Science Friday - Cancer Vaccines, Planting Wildflowers, Eating Copi Fish. August 5th, 2022, Part 1

Episode Date: August 5, 2022

White House Declares Monkeypox Outbreak A Public Health Emergency The Biden administration declared the monkeypox outbreak a public health emergency on Thursday. Earlier in the week the White House appointed Robert Fenton, regional administrator at FEMA to direct the federal government’s response to the monkeypox outbreak, along with a deputy director from the CDC. This comes after criticism from activists and public health experts, who have said that the federal government has been dragging its feet on access to vaccines, testing and treatment for the virus. Ira talks with Tim Revell, deputy United States editor for New Scientist, about the latest monkeypox updates and other top science stories including; new research into the shape of the human brain; how hand gestures can improve zoom calls and a plant that harnesses the power of a raindrop to gulp down insects.   New Steps Toward a Vaccine For Cancer Vaccines have long been used to prevent infection from viruses. But now, scientists are working on a different kind of vaccine—one that targets cancer. Dr. Kai Wucherpfennig is working on a cancer vaccine that would target tumors that tend to spread quickly and are resistant to treatment, like melanoma and triple negative breast cancer. This type of vaccine is intended to be used after a patient has had their tumor removed. The goal is to prevent the spread of cancer cells to other parts of the body, which is called metastasis. So far, this type of cancer vaccine is effective in animals, and the results were recently published in the journal Nature. Ira talks with Dr. Kai Wucherpfennig, chair of cancer immunology and virology at the Dana-Farber Cancer Institute and professor of neurology at Harvard Medical School, about his latest research into cancer vaccines, and how recent advances in understanding the immune system has jump-started research into new types of cancer immunotherapies.   Restoring A Sensitive Ecosystem, One Wildflower At A Time The New England blazing star is more than just a pretty blossom: it’s an integral part of a globally-rare ecosystem called a “sandplain grassland.” Just like the name suggests, sandplain grasslands have sandy soil with tall grass, no trees and an exceptionally high number of rare plant and animal species. That includes plants like the New England blazing star, an important food source for various grassland insects. Today volunteers would plant 1,000 of them to help restore Bamford Preserve, a 60-acre parcel of sandplain grassland on Martha’s Vineyard. As climate change threatens both human health and the natural world, experts say that protecting biodiversity hotspots like this one will offer the most bang-for-the-buck — protecting threatened species while offering other ecosystem benefits, like open space and flood protection. Read the full story on sciencefriday.com.   A Fish By Any Other Name: Inside The Effort To Bring ‘Copi’ To Dinner People who live near freshwater rivers or lakes are likely familiar with Asian Carp. The fish are not native to the U.S., but over the last few decades their populations have exploded in waterways like the Mississippi River Basin and the Illinois River. Over the last few years, there’s been a major PR campaign to move away from the name Asian Carp, in favor of a new name: “Copi.” The reason is two-fold: First, it joins a general trend of moving species’ names away from nationalistic associations, considering anti-Asian hate crimes during the COVID-19 pandemic. The other goal is to make the fish sound more delicious—creating a market that would incentivize fishing the Copi, hopefully reducing their populations. Joining Ira to talk about this is Jim Garvey, director of fisheries, aquaculture and aquatic sciences at Southern Illinois University in Carbondale, Illinois.   Transcripts for each segment will be available the week after the show airs on sciencefriday.com.     Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.

This is Science Friday. I'm Ira Plato. A bit later in the hour working on a vaccine for cancer, how recent advances in our understanding of the immune system are opening the door to new types of cancer therapies. But first, the latest on Monkey Pox. On Thursday, the Biden administration declared the monkeypox outbreak, a public health emergency. And earlier in the week, the White House appointed Robert Fenton, regional administrator at FEMA, to direct the federal government's response to the monkeypox outbreak, along with the deputy director from the CDC. This comes after criticism from activists and public health experts who said that the federal government had been dragging its feet on access to vaccines, testing, and treatment for the virus. Joining me now to give us the latest monkeypox updates and other top science stories

of the week is Tim Revell, Deputy U.S. editor for new scientist. He's based in New York. Welcome back to Science Friday. Hello, thanks for having me. And now that the White House declared monkeypox a public health emergency, what exactly does that mean? What opens up now? Yeah, so this had been coming for a few weeks now. I mean, if you recall that the World Health Organization declared monkeypox

a public health emergency almost two weeks ago now, and then there had been quite a lot of calls for the U.S. to do this as a national emergency. and then a few states like New York, California and Illinois, declared states of emergency for monkeypox. So the idea is that by declaring a national health emergency, that frees up some funding and resources to tackle the problem. So that includes things like extending the group of people who can administer vaccines, such as emergency responders,

pharmacists and midwives. It also gives the FDA more power. So part of that is being able to skip parts of its exhaustive review process to authorize measures for diagnosing, preventing, and treating monkeypox. And that was actually used quite a lot during the coronavirus pandemic. And there's talk that this power could perhaps make it possible to drastically increase the number of monkeypox vaccine doses that are available in the US without actually making any more vaccines.

There have been reports that the vaccines are hard to come by. Where are we now with this? Yeah. So the vaccine that's approved by the FDA for use in the US, it's called Ginios, and it's produced by a company in Denmark called Bavarian Nordic. And it's supposed to be that you get that with two doses 28 days apart. And it's very good. It can prevent someone from getting the disease completely. And it can also alleviate symptoms if you've already had it. So federal officials think that there's about 1.6 million people in the US at the highest risk of monkeypox, of catching monkey pox. But they only currently have around enough doses for 550,000 vaccinations. So here's where that additional FDA power could come in. So at the press conference yesterday, there was talk of a plan where you might be able to get five doses from a single vial of the genios vaccine. And this is called dose sparing. And in this situation, it would work by using a shallower injection than would typically be used to administer the dose. And there's a study

from 2015 that suggests that doing that you can use less of the vaccine, but you get the same amount of immune response. And that plan could be finalized in the next few days. That's really interesting. So who is eligible to get the vaccine? Should we all be anticipating the need for a monkeypox vaccine, just like we did for COVID? Yeah, not yet. So primarily Monkeypox is spreading in men who have sex with other men, and that's around 99% of cases. So at the moment, that's the primary group that's being targeted for vaccinations. So people who have sexual relationships with other men and who are at high risk, for example, people who have disorders that give you a compromised immune system, such as HIV, are being particularly

encouraged to come forward. The difficulty at the moment is actually getting hold of a vaccine is quite difficult. In New York, there has been instances where people have tried to get vaccines and the system's been all booked up or there's been a glitch. Currently, the advice is that vaccine appointments are booked up for the rest of the month. But if you're in one of the groups that's being asked to come forward, that you should keep checking the website and hopefully a cancellation will lead to free appointments. So it's a bit difficult and it's moving quickly at the moment. Well, I want to tell our listeners that if they have questions about monkeypox or misinformation floating around that you want us to debunk, send us your questions, and we'll get them answered by a monkeypox expert on the show next week. And you can do that by sending us a voice memo, sci-fri at science friday.com, sci-fry at sciencefriad.com, or find us on Facebook or Twitter.

Let's move on to our next story. It's one of these science marches-on kind. the stories where new research shows that the shape of the human brain actually hasn't changed much in the past, what, 160,000 years? That goes against all the theories we know. Yeah, absolutely. So we know the skull has changed in that time. You know, since early modern humans first arrived on the scene around 200,000 years ago, the actual size of our craniums hasn't actually changed that much, but the shape has. And we thought this was due to the brain. We thought what had happened is that behavior changes such as the development of tools and art had meant that our brains had become rounder and as such they'd made our skulls a bit rounder too. However, that's where this new research

comes in, suggesting that that could be all wrong. So this was a story that Luke Taylor did for us at New Scientist, and it's how researchers at the University of Zurich in Switzerland, they analyze and compared hundreds of ancient human skulls. And they found that the size and proportions of the skulls of homo sapient children from around 160,000 years ago, were pretty much the same as children today, but the adults were very different. And so as the brain reaches about 95% of its adult size by age six, that suggests that it's actually not the brain that's causing those differences as they come much later. So this does raise the question if it's not the brain changing our skulls. What did change our skulls over that period of time?

Huh, very interesting. And speaking of really interesting, we recently experienced the shortest day on Earth since the 1960s. Is the Earth spinning faster? Yeah, I don't know if you noticed. But at the end of June, we had a day that was our shortest day since the 1960s, and it was 1.59 milliseconds sooner than expected. So this is a really fun story from Ian Sampel at The Guardian. And we've actually seen quite a few records full of late. So in 2020, we had 28 of the shortest days in the past 50 years, which I don't know about you, but I actually had the complete opposite feeling in 2020. Yeah, they would not forever. Yeah.

This would make you think maybe is the earth spin it starting to spin more quickly, is that what's going on? But actually, it's doing the opposite. it. So in the, if you sort of look back in deep time over the last billion years or so, a day would pass in less than 19 hours and then it's been slowly increasing on average since then. So what caused these like little records that we've seen over the last 50 years, which is such a minute period of time compared to deep geological time, is all the little variations that we get on Earth. So things like the molten core sloshing about, the way the oceans move, earthquakes and tsunamis can all

affect exactly how quickly Earth is spinning, and that can cause these tiny little fluctuations day-to-day. Oh, that is really cool. Who knows it might, you know, get longer, what are these days? Yeah, well, that will almost certainly happen. We'll have it slightly longer, but it will only be for a very brief period. I want to end on some breaking news in the carnivorous plant world. Scientists have shown how picture plants are able to launch insects into their pouches using the power

of raindrops. You're going to have to tell me how that works. Yeah, hot off the plant press. You've probably seen these plants before. So picture plants are these carnivorous plants from Southeast Asia. And they have these sort of specialized leaves that look like elongated sacks with digestive fluid at the bottom. And so inside these sacks is like a nectar which attracts insects and a sort of slippery wax that normally sends the critters like tumbling down to their doom. But there's a second mechanism that we're now learning more about, which is that these elongated sacks, they also have a little lid. on top and sometimes insects crawl on the underside of the lid. And really, if you're a pitcher plant, you want a way to fling those insects into your digestive pool so you can eat them as a snack. And it turns out the way that they do this, which we're now learning more about, is that as raindrops land on the top, they have a sort of elasticated part towards the back that stores elastic energy and then it can use that to really catapult an insect. And it's a very similar

mechanism to when you get several people on a trampoline all at once. And if they bounce at the right time, it causes the person in the middle to really launch in the air much higher. And it's that same principle at play here where you can fling an ant into the digestive pool of a pitcher plant. So the pitcher plant then has to wait for it to rain. Yeah. Where picture plants live, it rains a lot, doesn't it? Yeah, it rains a lot where picture plants are. But it's also not their only mechanism. They can also use this slippery wax to get their food too. So it's sort of an additional way that they can eat their prey. Is this sort of a spring-loaded thing on the lid that it's waiting for the rain drop to hit and go boing?

The way it works is when it sort of hits on the top, that causes some elastic energy to reach towards the back of where the lid is. That sort of stores up, but only for a very brief period, which allows the leaf to sort of move jerk downwards, and upwards very quickly. And what that does is it means that the ant then sort of loses its footing and falls down below. And it's really unusual. We actually don't know of any other sort of carnivorous plant that uses external energy like this to power a movement to fling an animal towards its digestive pool. Love to learn something new.

Speaking of which, there's a new study that might make your long Zoom meeting feel a little more bearable. And how do you do that? using hand signals. Tim, tell me what the research found. Yeah, so if this is to be believed, we've all been video calling all wrong. And this is a fun story from Chris Stoker for New Scientist, where he spoke to some researchers at the University College, London. And they've been testing hand signals, which they taught to students during seminars,

which I do feel that could have gone a lot worse than it did. And they recruited 120 psychology students who were taught nine different gestures. So these included putting your hand over your heart to signify empathy, thumbs up and thumbs down for agreement and disagreement, and putting your hand on your head to ask a question. And then half of the group had seminars with the gestures and half of the group had seminars without the gestures. And then afterwards they did surveys and they did a big analysis and they concluded that the gestures like vastly improved the seminars for all involved.

Wow. Wow. Yeah. So it's like being in class a little bit more. Yeah, I guess it's like it was so used to just staring at a screen and not giving anything away that maybe you just need that extra prod to give the person at the other end of the Zoom call some sense of whether you're enjoying things, whether you have questions. Yeah. What you feel about it? Been there, done that, Tim.

Thank you for bringing that to us. Tim Revel, Deputy U.S. editor for a new scientist based in New York. We have to take a break. And when we come back, working on a vaccine for cancer, stay with us. This is Science Friday. I'm Ira Flato. Let's do a little word association. What do you say? When you hear the word vaccine, what comes to mind? COVID, monkey pox, maybe polio, right? One word that does not come to mind, I'm betting, is cancer, cancer vaccine. And while a cancer vaccine may not be grabbing headlines, my next guest is working on a vaccine that would target tumors that tend to be resistant to treatment. like melanoma, triple-negative breast cancer, and so far, this type of cancer vaccine is effective in lab animals. The results of the research were recently published in the journal Nature.

Joining me now to tell us more about that is Kai Wachafenig, chair of cancer immunology and virology at Dana-Farber Cancer Institute. He is also professor of neurology at Harvard Med School. Welcome to Science Friday. Thank you, Ira. Glad to join you. Let's start with the basics, should we? How does the immune system respond when it detects cancer cells? The immune system has a very sophisticated ability to detect trouble within cells that are within our body.

The cells that are particular relevant here are called T cells. These T cells have a special ability to detect proteins that are hiding within a cell. I can explain this best in the context of a viral infection. So let's say a cell is infected with a virus. A T-cell comes along. It crawls over the cells and detects proteins that display small snippets of many proteins inside that cell. And when the T-cell detects one of these snippets, we call them peptides,

then the T-cell becomes highly activated. it can kill that infected cell. Now, you can imagine that in the context of cancer, these T-Zols can be very powerful because they not only crawl through healthy tissue to detect any trouble, but they can also migrate into tumors and then detect abnormal proteins that are expressed by tumor cells

and then kill those tumor cells. Okay, so tell me about how they're, vaccine that you're working on works to prevent cancer from spreading and continuing to mutate? The challenge with cancer vaccines and actually any type of cancer treatment is that tumors continue to mutate. This is similar to viruses, for example, the COVID-19 virus, which continues to mutate and therefore can evade an immune response. The same happens within tumors, tumors generate a large number of mutations, and these variant tumor cells can escape our immune detection. And so what happens when T-cell attack tumor cells, they rely on these

proteins that can present these peptides from inside the cells, and when cancer cells mutate that process, the tumor cells become invisible to T-cells. So this is the problem that we try to address. And our hypothesis was that if we could generate a cancer vaccine in which there's a multi-pronged attack against the tumor cells, not only by T-cells, but also by other important immune cells, maybe it would be more difficult for those cancer cells to become resistant. And has that been successful? Yes. And so what we were able to do is to develop a vaccine that stimulates T cells and also MK cells. MK cells are natural killer cells, and they have the ability to detect and kill tumor cells. Now, what is important here is that T cells and MK cells

actually recognize cancer cells through different receptor systems. So it's very difficult for a cancer cell to mutate in a way that it's simultaneously eventually eventually, detection by both T cells and MK cells. Now, we're calling this a vaccine. Is that the true definition of what you're working on? We normally think of vaccines as being prophylactic, something that's preventative. Yes, so these are therapeutic vaccines, and therapeutic vaccines are more challenging than prophylactic vaccines.

For example, you know, you get a flu vaccine before you get the virus. it is easier to prevent an infection than to deal with an active infection. And the same applies to cancer. It is much more difficult to treat with ongoing established disease that may be widespread than to prevent the disease. And that's why it has been challenging to develop cancer vaccines. So do you give your vaccine, at least as you're testing it now, after you discover cancer? Yes. So the way we've done this in our mouse models is that we actually mimic an important clinical setting.

So the challenge in many cancer patients is that they have an initial surgery. The surgery is successful, but the tumor was already locally invasive. And frequently, there's a little bit of something left. Maybe, you know, 0.1% of the tumor. either locally or cells that have already spread. And so what we did in our mouse model is to use tumor cells that are very aggressive and that spread very rapidly. We let the tumors grow to a substantial size. Then we performed surgery in the mice. And only after we had done the surgery did we deliver the vaccine.

And what we found was that the vaccine was very effective in preventing the outgrowth of metastatic disease. Wow. This is how we envision cancer vaccines will be used in the future. So not waiting until the patient has a severe relapse with metastases in the liver and the lungs or in the brain, but actually giving a vaccine after surgery to prevent a recurrence. So this is, this is immunotherapy, right? You're tweaking the body to be able to search out, any remaining cancer cells? Yes, this is definitely immunotherapy. And the concept of immunotherapy is to empower the immune system to do what it already does very well, which is to perform surveillance of the body at all times and detect cells that are stressed. And so what we did

actually with our vaccine is to target a stress protein that is from, frequently expressed by cancer cells because they undergo damage of their genome. And these proteins are rarely expressed by healthy cells. And so what cancer cells do is to actually evade this immune detection mechanism and they cleave this molecule off the cell surface. And our vaccine targets a part of the protein that prevents this evasion mechanism. And the reason this matters for this combined. T-cell and then K-cell attack is that these molecules are detected by receptors on both T-cells

and K-cells. So with this approach, we can actually trigger a combined attack by T-cells and K-cells. Most people diagnosed with cancer, from what I understand, will undergo a few different treatments, right? How would this type of cancer vaccine work with the other available and cancer treatments. Given that cancer is a very complex disease, we definitely want to have many different tools and then select those therapeutic tools that are most relevant for a given patient. So the vaccine we've developed is most relevant for patients who upregulate these stress proteins on their tumor cells, and those we can actually detect in the blood of the patients. It's not vaccine that we think would work in in every cancer patient, but the pathway is relevant in the

number of important cancers that are very common. Yes, and you've chosen some really deadly ones like melanoma and triple negative breast cancer. Yes, so we tend to work on the cancers that are challenges for conventional therapies because we think that immunotherapy, has the potential to deliver, you know, long-term durable control of tumors. There is already substantial evidence that the immune system can do this. You probably had people previously on your show who are working on immune checkpoint blockade, which targets inhibitory receptors on T cells. And with those drugs, we have already seen that widespread metastatic disease can be

controlled long-term with these drugs. but unfortunately only in the subpopulation of patients. Now, I know this vaccine has only been tested in animals. Yes. And we've been doing this show over 30 years, and we have heard researchers cure animals of all kinds of diseases. But when they try to apply them to people, right? They don't work all the time.

What are the chances that this will actually work in humans? This is always the ultimate test. The way I think about cancer research is that we want to generate new ideas that can be tested in the clinic. And to develop successful cancer treatments, we need many shots on goal. I'm not going to be here claiming that our vaccine is going to be the final answer. But I think it's an approach that is worth testing. And so when will the tests in people begin? are you that close or close enough to see that end of the tunnel?

Yes, so we are collaborating with a leading pharmaceutical company to take this to the clinic, and we anticipate starting testing and patient next year. I've actually been contacted by a number of patients, and I always unfortunately have to tell them that I will not be the one who will be able to select patients for trials. The company that we work with will actually run the trial and they will select patients based on their criteria. This is really out of my hands. We develop the ideas and then other people take these ideas and take it to the next step. Other researchers are working to make vaccines that will actually prevent people from developing cancer using specifically tailored formulations.

How can the vaccine prevent someone from developing cancer? cancer, and how is your cancer vaccine different from these other approaches? Yes, so the ultimate goal of the field, of course, is prevention. But prevention is more difficult because not everybody is going to develop cancer, and you also don't know which cancer, if somebody will develop cancer, which cancer they will get. They're not all the same. So developing generic cancer vaccines is a pretty substantial challenge, in part because this vaccine would need to be associated with a very substantial safety profile.

The way we think about our vaccine is that we want to give it to patients with cancer who have, as I said, they've had a successful surgery. they have a high chance that there is disease left. And at that point, we want to eliminate it using both T cells and then K cells as a multi-pronged strategy. And I think this is an important way of thinking about cancer vaccines. Right now, cancer vaccines are frequently given to patients with advanced disease who have metastases in many different organs. And as you can imagine, the more tumor. cells they are, the more readily a few of these cells can evade an immune attack and then cause a relapse. So we'd like to, you know, target cancer when it's down and when the tumor burden

has been reduced, you know, more than 100-fold by a successful surgery. This is Science Friday from WNYC Studios. If you're just joining us, we're talking about a new type of cancer treatment, a vaccine with researcher Dr. Kai Wuchoffenig. You know, as I say, we've been talking about cancer vaccines for a while. And I'm thinking, well, just about, what, 10 years ago, a decade ago, developing a cancer vaccine seemed pretty implausible. We talked about it, but it was always somewhere way down the road. Has there been a paradigm shift in the field of cancer treatment that now we can talk about

plausibly? Yes. So, so, so, so, so, so, so, so, so, so, so, so, this is, you know, this is one of the big challenge and, and our challenges in biomedical research. So I think I would say 15 years ago, we weren't really sure that the immune system had an important role in fighting cancer, and, and, and we're now confident about that. So I think we're kind of confident about the biology that we're trying to, uh, manipulate. And now we're talking about, and now we're talking about the specifics. We're talking about what antigens do you want to target, how do you formulate the vaccine, which immune stimulatory agents do you want to use? And there are, of course, a lot of choices that the field needs to make when formulating vaccines and then taking them to

clinical trials. I do think that given our insights on the role of the immune system in cancer, that this will be eventually be successful. I cannot tell you whether it's going to be in five years or it's going to take another 10 years, right? Because... Yeah, I don't expect you to. This is a hard problem. Let me give that as my last question here.

It is a hard problem. What don't you know that you need to know? So we know how to develop vaccines against infectious diseases. that that field has matured for more than 100 years, right? But in infectious diseases, we're trying to develop primarily an antibody response or antibodies that can neutralize, for example, a virus. But in cancer, we actually need to induce a T-cell response. And so the technical aspects of how you optimally induce a T-Sall response,

and endow these T-cells with optimal cancer-fighting abilities. That is more complex. And it is sort of at the intersection of the biology and immune engineering. And there are a lot of details that are very important in developing these vaccines. And that's a very active field. And I do anticipate that the field will make progress. But as I said, I can't give you. specifics on the timeline.

Well, Professor, I want to thank you very much for taking time to be with us today. Thank you, Ira. A great pleasure for me. And good luck to you and your research. Thank you very much. Bye-bye. Dr. Kai Wuchafenig, chair of cancer immunology and virology at the Dana-Farber Cancer Institute, and he's also professor of neurology at Harvard Med School. Next week, we're going to be continuing our conversation about the latest in cancer treatment. We'll be talking about

CAR T-cell therapy, which is also based on recent advances in our understanding of the immune system, and people are talking about this very, very positively. We'll tell you why. We have to take a break, and when we come back, we'll talk about a monumental

effort to rehab one of the rarest ecosystems of the world located on Martha's Vineyard. Stay with us. This is Science Friday. I am Ira Flato. And now it's time to check in on the state of science. This is KERNO.

St. Louis Public Radio News. Iowa Public Radio News. Local science stories of national significance. Martha's Vineyard, you know it has a beautiful island off the coast of Massachusetts. And like many idyllic places in the U.S., development has threatened the island's ecosystem. In this case, it's the sandplain grassland found there, a rare ecosystem. But taking up the challenge is a team of volunteers, shouldering a daunting task to plant 1,000 wildflowers to rehab the area.

Joining me is Barbara Moran, Environment Correspondent at WBUR in Boston. Welcome back to Science Friday. Thanks, Ira. Great to be here. Nice to have you. Okay, give us some more information. The Bamford Preserve. Paint a little word picture for us. Will you please?

Sure. So the preserve is about 60 acres. And as you said, it's called a sandplain grassland. And what that means is the soil is very sandy. And when you look at it, it doesn't look like much, you know, I went out there and I was like, oh, grass. Right. So it's this huge grassy field with like sort of knee-high, tall grass waving in the wind. But there's no trees, you know, there's no nothing sort of, there's no magnificent sequoias or anything out of it.

But it's a huge open field with knee-high grass. But it's a really rare kind of place, right? Yeah, it's called a globally rare biodiversity hotspot, right? So this type of ecosystem is found only on the East Coast between New York and Maine, and most of the remaining sandplain grassland is actually in Massachusetts. And so when I went out there to the vineyard, I spoke with Mike Whitamore. He's the stewardship manager for the Nature Conservancy in Massachusetts, and he's overseeing this restoration.

These systems right here, these little sands, systems right here hold a high concentration of rare and uncommon species in the region. So it's not only the plants, but it's the wildlife, the pollinators, the things that you don't always see. So, you know, like I said, it doesn't look like much to the untrained eye, but there are a couple species of birds that depend on grasslands like this and a couple species of beetles and butterflies that are found almost nowhere else in the world. Right. So what's the development threat around the Bamford Preserve? So this area used to be a farm. It was a hayfield, and it came up for sale about 15, 20 years ago, and it was slated for development.

You know, the vineyard, like many places, is under huge pressure for people who want to build summer homes there. And the nature concerns he kind of swooped in and was able to buy it. So if they hadn't bought it, this would have been developed into, you know, condos or giant summer homes. Let's talk about the goal here. Now, this is to plant a thousand wildflowers. Tell me about that. Yeah. So the day I was there, that's what they were doing.

But the restoration started about 15 years ago. And what they had to do is take this field, which had been, you know, torn up and planted with non-native plants for years and years and figure out how to restore it, right? So they got the marine biological lab involved. They put out all these, you know, sample plots to see what to do. And they started a few years ago with planting. native grasses and then last year they started planting wildflowers and this year they planted 1,000 wildflowers called the New England Blazing Star which is

specialized to sandplain grasslands and even though it was like so much work I couldn't believe it like that they had to go around the vineyard and get seeds from the existing wildflowers and grow them for two years and then get them out to plant them and all these volunteers go out trudging through the grass and planting a thousand flowers by hand. So that's what they were doing the day I was out there. Right. So if you get all these thousands of plants growing there, does that make the area a little more amenable to the changing environment we're going through? Right. And that was my question. I was saying like, well, if the climate's changing, right, and it's going to get hotter and it's going to get hotter and

wetter or whatever, is this, does this make sense, right? Does this make sense to plant all these native species? Are they just going to die in five years, right? And I put that question to Mike Boland. He's the director of Polly Hill Arboretum on Martha's Vineyard, and he was the guy who went out and collected all the seeds and spent all the time cultivating these wildflowers. And he argues that native plants have a better shot at adapting to climate change. Here's what he said. These plants more than most have like a 14,000 year evolutionary advantage of growing in these ecosystems. So there will be plants that persist even with these rough conditions coming on. So it's really, it's doable.

Well, so the plants will be around probably a lot longer than maybe some of the people there. Yeah, that's what they think, you know. I mean, they've been through a lot these plants, right? been there for thousands of years as the ecology has changed and the climate has changed. So hopefully they'll make it through this next phase of the climate emergency. Well, Barbara, thank you very much, wishing you a cool summer. You too, Ira. Barbara Moran, Environment Correspondent at WBUR in Boston, Massachusetts. If you live by a freshwater river or a lake, you're likely familiar with the Asian carp. Yes, these fish are not native to the U.S.

But over the last few decades, they've gotten into waterways like the Mississippi River Basin and the Illinois River. A major PR campaign now is underway to move away from the name Asian carp and towards the name Kopee. One big reason? To rebrand the fish as a sustainable, responsibly sourced food. Joining me to talk about this is my guest, Jim Garvey, director of the Center for Fisheries, Agriculture, and Aquatic Sciences at Sartner. Southern Illinois University in Carbondale, Illinois. Welcome to Science Friday. Thank you for having me, Ira. You're quite welcome. There's a lot of thought that goes into changing a name. So what was the origin of the word

Copee? Did I get it right? Is it Copee? Yeah, it's Copee. Cope is short for copious. So when you're thinking about Big Hadder Asian Carps, as they're called, they're quite abundant. They jump out of the water, sometimes hit people in the face when they're driving a boat, for example. And so they're copious. There's a lot of them out there. And so what we would like to do is have people, when they think about copi, they think about a copious fish and doing their part by eating them so that they can control their abundance in the environment.

Walk me through how much, how much of a problem that this fish is in the Illinois waterways? Copie actually stands for four different species. of big-headed carp from Asia. One is the grass carp. One is the big-headed carp. One is the silver carp. And the last one is a fish called the black carp. These four species were aquacultured in China for well over several thousand years

because they are very valuable in what we call polyculture because they eat at different levels of the food chain. So they did very well in China and other parts of Asia. And so when they were introduced here into the United States, they found some really great opportunities in our lakes and rivers and did very well. They were introduced in the early 70s, late 60s, as food fish and potential fish that could control problems with water quality because they eat algae or tiny plants in the water. But once they escaped from ponds, they started to proliferate and became a real problem

when they reached the Illinois River in the late 90s, early 2000s. and their abundance started to explode. And then they began to get dangerously close to the Great Lakes. And the Great Lakes already have a huge history of invasive species that are very destructive like zebra mussels and sea lamp rays. I think the last thing any of us want is another potential group of invasive species to get in there and have negative economic and ecological effects. I'll bet.

And why is it so important to change the name from Asian carp? Well, there's a couple issues here. One is that, in my opinion, carp should be respected just like any other organism. Yes, they're invasive. Yes, they're a problem, and they can cause economic and ecological problems. But, again, they should be respected from the perspective that they are important to Chinese culture and other Asian cultures for a very long time. And so by placing the name Asian in front of it, they're could. be a negative cultural connotation to it. So I agree with this. There has been a push by the federal

government folks and then the rest of us biologists that are out there to maybe get rid of the moniker of Asian under that. We all know they come from the continent of Asia. So big-headed carps is probably a better way to describe this fish. Now, in terms of the name carp, common carp, which is not part of the four basic copi species, has been around for well over a century and has a very negative connotation, at least among some parts of the fishing public. And so because of this negative carp connotation,

the idea is, well, maybe we should move to a name that's more desirable to the consumer because what we're trying to do is get people to eat copy, eat them to extinction if possible. And so copy is the name that has been, introduced and hopefully it will stick. You know, it's part of an ethnic Jewish diet. There's something called the gefilta fish.

Oh, yeah. And you know, it's made from carp. Yeah. Maybe there's a market here. Well, there probably is. In fact, there is COPI processed and sent to Israel as one of the exports of this fish. There's exports all around the world from Illinois and other areas where they're

invading the U.S. They are sent to Africa and other places. So these fish are very valuable culturally and obviously nutritionally for many, many countries around the globe. It's just in the United States we're trying to get people to eat more of them because they are a good fish to eat. You know, when we talk about invasive species, we usually talk about them in context of them wreaking havoc on native species. Is that what's going to happen eventually if you can't get people to eat more Copee? Yeah.

In fact, there's a lot of research being done in the last 10 years or so that is suggesting that there has been a negative impact of these four species on native fishes here in the U.S. Maybe not as much as we expected because when an invasive species comes in, it usually pushes out the native species from their niche. What we found is that perhaps these species have sort of fit themselves better into the ecosystem than maybe other species have. But there are certain concerns. For example, the Black Cope, Black Carp, which is a lesser known of the four species, eats muscles. And the reason we should care about that is because the Central U.S., Mississippi River, for example, Illinois River,

has some of the highest diversity of freshwater mussels in the world. And so the concern is that these black carp are going to come in and bunch those native species. This is Science Friday from WLIC Studios. You know, when you describe the fish, it makes me think of Chilean sea bass. Yes. Which is also a name-changed fish, right? Yeah. So there's many species across the world that had bad rap, and it's usually reflected in their name.

I believe Orange Ruffy was called slime head, for example. Chilean sea bass was the Patagonian toothfish. So when you heard those names, typically you would potentially have a negative connotation to it. Someone wouldn't want to necessarily eat a slime head. But when you change the name, you begin to realize that, hey, this is not a bad thing to eat. In fact, it's quite delicious. and we think that the average consumer might take to the name Copee a little bit more than the name Carp, which might have a negative connotation to it.

Well, if I don't live in that part of the country, can I go to my supermarket and get a copy carp? That's a good question. Ten years ago, no. However, over the last six months or so, there has been a real push to try to get these fish into not only a regional market, but into a national market. So there has been talks among the processors to get the fish basically going nationwide. So that's the hope.

The biggest problem with all of this is that there's plenty of opportunity to fish Cope. The problem is that there are not enough fisher people out there to fish them and definitely not enough processing plants. to package the fish and get them in the market to meet, hopefully, what will be a growing demand. Wow. Well, I'd actually like to find some because I'd like to cook some up. What would be the best way to prepare my copy fight? Yeah, well, first thing, Ira, check your mailbox.

One day, maybe you'll get a package. I'll make sure it's on ice. I was going to say, make sure it's frozen. These fish are best prepared. in many, many ways. They can be literally, it's a blank canvas. They can be like a crab cake. They can be served traditionally in soups, believe it or not.

The heads, for example, you may think fish head soup sounds strange, but the head, if you watch any cooking shows or you cook yourself, you know that there's a lot of collagen in that head, which creates a lot of umami, really good mouth feel and broad. a few may, for example. So they can be used in a whole lot of different ways. Also, there's other products that can come out of these fish. For example, the collagen can be used in health care products.

So there's a lot of ways that you can use COPI, not just for food, but for other kinds of products as well. Animal food, dogs, cats? Absolutely. One of the primary uses of them right now is for fertilizer. or put into animal feed. That's perfectly fine, but that does not pay a lot. So when you're a person out there busting your behind to fish for these animals, putting them into fertilizer is not going to get you a good return on your effort.

By placing more demand on these fish and then hopefully the market increases so that there's a little bit more price, you're going to get more incentive for folks to go out and spend their time in their own money to fish these out of the water. Jim, that's about all the time we have for this fish story. I'm looking for that fish, maybe not in my mailbox, but Jim Garvey, Director of Center for Fisheries, Aquaculture, and Aquatic Sciences at Southern Illinois University in Carbondale, Illinois. Thank you for taking time to be with us today.

Thanks so much, Aaron. Take care. Just a final note to mark the passing of a public radio legend, Larry Josephson. Larry created free-form, freewheeling radio, full of political satire, puns, and a colorful Joker's story just to make you laugh. Not only was Larry a pioneer, but he was always ready to help you out. Years ago, when no one would give us a radio studio, Larry offered up his own, built in his New York apartment, complete with cat and couch. He is one of the last of his era, and his passing will be felt by all of us fortunate enough to have known him. Larry Josephson was 83.

And that's about all the time we have for this hour. Here's Diana Montana with some of the folks who helped make this show happen. Thanks, Ira. Charles Berquist is our radio director. Kyle Marion Viterbo is our community manager. Daniel Dana is our executive director. And I'm Diana Montana, Experiences Manager. Thanks for listening. Thank you, Diana.

B.J. Leiderman composed our theme music. Have a great weekend. I'm Iroflato.