which we live. So the vase is not interested in making incremental improvements to existing materials and devices, but in shifting paradigms. In this episode of Disruptive, we will focus on confronting sepsis. Sepsis is a bloodstream infection in which the body's organs become inflamed and susceptible to failure.
The leading cause of hospital deaths, sepsis kills at least 8 million people worldwide each year. It can be caused by six species of fungi and 1,400 species of bacteria. Diagnosis takes two to five days, and every hour you wait can increase the risk of death by five to nine percent. The treatment challenge grows more complex as the prevalence of drug-resistant bacteria increases while the development of new antibiotics lacks.
Even with the best current treatments, sepsis patients are dying in intensive care units at least 30 percent of the time, says one of today's guests, the senior staff scientist Mike Super, a new device developed by a team at Vees, and inspired by the human spleen may radically transform the way we treat sepsis. Their blood cleansing approach can be administered quickly, even without identifying the infectious agent. In animal studies, treatment with this device reduced the number of targeted pathogens and toxins circulating in the bloodstream by more than 99 percent. Although we focus here on treatment of sepsis, the same technology could in the future be used for other applications, including removing microbial contaminants from circulating water, food, or pharmaceutical products.
Now, let's explore the development process with Mike Super and Vees founding director Don Inger. Inger leads the biomimetic microsystems platform at Vees, in which microfabrication techniques from the computer industry are used to build functional circuits with living cells as components. He's authored more than 400 publications and over 100 patents. The seeds of Vees' therapeutic sepsis device go back over 20 years.
I asked Don to talk about some of the earlier explorations and findings that laid the foundations for the current work. I was interested in mechanics and biology. This idea that mechanical forces are as important as chemicals and genes and that the shape of the cells is important. To get at testing that, I come up with the idea of using little magnetic particles that I would coat with molecules that would bind to specific receptors on cells.
I had developed this technology with getting very specific interactions between magnetic beads and cells. So we had ways to pull on cells to collect cells to move cells. Many labs have used that for diagnostic purposes. In the early 90s, working with chemistry professor George Whitesides, later a Vees founding core faculty member, Inger imported the use of photolithographic microfabrication from microchip construction to cell biology.
That now got me into this world of microfabrication and cell biology. I think that was the first time I think those two fields really connected in a big way. I think that was a major opening of a spigot that's become on firehose. Whitesides group later developed what they called microfluidic channels with tiny inlets and outlets.
Very interesting thing about it is that if you put, let's say, a red dye in one inlet and a blue dye in the other inlet, when they join in the bigger river, they don't mix and they go pass out the outlets and they don't mix. That's because turbulence, which you'll learn about in high school, like you see, you know, smoke mixing in the air is a function of radius. If you have a very small radius less than about a millimeter, there's no mixing. It's called laminar flow.
So that, George and others, have used to miniaturize all kinds of instrumentation and big things the size of a refrigerator and now the size of an iPhone and toaster and use for analytic labs and diagnostics. But I have a medical background and I thought, this is really interesting. You have two things moving by and they don't mix. Well, what if you had blood mixing by sterile saline in like a dialysis type of a format?
What could you pull out of blood? That would be cool. And how would you pull it out of blood while I had these magnetic beads and I know if I had magnets, I could pull things. So what if we could have magnetic beads bind to things and pull them out and I thought what would be useful to pull out?
And I thought of sepsis and I started to talk to clinicians and basically it was very interesting. The medical clinicians said, no, that's not sepsis. It's an inflammatory cascade. That's what kills patients.
And all of them were working on modulators or inhibitors of the inflammatory cascade. The surgeons said, this is a great idea. I'll test them to patients because they're just like, can do cowboys. And they said, actually, one of them said, I had a small child and everything was failing and we did a complete blood transfusion and actually saved the patient.
And I think it's because we got rid of the toxins in the bug. So here's critics, 99% of the medical people because that's who fund sepsis and reviews grant. I went to medical school. I saw patients.
Some of them get better just with antibiotics. Well, that means that what triggers the inflammatory cascade? It's the bug and the toxins it releases. So it's got to help to get rid of the source because it's all in equilibrium.
One of the amazing things about medicine people don't realize and everything biology is all tipping points. So in medical school, you learn if you think a patient has urinary tract infection, you do a urinalysis. If you do urinalysis and you count the number of bugs, if you have 100,000 bugs, you treat that as a patient. If you have 99,999, you send them home and you watch.
Because empirically, experientially, we know that if about 100,000, it's going to propagate, not if your body will bring it under control. Well, to me, that must be what sepsis is like, except you have these bugs proliferating more and more toxins you're fighting and if you can get rid of them, it's got to help. And it's not just the live bugs, right? It's also the debris of the ones the body has already killed.
When the bugs die, they release toxins. The toxins are often cell wall molecules. So yeah, so this is another key point, which is that the reason that the clinical people say it's not important is that their blood cultures are almost always negative. So I think they thought, again, no questioning or their assumptions.
They thought there are no bugs in the blood culture. So the bugs must have started the cascade and now they're not really there. They're not relevant anymore. They're not relevant anymore.
It's like 70 to 80% of blood cultures are negative. So they treat blindly, which is one reason why people die. But that was hard for me to believe. And the more you learned about it, the more you realize that even if your body's killing the bugs, they release these toxins.
And the toxins are what trigger the cascades. I got some funding to explore this. And we use these little microfluid devices and in fact we could pull bugs out with magnetic beads if we put antibodies to the known bug on it. And then we even put human blood through and we could pull bugs out of human blood.
And this little device, the problem was incredibly slow, be incredibly low volume. See, the device with that laminar flow, if we were off at all in the flow rates, we would dilute the blood or lose blood, so it was not very robust. And then finally, I know this clinically, when a patient comes in with sepsis, 80% of blood culture are negative. You don't know what the bug is.
I can't use an antibody against it. So we had to think of something that would capture the bug without knowing what it is. And this is really where the key technology enablers. Now, I being trained in medicine know that there are things in your blood called opsinins that are part of your primitive immune system, your innate immune system.
And the nature has evolved before antibodies to capture bugs. Now, I didn't know much about it, but I did write that on my grant and said, if this worked, that's how we get over that problem in the future. Now we're getting close to around 2008, 2009, which is when I started the VS Institute. And so I had this little project going, but I knew that it really wasn't going to go anywhere unless we could get around the efficiency and the flow problems.
In other words, you had the principles working. I think it was there. But they weren't working in a way that would actually be useful. It's not be translatable, exactly.
So when we did the VS Institute, it really needed to be an institute that focuses from fundamental to translation. And the translation was the most novel thing that isn't not normally done in academia. To do that, I set out to hire people from industry with had 10, 20 or more years in product development experience and integrating with students, fellows, postdocs, and so forth. One of the first hires was Mike Super, who had been in the infectious disease field and then worked in monoclonal antibody therapeutics for drug companies.
Mike Super grew up in South Africa and then in Namibia, which was then called Southwest Africa and got a PhD in medical immunology at the Institute of Child Health University of London. In my PhD work, which was at Great Ormond Street Children's Hospital, I took on a group of children who had what they called non-specific childhood infections in the first 18th century or 18 months of life. They had otitis media, they had fungal infections, they had bacterial infections, and then they seemed to get better. So for my thesis, the purpose was to find out what was missing in these children and to find out if eventually one could come up with a therapeutic application to help these children.
The thought was that there was something that was wrong with their complement system. Complement is a very ancient part of the immune system. And we knew this because we could treat the blood, we could heat it, we could do things like that, and we could actually show that this protein, we thought, in the blood was sensitive to, let's say, 56 degrees heat inactivation, whereas an antibody could withstand that. So we knew it wasn't an antibody.
So to cut a long, long story short, what I found was that these kids were missing this protein, which we later called Manos binding lectin. Manos binding lectin, or MBL, binds to sugars on the surface of pathogens. And it's also involved in the activation of complement and clotting. I was invited to Harvard Med School to do a postdoc based on the Manos binding lectin work that I had done in London.
And unfortunately, Harvard wouldn't get me a green card. And so I had to go to industry. And that actually was a very good switch in that I learned certain things that are necessary in which I use day to day now. Mike Supers spent 17 years in the biotechnology industry in companies ranging from startups to large pharma.
His industry work focused on the design, development, and production of therapeutic antibodies for cancer and autoimmune disease therapy. I asked why he decided to leave industry. I decided to leave because industry was getting very, very restrictive. I had worked in biotech where essentially I had five to ten different hats.
One moment I was talking to the FDA, the next moment I was traveling the world looking at production sites. The next time I was talking to the protein engineering group or the molecular biology group and really had a broad reach and enjoyed that very much. But as my company got bought by larger and larger companies, my role got smaller and smaller. So at the end, they just wanted me making monoclonal antibodies again.
And I didn't sit here. Let's put it that way. And then the offer of the beast came along. And this was transformative to me to hear about something that was in Harvard.
But with access to that tremendous brain power of Harvard, but wanted people like me who had a track record in industry who had actually led teams. And so this fitted very nicely because the idea of taking a well-developed project from academia and move that quickly forwards as to something that could be presented to the FDA really appealed to me. I've read before. You said you were also finding that industry was getting risk-averse.
So when I was in biotech, we weren't risk-averse. We had to take risks. The whole field is not risk-averse. But as my company got acquired by larger and larger pharmaceutical companies, that's when the risk aversion became very clear to me.
How did you get involved with the sepsis project? Donning the sent-around an email that said, I've been writing my grants and all the time I talk about an obstinine that could be used to bind pathogens. The proteins which are obstinins will bind to a pathogen and will tell the immune system, oh, he has a foreigner. Let's attack him.
Let's clear him out of here. Now, antibodies are obstinins. MBL is an obstinine, right? Antibodies are different in that they bind to a specific target.
What Don was asking for is something where you didn't have to know what the pathogen is before you started to remove it. Okay. By end. And I wrote back and I said, well, Don, I did my thesis on manos binding lectin.
I think that we can use that to address your question. Inberg explains how in a human body, MBL works with the spleen. So normally, it's in your blood. It will bind to things like microbes over 90 different pathogens and toxins.
What happens is they bind and then because other parts of the molecule are exposed, when it passes through the spleen, and the spleen is this incredibly vascularized organ that literally has sinusoids where it's kind of trickles slowly just like a marshland can filter water because it slows and has huge surface area on the reeds. Your spleen does the same thing. It slows and has huge surface area on the blood vessels and slits in the blood vessels and macrophages that they capture this complement MBL bound bug and then they engulf and kill it. Okay.
So that's how you normally clear. And when we were doing studies, we actually tried this device in a rabbit and we gave it a huge amount of pathogen of fungus. And we could never detect it in the blood. And when we stained the spleen, it went all in the spleen.
The spleen is incredibly efficient. It's just that when you get infected, you overcome that balance. But Mike Super wasn't satisfied with MBL as it naturally occurs in the body. What I then did was to take what I had learned in academia and what I'd learned in industry and put them together.
What do I mean? I made a fusion protein, an FC MBL fusion protein that had the capability of binding that MBL has. So it binds to many different pathogens. But it also has the high level of expression, the ease of purification of the FC protein.
We made a fusion protein of that. We managed to put that on magnetic beads and on other surfaces. And we have shown very nicely that that binds and captures pathogens from many different media. The first thing to do was then to see, did it bind to all these pathogens, that normal wild type MBL bound.
So we set up what has turned out to be the largest collection of pathogens in private collection. And we have been testing systematically to make sure that the FC MBL binds to all of them. That's one point. A second point was when I was working in industry with therapeutic monoclonal antibodies, I was actually often making something called immunofusions.
I was fusing a cytokine to the antibody. And I was trying to use this in cancer therapy. The problem that I found is that the standard of care for cancer therapy and our new therapy worked against each other. How so?
The standard of care was to do chemotherapy, which turned out kills the immune system. So if I added an immune stimulating therapy, at the same time as I just killed off the immune system, that wasn't going to go anywhere. Interestingly enough, immunotherapy is becoming the big deal in cancer, as you know. Right.
Now, a bit late. But a little bit late. Maybe I was a bit ahead of the curve. Or an opportunity for your next project.
Very good point. So what we found that's very encouraging with FC MBL is that treatment with antibiotic actually sensitizes gram-negative bacteria for binding of the FC MBL. So how does that come into play? That means the standard of care that they are giving at a hospital is actually helping our dialysis machine take out the pathogen.
But that was just step one. Don Inger picks up the story. So he bought some and it worked really well. But then, being somebody like Mike, who's a development guy, he had a team of people, they took it, they genetically engineered it because there could be problems.
There are parts of the molecule that induce blood clotting. There are parts that induce, I think, complement fixation, which is part of the inflammatory cascade. We wanted to retain the binding function, but we wanted to remove completely complement activation and coagulation activation. So this is where engineering comes in, biologically-inspired engineering is being inspired by the way nature builds.
Then we want to take the best technologies we have for, you know, man-made approaches in engineering and science to now do it even better for our purpose. So yes, so he took out the bad parts, kept in the good, put a bit of a molecule from an antibody at the bottom because in the pharmaceutical industry they learned that that makes it incredibly easy to isolate it, purify it so you can make large amounts of it cheaply. It also stabilizes it if you ever want to inject it in blood. So there again is where that translation approach.
You would never have done that in academia, but when you're thinking translation you pick and choose and do what will move things forward the most. And the fastest. So he basically made that. We tested it and worked incredibly well.
And about this time DARPA, which is the Defense Advanced Research Project Agency, the part of the Department of Defense that is tasked with keeping America ahead technologically by 30 to 50 years for the defense of the United States. And this means economic defense, medical defense, everything. They put out a grant opportunity that used my papers and my review articles, pictures, my device as a paradigm and basically said we need to have dialysis like therapeutic devices for sepsis because our soldiers in Afghanistan, Iraq were discovering that they're getting injured but then they're getting infected and they're dying of sepsis. And also we used to think we have to fly them home to be dialized to go into intensive care.
But now we have these little portable devices. You can do it by the bedside at this site. And so they want to have things that would integrate into dialysis units that would be able to cleanse their blood. And they also want us to do it without use of anticoagulants because injured soldiers can't be anticoagulant.
They bleed out while they're on these machines. I ask how they solve the problem of keeping the dialysis moving without anticoagulants. Joanna Eisenberg at the V's in another platform for non-medical purposes, literally to prevent ice from sticking airplanes. We used to develop something called slips, which is inspired by a picture of plant in Africa.
It can have insects walk over it when it's dry but when it's wet, they just slip and slide and fall into it like a black hole and it eats it, like a Venus fly drive. It's kind of amazing. And I realized that was due to surface texture and topography and then with a liquid held on by capillary action, she made artificial substrates by using micro manufacturing to etch substrates and then put liquid oils on it that were biocapatible and she could prevent anything from sticking. And that was commercialized in a company called Slips Technology.
I was aware of this and had this grand opportunity. And actually was speaking at a meeting on architecture, Ben Hatton, who was working with Joanna was there. And I said, you know, do you think we could use your slips for preventing blood from sticking and we went back and tried it and it worked? Mike Super.
I'm not saying that we prevent a clotting. I'm saying that we prevented clotting from sticking to the surface. Now, this is a big deal in medicine because you don't want clots to form in artificial valves. You don't want clots to form in dialysis.
There are many, many places where clot formation is terrible but also it has been shown that clots form and bacteria clump in the same place. And what we've been able to show with the slippery surface is that bacteria fungi et cetera do not stick to this. So we have done hours in vivo and weeks in vitro in the lab. In other words, to show that we can have very high levels of bacteria, a sticky bacteria like pseudomonas, which is not sticking to the surface.
Inber tells me, these got the DARPA grant and exceeded everyone's expectations. We hit four-year milestones in nine months largely because we had this team of guys from industry who knew what milestones were and how to bring full force to bear. Whereas academia, graduate, and spousal stocks, they get a little derailed. You have to let them follow the paths as you should.
But by this mixed model, it really worked incredibly well. And to the mix, the FDA. FDA, as being a partner, we talked through a lot of issues about if you want to bring this to the clinic, what are the challenges you're going to face? And the challenges you're going to face, nothing in a translational site is you've got a biological molecule that's engineered MBLO.
It's a natural protein, that's okay. But then you have magnetic beads, that's a danger. What happens if a clot's a vessel gets out? Then you have this flow system in all the surface contact area.
So can you simplify it? It's simplicity and impact. And so can you make it simpler, simpler, simpler. And so in this case, we decided, it's a dialysis like their pigg.
Why don't we just put it on a dialysis cartridge? And it works incredibly well. And so that would be a paper's in review, but we're already in pigs. And we're about hopefully to do a startup very soon called Opsonics.
Opsonics is what MBL is what Opsonics that will bring this through the large animal testing to get to humans. So to overcome the projects and heron obstacles, others that emerge in the translation process and steal more in response to input from DARPA and the FDA. They're now testing the device with large animals. Because we basically want to use a human-sized dialysis machine and a human-sized filter with the FCMBL protein, and to check this in a large animal model of sepsis, unfortunately, for the animal that is, we have to make it sick, but fortunately for the animal we then cure it.
Don Invers says the beginning to see some promising results with pigs. They're still early, but we have a lot of success in rats. The other thing that's interesting in rats, we've shown that it synergizes with antibiotics. So if you use an antibiotic, you actually kill the bugs, but you release the toxins.
Because we capture both the bugs and the toxins, when we release the toxins, we capture both. Now, the other exciting thing is that I told you 70 to 80 percent of patients have negative blood cultures. And what that means is you've done a blood sample of the patient that's waited for it to culture all that time, and now it doesn't tell you anything. So there's a couple of things there.
You mentioned earlier that mortality rate can increase 5 to 9 percent every hour you run the wrong antibiotic. And they just give you a broad spectrum antibiotic when you've come in because they don't know. And 80 percent, they never know. So they just keep trying things to see if it works and it often doesn't.
But even if you have a positive blood culture, it can take two to seven days. So every day with that kind of mortality rate. So we found that because we're pulling out live in bed, if we just measure MBL binding material in blood, we've now done a large number of patients in a study in the lab with human patients from emergency rooms. Now, it looks like we can detect a very high percentage of those.
We can't yet tell you what the bug is, but we can say yes, you have sepsis. Now, for our device, what's valuable again for going to clinical trials is it's very powerful to increase the likelihood of success of a therapeutic, whether a device or a drug, to have what's called a companion diagnostic, which means make sure that this patient you think really will benefit from your therapy and that show that when your therapy is working at scales with what you thought was causing it. So if this ever goes to clinical trials, which we hope, if we have a diagnostic, we could say, well, here are 10 patients, but we don't detect this, these MBL binding materials in these two, but these eight, we do. So let's test those because we think we'd help and then we could follow it and we say, oh, it's high and now we try it to treat it and now it's going down, down, down.
Now we can stop there. Like you don't know when to stop there. And then you can see if it comes back and then we should need to start there. So that's how we're thinking about it right now is as a companion diagnostic.
So the future could be used in any lab to basically determine whether, you know, there really is sepsis and this patient should move to the intensive care unit to be watched and really be tried with antibiotics or go home. And that's a big problem. And clinically, as you see a patient, they're old. Sometimes they don't get a fever.
They don't really express the way a young person does if they're sick and things go very quickly. I think it has real value. And so just to bring it up to today, what are the next steps, the next developments and kind of the timeline you're looking at? For you to move towards clinical trials, you have to show safety in an appropriate animal model and some degree of efficacy.
But you also have to be able to manufacture materials that are quality controlled that would be appropriate for clinical use. So that's something we are starting to do and we need to really form a company to get that done right. So that's one thing that's being done. The other is developing an animal model for sepsis, which believe it or not, really are not any good animal models.
So that's one thing we have done with a pig model. We have a pretty good model of sepsis where they have clinical signs that look like in patients. And then this diagnostic similarly get it in a form that's robust that can be mass manufactured so that if it works, it can then go out clinically. All that requires a different know-how dollars, big dollars, but also, you know, people have regulatory experience, people who know how to do manufacturing.
I ask Mike super, if everything goes well, how soon might human clinical trials start? Usually we're talking about two years from now. And as you say, in some ways this process started in 2006. Yes.
So we're talking 2017. Yeah, well. And things with things with Quaker and Vees that are still 11 years. Yes, I know.
But let me push you back on that because Don's ideas on the microfluidic in 2006 and my ideas on MBL, which were also way back, we're working in isolation. That's right. But from the start of the project at the Vees, we're talking less than four years from then, from the start of the project in August 2011, until now. And then plus two.
And plus two. Now that is incredibly fast. I want to know. Does he have visions of the future, of how things might be different or better because of the work he and his colleagues are doing?
I hope so. I mean, one of the things that we are also working on is being a guinea pig with the FDA. Why? What do I mean by that?
I mean that they are very interested in other examples of coming into a project early to see how to transition that through the FDA. For example, here we have a protein on a device. Which department of FDA does that though? Is it devices?
Is it CDA? Is it CBAs? How do you deal with that? And this could get lost in the weeds.
So having good advice, hopefully in examples like this where there are huge unmet clinical needs like sepsis will allow us and the FDA to work together to getting drugs and devices approved much more quickly, go smoothly through this difficult process where you still have absolutely their requirement and hours of safety for the final treatment, for the final device, for the patient. But at the same time find a way to do this in an interactive collaborative even way to speed this up. As super and I discussed, some of the discoveries, the research, the academic papers go back years. I asked Don Inger how the V-S model accelerates their coming to fruition.
Call it a technology translation engine. Measures of success in our original founding included IP portfolio patents and we're up to a thousand patents after six years. Corporate alliances, licensing agreements and new startups and having your term impact because you can't have your term impact. Academics don't produce products.
You have to develop a seamless interface with the industrial world. Now we did that partly by bringing in technical expertise with Product Development. We have a program called Institute Projects where essentially we use a very organic approach. So people often say how do you decide what to fund and what to kill.
And we don't. We use self-assembly and self-organizing principles of biological principle which is basically if you have faculty and students and fellows come up with an exciting technology to them and then they start interacting with these guys from industry and the guys from industry will either say it's already been done. I've heard of a technology that's about to come out. No one's ever heard about but it does it better or they can say that is really exciting.
It's not to say it's really exciting and we start submitting intellectual property patents and lawyers who look in the outside will say this is novel. You can really, this is unique. Then we put more investment and we call it what we call platform projects. Now if we start talking to industry, why do we talk to industry?
Because they know what the real challenges are. They know what the competition is. They know what has been done before. They know the regulations.
They have nothing to do with technology. Some people say that the success of the startup is only contributed about 10% by the technology which academics don't get. It really you got to get good management and regulatory and marketing and business manufacturing and so we actually bring entrepreneurs and residents in when we get feedback from industry and venture capitalists and so on. It's really exciting.
We want to see more de-risking more importantly commercially. Right. That's one thing that I would imagine is one of the real distinctions of these. Others will de-risk scientifically or de-risk academically.
You want to de-risk commercially so that you can hand it off. So that is the value of death that everyone talks about. Which is how this great technology but basically the investors won't take risks. They want to validate it.
So how do you get over that? So we get over that by wondering if people like Mike Zupur do the technological de-risking. But then when we really see we think this is really exciting. We have strong intellectual property or patents.
We have strong interests but they want to see it de-risk. And we get the same message. We triangulate it and we get the same message. We need to do this, this, and this from all these different groups.
Then we'll move into what we call an institute project where we form a triad with the faculty inventor, in this case with me, with a member of our staff with industrial experience who's the technology lead which in this case is Mike Zupur. And then we'll either use one of our internal business development people who've been in the outside world as entrepreneurs or we will recruit an entrepreneur in a business that has experience and is excited and we think could bring it all the way who will be our interface with the outside world and understand what they're talking about when we sometimes don't. And that was Eric Devere on this project. And that it takes time but you are constantly iterating in the process and that has been quite successful and we're very close to closing on a startup that will be very focused on commercializing a sepsis therapeutic with a diagnostic as a companion diagnostic.
How many of these institutes platforms and how many of its novel technologies does this one effort draw on? It involves my platform by my micro systems which started from the flow and the bioswink concept. Mike Zupur is now in my platform. He actually started in what was called biomaterials evolution where we're going to do protein engineering.
We're not able to protein engineering group but as this project grew and that platform moved more towards genome engineering and synthetic biology he joined my platform and then joined his platform on the anesthetic surfaces called adaptive materials technologies. We're now collaborating with the anticipatory medical and cellular device platform. They developed a way to diagnose Ebola with literally engineer the gene circuits in microbes and then break the microbes open and put all the chemicals on a piece of paper and dry it and then add water and they could get programmable activities and they could program it to sense Ebola very quickly. But the MBL may be a friend and capture agent.
The way technology is developed at the V so I think in all good scientific labs is that there's a natural flow. It's like a blood vessel that branches and branches and branches and so you have creative people and we have a goal but then it's like oh we developed this technology could also be good used for that or that. It's like I developed magnetic beads. I wanted to pull on receptors but hey I have these magnetic beads.
I could use this for other things. What else could I use it for? And it's who's around you that usually not only you can think about hundred ideas but you only pursue ones that you have tools to pursue. It's like you can think of great ideas in your house to build something when you have some free time but you never do it because you don't have the right materials.
And at the V's we have the right materials to do anything because we do medical, non-medical. We do synthetic biology, genome engineering, polymer chemistry, nanotechnology, material science, computer engineering. We just do it so there's someone around to do everything and bring their own creativity to it. You've been listening to Disruptive, Confronting Sepsis.
I'm Terence McNally. My guests have been Don Inger and Mike Super. You can learn more about this sepsis therapeutic device as well as an exciting range of other projects at the V's website, v's.harvard.edu. That's W-Y-S-S dot harvard.edu where you'll find articles, videos, animations and additional podcasts.
If your podcast delivered to you, you can sign up at the V site or on iTunes or SoundCloud.com. My thanks to Seth Crowell and Mary Tolicus of the V's Institute and to JC Swatkin Production and to you, our listeners. I look forward to being with you again soon.