Western Science Speaks
We live science every single day but we take for granted that the world around us and how we think about it is constantly changing. Join Western Science Speaks with host Henry Standage talks with geneticists, astronomers, software developers, evolutionary mathematicians, synthetic chemists, geologists, and a variety of other experts working together to answer humanity's most interesting and important questions, because, behind all the formulas and graphs, sciences is our past, our present, and our future
Miss an episode? Catch up today on our wide range of topics in science, relevant to a broad spectrum of listeners. Our podcast is carried on many streaming sites for you to enjoy at any time!
Click to listen today on your preferred platform:
S4E12: The Next Hubble: The James Webb Space Telescope
One year in advance of the James Webb Space Telescope's official launch, Western Science Speaks is thrilled to be joined by Prof. Els Peeters, for an all-you-need-to-know audio exhibit of the revolutionary telescope that will follow in Hubble's footsteps.
Dr. Anne Simon joins Western Science Speaks to talk about the processes within group behaviour in a variety of animals. Later, Dr. Simon talks about her own research with fruit flies and the impact of experiences on genetic predispositions.
Just in time for Valentine's Day, Amanda Moehring and Geoff Wild join Western Science Speaks to discuss mating, courtship, and everything you need to know about love. Listen for the contest phrase and enter to win through our "Will you be my Valentine?" podcast contest. Contest opens February 10, 2020, and closes at 12:00 pm EST on February 12, 2020. *Contest is now closed*.
Professor Dani Way from the Department of Biology joins the show to discuss her work predicting future climate realities on Earth - and what that means for our plants and trees.
With a population in the millions of trillions, parasites are able to evolve at a faster pace than just about anything on Earth. Beth MacDougall-Shackleton, joins the Western Science Speaks Podcast to discuss some of the innovative mechanisms used by parasites to attach to a host, some of the warning signs of infection across different species, and why we wouldn’t want to completely eradicate parasites from our ecosystem.
Dr. Jan Cami joins the podcast to discuss the origins of life on Earth, the process of finding other Earth-like planets, and the likelihood that we will ever find company out in the Universe.
Dr. Nigel Blamey joins the podcast to discuss the challenges facing the mining industry, what a mass extinction caused by gas would look like, and how oxygen has evolved.
Dr. Desmond Moser joins the podcast to explain how his latest paper, detailing the analysis of meteorites, can explain the history of Earth, and all our neighbours in the solar system.
You're listening to the Western science speaks podcast. Presented by Henry Standage.
Henry Standage 0:28: All right, welcome to the Western Science Speaks Podcast. One of my favorite clichés of science fiction movies is the discovery scene where a character find something supernatural, but has no idea where or what it came from. This week on the podcast we have as close to a real life version of that as you're likely to find, except we're lucky enough to actually know where it came from. Dr. Desmond Moser has been studying Meteor fragments that landed on Earth from Mars. These findings can tell us a lot about the history of the planet, including dispelling some existing notions that the academia community had. He came on to the pod to talk about his findings, take us through the journey that these supernatural artifacts went on to get to Earth. I even got him to give his take on Elon Musk, and his proposed Mars venture. Here we go.
I'm sitting down with Dr. Desmond Moser. It's a beautiful day outside, sometimes when you're with the earth science people, it'll be super ugly outside and it's not as inspiring. It is lovely today. So thanks for coming. I guess by the time this podcast comes out, your work will have been published for a couple months now. But this is kind of the calm before the storm, if you will. So, yeah, so let's hop into it. You look at minerals and you look at them on a large time scale. How is it even possible for us to get our hands on minerals from millions years ago from other places in the solar system.
Desmond Moser 2:03: Okay, yeah, well, there are some minerals that are just naturally long lived and they've got incredible survivor characteristics. And they occur on the rocky planets. Of course, we're not talking about minerals and planets like the gas giants, because they're made of light elements, but for the rocky planets from, you know, basically from the asteroid belt inward with Mars, or Venus etc., there are these minerals that form as some of the first formed phases to condense out of the solar system cloud, when they're pre solar discs first starts out in the sun, it's just forming. So they continue to form through natural processes through you know, volcanic activity throughout the last four and a half billion years, and now so there is just to say that these minerals occur, they're very tiny, but they occur on most of the planets that we have samples from. Now, how do we get those samples that's the other part. That's pretty cool. Of course, we go outside the building here today on campus and, and dig up some sand or, and we would find these minerals, and some of them will be quite old from the Canadian shield washed down here by glaciers, but from other planets we need a piece of the planet's surface to make it here. From the moon, we've got samples that humans have brought back. But by and large, most of the samples we have are in the form of meteorites, so that pieces of other planets, where there's been an energetic event usually a meteorite strike on another planet that knocks pieces out of the escape velocity of that planets gravitational field. And then they start wandering around the space until the earth comes and grabs them.
Henry Standage 4:07: That just seems so absurd to me, what are the odds they would land here? Out of all the places? I mean, I'm sure they're floating around for a while, but it just seems incredible.
Desmond Moser 4:17: Yeah, well, there's actually little bits falling all the time to earth, and there's a steady flux of material going between planets, some planets, of course, the larger planets can attract more, if it's nearby. But it is pretty amazing. I totally agree with you. Some of the facts, some of the pieces of Mars that have been found - there's about 120 or 130 known pieces of Mars that have come to earth in that way. And there's actually been a few falls recently where they've actually been observed. So they've seen a fireball coming into the northern Sahara Desert. And they go the next day, and they find bits of the meteorite, and turns out is from Mars.
Henry Standage 4:57: When it falls to earth, and then it's discovered, what's the process there? So somebody finds it that brings the bring it to a lab, it gets identified. And then is it an antique? Is it put away somewhere safe? How do you as a researcher, get the opportunity to have a look at it?
Desmond Moser 5:16: Yeah, this is a nice case of a win-win between market dynamics and science. So well, a while ago, meteorites started becoming quite collectible. People were interested in them, so they had value and more people wanted them, the more value they had. And historically, a lot of the collecting was done from places like the Antarctic ice caps. Although meteorites were found everywhere, through large government organized expeditions to remote places, but increasingly in the, in the of 80s, 90s more findings were made in the northern part of Africa, in the Sahara, and desert region. And so once it became known as these stones were value, then local people's nomadic peoples would keep an eye out for them. And so now there's been a huge treasure trove of meteorites that are available from collectors, artisanal collectors wandering around the desert, spotting these things with very skilled eyes and bringing them to dealers in places like Morocco, where people from around the world will come to, deal with the collector and make deals with dealers. Now, the other part of your question was, how do we get access to them? So now they're in the hands of the dealers, but it doesn't have true value until it's officially -
Henry Standage 6:43: So the dealers, it's the same thing as saying art collector?
Desmond Moser 6:46: Yeah, exactly. Exactly. Exactly. But if you want to purchase a piece of art, you want to know it's a Rembrandt? So you want to have it authenticated. And so that's where the scientists come in. So there's an international Meteor meteoritic group that will analyze, your meteorite and tell you where it's from, and tell me if it's an asteroid from the moon, and then give it a unique number. And the cost of doing that is that you have to leave a reference slice of the meteorite with the international organization and then sciences can study those pieces. So it becomes part of the scientific community, a small piece of the meteorite. And of course, the more research is done and the more special a meteorite is, the more value it has. The he media collectors are usually very excited to get research and not just for monetary value, a lot of them are genuinely thrilled to have a piece of space, another planet in their possession. So it's a winner.
Henry Standage 7:53: Okay, so let's take it back, when these meteorites are first sent flying through space down to earth. How did they survive and their signature, how are we able to identify them? And how are we able to pair it with a planet, say, this is from Mars.
Desmond Moser 8:13: OK, so the surviving part, it's kind of cool. They'll launch from another planet as a fragment. And if that planet has an atmosphere that will undergo some heating, from the energy of the event that launched them in the first place, and maybe a little bit of friction heating as they leave the planet, then they're, they're basically at Space temperatures, ultra-low temperatures, until they get captured by a planet like Earth, in which case you've seen the fireballs etc. in space. There's that heating of the outer part of the meteorite. Heating is so short, and the speed of diffusion of heat into the meteorite is so slow, because rocks are really good insulators that you only really modify the outer margins of the meteorite, you know, a few millimeters. And so the interior of the meteor, it stays intact. So there is a chance for some partial melting or, you know, some fracturing and things, during that whole process. Although not always, like the piece of Mars that we studied is remarkable in that it has very little, or has been very little affected by that ejection from Mars landing on Earth.
Henry Standage 9:27: Where did the piece you looked at land on earth?
Desmond Moser 9:30: It's also from Northwest Africa.
Henry Standage 9:32: Okay, is there a reason why they tend to fall in that region?
Desmond Moser 9:36: They're falling everywhere, but that's because it's dry, you know these things are not, you know, formed on Earth. They're not stable under water rich environment, so they'll start breaking down.
Henry Standage 9:46: How have people primarily been looking at these minerals in the past? And how did you and your lab look at them differently?
Desmond Moser 9:54: All right, well, we haven't named these minerals yet and there's thousands of different minerals types. People around the world use these minerals on Earth to date events in our history. But what fewer people do, aside from getting an age on these minerals is to look at the micro scale and nanoscale structures within these minerals, in addition to getting their age, and that's what we've done differently with our lab here at Western, you know, developed, assembled some electron microscopy tools, and, together with other groups around the world, used a technique called atom probe microscopy, where we can actually make a 3d image of the atoms and their distribution.
Henry Standage 10:44: What do these structures tell us?
Desmond Moser 10:46: Well, you can imagine with the meteorite impact, there's a lot of force and there's a lot of heat. And those two things, do very specific things and leave very specific signatures within the crystal. Sometimes it scrambles the atoms, sometimes it organizes the atoms into clusters that we don't normally see. So there are all these special micro and nanoscale features that tell us that, oh, this crystal has actually seen a giant impact event of incredible forces that we only see in the interiors of planets for a microsecond. Or from a shock wave, or the intense, you know, thousands of degree Celsius temperatures that the impact energy creates.
Henry Standage 11:32: Is that the photo that you had that you showed me before?
Desmond Moser 11:38: Those photos were up one of those crystals sitting in a rock fragment from Mars
Henry Standage 11:43: There're all these colors which I assume tell you different things about the properties.
Desmond Moser 11:48: Those colors were differences in light at the rate at which the light passes through or the vibrational directions of light going through. I didn't show you some of the these other images of the atoms, they're in our paper. But basically, you would see it would look like a gumdrop with a clump of sugar with all those little tiny sugar particles, the anatomy, and you would see little clusters of certain types of elements. Sometimes they form little strings. Sometimes the crystal itself is, shifted like a deck of cards, so you get a little zones between material within. So all those things we don't know of any other way to form those except by mirror and impacts.
Henry Standage 12:35: Yeah, we're going to have to find a way to post the pictures with this podcast is for listeners. They're awesome. They're pretty cool to see. What did the crystals tell us about the history of the solar system?
Desmond Moser 12:49: Yeah, they can tell us a lot. And they can tell us, as I just described, whether a giant impact had occurred within the vicinity of that crystal when it was a mineral on the inner crust of the planet. There are also other chemical indicators in their isotopic compositions that tell us things like; did that magma that generated that crystal come straight out of the interior of the planet? Or was it recycled near the surface of the planet? The most impressive thing I think, from these crystals, you can tell whether there was an ocean around or not, whether there was liquid water on the planet at the time.
Henry Standage 13:33: That's huge!
Desmond Moser 13:34: Yeah, so you can use it on earth to show that liquid water was was here on Earth at least 4.3 billion years ago. So that was already a huge advance. And what we've seen with these tools and crystals from Mars is that they're actually even older, they're the oldest known minerals like this from a solar system body that we know of from a planet. You can get slightly older from the first asteroids formed, but the planets didn't make it. But for the planets that made it, these are the oldest planetary reocon crystals. And they tell us that actually not much has happened to them since 4.48 billion years ago, we get the age of the crystals, and then we don't see any of these signatures of these giant compartments. So to get to your second point, what does that tell us about anything new about the solar system? There's been a debate raging for 50 years since since the Apollo samples came back about whether the inner solar system suffered this massive bombardement. Long after, 500 million years after the planets originally formed, was there a second bombardment and would it have sterilized any life forms that would have existed at that time? And what the survive of the presence of these little 4.48 billion year old crystals from Mars in near pristine conditions, tell us Is that, no that didn't happen didn't happen on Mars. And if it didn't happen on Mars, then it probably didn't happen on Earth. They called it the late heavy bombardment. But there's been growing evidence calling that into question. And that theory and question and now we think are results supported by the trend that there was no nothing sufficient to rework and rebuild the whole planet.
Henry Standage 15:29: So that squashes any conspiracy that we had life on Mars before Earth.
Desmond Moser 15:37: No, it doesn't actually. Actually that's the purpose of the paper, saying that based on the Martian evidence alone, forget the rest of the solar system, as early as 4.2 billion years ago. Things that cool down and become low impact, could host life as we know it potentially. We can say life is there, and certainly the platform had the right conditions to allow life as we know it to live there 4.2 billion years ago. And then the next part is that extends to the Earth. You know, if we had water then this bombardment didn't occur on Mars, and there's no reason why it would occur just on Earth.
Henry Standage 16:21: Yeah. And we've known for a few years now that there's water on Mars. I remember I think finding that out in elementary school, or maybe early high school, sounds like that could have broken the news if we found out. That was a big one.
Desmond Moser 16:35: Yeah, the water we have on our Mars today is mostly ice and then subsurface because Mars lost its atmosphere. Early on, though, is probably more clement and more habitable than today. Now it's a dry, relatively arid surface, getting bombarded with lots of cosmic rays that destroy organic molecules. In the early days, it would have been a lot more favorable.
Henry Standage 17:04: And I imagine the likelihood of pieces of Mars coming down to Earth is much higher than other planets because Mars is our closest companion. But could say, a piece of Jupiter fall onto Earth?
Desmond Moser 17:21: Probably not, it's made of ice and light elements that probably vaporize before that and other properties. Yeah, you need something with a really high melting temperature and material like that, from one of the large planets is buried so deeply in the interior of the planet. I can't see any surface bombardment, reaching deep enough to get that stuff out.
Henry Standage 17:43: But it is possible that a planet that far away, we're talking really far away when we get past Mars could still fall to Earth. Like if we get a piece of Uranus or Pluto.
Desmond Moser 17:53: I guess when you're getting out there, you're getting to, you know, the Kuiper Belt and you know, it's particles. So yeah, you could get to material. So there are the really primitive meteorites that fall on Earth that come from further out. Another famous one here for Western was the was the one that fell in the Yukon. Tagish Lake, which was a very primitive meteorite with clay particles. And no ice.
Henry Standage 18:24: Do we know where it was from?
Desmond Moser 18:30: Outside of my part of the solar system.
Henry Standage 18:32: True. How has Mars changed as a planet from when these minerals first came to exist? I guess we kind of talked about that a little bit.
Desmond Moser 18:45: Yeah, it has changed. In the early days, Mars would have been more like Earth, and that it had a core, a molten core and a magnetic field. Why does that matter? The magnetic field actually creates an atmosphere that protects the planet from incoming cosmic and solar radiation, the type of stuff that destroys life forms and largely erode an atmosphere. So by having that spinning Molten Core, you actually have this, this force field around the planet that protects the atmosphere and the water and makes it more viable.
Henry Standage 19:28: You seem like a good person to ask - what's your thoughts on Elon Musk wanting to live on Mars?
Desmond Moser 19:40: Well there's a whole bunch of layers to that, you know. I'm planetary geologists, but I'm also an Earth scientist. And I was at one point in charge of the graduate program in environmental sustainability here. I loved the idea of going to a place that's relatively uninhabitable because you will learn something about technology. Same way we learned a lot with the Apollo missions, on the other hand in terms of a mass migration, I think we were just going to mess up another planet.
Henry Standage 20:24: Well, you said Mars hasn't changed that much in the 4.2 billion years, right?
Desmond Moser 20:32: It has changed quite a bit in that it went from this period when it had flowing water. In the early times when they had an atmosphere it was protected for about three and a half billion years, then it started losing his atmosphere started drawing in
Henry Standage 20:45: Right but it's beautiful that it hasn't like changed that much compared to say Earth which we've totally messed up.
Desmond Moser 20:53: Yeah, that all depends on where you're looking at it from. The Earth is is changing a lot. But it's not changing beyond the limits of where it's been in the past. It's not about the earth is about us. After we're gone, the earth will be stabilized.
Henry Standage 21:18: The new year I keep reading everywhere is 2050.
Desmond Moser 21:22: It's pretty scary.
Henry Standage 21:30: Are these pieces of Mars the furthest back we can find conditions supportive of life outside Earth in our solar system?
Desmond Moser 21:42: Probably right now. Yes, the there aren't many ancient fragments of say they're known for age but fragments of the earth left. So the oldest pieces of the earth that we have are these tiny little Zircon crystals. The rocks that they formed from are totally gone. All we have are these little survivors. So we don't have any rock record from this period of, you know, 4.4 to 4.2 billion years. The oldest rock on Earth known is 4.0 billion years. When we get back to other bodies, the moon's rock record has been modified, But certainly there's more old material on the Moon, and Mars is really probably the best place. We haven't been to Venus we haven't, you know, that's an extreme place of mercury as well. Temperatures are getting near the melting temperatures of some rocks. But in terms of Mars, what are the odds that we get a piece of the oldest crust known in the inner solar system, the hundred and 20 or so pieces of Mars that make it to Earth. So, the odds are there's probably a lot more of this stuff up there on on Mars. And this is what we highlighted, the close of the paper, is that if this can be sampled by a relatively recent meteorite impact with Mars, a small one that sent this thing to Earth, It's probably accessible to human missions and rovers.
Henry Standage 23:20: How far back do you think this piece could be from? When do you think it flew off?
Desmond Moser 23:25: Oh, they've actually done that. So once it gets out of the atmosphere or away from the planet, it actually gets bombarded with cosmic rays and changes the meteor chemically so you can date you know, the space and these changes happen so you can actually get a rough age of when it was launched. So it's the estimate is, you know, on the order between five and 20 million years ago, is when the piece that we studied left Mars.
Henry Standage 23:49: So long trip.
Desmond Moser 23:50: Long trip, and then it's probably been on Earth, you know, at most 100,000 years.
Henry Standage 23:57: I thought going from Kingston to London was bad.
That's it for us this week. Hope you enjoyed the interview. As I mentioned, there are some stunning photos from Dr. Moser’s research. If you want to check them out, they'll be on our website, I highly recommend you do. But for now, I'm Henry Standage, signing out. Thanks for tuning in.
Dr. Bryan Neff from the Department of Biology joins the podcast to discuss the rise of sustainable fish farming in Canada, why we’re hesitant to eat genetically modified food, and his research in restoring salmon to Canadian lakes.
Hey, welcome to season four of the Western Science Speaks podcast. We're kicking this season off with an interview with Brian Neff from the Department of Biology here at Western. Brian is one of the smartest fishery researchers we have here in Canada with work scoping from understanding evolution from a gene perspective, all the way to aquaculture sustainability. A lot of people don't know this, but fishing in Canada is going through something of a cultural referendum. On one side, the fish hunters have been doing this for generations. It's built into the fabric of their families. And on the other side, you have fish farming; the more analytically driven, slightly less personable method aimed at creating higher efficiency in aquaculture. Brian and I discussed that at the beginning of the episode and then moved on to a whole bunch of other cool stuff about his research. Here it is.
Let's start with a topic that has become increasingly contentious in recent years: fish farming, replacing fishing as the primary form of aquaculture. Can you take us through the differences in this process?
Bryan Neff 1:42: Sure. So traditionally, most of the fish that we eat or ate came from what's called the capture fisheries. So we went out there and effectively hunted for the fish. They were wild fish, and we would use different techniques. It could be using long lines with hooks, really large nets, or even dragging really large chains across the bottom and collecting all the fish that we stir up. So that's a form of fish for fish. Edit that right, that's a form of fishing and it used to encompass almost 100% of the fish that we ate. And most of that came from the ocean. So it's marine fisheries as opposed to inland freshwater fisheries and the oceans about maybe 25 years ago, were fully tapped, so we were catching every possible fish that could be caught to eat. And it yielded about 100 million tonnes of fish, most of which we would consume. Some of it would be used for other products, dog food, or even feeding other fish. Well as we saw aquaculture emerge, aquaculture as fish farming is exactly that, it's farming. It's like farming a cow or a pig. Most farming involves inland waters so you dig a hole, fill it with water and put some fish in it and grow them, and then you harvest them so you collect them and put them on market. Some fish farming involves net pens that float in the ocean. And that's the farming were probably most familiar with in Canada it's the biggest form of farming in Canada but not globally. So globally, the common form of farming is you know, dig a hole, fill it with water and put some fish in it. No net pens. But the net pen fisheries is fairly controversial particularly in Canada because it often comes up against the traditional fishing for fish and people who fish traditionally generally don't want to farm for fish. They're two very different professions. And sometimes the agriculture of fish farming has been implicated, albeit the evidence is not conclusive, in affecting or being detrimental to fishing. And so the two different types of Fish production sometimes come at odds.
Henry Standage 4:05: And when would you say the pivotal moment where you start to see this transition from fishing being the dominant form, and then the rise of fish farming coming in?
Bryan Neff 4:17: Yeah, it was probably in the 1980s. And really, the change was in the collapse of the world fisheries. You know, the Oceans Bounty, we had fully tapped it, we had over tapped it, so it was no longer sustainable. And we saw some of these very lucrative fish stocks collapse and it made you know, global news. The one in Canada that were probably most familiar with would be the collapse of the Atlantic cod on the east coast and around 1990 this was you know, a huge bounty for Canada and for international fishers to tap and then eventually all the cod one day were just gone. And there weren't any more to catch. And so as a result of the collapse, you know, so we were at globally about 100 million tonnes per year being pulled from the ocean that was, you know, most likely unsustainable, we saw a lot of catches just declined. So fishers would go out there that put out their nets, but they wouldn't come back with any fish. Those fish were needed in terms of feeding a hungry world. And so we saw aquaculture start to emerge. So more and more farms were developed to replace those fish that we could no longer take from the ocean. Most of that originated in in Asia, in particular, China, China's the single biggest farmer of fish in the world, they produce about half of all the fish that come out of farming. And that's important for food security globally, in part because they're feeding their own very large population and therefore not in competition for exports of other people's fish, but also because they're also an exporter of fish. So they provide that farmed fish to other nations that needed to to put in their stores for people to eat.
Henry Standage 5:59: So these fish that have been farmed are almost being reborn because they're having the chance to start a new family albeit very small. And so I think something people underrate is that a lot of it is preservation of the fish, rather than a GMO genetically modifying it.
Bryan Neff 6:17: Yeah, that's very interesting. And, you know, you're right, that most of the fish that are farmed, are basically, you know, a wild fish at least originally, unlike the cow or the pig, which, you know, through many, many generations have been domesticated. So you don't really find a wild pig anymore, you know, might be the wild boar, but it's not the pig. It's not the cow out there in the wild, whereas in the case of fish farming, it's still young enough, you know that there hasn't been a whole lot of domestication that if we look at a fish like Atlantic salmon that's, you know, heavily farmed in Canada and say, Norway, it's still very similar to the wild Atlantic salmon. That said, it's a hugely controversial question. And when we look at conservation of wild fishes in Canada, the species at risk act, for example, is one way that we monitor species that, you know, have been overfished and may be threatened for extinction. They actually delineate what are called evolutionary significant units. And so Atlantic salmon is a species, but they'll distinguish different stocks. So an Atlantic salmon from Maine, may be considered different from an Atlantic salmon from Newfoundland. And so they've managed accordingly. So they're considered different species and we want to preserve both of those stocks. So when you throw the Atlantic salmon that's now in a net pen, they're usually viewed as a domesticated species they're not a wild species, even though they haven't been domesticated, not like the cows, the pigs or the chickens have been.
Henry Standage 8:00: The first GMO fish for human consumption was approved in August 2017. Have scientists recently discovered how to make GMO fish safe to eat? Or was it an issue of overcoming the stigma attached to it?
Bryan Neff 8:13: Yeah, that's an interesting story. And it goes back about 30 years. So the first fish that we can consume, you know, as a GMO, was an Atlantic salmon and it goes back to your point is it still an Atlantic salmon. The researchers, much of it was done in Newfoundland, so here in Canada, and then it was commercialized eventually by Aqua bounty, which is a company that has an office in Prince Edward Island. There was such a new technology, you know, this idea that we could create a fish we could manipulate the genome and change it and put genes into that fish that we wanted, desirable genes, that it was treated as a drug, not a food and so to get a drug approved, and they focused in the US because if they could tap the US market then Canada would follow suit but also because the US markets far bigger
Henry Standage 9:04: Was it approved by the FDA?
Bryan Neff 9:05: Yes.
Henry Standage 9:06: Interesting.
Bryan Neff 9:07: So you know it to get a drug approved is a far bigger challenge than to get a food item approved. So the FDA requirements are very, very rigorous. And so they were held to a very, very high standard. And it took basically 20 years to meet all of those regulations, just like it would if you're developing a brand new drug - it can take 20 years from the discovery of the new drug to the point where we're actually using it for human health. So, you know, fast forward 30 years, it was finally approved and, you know, then enter the stigma and GMOs generally are not well received by society. So we see a lot of backlash for GMOs to a point where companies that produce a GMO usually try to hide that it's a GMO, it's usually not a seller. You know, put on your package: This is a genetically modified organism. It's generally not what you look for when you're in the grocery store. But yet, I would argue that it's a necessity moving forward. We've had GMOs for decades, most of them are plants. Most of the vegetables we eat are genetically modified. Usually, it's just around, you know, having resistance to particular pesticides so that they can grow them effectively and not have insects eat all the crops. But in the case of the fish, this Atlantic salmon that was approved, they manipulated genome by introducing genes from other fish. And so that makes it a GMO, albeit it one could argue, you know, if you naturally breed two different species and create a hybrid, no one would probably argue that's a GMO. What the researchers did is they just took out a gene from a Chinook salmon, a promoter from an eel white fish, and put it into the Atlantic salmon. So we have two genes from other fish in the Atlantic salmon. It's still a fish.
Henry Standage 11:04: Yeah, I think it's incredibly important to note how important it is how something enters the public consciousness. And so the fact that it entered as this drug and freaks people out I don't want to eat some drug fish. It's like some scaled-down Jurassic Park-esque thing. And I think changing that perception is incredibly hard. I think this is why you still see it as a super controversial issue.
Bryan Neff 11:30: Yes, and the case that the Atlantic salmon too, the gene they took from the Chinook Salmon was a growth hormone gene and so it does speak to what you're getting at - it was a hormone and that basically just causes the fish to grow faster and that's a good thing for aquaculture. You know you want to harvest it as quickly as possible so we can eat it. Interestingly, the growth hormone levels in the Atlantic salmon are no higher than the Chinook salmon and the Chinook are these big salmon, you know. I love to eat, lots of people love to eat their Pacific salmon. They're, they're part of the capture fisheries in Canada. But the growth hormone levels although not higher than the Chinook salmon are higher than the Atlantic salmon and that's why those salmon are smaller. And so it was treated as a drug in that sense that they didn't compare them to Chinook Salmon they compared the growth hormone levels to other Atlantic salmon that live in the wild.
Henry Standage 12:25: There are other ways to genetically modify fish other than for consumption like human food. Such as fish technologies that allow zebrafish to express jellyfish and sea coral proteins, giving the fish bright red fluorescent colours when viewed in light. And nobody has a problem when it's for entertainment purposes. It's when consumption comes into play that you see issues arise. To follow up, are fish the only animal to have their DNA changed for consumption. You mentioned cows and pigs earlier in our talk but as it solely fish that can be modified for consumption.
Bryan Neff 13:03: Yeah, that comes up an issue of perspective. So, when we use these really advanced techniques like these really, really micro needles to introduce a gene into an egg that manipulates the genome of the fish as they did in the Atlantic salmon, or sometimes they use viruses, you know, to introduce the new DNA or RNA into an organism to manipulate its genome. It's very, you know, that gets labeled immediately as a GMO, you know, we're using these highly advanced technologies to manipulate the genome. But humans have been manipulating the genome of animals for centuries, you know, thousands and thousands of years. This could be anything from our pets. You know, if we think of cats and dogs, they've been widely bred for particular trades, like the dog is a single species, but think of all the different types of dogs, very different. Their genes and their genomes have been manipulated. Much of the food we eat, you know, grow the crops were manipulated by breeders, they would pick crops that had certain traits, you know, maybe it was more corn or more tasty corn. And they would then breed those individuals to produce their crops in the next generation. And so that's a form of selection, even natural selection, where we're manipulating the genomes based on the phenotype. So the traits that particular organism has, just picking the ones with the best traits to breed, and consequently, we change the genome of the population. And that's a form of genetic modification, but it's not labeled GMO and nor should it be.
Henry Standage 14:51: Right. And on the surface, this entire issue feels like an issue of class stratification where you've had Blue Collar families, where fishing has been something they do for generations. And then you have fish farmers and maybe it comes across as this elitist way to fish. Am I looking too far into it? Or do you think that's a real concern with some people?
Bryan Neff 15:17: Yeah, that's an interesting perspective and probably a Canadian and North American perspective because most farming in the world is done in Asia and in particular in China and it is not an advanced industry by any means. It's done by locals, by peasants, by people who live in towns that have you know, very little electricity or clean running water. That farming is literally you know, dig a hole and fill it with water, you find a pond, and you remove all the stuff that's in it, and then you put fish in it and the most commonly farmed fish is carp. And so they fill a pond or even a rice paddy with carp and they don't feed them, they just tend them. So they make sure they don't leave or go anywhere. And when they're big enough they harvest them. The perception is, in North America might be that, you know, aquaculture is an advanced industry and so much as, in the ones that we hear most about are these ocean net pans where we're fishing, you know, these highly expensive crops, so to speak, salmon, the Atlantic salmon or the Pacific salmon, and those are our cash crops like that's an expensive fish. And so it might have that, you know, that idea notion that fish farming is you know, a super-advanced industry and it's putting, you know, some advanced industry against the traditional fishing ways of life. I would argue though, that fishing in North America is a hugely advanced industry. You know, some of the lucrative salmon fisheries, the tuna fisheries you know, these are massive boats that they go out to fish with. And they have, they have helicopters on them and the helicopter pilot flies around looking for the fish and radios back to the fleet: Here's the fish. Then they come out, the big trawlers come out and they, you know, unwind thousands or hundreds of kilometers of net to catch the fish. Some of the big boats that are offshore fishing boats have the full processing of the fish right on board the boat so the fish comes in the back, they process it, out the front comes to your canned tuna or your frozen fish. So it's also, it can be a very advanced industry as well.
Henry Standage 17:40: I think my generation and your generation, make the optimization of certain fields, and not just fishing, whether it be sports, or any sort of hobby in any field, how the next generation uses technology to get higher efficiency. That always frustrates people with tradition, I think. Anyway, let's switch it to your research. You look at some of the genes underlying certain adoptions. One of the major themes in your research is understanding the genes underlying adaptation. Can you discuss that?
Bryan Neff 18:20: Yes, sure. So I take an evolutionary approach to understanding adaptation. And what an adaptation is, in my field, it's defined as basically the gene of the gene variants, what we call eels that allow an organism to persist well in its environment and to reproduce. So basically the live and then to reproduce, produce lots of kids. The gene, the genome, and the genes underlying adaptation. There's been a long history of work looking at the genes that underlie adaptations, but really in the last 10 or 15 years with the advent of technologies that allow us to actually look at the DNA of the organism. So for example, the sequencing that we can now do, it opened up a new understanding of adaptation. So we could really get at these different levels, the different base pairs that are in the genome, and how that affects, you know, one fish versus another fish ability to survive in its environment, perhaps to guess at how it will survive in a future environment, and ultimately, to reproduce, which is important if you want a fish to persist. Some of the genes that we looked at in my lab pertaining to thermal tolerance and is one example. This is something that's getting a lot of attention in terms of global warming, so we know that our waters are warming. And that's a question given that fish are ectotherms so they don't regulate their body temperatures like you ot I would, they're very prone to changes in temperature of the water. And so we tried to get at the genetic basis of what we called thermal performance or thermal tolerance. So their ability to perform well in water of different temperatures. And so that's going to be important in understanding whether or not a fish will persist, say 50 years from now in a particular water body, and or what we might be able to do to allow it to persist, including maybe going back to that idea of GMOs, do we go in and actually start manipulating the genomes of these fish to ensure that they have future adaptations, you know, to this changing environment?
Henry Standage 20:30: And your group specifically works at restoring salmon. What are some of the difficulties you face regarding the evolutionary resilience of salmon?
Bryan Neff 20:39: Yeah, the salmon fisheries in Canada is a complex issue, one, because it's multifaceted so the traditional challenges so that the populations have been decimated, you know, the Pacific populations are now down to around 5% of their historic run sizes, run size is basically the number of fish that come back to reproduce and it's a nice easy way to track how many fish there are, so they go out to the ocean, they feed, they grow. And then when they reproduce, they come back to the freshwater streams. And we can count them pretty easily as they swim up these streams. So the historic run sizes are down around 5%. And basically, you know, they're gone or they're almost gone. So a lot of them are threatened or endangered. And so this is a serious concern. It's a multifaceted issue starting with for one, we just caught too many of them, you know, we ate too many of them. So we fished them unsustainably, not enough came back to reproduce to produce that next generation of fish for us to fish. Other issues though are around habitat destruction, and so in particularly with salmon because they come back and breed in these streams. We also live around these streams, we built big cities like Vancouver, and other cities, that we change the landscape and the ecology of those streams and that to can affect whether or not the fish are able to persist in them. For example, if we build a dam for hydropower, which we do a lot of in Canada and globally, the fish can't, you know, jump over a giant dam, and so they can't get back to where they want to reproduce. And how do you compensate for a shortcoming such as that? Yeah, so there's a big movement now to actually get rid of as many dams as we can, particularly for fish that live both in the streams but also want to go up to the ocean. That's not going to that's going to take a long time. There's a lot of dams but there's a movement to move away from damming rivers for whatever reason, whether it's just a whole backwater or whether it's for hydropower. There's a lot of restoration work now going on around streams to try to rehabilitate the riparian zones which is the shores of the streams to make them more natural. But also there are more significant interventions where we might go in and take the last fish that would swim up a stream and we put them in what's called a live gene bank, so you can think of it as almost like a zoo, or an ark, where they're all brought in and they're kept in captivity. So they're kept in, you know, big ponds or something. And they're bred in those ponds with the hopes of one day re-releasing them back into their natural environment, once we've had time to restore that natural environment to a state where they could survive.
Henry Standage 23:26: With respect to aquaculture and Canada's role at the forefront of that transition. What are some of the new practical technologies that your lab is helping to implement?
Bryan Neff 23:36: Yeah, again, this is quite a distinction between North America from you know, the rest of the world, particularly Asia where most farming is done. So if we go to Asia, their movement is actually away from the high tech agriculture and so they want to remove net pens, and instead focus on fish that you don't have to feed. So you put them in a pond, and they feed on the natural foods that are produced by the water. So they tend to eat very low in the food chain. So they're herbivores, so to speak like a carp. In North America, our movement has predominantly been around net-pen farming of these high cash fish like salmon. And they're the technology that the movement the technologies is really to ensure that these net pens and the fish themselves minimally impact the environment where the net pens floating, so they're typically in the ocean around the coast. And the idea is to make sure that they don't pollute the environment around the net pens too much. And that pollution is, you know, just all the poop that the fish release, because there could be millions of them held in these net pens, all the food that isn't eaten, so they throw in the food, they tried to make sure it gets all eaten, but eventually, some of it floats away or sinks out of the net pen and so that can be significant organic loading in the area, as well as potential disease, and that's a major concern. So those diseases can be treated sometimes with therapeutics in the net pens. But the concern is that they might transmit those diseases before they're treated to wild fish that are swimming, you know, by the net pens. So there's been a movement to try to create fish that don't need those therapeutics so that have these heightened immune systems. And that's something my lab works on. But also to try to reduce the impact or the creative barrier between the fish in the net pen and the fish that aren't in the net pen. And so new technologies include not using nets anymore net, you know, are obviously very porous, lots of water comes in and out, but instead using a closed containment technology, and that's where you basically have what's like a giant floating Tupperware in the ocean, something made of a plastic where the water is controlled the water that comes in controlled, the water that goes out is controlled. The problem with that technology is that it requires that we pump water on like a net pen which just uses natural parents to water. pumping water requires electricity. Electricity is expensive. So it's more expensive than traditional net-pen farming. And so the profit margin, you know, it's going to shrink and there isn't a high-profit margin in fish farming. And so right now it's not economical to switch to these new technologies.
Henry Standage 26:32: Last question, Are you optimistic or pessimistic about Canada's aquaculture future?
Bryan Neff 26:38: Yeah, that's a that's a tough one. I'm optimistic in the sense that globally, we must invest in fish farming, you know, the human population is growing. No other food industry is growing like fish farming. It's the only way that we're going to feed a hungry world that needs animal protein. Canada is a leader. It has great environmental policies. So I think we can be a leader globally around fish farming. That said, there is a social element as well, that needs to be tackled. And there's no real timeline when you're dealing with, with issues that are controversial or seen as controversial in society. And so Fishers and fish farmers are generally different people, their different professions. And at the moment, there's still a lot of tension between fish farming and traditional fishing. And, you know, I don't know, it's going to be a long time I think before those challenges are reconciled.
Henry Standage 27:44: All right, that's it for this episode. I hope you enjoyed we'll be releasing 12 more episodes bi-weekly until we get to 2020. If you did enjoy this and feel compelled to share it with your students, your prof, or whatever it be. We really appreciate it. And I'm really excited for you to hear from our team at Western this semester. I'm Henry Standage, signing out. Thanks for listening.
Evidence suggests that metabolism is connected to Alzheimer's disease. In fact, lifestyle habits contribute to your susceptibility of getting Alzheimer’s. But exactly how remains a mystery. Robert Cumming and his lab research how age-dependent alterations in brain metabolism affect memory and contribute to neurodegenerative disorders, including Alzheimer’s disease.
Henry Standage 0:28: Hey, thanks for tuning into the Western Science Speaks Podcast season four. Today we're going to be talking to Dr. Robert Cumming from the Department of Biology. Rob told me he starts the cell biology class the same way every year. He asks the students to raise their hands if they have a family member who's been affected by Alzheimer's. When 30, 40, 50% of the class raises their hand, he tells them, that means there's a pretty good chance they might inherit an age-related brain disease themselves. It sets a tone and shows how high the stakes are for the next generation of scientists. Diseases like Alzheimer's don't have a cure yet. So if you're going to inherit it, you might not even want to know - you might just want to continue to live your life. These inheritable diseases are what we talked about when we sat down, as well as a couple of other things like how memories are formed, how your lifestyle choices can affect your brain. And then at the end, we shift into the topic of cannabis and what it's legalization means. Anyway, here we go.
A lot of your work originates from you having a background in inheritable blood diseases, how does a gene get passed on?
Rob Cumming 1:44: Well, it's not that everybody has their genetic compliment. They get half from the mom and dad, and if all the genes are working fine, then you have no problems. It's when there's a mutation in a certain gene, that male critical function. So I did my PhD studying a rare disease called Franconia. So turns out there's about 17, or 18 different genes, that if they're mutated, and when I say mutated, both versions of the gene, one that you get from your mom and your dad have to be mutated in a way that they're not functional. And in that case, that's what we refer to as autosomal recessive. So you have to have two non-working versions of the genes, and you just don't get a functional protein. Whereas there are other types of diseases where you just have one mutation in a particular gene. And that mutation causes the function of the encoded protein to not to work in a manner that is harmful. And so that's what we call the dominant mutation. So when working on that rare blood disorder, this was one where you needed two defective versions of the gene. It's a bit of a rare event when you have that. So we usually have two parents who are carriers, they have one normal version and one new version, and you have about a 25% chance of getting two bad versions. So it's really bad luck of the draw when that happens.
Henry Standage 3:18: What are some examples of diseases or mutations that we might be surprised are inheritable that can be passed down?
Rob Cumming 3:27: Well, there's many of them, I now study Alzheimer's disease. And there are a very small number of individuals, maybe 1%, maybe 2% of the population of people that have Alzheimer's actually have an inherited form. And that's the type where you just have to have one bad version. And that bad version, ultimately will result in an individual getting Alzheimer's disease, maybe they could be in their 40s or 50s. That's what we call it early-onset Alzheimer's. So what's interesting, though, is that most of the research on Alzheimer's disease has been had been using these rare forms of inherited Alzheimer's disease to sort of model it. And even though the vast majority of people that have Alzheimer's disease don't have mutations in these genes, so there are about three genes involved. There's a precursor protein, there's presenilin one and presenilin two. So these three versions, these three genes, if you have a certain mutation result in the production of a harmful piece of a protein called the amyloid beta. And that amyloid beta, if it accumulates at very high levels in your brain, it forms these things called plaques. And the plaques were long believed to be what caused Alzheimer's disease. So because the original description of Alzheimer's disease by Alois Alzheimer, when he examined a woman who actually had the rare inherited form, this is back in 1905 - when they looked at a brain, they found there were all these sticky proteins, plaques, and another protein called tau, which accumulated in something called tangles. And so this was sort of the first clue that this kind of brain disorder is associated with the accumulation of these bad proteins.
Henry Standage 5:25: That's the luck of the draw you -
Rob Cumming 5:28: A little bit, yeah, in a way, in this case, you have a 50% chance of getting it, because it works in an autosomal dominant manner. So just, you know, you're here, you may have a parent who has one bad version of the gene. And it's a type of gene that you don't show the disease until your maybe in your 50s, you've already had kids by then, right. So there's, there's a number of diseases that are like that, where you may not necessarily know that you have it. And by the time you have it, you've already had kids, then you possibly pass it on to those children. So another example is Huntington's disease. And in that case, that usually affects people in their late 30s, early 40s. And again, they may have had children at that point. So now that we know that some of these diseases can occur in a heritable manner, if you have a history in your family, then you really need to get tested. And so what they're doing now, certainly in these rare, Alzheimer cases are getting tested. And then it's the one of the types of things where you know, you've got the mutation, you know, you're going to get it. And that's frightening, it's even more so frightening for people with Huntington's disease. So there's actually kind of ethics rules related to this. So let's say you're, you're 40, and you discover that you have Huntington's disease. And you have a kid who's maybe 15. And you, you think, oh, my God, I want to know, is my kid going to get it. I need to go to the doctor, he asked the doctor, can you test my kid to see if he or she's going to have Huntington's disease? And they say, No, we can't. Because the child has to be 18 years of age to be an adult. And then that child can make a decision whether he or she wants to be tested. So it's an interesting kind of dilemma. Because as a parent, you want to do everything you can for your kid. The problem is, if you have inherited form of a disease like Huntington's disease, or Alzheimer's disease, and you want to see if your kid is going to get it. Well, the problem is there's no treatment for so there's nothing you can do. So the kid can say hey, I have the gene, I'm going to get it. Well, how's it going to influence your life?
Henry Standage 7:49: So that's why there needs to be approval for that. So if it was something that could be treated like the flu -
Rob Cumming 7:58: Could be a different situation, if you can intervene earlier, and actually have the treatment that can prevent the disease or delay it. So when you have diseases where there's no cure, then it becomes an ethical dilemma. What's up, there's actually no point in knowing, because it actually causes a lot of emotional distress for an individual. And so they can determine whether they want to know and there's some kids who say, I don't want to know, because I'm going to live my life to its fullest. And if it happens, it happens.
Henry Standage 8:27: So it's like, the big hypothetical question people like to ask is; if you could see the day you die, like in the future would you choose to? And I think people generally say no.
Rob Cumming 8:38: It is a little bit like this. Do you want to see whether you're going to have a long prolonged agonizing death? Yeah, because that's generally what happens. Yeah, right. So the getting back to Alzheimer's disease. What's interesting is that when they found that there's these rare group of people that have inherited forms of Alzheimer's, and it leads to the increased production of this amyloid peptide that basically all the animal models have been engineered to recapitulate that rare form of Alzheimer's disease. And all the investment in drug discovery has focused on amyloid. And they spent billions of dollars and it's amounted to nothing.
Henry Standage 9:23: And by that, you mean testing on animals?
Rob Cumming 9:26: Well, they started with testing, like we've cured Alzheimer's disease in animals many times, in my mouse models, for example, the rodent models, but the problem is that that's not the type of Alzheimer's disease most people get, they get what's called sporadic. And when you have sporadic Alzheimer’s disease, you don't have a very clear defined mutation, that means this is the sequence of events are going to happen, and ultimately resulting in Alzheimer's disease. So the brain, even though it only represents about 2% of your body mass consumes about 20 to 25% of your energy reserves. So it needs both the fuel in the form of usually carbohydrates, sugars, and also oxygen. And so it's an incredibly demanding organ. And the reason it needs so much energy is that you've got, you know, a trillion cells, I don't know, I can't remember the exact number. But there's a lot of all the cells in your brain, you've got neurons, and glial, those are the two main cell types. And they have to work together, the neurons have to talk to each other through synapses, these are little close connections, and it's sort of like electrical signals that go back and forth between neurons. And all that activity requires an enormous amount of energy, even when you're not even doing anything, your brain is active all the time. Once you start to get engaged into, you know, writing an exam or coordinating your movement while you're doing a dance or any kind of task, your brain activity increases, obviously, a lot more and depending on what you're doing certain parts of the brain become more engaged, more active. So you need a continual source of energy in order for your brain to function. And that's well understood. If, for example, you get a blockage of blood flow to a part of your brain, that's what's called a stroke. And so not having enough oxygen and nutrients going to part of the brain. If that goes on for a great period of time, that part of the brain will actually start to die off. So people understand that. But what happens when you get older, and one of the biggest risk factors for Alzheimer's disease is actually age, the older you are, the more likely you are to get Alzheimer's disease. So like from the age of 65 on, every five years, likelihood of getting Alzheimer's disease almost doubles. So the fact that North American Western society individuals are getting older, we're living longer. Now we're seeing a progressive increase in the cases of Alzheimer's disease simply because people are getting older.
Henry Standage 12:01: Which takes away the upside of being able to live longer.
Rob Cumming 12:05: Yeah, I mean, it's sure we can live longer, but to what extent, you know, you're now being afflicted with a whole bunch of diseases. So it's certainly you could say, well, I want to live to 90. But like from the age of 80, to 90, you’re in horrible pain, or your mental faculties deteriorate substantially, it's not really living, you're just prolonging death, that's all you're doing. So the idea is, we can, instead of focusing on lifespan, we should be focusing on healthspan, and being as active and as functional as long as we can. Because that insures the best quality of life.
Henry Standage 12:41: You've already alluded to the metabolism, the idea of processing energy in the brain using nutrients, oxygen for fuel - talk about what the metabolism means in your work.
Rob Cumming 12:53: I kind of inadvertently got involved in brain metabolism by studying the older kind of train of thought with Alzheimer's disease, which is to look at amyloid. And one thing that has puzzled people, well I wouldn’t say puzzled, people have ignored or conveniently ignored in some cases, is the fact that there's many elderly people who have had normal lives and had no form of dementia, memory loss. And when they die, they may have donated their brain to science and somebody cut into it. And a pathologist looked at it and went, Oh, my God, this person must have had Alzheimer's disease, they had all these plaques in their brain. They didn't have Alzheimer's disease, anywhere from estimates 25 to 40% of the elderly population are walking around with all this plaque in their brains, and they're not getting Alzheimer's disease. So does that mean, the amyloid theory of Alzheimer's disease is wrong? It's possible, or we need to rethink is that some individuals may be able to tolerate very high levels of this particular protein. And there's lots of evidence suggesting that the protein itself is bad. In different experimental models, it causes harm to put to neurons, they don't function properly, or they actually start to die off. And that's a big part of Alzheimer's disease is you have a mass as it progresses, you get massive loss of brain cells. So why are individuals who have all this amyloid not having all that brain cell loss? And so we thought, maybe it's because they have a natural adaptation mechanism to become resistant to it. So we mimic that in a dish. So the cultured nerve-like cells, in addition, we've exposed them to the amyloid peptide and most of them died. And then the ones that survived, we looked at them and said, well, how are they different from the original starting population of mostly sensitive cells. And it turns out that those cells became very good. They took up lots of sugar, and then they process it to make lactic acid. And so that's sort of where I initially got interested in this. And we thought that perhaps this type of metabolism, which is a unique form, and it was originally discovered in cancer cells, by a German researcher called Otto Warburg, and this is in the 1920s. And he found that cancer cells are very sugar-loving, they take it up at very high levels. And they don't process it in a manner that would normally be dependent upon oxygen, they process it in a non-oxygen dependent manner to generate lactic acid, and anybody who maybe runs too hard or isn't in great shape, and they get a cramp. That's an example of, for example, your muscle tissue, not having enough oxygen in order to sustain the type of energy production and by default, you start to produce lactic acid and the lactic acids are what causes the cramp. So this lactic acid phenomenon was what I initially discovered in a very artificial model and culture. And then I started to ask, does that have any relevance to what really goes on in your brain?
Henry Standage 15:59: And what is the connection with memories to lactic acid?
Rob Cumming 16:04: Well, this is a controversial theory. And it was proposed in 1994 by a fellow by the name of Pierre Magistretti, and he proposed something called the astralcyte neuron lactate shuttle hypothesis, which is a big mouthful. And in essence, what their saying is, there's as I mentioned, there are two main types of cells in your brain. There are glial cells, also known as astrocytes. And then the neurons, the neurons are the things that fire and so the support cells are astrocytes. And the theory is that the astrocytes basically sup up all the sugar out of your bloodstream, and they process it to make lactic acid, and then they feed the lactic acid to the neurons. And then the neurons use that in some not very clear manner, maybe for energy production, or for some molecular process evolved in memory. And there is evidence in support of this. But then there's also some other evidence suggesting it's not that straightforward. So there, the evidence to support of this is that if we experimentally modify a mouse brain, and we can do it chemically, where we put probes or little tubes into the brain, and we administer drugs that actually prevent the ability of lactate to transport between cells, and those animals have problems with learning and memory, or we can do genetic intervention, and we monkey around with things that transport the lactate the transport channels, and that also causes problems with memory. So that's sort of been the basis of this theory. But it's always assumed that it's like, we go from sugar in your blood, it gets taken up by astrocytes, the astrocytes then break it down to lactic acid, then feed it to the neuron. And then the neuron without lactic acid somehow does something related to memory. That's the theory. And it could be true, but it may also be dependent upon which part of the brain which kind of task you're involved in what type of learning you're undergoing. So I don't think it's black and white. And we've done some studies where we administered a drug that actually prevented the creation of lactate. So the animals couldn't actually generate lactate, lactic acid, or lactate. And what we found, depending on when we administered the drug, is that in this case, that we do a learning spatial learning task called the Morris water maze. And mice don't like water, they want to get out of it, you throw a mouse in a big tub of water, he swims around like crazy, not very happy. And there's a little personally submersible platform. And the mouse learns where that platform is, because we have some cues around the big top of water. And so he uses the spatial cues or little signals like there's a star, there's a circle over there is where that hidden platform is, and he swims to it. And then once he gets on the platform, it can rest. So in the process of learning where the platform is, takes some time, it takes a number of days, we have to do what we call trials, where we kind of teach the mouse where the platform is, and he learns. And then at the very last stage of the test, we kind of do a sneaky thing and take the platform away, and throw the mouse in the tub. And then we see how much time does he spend in the area where the platform was previous. And that's an actual reflection of memory itself. So the first stage is learning. So that's our working memory. So you, if somebody says, Okay, here's my phone number, you know, 519-226-4535, whatever, you have to repeat it a number of times. So through repetition, you start to lay that memory down. And so what we, what we found is in the learning phase, is if we administer the drug, so the animals can't make lactate, they don't learn, and they don't have a memory. So it's kind of like building the road memory, it's like a memory is just doesn't happen spontaneously, you kind of have to lay down tracks. And it literally in a way, it almost is like laying down tracks, it's connections in your brain. And those connections have to be strengthened through repetition. And through the repetition to become stronger and stronger, you end up building a road. Once the road is built, then it's easy just to run right down the road and grab the memory and come back. So what we found is the lactate, based on our experiments where we didn't allow the brain to make it during the learning phase, they didn't learn and then they just simply there was no memory to recall. But if we allow them to learn appropriately, and at the very last, we injected them with the agent that wouldn't allow them to make lactate, they could still recall that memory of where the platform was. So what that suggests is that lactate isn't so much about retrieving and establish memory, it's about making the memory and laying down the tracks. And that actually makes a lot of sense because lactate in the metabolism associated with it is involved in building cells. It's one of the reasons why cancer cells use this metabolism. Because they can and you say well, why would they use this metabolism make lactate lactic can't be very good for you? It's not a very robust, efficient way of making energy. But it has a side benefit. If it makes all these little intermediate building blocks to make more cells, it could be more DNA, more protein, more fat. In the case of your brain and neurons, it's about making connections and the connection between neurons are called synapses. And so those are actually structural changes to it to a neuron, they're actually making more synapses in order to make extend a piece of the cell outward to make a little pokey projection, you have to have protein, you have to have limpid and to actually physically extend a piece of itself. And so we think that that metabolism is really important for actually structurally changing the connections between neurons and making them more stable. It's part of what's called synaptic plasticity. So when you learn something, you actually start to create new synapses or strengthen existing ones or make them more functionally connected. And so we think that the lactate and the metabolism associated with it is really important for that. Once that's been established, you build the road, then you don't need them.
Henry Standage 22:54: In Alzheimer's, it's the new memories that go first. That's right. Yeah, when you build a strong bridge there, it's, it's more durable.
Rob Cumming 22:57: Right. So long term memory, or what we might call semantic memory, remembering two plus two is four, or, you know, how you start a car, and how we operate a car, you don't think about it, it's kind of built-in memory. Those types of memories persist the longest Alzheimer's, where people that start to show signs of Alzheimer's, it's there. The recently established memories, like, oh, you know, a friend visited me in the morning, or I had toast, and eggs, you know, in the morning, you don't remember that stuff. So these sort of short term new memories just don't stick. And so, you know, there's a lot of theories as to why that is. Certainly the neurotransmitters. Those are the chemicals that allow neurons to communicate with one another, they become very imbalanced. Acetylcholine is a really important neurotransmitter that's quite messed up, glutamate, is another. And so people kind of focused on the neurotransmitters. And certainly they play a big role in it. But is it simply a case of they don't make enough neurotransmitter? Or is it a case that they're just not really able to form those new connections very well. And so what we're kind of exploring is, well, what happens this lactic acid is not like your brain is churning out buckets of lactic acid all the time, it does in very small amounts in a very controlled way. And we think that these little small bursts of lactic acid production are really important for making those new memories. The question is, what happens with age does that not work as well, and what happens in Alzheimer's disease. And what we found with age is the animals - some of the enzymes that are involved in making lactate, the enzymes itself diminished with age. So it looks like animals don't have the ability to make as much lactic acid in memory, your memory gets a little dodgy. Even if you don't have Alzheimer's disease, the older you get your ability to form new memories, and recall memories is not as strong. It's just part of the natural ageing process. But it's really dramatic in Alzheimer's disease.
Henry Standage 24:18: What happens if you produce too much lactic acid?
Rob Cumming 25:18: Well, certainly producing too much lactic acid is bad. People that have epilepsy produce very high levels of lactic acid, its associated with seizures. So having high levels of lactic acid can actually induce a seizure, or trigger unwanted neuronal firing. So that's an example of too much. But the question is, well, what's happening in Alzheimer's disease? Is it too little or too much? And that's what we're trying to figure out. So right now, we have somewhat crude tools to try to measure. Lactate is not an easy thing to measure. If you were to euthanize a mouse, and then try to go into the brain and assess how much lactic acid is there, well, part of the problem is when you euthanize an animal, you put it to sleep. And, and then, you know, if you give it a lethal injection of a drug that eventually will cause it's hard to stop. Well, the problem is, now you're going to have a lot of lactic acid because there's an adequate blood flow and oxygen to that tissue. So it's very difficult to try to measure lactate in an animal that has died. So helping you measure lactate, in an animal that's still awake or still alive, is not sedated. So if an animal is sedated, that's going to affect lactate levels as well. Very difficult. One of the things we've been doing, working with researchers at Robarts Research Institute, is to do MRI scans. And these are special magnetic resonance imaging. So we do a slight variation of it called magnetic resonance spectroscopy. And this is a way to actually measure metabolites within the brain of animals and their alive. So we still have to sedate them, because a mouse isn't very cooperative, I guess, in a scanner. But we can at least make some relative comparisons, we can look at young animals, we can look at old animals, we can look at animals that are engineered to develop high levels of the amyloid with all its flaws, and sort of the only model we've got right now for Alzheimer's. And what we found is when we use this form of imaging, that the lactate levels and old mice declined with age, and parts of the brain that are involved in memory. But unexpectedly in the quote Alzheimer mice, we found that the lactate levels didn't go down with age they remained elevated. It's a tricky one. So yeah, I mean, that was not what we expected. That was the complete opposite. So if I made this case about lactate is really important for forming new memories. Well, then, why would the quote Alzheimer mice have higher levels of lactate, even though they have memory problems? And there's been more recent studies in humans also corroborating this where lactate levels seem to be higher, in Alzheimer's patients. And if I've just told you that lactate is really important for forming new memories, and new memories are compromised in Alzheimer's patients, why would they have lactate levels that are high? And I think it gets back to the sort of sweet spot, if they're making it, but they're not consuming it, it accumulates, and that's actually a bad thing. So we think, and this is still a bit speculation, that certainly the mice, maybe humans, it remains to be seen, that they are producing lactate, but they don't seem to be able to utilise it properly. So if it persists, where it's persisting, which parts of the brain inside of cells outside of cells, we still don't quite have that answer. So we think that in the Alzheimer's model, for some reason, the lactate levels are high. And that actually can lead to a whole bunch of problems. And there's actually evidence suggesting that in the early stages of Alzheimer's disease, they actually have hyperactivation of neurons. And so they're getting firing, where they shouldn't be firing. And so there's a theory perhaps that this hyperactivation may be associated with higher levels of lactate, a thing that very few people realize is that there's actually a strong association of epilepsy or seizure-like episodes in Alzheimer's. So if you were an epileptic patient, you have a greater likelihood of having Alzheimer's disease. If you have Alzheimer's disease, you may have episodes of what are called nonconvulsive seizures. So you're not necessarily, you know, pass out and you're on the floor and you're frothing at the mouth. They may just have these sort of fugue-like states where they're just confused. They don't have what appears as a classical type seizure. But if you were to measure their brain activity, you would see it firing in a sort of uncontrolled manner. So, again, does this have some relationship to the high levels of lactate? Possibly, we don't have those answers just yet.
Henry Standage 30:20: In one regard, it's helping people make new memories and on the other it's given people seizures, which are just two polar opposite things. How can research on brain metabolism translate to possible therapies to Alzheimer's disease?
Rob Cumming 30:35: Well, there's a lot of people that are now viewing Alzheimer's disease as a metabolic disorder. And there's something that's been kind of floating around; a term called type three diabetes, which is the inability to respond to insulin appropriately in your brain. And so insulin is really important for taking glucose, and then processing it. And so the train of thought for many years is that insulin is certainly really important than most tissues in your body, but a lot less important in the brain. Because the brain doesn't have as many, what we call insulin-dependent transporters for glucose. So a lot of the glue, they don't need to have insulin in order to have those transporters working. But that's not entirely true. And now they're finding more and more evidence that we do have what are called insulin receptors in the brain, and in certain parts of the brain that are really important for establishing memories. And they're now starting to do things like administering insulin into the brain. So they do these intra nasal administration. So believe it or not, if you screwed, sort of an aerosolized type of spray up your nose, in your olfactory epithelium, so isn't that the very upper part of your nasal cavity is permeable to certain agents, and that can actually get into your brain. So they've been doing these studies where they're using intranasal insulin injection, and there has been some improvement in some individuals. So the argument is, well, is it because insulin has a whole bunch of other properties that don't necessarily involve glucose? It could, it acts as a signal in a way and triggers molecular changes inside of cells? Or is it because it's helping facilitate more glucose uptake? So there's a lot of evidence that glucose does not get processed properly. And Alzheimer's brain is actually sort of the earlier studies using Positron Emission Tomography, where you use radiolabelled glucose, and you see it doesn't get taken up. So we know there's a problem with getting glucose inside of the brain cells of Alzheimer's disease, you're not getting glucose - that's a bad problem. What's what researchers haven't really tried to parse apart in a little more fine-tuned manner is asking if the glucose getting taken up in astrocytes or is the glucose going up in neurons, and the technology is slowly getting there, we can start to look at that. So a lot of this is just we didn't have the tools to try to figure this out. But we're getting there. And we have a lot of genetic models and mice where we can modulate certain things. And then see how does that affects the ability of the animal to process sugar or make lactate? So getting back to well, how does some of this data with lactate? Is it translatable to a therapy? We're not there yet. I think we have to establish that too much lactate is bad. We need to ask, where the lactate coming from? And when we start to have answers to those questions, we can say, well, where's the source of the lactate? Is it producing too much? Is it not being utilized? Is there a way we can fine tune the lactate like a thermostat to turn it down a bit? And does that actually help? So there are potentially some drugs out there that we could potentially repurpose to try and treat Alzheimer's disease. So I mentioned seizures. For example, a few years ago, there was a paper suggesting that drugs that target an enzyme called lactate hydrogenase, which is the enzyme that makes lactate could be used for the treatment of epilepsy, or seizures. So right now, that's still in the experimental stages. But could we try to test those drugs and Alzheimer mouse models? And if do they indeed lower lactate levels? Does that actually correlate with improved memory, but it's a really tough one. But the fact that people are trying these strategies, using metabolic intervention to treat Alzheimer's disease 10 years ago, people would say that snake oil, you know, but now papers, because all of the trials, clinical trials targeting amyloid have failed. All of them. So we're back to square one, we have to try something different. And I think there's ample evidence that metabolism is messed up in Alzheimer's disease, nobody argues that where the argument comes is well, how is it messed up? And which form of metabolism is more adversely affected? And if we're going to intervene from a metabolic perspective, where do we start, you know, which strategy, and those are all valid concerns and research directions that people could explore. And the funding for that has not been great. And I'm hoping that it's going to change over time because people could recognize that metabolism is something that you can target and modulate from a therapeutic perspective. I think where it's, it's taken a hit as people perceive as some fad diet, like a ketogenic diet, and that's going to help. And, you know, this isn't really about diet, per se, although there's ample evidence suggesting that your diet can dramatically determine whether you can get Alzheimer's disease, you eat crappy food, you know, high carbohydrate, high fat, high fat, processed foods, you start to become obese, you have insulin insensitive type two diabetes, all of these things make you way more susceptible getting Alzheimer's disease. So anybody that says, well, metabolism is kind of a hokey thing. No, it's not. I mean, all the epidemiological data shows very clearly, unhealthy diet, unhealthy lifestyle renders you way more susceptible to Alzheimer's disease.
Henry Standage 36:55: That is something that not enough people know.
Rob Cumming 36:59: Well, I think it's going to change because I'm, I'm hearing a lot more on the media, this talk about what can we do to prevent Alzheimer's disease, and there was a recent sort of study, and it was covered in the news media quite extensively about what are the things that you can do? And certainly, they talked about diet, they talked about, you know, eating more healthy, getting your diet down, being more active, be socially engaged, you know, the whole idea about these crossword puzzles, and, you know, brain training. Actually, it's not that great. What being engaged with people actually, is far more preventative. So you could sit at home and do all the crossword puzzles all day long, that isn't necessarily going to stop you from getting Alzheimer's disease going out and having coffee with friends, actually will. So this aspect of social engagement seems to be really important. Getting out and moving. Getting a little bit of cardio and the diet. It's a really big one eating fresh fruit and vegetables, lowering your carbohydrate intake, avoiding lots of processed foods. Yeah, I think that that that data is, is quite convincing. But the problem is, you know, people want to eat their Doritos and they want to, you know, have a big pint of beer.
Henry Standage 38:20: I feel attacked.
Rob Cumming 38:22: Yeah. So it's, it's difficult to change. Those lifestyle changes are very difficult. Of course, people would like to just take a pill.
Henry Standage 38:31: That was the interview with Robert Cumming. There was a lot to take on board there. Humanity's defining characteristic is its capacity to learn. When we don't take care of our brain, we damage ourselves and our loved ones. That's it from us for this week. In the meantime, like, share, subscribe to the podcast. I'm Henry Standage, signing out. Thanks for listening.
On this episode of Western Science Speaks, Dr. Dan Lizotte and PhD Student Brent Davis discuss how they are using artificial intelligence (AI) to identify people on social media who may be struggling with addiction.
You're listening to the Western Science speaks podcast. Presented by Henry Standage.
Henry: Hey, welcome to the podcast. Today Western Science Speaks expands its horizons as we have not one, but two guests: Dan Lizotte who came on to the podcast last year to talk about his research pertaining to artificial intelligence and using it to diagnose and treat physical injuries and we're lucky enough to be joined today by his PhD student, Brent Davis. They're working on a software program that identifies people on social media who appear to be struggling with drug abuse. The whole project, in concept and execution, feels like such a fantastic modern remedy to some of the cries out for help we see online. So I hope you enjoy it. Here's the interview.
Henry: All right. A couple of firsts on the podcast today, our first two-time guest: Dan Lizotte, and our first three-man podcast. Thanks for coming, guys. And we'll start with Brent, why don't you tell us a little bit about the research and what you and Dan do together.
Brent: So the research we're doing is a way to search social media for a topic of interest that you might not know the keywords for. Like if you go on Google and you type in ‘cat pictures’, you're going to get cat pictures. If you're looking for something a little more relevant to research elsewhere, you might be involving a community of people that you don't really know, so you also don’t know their speech patterns. If you're trying to find posts that are related to a topic that is most relevant to that group, it can be very challenging. So, we're trying to design an AI technique that facilitates that kind of research for other people.
Henry: I see. Something that I always see made fun of is: "Parents: how to catch your kids' internet slang." And the advice is always incorrect! And so how do you build a program, that, as this stuff changes fluidly, keeps up with it.
Brent: The kind of new technique that's coming out for that is a technology called ‘Word Embedding”. As long as you can find a sample of the kids’ speech, their slang, you can develop a technique that will go in and learn a machine-oriented understanding of what that word means. And it'll at least (usually) associate that slang with other slang that can be used interchangeably.
Henry: And where do you move from there? So, you figured out how to embed these words, and then what are the next steps.
Dan: So, once you've got that representation built up of how people are using language online, you can take a lot of different next steps, which is actually kind of a fun thing about this piece of research. One of the next steps is to look for more occurrences of that same kind of discourse - that same kind of way of talking. And, you can move to different platforms. You could learn about a discourse on one platform, like Reddit for example, and you could use what you learned there to maybe search on Twitter for similar kinds of conversations that are happening.
Henry: Right, and you guys are starting off on Reddit, right?
Dan: Yes, we are.
Brent: Yeah, one of the big differences about Reddit is that everything is more likely to be anonymous than Twitter. So the odds of you finding someone that's like put up, this is where I live, this is what I do for a living, usually Reddit accounts don't have that much detail, whereas on Twitter, most people tend to label it with everything; mine has what I do, where I work, a picture of my face. You don't really see that on Reddit, which I think is an advantage for getting this started.
Dan: Because we think that people feel a little bit more free on Reddit to speak their minds and to speak in a way that they know to be understood by the community of people that they want to interact with, we feel like we're getting a better picture of how people are using language.
Henry: Yeah, on Twitter, you could have work colleagues or even family whereas on Reddit you can keep it as low-profile as you want. It's narrow in scope on the subreddits too.
Dan: Exactly. Brent can tell you a little bit more about how we're using that. The other obvious difference, too, is the forum. On Reddit you can post can be as long as you want long as you want, more or less, whereas on Twitter, it's different because you're restricted.
Henry: And you're looking solely at mental health here, right?
Dan: So far.
Brent: Yeah. And mental health and substance abuse in particular. So, one community that is out there, that came up from talking to the health units and seeing what might support them is the opioid users; there's still the opioid epidemic going on. I think it was up to 3000 overdoses in Ontario in 2018 - not sure on the number, I could have gotten that number wrong. But it's been steadily going up. And, they are a hard to reach population; no one's going to go on Twitter, on their work account and be like: "Hey, guys, I'm about to go home and do [whatever their drug of choice is]". But on Reddit, they have a way to talk to each other. And you see some surprising things like safety tips, the overdose kits; it's not what you would expect of people; there's kind of an active community around what they do. And, that's where we're getting the language they use to be able to understand what's going on.
Henry: Can you give me an example of this language? What's something that would pop up on your system as a red flag?
Brent: One of the big ones is the word ‘fentanyl’. Right, you just call it ‘fent’. So, if you didn't know that, and you're trying to do a keyword search, you search for fentanyl you may not find much. It is very common that short forms get used, informal names get used.
Dan: Oh, yeah, a lot of language around buying and selling. And I can't think of any of the specific words right now. But a lot of that language around buying and selling is different than it is in other communities. And, I should say, you could just read a whole bunch on the subject. and eventually you would get it right, or you would identify some of these things. But yeah, I think one of the things that we're providing is a way to use the computer to highlight the words that are most distinctive of the discourse in that subreddit without having to read through it all manually.
Brent: Who is this information for? So, you're kind of making a shortcut for people so that they don't have to go on a full method investigation for a year to figure out that ‘fent’ means fentanyl. So, who are you supplying this to?
Dan: This project was really instigated by an epidemiologist with Ottawa Public Health - Cam McDermott, he's a great guy. And we were talking about different ways in which AI techniques might be able to help people working in public health. He really expressed his frustration over how hard it is, for folks working in public health who want to be helping and delivering services to these vulnerable populations, to actually get in touch with them. It's really hard. And so that kind of piqued our interest. And so, they've always been our kind of number one client, not just Cam, but public health organizations in general. So, they're definitely at the top of our minds.
Henry: And they've got two major universities there, as well as Algonquin college. I don't know what else is there, but have they used it toward student life there at all yet?
Dan: No, they haven't but we are collaborating with folks at Carleton University in the Geography Department because they're really interested in how the place where you are interacting correlate with the vulnerabilities you have. What do you have access to? How does it impact what kind of services you can get? The folks at Carleton have a lot of expertise in working with these populations and really helping them tell their own stories about what their experiences are like, which we really like. Working with the social scientists at Carleton, I think, is going to give us a way to really bring this beyond helping the health units to help the people on social media tell their stories; help them tell the rest of us what they're really going through.
Henry: Right- without the veil of anonymity. Yeah. So the problem I've had is that Reddit doesn’t like it when I promote the podcast on their subreddit’. Apparently, I don't add to the community, I just plug the podcast. But I imagine for you guys, with the Ottawa people, it's probably pretty rare that you find someone who talks about their location, being in Ottawa, and then kind of being the ideal person for who you're working with. So how are you going to be able to find lots of people in that demographic?
Brent: The kind of bewildering part is there are many more addicts than you would expect. There are people on there that are not thinking that someone's going to come and find their comments. And, they do they say “I'm in Ottawa, and I bought this”; not exactly in those terms, but spread out over 20-30 posts, you can sometimes find something that explicit. The other part of what we're doing, involving public health news, requires the expertise of the geography folks. They want to look in an area. And like you said, there are subreddits dedicated to particular areas; Western is in area, Ontario has its own subreddit, Canada, London, we've got Western and London, Ontario. So those are all spots where you can go and find the same usernames used in different areas, because usually, someone doesn't do all of their posting on London, Ontario. You can identify some people that likely have a tie to London, Ontario pulling usernames from there. And then you can retrieve their history. And that's where we started to bring in the machine learning apparatus to help us out.
Henry: Right, so they're prominent on Reddit, Ottawa Senators fans or something and then yeah, you have a pretty big hint there or something like that.
Dan: Yeah, exactly. And with that was one of the things we started thinking about at the beginning of this: what would be those flags [hints]? And it's like, since fans, and maybe government stuff, maybe [tags like] Ottawa Blues Fest, like there's a lot of things that folks in that region, for example.
Henry: Right, definitely better to start off with a major city.
Dan: Yeah, I think so. But we're not just interested in identifying people so we can go to their house, and I don't think we'd ever be able to do that, which is just as well. But the cool thing about this is that it’s a two-way street. Through social media, the health units can reach out to these individuals without exposing them, without having to know exactly where they're at, without having to know their name. Even just with things like, “did you know, we have this program? Did you know, safe injection sites are here, here and here?” Even stuff that basic is stuff that they can't target right now because they're not sure who really needs it. So that's really the goal of the project in terms of what we hope we can deliver to them.
Henry: Have you thought about how you would ever possibly expand to other social media sites?
Brent: The advantage of how we build the AI technique is that as long as it's from a social media site that has text, it can be used. Nothing that we are doing so far as specific to like Reddit score, karma votes, it's entirely based just on the words they use. So it actually translates to Twitter very easily, and potentially other social media, too.
Henry: Yeah, weirdly, I see a lot of heavy stuff on Facebook these days, which you would assume wouldn't be the case. But Facebook is like if I'm feeling like particularly strong that day. I'll check out Facebook and see what old people from high school are doing and maybe stuff hasn't panned out perfectly.
Dan: I agree. And I wonder if that's something that's changing over time. We have some great expertise at Western too who are thinking about the impacts of social media on different aspects of people's lives. Jackie Burkell in FIMS is a great example. She's a great researcher and she looks at different aspects of social media. One of them I think, being the idea that you don't always present your best self on social media; you pretend that things are always super sunny, even when they're not. But I wonder if we're seeing that change over time. That's the other thing about this project. And the thing about social media in general, that everything is evolving so fast that we're kind of watching it happen in front of us as we develop these techniques. And it'll be interesting to see where it goes and how we must adapt the work.
Henry: Yeah, and Reddit as kind of an intellectual community, in a way. You guys said they have all these safety tips and there's actually a real discussion going on. If I were to do an opioid, that would be the place that I would trust to talk about it. With Facebook, I think you have people more just shouting out into the void if that makes sense.
Dan: Yeah, I agree with that. And I think, like what Brent was saying, but the opioids community is really remarkable; there are people on that subreddit who are public health psychologists and people who care about harm reduction. So, professionals are already using that subreddit, for example. So, we're seeing people with a lot of expertise and a huge amount of lived experience having these conversations. It's an amazing thing that's being captured right now, as people are going through this.
Henry: When you came on last summer, we talked about physical AI diagnosing stuff? Have you noticed any similarities or major contrasts between the two projects?
Dan: I feel like there's one big difference and one big similarity. In the diagnosis setting, you usually have measurements of what we call health outcomes -what happened with somebody- and you're trying to figure out the causes that led to whatever that outcome was, whether it was good or bad. Then you're trying to figure out what you could have done differently. We can sort of do that with this project, but not nearly as well. And it's a lot more about just saying, "look, there's this whole big bunch of data and we're just trying to understand what the patterns are in it. We're trying to relate that to what's happening in people's actual experience." So this project, in a lot of ways, has been a lot more open-ended, which has been exciting and interesting, but really challenging. It's a lot more difficult if you don't have a problem, like, here's your specific problem, and I'm going to do this, this, this, and then I'm going to solve it. And then it's going to pick a treatment for somebody. This has been different; it's really tools for exploring the data and trying to make use of it when you can't necessarily get that kind of clear goal. So it's been cool to be doing both of these kinds of research. We're lucky working in AI to have different aspects to explore. But I think in both cases, you always have to be so careful; to do your best to understand where the data are coming from, how they're being produced, and what they really mean. And, whether the data comes from Reddit, or electronic health records, if you're going to do a really good job, you really need to take the time not just to understand the AI methods and stuff, although that's key, but to appreciate what that domain of knowledge is and, how can you add to that.
Henry: How much data are you getting on a daily basis?
Brent: We're not doing the data collection, but the repository that hosts this, per day, there's probably two or three gigs per day going up; gigabytes of just pure text going up on Reddit every day. I think someone was saying there's something like 2000 or 3000 posts every second. Not all of them are going to be relevant. And that's part of the challenge of working in social media, dealing with the huge sea of information that's out there. I think it was something like there was 3 billion Reddit post last time we did a full count of everything we had. So, there's, there's a huge wealth of information. And that's part of why we build the search technique. Because really, until you go and see what's on there, in a lot of ways you have no idea what you are going to find. There's definitely a lot of communities on there that posts all kinds of things.
Henry: I guess. So is it levels of filters, and you kind of narrow it down slowly?
Brent: I think that's a good way to describe it. And then the last stage of the research that I find the most interesting is when we build a Smart Filter that's customized to seek what we want to look at. Because there's a lot you can find by just grabbing a subreddit, grabbing a list of usernames that are associated with what you want. But when you can find relevant information with something that has no idea or understanding about any of these topics, well, that's the fascinating part to me.
Henry: I think this is super interesting research. And I think you guys are kind of getting in on the ground floor, but it's probably going to be one of the most prominent forms of research over the next two or three decades. It’s important to be able to figure out how to identify people on social media, because I think one thing we've seen from recent tragedies where people are overwhelmed by stuff on social media is that there are always warning signs when you look back.
Dan: Thanks. That was a lot of fun. We have got our website under construction. It is at philab.uwo.ca and we're slowly getting research projects up. So, if people are interested to know more, go check it out.
Henry: That concludes this episode of the Western Science Speaks podcast. I think with a research area like this, you're going to see it blow up where people try to figure out how can we deal with some of the mental health issues we see from people in my generation. And Dan and Brent are at least the first I've heard properly, addressing part of the problem. So, definitely a research project to keep your eyes on. I'm Henry Standage, signing out. Thanks for listening.
Malaria is a serious disease that threatens human life. This illness, however, is not unique to us and understanding how it effects and is transmitted among other species can be important for controlling it among our own populations. On this episode of Western Science Speaks, our guest, Leticia de Souza Soares from the Department of Biology, talks about how birds specifically pass Malaria to one another through a middleman; the infamous mosquito.
- Downloadable Transcript (Coming Soon)
You're listening to the Western science speaks podcast. Presented by Henry Standage.
Welcome to the Western Science Speaks Podcast. Today we're with Leticia de Souza Soares from the Department of Biology. Leticia works at the awesome aviation center here at Western. We sat down to talk about how birds pass parasites to one another, which led us down a bunch of interesting alleys about the history of islands being exposed to parasites that the native bird species weren't equipped to handle. Small spoiler alert - it doesn't look great for my native English blood here. And then we moved on to talk about how as people lucky enough to live in a first world country, how can we become better tourists? Anyway, here's the interview.
Henry: Okay, what bird do you primarily look at in your research?
Leticia: So I it's easier to answer that question just not thinking about a specific bird but thinking about more systems rather than an individual bird species. So I have worked with birds in the Caribbean region, mostly across the islands off the West Indies, in the US, in the Amazon, and now in Canada. I'm mostly interested in birds in the tropics that live year round they are so they are born there, they reproduce their they died there. And also birds that breed in Canada or in the US. And then whenever temperatures go down, it gets cold, and we start complaining about how miserable we are, they just fly to the south and then spend the winter months in tropical regions. So they are migratory birds.
Henry: And your work specifically looks at the disease, malaria. So what makes malaria different from other parasites or diseases? Or more prominent in birds?
Leticia: Yeah, I think for bird malaria, I think we just know a lot about it. And we know little about other avian diseases. And the difference is probably because of the similarity of malaria in human malaria. So a lot of the major discoveries in human malaria started by looking at malaria in birds and looking at doing experiments in birds and looking at which vectors transmit malaria to birds. And then carrying this knowledge over to human malaria and trying to understand it. So the bird malaria field takes a lot of advantage of the advances in terms of research of the human malaria field, and vice versa. So it's a really good system to study malarian birds, because it's almost like an uncontrolled system because in humans, you have obviously we treat malaria, and we have all sorts of measures to control. So understanding how the system would evolve naturally, so a lot of these ideas come from natural systems like in the bird malaria system.
Henry: Can you give an example of how the process is the same between birds and humans with malaria?
Leticia: Yeah. So they're both transmitted by mosquitoes. Different mosquitoes, there are mosquitoes that only feed them birds and their mosquitoes that just pretty much anything with legs and warm blood. But there's many, many mosquitoes that just take a lot of meals only from birds. Same thing for humans there are mosquitoes that are just specific human-feeding mosquitoes. So they're both transmitted by a vector, which is like this middleman that carries the parasite from one host to the other, and they have the same symptoms. So right after a mosquito - when a mosquito take a blood meal - it can inject the parasite through the saliva because the parasite gets lodged in the salivary glands with a mosquito and then a mosquito injects saliva into the host and then the parasites just get in the host through that way. So it's the same thing for birds as well. The path that the parasite takes into birds is the same thing as it takes in humans. So first goes to the liver, spend some time in the liver, and all they do pretty much is produce clones of themself, they just make clones after clones after clones. So, initially, they do it in the liver, and then they leave, the liver and then go on to factoring red blood cells and then destroying red blood cells. So a cloning phase of red blood cell and make tons of copies of itself, burst the cell and then goes on to infect other cells. So those are parallels that happen in the bird system and then in the human system as well.
Henry: Are they treated the same way medically?
Leticia: Yeah, the there are drugs that people can use - the same pharmacological mechanisms apply, and the way the parasites invade the cells is the same, that there are many, many parallels.
Henry: Can malaria only be transmitted by a mosquito? Is a bird contagious after getting a can it spread it?
Leticia: So, if you handle a bird with malaria, you can't get it for two reasons. First, because the malaria needs that intermediate - the mosquito middleman guy who will transmit the malaria from one bird to the other. The parasite actually needs the mosquito it needs to pass through the mosquitoes so he can change his shape. So you can see the parasites is kind of a shapeshifter a little bit. It actually has sex in a mosquito, so it makes clones in the birds produces tons and tons of itself. And then in the mosquito is where sexual reproduction actually takes place. And after it reproduces inside the mosquito, it has this specific form that is the infective form. So they needed to pass through mosquito to go onto a different host. And you also wouldn't get malaria because it's a different parasite that infects birds so it's completely different, but also other birds that if it's just like direct contact with each other, they wouldn't get malaria because they need this mosquito intermediary.
Henry: There's probably a funny joke to make about the mosquito serving as a home. Yes, well reproduction but it's a school podcast so I'll hold off. Tell us about your paper documenting the extinction of endemic bird species in Hawaii.
Leticia: So, that paper we were interested in looking at, specifically, the type of parasites that were in Cuba. So islands in general are very important ecosystems for all sorts of organisms. So Island populations are vulnerable, because first they're isolated from everything else. Some islands more isolated than others. Second, many of these organisms they evolved from one ancestor, but they are unique organisms. They have evolved on an island and they're not found anywhere else. So they have this uniqueness to them. And they have this naiveness to them too, because they have never been exposed to things that are found in a continent, right? So we have this extra interest in monitoring island populations because they are more prone to threats of things that people bring into this islands. So, Hawaii is a very sad case in terms of bird malaria because the mosquito was introduced in the island in the early 1800s. And a mosquito came with British colonizers - it was in the water that ships collect - like to balance - so that shipped they know the precise ship that sailed from Mexico to Hawaii and brought in all those mosquito eggs and then whenever this ship anchored in Hawaii it released the water into stream. And then the mosquito eggs just got all over the island. It was Maui and then the mosquito populations just established there. But before the mosquitoes got there you have all those Europeans arriving in Hawaii bringing just ducks and chickens and all sorts of domestic birds and animals that likely already had malaria and we're just reservoirs for the parasite. And then so you have like the pool of parasites and then you have the mosquitoes and that's the perfect combination for infecting the birds from the island. And Hawaii has many birds that have evolved with, they're endemic of the island and they just never handled anything like that before. So there are these reports from naturalists from the 1800s that they write about their everything in their life like what they eat for breakfast, their hikes and all that and they report like seeing birds dead on the forest grounds, which is something that if you do hikes, you don't really see birds that often you don't see animals that because something else just eats it or it decomposes super fast. So I think it gives us an idea of how impactful that was. So there were many extinctions reported, and many populations declined tremendously. And until today, people have been monitoring Hawaii's malaria and the parasite that caused disease this extinction and decline of this Hawaiian birds is actually globally distributed. But there are very specific strains of this parasite that are more lethal to birds, they are more invasive, whenever they are inside a host they reproduce faster, they cycle faster than others. And so when we were working in Cuba, we were just describing the malaria parasites of Cuba and then we found the same strain that was present Hawaii. And I was like, "Oh, this is bad." This is not good. So what we decided to do is to go a little further in terms of understanding the genetic fingerprint of the parasite, so we looked at a very fine scale variation in the genome of the parasite. And so by looking at a specific region of the genome, we were able to just go a level further in terms of specifying which strain of parasite we're dealing with. And we found a match with the Hawaiian strain. So the same strange that was in Cuba was the strain that was in Hawaii, and it was the strain that had caused extinctions in Hawaii. But what is interesting about the story is that we had to go back and actually read books about the history of colonization in Central America and in the Caribbean to understand kind of the timeline of human occupation in those areas. And we think that this introduction of the mosquito in the parasite happened much earlier in Central America and in the Caribbean. (Henry: And it's really bad though, right?) Um, it's very common there, this specific bad parasite is not so common. It's actually very rare. So we have sampled more than 20 Islands in their archipelago and we have only found it on Cuba. Just so you can have an idea. So it's not it's not super common - this specific bad one. So that's why we were concerned and we were trying to understand what was going on. So we think that if you put this event in a timeline, so Europeans started this sugar cane plantations, in the in the Caribbean region, in the 1500s, and it was later on in Hawaii. So it is possible that ships that were doing slave trades from West Africa where the parasite actually is originally from. So they brought the mosquitoes and birds to to Central America and to these islands into Western this. And we probably missed a ton of extinctions, right? Because at the time, there weren't that many naturalists reporting these things and doing these expeditions, and in Hawaii happened later on, and there were tons of naturalists that we're living in the island and just reporting this things as events of mortality and possible extinction. So with that, we think the first parasites, hitchhiked with the the ships from West Africa to the Caribbean region, and the established there, we probably missed a ton of extinctions. We still don't know exactly what's going on in Cuba because our sample is from Guantanamo Bay only so we don't have a comprehensive assessment of Cuba, unfortunately. And then the parasites probably moved from Central America, in the Caribbean region to Hawaii later on.
Henry: Now, as with most historical stories, it comes back to British colonizers. Is there is there anything they could have done to not bring the mosquito over? Is there anything I can do as a potential traveler going to a part of the world that might be particularly sensitive to mosquitoes coming over? Is there any steps you can take?
Leticia: I think that's a really good question because I don't know what these people were thinking at a time, my general personnel perspective is that they didn't care. But now I think where there is a threat many countries have policies of what you can bring. And you just have to be respectful of these policies, understand them before you go abroad, and follow them - be compliant with what they're suggesting because they know what they're dealing with. (Henry: Right, don't bring your pet mosquito; Leticia: Yeah, or your pet bird.)
Henry: Speaking about climate and different parts of the world, are there some regions that offer more nutrients to birds that help fight against diseases like malaria.
Leticia: I think this, this is a complex question that I don't have the answer for and I don't think anybody has. I think there is a different way of looking at this problem. And I think Malaria is just one more thing that birds are dealing with, right. So they have now just a reduction of food sources, they have reduction of their average dead, they have all sorts of like toxic contaminants in their habitats, they have other types of parasites that they have to handle. So they have this constant moving target of like new threats that they have to respond and adapt to. And this change from one place to the other some species are more vulnerable than others. And I think our role now is to try our best to buffer all the threats that birds are facing, which include things like keep your cats indoors. They are simple.
Henry: Do you have any trips coming up? Are you going anywhere in the future?
Leticia: Oh yeah. I'm always going somewhere I was just in the Dominican Republic a month ago. In the fall, I going to be working a long point. And I'm going to be working in Bruce Peninsula as well with migratory birds.
Henry: Alright. Well, thanks for doing this.
About 1% of the Canadian population is affected by Autism Spectrum Disorder; 100,000 Ontarians alone currently live with ASD, which presents with a number of symptoms including difficulty with social interaction. On this episode of Western Science Speaks, graduate student Wes Robinson from the Department of Biology shares his insights the how the brain deciphers social cues, what has happened when it can’t, and how his research may contribute to a better understanding of how to treat autism.
I'm Henry Standage, and you're listening to the Western Science Speaks podcast. The Three Minute Thesis (3MT) competition in Canada gives graduate students a chance to pitch their research in a condensed manner. In the next few weeks, I'll be sitting down with a couple of the participants from Western's field. Today, we talked to Wes Robinson, about his talk "X marks the spot" that focuses on how our brains understand social cues. Here it is.
Henry: Tell us about your work.
Wes: So, I'm studying a specific protein in the brain that we use to control information flow. So to take a step back let's see you're imaginin yourself standing in a line or standing at the bus stop, and you can feel people that are getting a little too close to you, and you can actually feel them in your personal space. So that is essentially what I'm looking at in my master's program. So, in that feeling, you're using your eyes, your ears, or your smell, or you're receiving input of what's around you. And so when your brain that takes that in and then deciding what you want to do, and so that's, that's that feeling you get of somebody being too close from you. So I'm actually looking to study this in the fruit fly, which seems like a large jump - from the human-feeling personal space to fruit-fly-feeling personal space. And so what's interesting is we can study in the fruit fly because we have set up an experiment that allows us to test what the fruit fly's preferred social spaces is. So we set them up in the chamber and we let the fruit flies explore and then they actually settle at our preferred distance, which is about half a centimeter. And we do it over and over and over again, we see that they were repeatedly settling at half a centimeter. So you know, that's their preferred social space.
Henry: Do you work with Anne Simon?
Wes: Yeah she's my supervisor.
Henry: A regular podcast listeners quite familiar with the fruit fly. Taking it back a bit - where did this idea come from? Is it a natural thing that's inherent that we're born with it's a space or is that something we learn and developed?
Wes: The short answer is both. So it's an innate behavior that we have to want to be a certain distance to other people but the environment can influence whether we want to be closer or further. So a colleague of mine studies flies in isolation versus flies that are enriched and they actually they have different personal spaces that they prefer depending on how they were raised but it's actually already innately encoded the behavior of a preferred distance. So looking back into my project specifically, I'm looking at a protein in the brain that helps to control the information flow through to the brain and then helps you to decide what you want to do with that and so why this protein is interesting for me is because mutations in this protein in humans are people with a predisposition for autism. So that's where I'm looking at that angle. It's really cool because we can study this protein in fruit fly. And this specific gene and protein is very, very similar to humans, as well as the neurons, which are the basic units of the brain. They're very similar between flies and humans. So not many people would think about that, but flies have a nervous system, they have neurons. And if you were to have a neuron in a microscope of a human and the fly side by side, you almost couldn't tell the difference. You can study one and have an impact on us as humans.
Henry: To me it feels like something that's not just related to sight because if I go behind someone really close just to their back, they're going to notice there's gonna they're gonna know something's up. And is that brain-related? Is there another sensor that goes past the site?
Wes: Yeah, for sure. Your brain actually takes all your sensory modalities, combines them, decides what to do, and then goes from there. So you're right. And even in the fly specifically, we have a way of doing it, we basically do it where they can't see. And they still have their preferred social space of centimeters. So even without sight, they do go to that preferred space. So it's just taking all of your feelings - so like your sense of touch, your sense of smell, people getting too close you can even smell them. And so that's what's contributing to that space.
Henry: What are the signals you look for in the flies? How do you know that one is uncomfortable with how close another is?
Wes: You can't really tell how comfortable they are. That's sort of putting a human feeling to it. I specifically just look at the distance. So one fly, how close is it to another fly? But we actually recently expanded to look at when you're looking at one fly, how many other flies are within for body lengths of that fly? So we're trying to see as a group as a whole, are they getting close together? Are they getting further apart? And so our recent experiment of mine where we mutated this protein that I was talking about - that's a candidate for autism - we mutated this protein and we're seeing that flies in females actually getting closer together, and flies and males actually get further apart. So we're getting a sexually dimorphic response from the fly. Which is really cool.
Henry: What are the limits of using flies for this research? Because you said with neurons, there's really astounding similarity with humans. What can humans offer in research that would go past the flies?
Wes: When we're looking at flies, there's always only so much you can extrapolate to humans. So the behaviors we have to look at to be very simple. The behavior of just how close is it? How much does it move locomotion? When in humans, there's conscious thought, there is deciding things, there's higher thinking. So we can only extrapolate so much to humans. But that being said, when you're looking at people with autism, the clinical definition of autism is having an abnormal social behaviors. So when we're trying to quantify that in the fruit fly, we're just going to look for abnormal social behaviors, not necessarily whether we want to hang out and play video games as humans, but whether they're doing social things like they're getting closer together.
Henry: Do you see an impact? If one flies getting closer to the others does it affect, say two days later how the other flies interact with this one fly?
Wes: We hadn't looked at that specifically. But what I was telling you earlier about with my colleague who's looking at what we do is right from birth, or we call it eclosion. As soon as a fly ecloses, we separated from everyone else. And we find that those flies are generally less social. So they want to be further from other flies and when we actually sort of forcing them in closer spaces, closer places, they become more aggressive to other flies.
Henry: About this protein, I want to know a little bit more about that. Run me through what exactly it is again.
Wes: So the proteins called neuroligin and the simple explanation of what the protein does is it helps two neurons connect to each other. And it allows the two neurons to talk to each other. So a neuron can go from your brain to your leg, and it can tell you: "hey, I want to walk", so you lose your legs. So for them to be able to communicate from the brain to the leg, they have to be able to talk. And so this protein, while you're developing while you're growing as a human, you have to form these connections. So the protein forms the connections and then helps facilitate the communication across.
Henry: Do people, you say it's directly related to autism, is that they have a smaller one or mutated one.?
Wes: So they actually found this mutation in a family. I think it was a Swedish family that they saw had hereditary autism. So there were multiple people in the family that had autism and they were trying to look at what might be the link in the family. They found a mutation in this gene, and that's where they saw that in each of the people affected with autism, they have this mutation. And one other thing about autism is it isn't a one-gene disorder. It's a multi-gene disorder. And so I like to think of it as puzzle pieces. So, the more puzzle pieces or the more genes that are mutated, the more severe autism. And that's why you've heard of autism spectrum disorders. So there's the more mild version of autism, which has Asperger's, and the more severe version of autism, which is autism. And so the more puzzle pieces or the more mutations in these genes that come together can lead to a more severe, or if you have fewer mutations, it's more of an Asperger's disorder.
Henry: So it's not something like Down Syndrome where there's a difference in the number of chromosomes? So they're not lacking this protein, it's just different?
Wes: Correct. You said it, right. It's a mutation in this protein.
Henry: Okay, let's talk solution because you're doing the Three Minute Thesis. Ambitious as possible, 10 years down the line, what do you want to be able to say about this research?
Wes: As much money as I can have (laughs). So what would be the ideal solution, and this is what I'm pushing for and I'm going to start my PhD and continue to look at this, is I've mapped in the fruit fly brain where this protein is. So I've actually found a specific structure in the brain called the mushroom bodies. And that can be translated loosely to the human hippocampus. And so I've located that this protein is in the mushroom bodies. Now I'm trying to follow the flow of the information. So the sensory information, so how close to somebody standing to you goes into the brain, and then it goes to the rest of the body and you decide something like if somebody's standing too close, you move. So I'm trying to figure out what downstream of this protein is going to the rest of the body or is it going somewhere else in the brain? So I'm trying to map it, maybe even down to single neurons or single clusters of neurons, where is this information going? And the ideal solution for humans is if we can find a downstream very succinct target of where this information is flowing. This could be a possible therapeutic. So people that have autism, the current treatment they have uses medicine to either recover impaired signals or to repress overactive singling from the brain. The issue arises with these complex networks, but there's often a widespread effect of the drugs - you often get unwanted side effects like sleeplessness, nausea, depression. So if we can find a more succinct target downstream that we can manipulate with some sort of drug or some sort of chemical, then we may be able to reduce some of these unwanted side effects.
Henry: By understanding where exactly fly's brains and human brains or similar, Wes hopes to provide a solution for people with autism who may lack the awareness of social norms. You can check out more three-minute theses on the Western University YouTube page. I'm Henry Standage, signing out. Thanks for listening.
Rebecca Clark came to Western for her Masters of Environment and Sustainability (MES). As her time at Western comes to close, she has left her mark on campus by leading all Science Faculty masters students in volunteer hours. Rebecca joins Western Science Speaks to talk about her experience volunteering, and why with the right organization and time-management, it can be worthwhile in the short and long term for any student looking to get involved.
- Downloadable Transcript (Coming Soon)
Power outages disrupt modern life, making the speed of repairs to electrical wires absolutely crucial. Unfortunately, the technology behind power outages is dated, leaving families and businesses in the dark longer than they should be. Western Science Speaks is joined by Dr. Hanan Lutfiyya, Chair of the Computer Science Department at Western University, to discuss the flaws in our current method of power repair, and her proposed solutions to the issue.
I'm Henry Standage, and you're listening to
Look, I don't need to convince you how important electricity is to our day to day lives. To live without electricity is to live in a world without an economy, entertainment, or just plain old comfort in your at home life. That's why it might come as a surprise that the technology we use to detect and fix power outages has barely progressed since electricity first came into our homes. Dr. Hannan Lutfiyya, from the Department of Computer Science, researches how power outages are repaired, and where she believes the technology needs to go. She joins this episode of Western Science Speaks, here's the interview.
Henry: How is our power distributed?
Lutfiyya: Power is distributed, it starts with the power plants. So a power plant actually generates the electricity, whether it's from coal, hydro, nuclear, or whatever, then what it does is it has to transmit that power to the consumers. So it does that through transmission lines. And those are the things she's you often see these long transmission lines, you know, the electric poles. But the thing is, so when it does that transmission, what it does, it has to increase the voltage a lot, so that it can be transmitted over a long distance. Then when it gets closer to the consumers, what happens is you actually have to decrease that voltage, because the high transmission voltages are dangerous. So what they do is they go to a distribution grid, where it starts to decrease the voltage before making the final delivery to the consumers.
Henry: Right. So it comes out extremely high voltage when it leaves the plant.
Lutfiyya: That's right. And then when it gets to closer to the consumers, they have to start decreasing that voltage before they can actually power your home.
Henry: What happens when we have an outage?
Lutfiyya: What happens when we have an outage, well, you every you no longer uncle have electricity, right? And usually, what happens is that it's very difficult to detect. So what they [providers] have to do right now, is they send crews to the area that's been affected by the outage, trying to find out what's the cause? You know, is it something that one of the substations that's reducing the voltage, did a tree fall in a branch or whatever? So they actually have to send crews out to sort of manually search for the outage.
Henry: There's no automatic sensor or anything?
Lutfiyya: No, nothing. It's very manual right now.
Henry: And so I imagine that when there's severe wreckage in some sort of community, such as a hurricane, or tornado, locating the pivotal spot must be extremely
Lutfiyya: It is, there could be actually multiple causes, right? If you have two trees falling on the line, right? But yeah, it can be very difficult to find out.
Henry: Is that a universal method? Or do different cultures have more modern advanced technologies for this?
Lutfiyya: No, everyone is pretty much doing it the same way.
Henry: What are you proposing as a solution?
Lutfiyya: The solution we're looking at is we're saying, "can we pinpoint what's causing the outage?" And it turns out that there are techniques on the transmission network that people do use for that. The reason it doesn't carry over to the part of the grid distribution network, which is closer to our homes, is because they're much more complicated. Because every time if you are the neighbourhood, you may have a line. And then you have to have a bunch more lines, they have to branch out like a tree, or radio network, just so that they can actually deliver it to different homes. So the approach we're taking is that whenever there is an outage, it will emit some sort of signal. And our centres are going to detect that signal. And then based on that, they will be able to figure out based on that signal also get the reflection. Because when a pop happens, it will send out signals throughout the distribution network and they start to bounce. So the sensors, they'll get the initial fault and they'll get off the bounces or the reflections. And so you can use those signals - you can use the time between them - to sort of help you figure out what were the actual location is.
Henry: Is that what you call the x-fault?
Lutfiyya: Yes, you're trying to pinpoint. So that's what's actually causing that outage. What makes that actually very hard, is that the way this works, is if you have a fault somewhere, it's going to take out everything, right? It's going to cause an outage everywhere, within a certain area, the reason is they are trying to protect the equipment. So I can have two faults in one area, and they cost the same outage, right? And that's making it very challenging.
Henry: I think this will surprise a lot of people because we're talking about a billion-dollar industry, where when there's a fault, more money can be made in other industries because
Lutfiyya: That's absolutely true. And it's not even 20th century, I mean, the electric grids are really based on a concept from almost the first days of the grid. Now we're talking more than 100 years, sure the equipment gets upgraded and they will, you know, buy new stuff and it's more modern and faster and all that stuff. But, the basic structure is the same. What's changed, I think now, looking at the possibilities of using cheap sensors, analytics. And they're looking at trying to take advantage of it and in this environment. But you're right, it's an old infrastructure, and yeah, we still have it and we're still using old technologies.
When a power outage strikes, it takes down the entire community and won't be fixed until the exact sweet-spot is manually found by workers. Power outages are inevitable. But prioritizing the technology behind repairing them faster, so that hundreds of families aren't left in the dark is more crucial than ensuring top-speed WiFi. The world has primarily shifted to automatic detection methods for industries as lucrative as electricity. And considering the impact outages have on a wide range of people and businesses. A modern shift and how we fix them is imperative. I'm Henry Standage asking you do a warm up and chill out. Thanks for listening.
Predictive mathematical models are a useful tool for just about any type of research in science. Just how useful can they be in helping us to understand the nature of evolution? Dr. Lindi Wahl from the Department of Applied Mathematics at Western University develops models to help capture the evolution of microbes, specifically viruses, and bacteria. Western Science Speaks host Henry Standage chats with Dr. Wahl about the mechanisms viruses have or develop in order to avoid extinction. Discover how a better understanding of microbial evolution allows humans to stay one step ahead in the evolutionary arms race.
We all know someone who has or is suffering from cancer. This week on Western Science speaks, Dr. Eugene Wong, a medical physicist at Western University, tells us about the wide variety of imaging technologies he uses to better understand the contexts in which cancerous tumors grow.
This week, Western Science Speaks brings you the magic of synthetic chemistry – mixing molecules to create new materials! Dr. Joe Gilroy from the Department of Chemistry at Western University shares his insights about a new, cheaper, and more efficient imaging dye designed in his synthetic chemistry lab. The molecules that make up the dye are red and they glow! Listen here to find out more.
Chemists never rest on their laurels. 159 years after the invention of the periodic table, they are still looking to find revolutionary ways to apply and organize elements. This episode of Western Science Speaks focuses on the dexterous ways in which Western chemists are manipulating the element Phosphorus, in order to create a brighter, greener future for our planet.
With a population in the millions of trillions, Parasites are able to evolve at a faster pace than just about anything on Earth. Through this extreme and rapid evolution, parasites are able to come up with increasingly innovative ways to attach to a host species; whether it be in the sky, or down on the ground. Beth MacDougall-Shackleton, a professor at the Western faculty of Biology, studies the way in which parasites evolve in order to find hosts. She brings her expertise to the Western Science Speaks Podcast to explain how parasitism became the most popular lifestyle choice on Earth.
In honor of International Week at Western University, Western Science Speaks podcast is proud to present a special podcast, celebrating the students willing to go the extra mile for a unique and foreign academic experience. Beginning with an interview with a student who spent 6 months in Stockholm, Sweden, and concluding with a student who spent 10 months in Singapore, this podcast unveils the tips and insight needed for any student considering studying in a new learning landscape.
On this episode of the Western Science Speaks podcast we explore why attributes such as kindness and selflessness have triumphed over some less altruistic traits in evolution. Geoff Wild from the Department of Applied Mathematics stops by the podcast for a discussion ranging from the evolutionary benefits of "niceness" to how to the incorporation of social media into our daily lives has changed our perceptions of one another.
DNA is our biological signature. If our DNA changes, naturally so do we. So what causes these changes? Listen to this episode of Western Science Speaks to have Kathleen Hill from the Department of Biology break down how DNA is the thread that joins us to our ancestors, plus a conversation about the biological impacts of modern life.
There's nothing better than losing yourself for a couple hours in a foreign, thought-provoking virtual land. Those experienced in video games will know this typically ends with an irrational rant at a bunch of animated characters on a TV screen, and on truly antagonizing days, a broken controller to boot. So how do video games manage to create a sense of real-world importance? On this episode of Western Science Speaks we hear from Michael Katchabaw of the Computer Science department at Western University. He discusses how his lab develops hyper-realistic methods for creating believable online landscapes, how online multiplayer has changed the industry, and where video game technology is heading.
Few would argue the magnetism of space and its mysterious nature. An endless puzzle looming over us, begging to be solved. At the heart of our extra-terrestrial conundrum are black holes; an irresistible juggernaut, seemingly capable of so much - yet barely understood. Western Science Speaks hosts Western's resident black hole expert, Dr. Sarah Gallagher from the Department of Physics and Astronomy, for a discussion about what we truly know about black holes, some of the common misconceptions about them, and a few of the most interesting theories Dr. Gallagher has came across.
Western Canada is one of the world's largest oil manufacturing regions, but in the last half-decade the industry has experienced a significant downturn, and is only just starting to recover. Western Science Speaks brings in geologist and former oil exploration CEO, Professor Burns Cheadle, for an objective breakdown of Canada's oil sector woes, the head-scratching reality of half the country importing oil from abroad, and how the sector impacts our relationship with the U.S.
We rely on metal to power our daily lives. The good news is, Canada is one of the world’s largest producers of this vital material. However, balancing that productivity with the obligation to protect our increasingly fragile environment is a challenge that leaves Canadian miners and environmentalists grappling. Professor Kim Baines from the Department of Chemistry joins Western Science Speaks to discuss metal’s national importance, the common mining and separation techniques, and how chemists approach the obstacle of assembling an environmentally friendlier mining process.
Are you concerned about the impact rapidly advancing AI technology on your privacy, wealth and our democracy? If so, you need to hear from Dr. Dan Lizotte from the Department of Computer Science at Western University. Dan joins the podcast to dispel the evil-robot narrative, talk about his medical AI research and illuminate the life-saving upside that robots can contribute to the health of Canadians in the very near future.
Meeting someone special is an undeniably worthwhile and necessary part of life. Unfortunately, it can often be awkward, flustering and at the worst of times, cringe-inducing. Determining how much of our success (or failure) in that domain is dictated by free will, rather than deep-rooted peculiarities is a question that fascinates researchers of behaviour. Amanda Moehring, from the Department of Biology, joins the podcast to break down the role genetics play in our courtship and mating process.
When you live in a fish-eat-fish world, the complexity of your environment and how you use it to survive and thrive is of critical importance. Neff Lab researcher, Chris Therrien joins us for part two in a series about the revival of Atlantic Salmon in The Great Lakes.
Western students, professors
Our world is supporting less natural life forms than ever before. How do we revive a once thriving species, that perished at the hands of man? Western Science Speaks talks to Nicole Zathey, who is working to restore the previously native Atlantic Salmon back into Ontario waters.
Western Science Speaks takes a tour of the Advanced Facility for Avian Research. This cutting-edge research facility has it's own wind tunnel and is able to simulate almost any environmental condition. We talk with Jeff Martin who's looking how climate change is affecting birds in Canada.
Sustainability, alternative energy, profitability