Being Healthy: August 2010

Tuesday, August 31, 2010

Pregnant women should receive more vitamin D

The vitamin's support benefits. Journal of nutrition wrote the researchers in the British that vitamin D benefits pregnant women and the risk of diseases such as infantile hypocalcemia and rickets.NutraIngredients reports:

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Chicken McNuggets Contain Disturbing Additives

Vorherigen Post Next Post In Reaktion auf Berichte, dass die Zutaten Gesundheitsrisiken darstellen können, behauptet McDonald's China, dass Zusatzstoffe in seiner Huhn McNuggets sind

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The reckless self-interest of the fragrance industry

Previous post next post the cancer prevention Coalition warned must protect people from exposure to fragrance ingredients that occur cancer or fetal, hormonal or reproductive toxicity. But federal agencies are not to regulate these ingredients, leaving the public at risk. Perfumes and fragrances are the single largest category of cosmetics and personal care products. They are also often in a variety of household cleaning products.According world large used:

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Monday, August 30, 2010

Go outside and enjoy the nature to improve your immune system

Previous post next post spending time in nature could benefit your immune function. Stress is one of the reasons, but another is the presence of Phytoncides that emit airborne chemicals, the plants themselves before a rotting and insects to protect. A study found that nature plants in lower concentrations of cortisol, lower pulse rate and lower blood pressure.According the New York Times led:

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Salmon in hot water

Previous post next post rearing juvenile salmon at relatively high temperatures caused skeletal deformities in fish. This issue occurs, when the salmon that use farmers to increase water fish growth rates.Production of bone and cartilage were interrupted when the high temperature water was used.According to EurekAlert:

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Olive oil's benefits associated with gene expression

Previous post next post phenolic compounds in olive oil could genes that linked suppress-related of inflammation, the molecular basis for heart disease risk reduction already to olive oil. A new study tested the effects of people suffering from a rich breakfast of olive oil in metabolic syndrome, a cluster of conditions associated with heart disease and diabetes. The study showed that the inclusion of Virgin olive oil was able, the expression of several pro-inflammatory gene, the switch-to suppress the activity of peripheral blood mononuclear cells to a less damaging inflammatory profile. NutraIngredients reports:

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Sunday, August 29, 2010

Where do you store in your fridge produce for maximum durability?

Back post next post Americans take the from 14 percent what kaufen-- and this is before factoring in the leftover food from your plate to scratch that. Mint life suggests some tips to extend the shelf life of fruit and vegetables: Apple store on the counter for seven days. Not revealed, hold you close to other fruit or vegetable-the ethylene gas which produced by apples can ruin them.AsparagusStore, that you maintain in the refrigerator in a plastic bag in inches of water or with a damp cloth wrapped around the base.BerriesRefrigerate berries, unwashed and in their original container.CauliflowerRefrigerate you page after below in a sealed plastic bag.CeleryKeep stem it to the front of the fridge where it inclined to freeze.GarlicStore is less in the pantry or anywhere from heat and light. It will take up to four months.PeachesLet you tyres at the counter in a paper bag perforated with holes, from sunlight.Summer SquashRefrigerate it in a perforated plastic bag.TomatoesSpread out on the counter out of direct sunlight even ripening. Sources:

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Vitamin D fears lead to Sun alerts review

Previous post next post warning people out to stay the Sun independent can vitamin D deficiencies.The British newspaper, the a confidential report by cancer research UK, cited, which showed that love their advice on avoiding the Sun review was led. The charity was responds to concerns the risk of a lack of vitamin D.According on Fox News people were:

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San Francisco forbids soda vending machines

Next post under an executive order of Mayor Gavin Newsom, drinks such as Cola, Pepsi and Fanta Orange in vending machines on city property no longer allowed. Some of your diet colleagues are still erlaubt.der prohibition includes, not diet soda, sports drinks and artificially sweetened water. Juice 100% fruit or vegetable juice with no added sweeteners, and diet soda not more than 25 percent of items offered.The reported San Francisco Chronicle:

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Saturday, August 28, 2010

Take the sizzle out of summer in the city

Enlarge courtesy of sustainable South Bronx

The EPA estimates the 'cool' roofs, such as the bank note can reduce in the Bronx, n.y, building this one air conditioning costs from 10 percent to 15 percent.

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Charles Darwin-advice for walking upright

by Kathleen Masterson

Millions of years ago, our ancestors that were adapted to living in the trees to experiment with started walking upright. This chance experiments proved a useful skill, and in the course developed we humans face time, for upright walking built. From our neck at our feet, this brought many changes to our skeletal structure. We developed also hands, the better for fine motor skills adapted and large heads, which ultimately helped develop language.The beautiful Emma Darwin, wife of Charles, has you graciously voluntarily, to the differences between humans and chimpanzees to demonstrieren.Klicken easy on your body parts for more.

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Emma

Credit: Kathleen Masterson, Gregoire Vion, Adrienne Wollman, Maggie Starbard, Vikki Valentine, Christopher Joyce/NPR

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Millions of years ago our ancestors that were adapted to living in the trees to experiment began with going aufrecht.Diese proved chance experiments a useful skill, and this throughout the developed we humans make time our neck at our feet for upright walking gebaut.Aus led many changes to our Skelettstruktur.Das beautiful Emma Darwin, wife of Charles, has graciously volunteered, to demonstrate the differences between humans and chimpanzees.

Similar NPR stories A fishy take on human skin tones July 5, 2010 the human edge: finding our inner fish July 5, 2010 building A human body July 5, 2010 e-Mail share comments print Facebook stumble upon reddit Twitter Digg what is this? share more of this series podcast

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Presidential Panel Scrutinizes Synthetic Biology

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Scientists are cutting and pasting genes to create engineered organisms that may yield new vaccines and biofuels, but what are the ethical implications of toying with DNA? Geneticist George Church discusses synthetic biology, and why scientists need to be careful with the technology.

IRA FLATOW, host:

You're listening to SCIENCE FRIDAY, from NPR News. I'm Ira Flatow.

We're talking this hour about something new. Craig Venter - remember Craig Venter's Synthia, the cell completely made up of computer-generated synthetic genes?

Well, following Venter's announcement, President Obama called a commission to look into the ethical issues surrounding this technology, called synthetic biology. Synthetic biology is the creation of standard genetic pieces, like DNA. You take them, you cut them up, paste them together into living systems. It's sort of like building with LEGOs or transistors, and the idea with synthetic biology is to engineer a biological circuit, let's say, to manufacture what you want it - what you want the circuit to do. Maybe it makes biofuels or a vaccine, for example.

But with the potential benefits also come risks, and that is what the president asked the commission to look into. He asked them to consider the implications and the risks and return with a recommendation for policy. And he gave them six months to work on this, and they've done it in record time.

The President's Commission on Bioethical Issues met yesterday and today to discuss these issues and how they relate to synthetic biology. And one of the speakers at yesterday's meeting is my guest, George Church, director of the Personal Genome Project and professor of genetics at Harvard Med School in Boston. Welcome back to SCIENCE FRIDAY.

Professor GEORGE CHURCH (Genetics, Harvard Medical School; Director, Personal Genome Project): Thank you, Ira.

FLATOW: Was it a good meeting, do you think?

Prof. CHURCH: It was really terrific. I think many of the participants in it, both on the commission and the people that were just there for the day, were very pleased with the fact that the executive branch was taking an interest in this, and I think we and seeing all the progress that's been made recently.

FLATOW: Mm-hmm. Our number: 1-800-989-8255 if you'd like to talk to us about synthetic biology. We're talking with George Church. George, define that term better for me. I didn't do such a good job. But what is synthetic biology?

Prof. CHURCH: Well, it's an effort to apply the engineering principles that have been applied to many other sectors - civil engineering, biological engineering, mechanical and electrical engineering - specifically to synthetic genes and genomes that are made from data in the computer. So basically, we're going from bits to genomes, and doing that in a way that includes some of the things that you take for granted in other engineering fields, like safety engineering, computer-aided design, large-scale testing, and so on.

So it sounds at first blush a little bit like genetic engineering, which we've had for decades, but the difference is that it's much more of an engineering discipline now.

FLATOW: Well, if it's an engineering discipline, I'm picturing in my mind that you could sit at the computer and dial up the parts of DNA that you want to put together. The computer makes a little picture, you press a button, and it goes into little vats of chemicals and pulls out the pieces.

Prof. CHURCH: That is certainly part of not just the vision, but some of the day-to-day practice. That's it's not the case for any realm of engineering that you can simply design something and press a button and you've got a bridge or a car. There's trial and error in every field, and it's certainly true for the latest, most exciting fields, this will particularly have troubles with prediction and models and so forth. But it's very, very conceptually, a lot of that is in my place already.

FLATOW: So what's to prevent me from buying a kit or a machine that can do this and putting, you know, putting the little numbers in there and creating my own virus, if I wanted to?

Prof. CHURCH: Well, it's sort of like what's preventing you from, you know, building your own cell phone, building up a manufacturing facility that will build I mean, to some extent, it's not cost-effective for you to do that, and there is all kinds of secret sauce. It's not or just things that are complicated to do.

Now, people will say, oh, you know, biology is very simple and or at least the practice of it is simple. But there many things that actually require a great deal of education and infrastructure to do with any accuracy.

FLATOW: I guess the fear here is having this kind of technology being turned against us, or if someone wanted to build a virus that infected us, that was a harmful virus, you could use this kind of technology to do that.

Prof. CHURCH: Well, absolutely. I mean, almost all fields of engineering - I mean, you can turn a car into a car bomb. You can turn fertilizer used in agriculture engineering into a bomb. This is more serious in the sense that these are replicating entities, while, you know, a bomb is localized, a pollutant is localized, all of it can spread and become dilute.

There are elements - and I don't mean to say that this is so complicated that people - that anybody can't do it. We have, you know, undergraduates doing this. There are simple exercises that can be accomplished in short periods of time with low budgets. But overall, this is something the most hazardous things tend to require pretty large teams, with a great deal of structure and expertise.

But I think it's very important that we have commissions such as this presidential commission looking at this, planning for the future, as the costs drop and as the expertise starts to permeate throughout society.

FLATOW: Mm-hmm. I remember back in the '70s, when gene splicing was invented. There was a conference in Asilomar. I think it was 1974.

Prof. CHURCH: Right.

FLATOW: And the scientists said hey, we'd better stop our work and talk about where this is heading, and the ethical and the health implications of all these things.

Prof. CHURCH: Right.

FLATOW: Are we at a similar stage with this, and would scientists think of doing that kind of thinking?

Prof. CHURCH: Well, I think we've matured in two senses. One is in Asilomar, they were mostly worried about accidental problems with the technology, where we really didn't know what we were doing, and maybe we could do something that would go wrong.

For the most part, those fears have turned out to not be of any substance, but it was good that we went through that process. Now, there's because of 9/11 and other events, there's more concern about purposeful misuse, but even those are not considered major public health threats. The major threat is that we won't act and we won't solve our energy problems and our emerging disease problems and other problems of cities and so forth by not taking the opportunity and expanding the technology.

FLATOW: What does working in an ethically responsible manner - which I know that term has been used - mean for synthetic biologists?

Prof. CHURCH: Well, I mean, I think here, there's some blurring of ethnically responsible policy decisions and so forth, but basically, you should not be risking the health of the researchers, you know, by exposing them to, say, hazardous agents. And these could be non-synthetic agents. They could be natural agents that you begin to do research on, or they could be synthetic agents - not releasing those into the environment until they've been through proper testing, engaging a large number of different people in the conversation, I think, is something that's increasingly considered part of the ethical behavior.

I mean, it used to be that a scientist would try to become an expert on everything and would feel that they could think of every way that something could go wrong. But I think that now, it's much more a matter of inviting a large number of people who can think out of the box in different directions and really think of negative scenarios and positive ways of working around those and coming up with solutions.

And so what's really interesting about this presidential commission is it is public. So yesterday and today's sessions were open to the public, and people attended, and they were allowed to go up to the microphone. And there's a website, bioethics.gov, very easy website, that people can participate in.

So it's really intended to part of this ethical behavior is engaging people that can look at it from different angles, including international discussions.

FLATOW: We don't expect any treaties, laws, regulations to come out of this.

Prof. CHURCH: I think we do. I mean, I think that there is a lot of influence that comes from carefully reasoned discussion, and then summary in written documents that all people, not just American citizens, can refer to this document.

I think a very influential set of documents will come out of this, and there is already significant interest all the way to the level of the United Nations secretary general.

FLATOW: 1-800-989-8255. Let's go to Greg in Syracuse, New York. Hi, Greg.

GREG (Caller): Hi, how are you doing, Ira? Thanks for taking my call.

FLATOW: You're welcome. Go ahead.

GREG: I am a big science fiction buff. And what comes to mind when you talk about this is replicator technology where they take over the ship and have the artificial intelligence and basically decide that they want to make their own stuff instead of the stuff we tell them to make. How far off is this? Are, you know, we at that level of technology today? And what is the most practical use that he sees from this technology long term?

FLATOW: All right.

Prof. CHURCH: So restate two question there.

FLATOW: Let's go to reverse.

Prof. CHURCH: One is the replicators...

FLATOW: Right.

Prof. CHURCH: ...and the other is what are the most use for long term. In a certain sense, almost everything to do with synthetic biology is about replication. And so we don't need to develop artificial intelligence or replicating machines. In fact, replicating machines is still a very challenging and interesting engineering task and may be quite useful in the future. But that's a separate thing.

We have replicating bio-machines already, almost everything we produce in synthetic biology. And that's actually part of the promise and the risk. They won't have a mind of their own very easily in the sense that, you know - not even the most advanced animals - and most of this is done in microorganisms. But we can certainly make hazardous replicators that aren't intelligent.

FLATOW: Mm-hmm. And part two is about what use is this, what practical...

Prof. CHURCH: Right. So the uses are actually - are going to be quite - are actually already arriving. So they are in less expensive and higher quality manufacturing of pharmaceuticals, of all sorts of specialty chemicals, of fuels, of materials. Some of those materials will be things that you recognize as biomaterials and others will be materials that you normally wouldn't think of as biological.

But the biology is the nanotechnology that works. It's something that's capable of atomically precise manufacturing that scales well partly because it replicates. And really, almost any complicated material you might want to make, maybe even things like large-scale integrated circuits to beat Moore's Law, all kinds of interesting smart materials, these are all within the realm of synthetic biology. And many of them are being delivered already, including fuels and chemicals and materials.

FLATOW: But we - but you're saying that we could have biology-making computers for us.

Prof. CHURCH: We could have biology-making sensors and either electrical or optical components that can compute in all sorts of ways that interface better with the real world or simply are smaller and more complex at higher density.

FLATOW: Talking about synthetic biology this hour at SCIENCE FRIDAY from NPR.

I'm Ira Flatow talking with George Church. Tell us about some of the work that you do in synthetic biology.

Prof. CHURCH: Well, so we - both in synthetic biology and in personal genomics, a lot of our focus is on bringing the cost down. It's easy to scale things up by just spending more money. But in both of these fields, we've seen dramatic cost reductions partly through the work that we've done collaboratively with many other groups and companies, where we've seen as much as 100,000-fold reduction in cost over as little as five or six years. So this is - blows away that computing industry, Moore's Law curve where you have about 1.5-fold exponential improvement per year, this is more like tenfold exponential improvement per year. And that really opens up all sorts of new opportunities when you have something that's 100,000 or a million times less expensive than it was half a decade ago.

FLATOW: Mm-hmm. You're also director of the Personal Genome Project at Harvard.

Prof. CHURCH: That's right. Yes.

FLATOW: What's that project trying to achieve?

Prof. CHURCH: So that's taking off where this technology improvement starts. So the first thing is bring the cost of the human genome down from $3 billion down to where it is about now, which is around $3,000 to $9,000. And it will be down to less than $1,000, almost basically free to the consumer very soon. And - but ask, how do you add value to that? By making it interpretable.

FLATOW: Mm-hmm.

Prof. CHURCH: And that requires that, in a certain sense, requires a lot of community involvement where every person who wants to can participate in science because they know their - they know how their genes play out in terms of their body. It's that kind of community involvement and...

FLATOW: But what if...

Prof. CHURCH: ...interconnection between genes, environments and traits.

FLATOW: What if people don't want to have their genome sequenced?

Prof. CHURCH: Well, there's absolutely no reason why someone should get it if they don't want to. Some people will want it so much that they'll pay for it up to, in the past, up to $300,000.

FLATOW: But you're saying it's going to be almost cheap or nothing.

Prof. CHURCH: It could be quite - it could be - it's already getting into the range where a variety of other entities in the medical community - insurance companies or employers or, you know, your health care providers - could pay for it for you and then recover their costs in various ways in reducing the overall health care cost.

FLATOW: Well, you just named three of the most scariest things to most people.

(Soundbite of laughter)

Prof. CHURCH: Well, they're less scary than they used to be. I mean, we don't want to understate the scariness, but the Genetic Information Nondiscrimination Act of 2008 actually made it illegal for them to discriminate against you. So the only way they can make money now is by helping you save them and yourself money and avoiding drugs that aren't good for you or are - you know, that either don't help you overcome whatever it is you want to overcome or are toxic.

FLATOW: Mm-hmm.

Prof. CHURCH: So that can reduce medical costs, and it can be a win-win situation. But the - but this new law, in principle, prevents health care insurance discrimination and employers from discriminating.

FLATOW: Dr. Church, thanks for taking the time to be with us today.

Prof. CHURCH: Thank you.

FLATOW: And have a good weekend.

Prof. CHURCH: Bye-bye. Yeah.

FLATOW: George Church is director of the Personal Genome Project and professor of genetics at Harvard Med School up there in Cambridge, Massachusetts.

We're going to take a break. When we come back, we're going to talk about replenishing our ever-diminishing number of brain cells. You know, we actually do make new brain cells, and now there's a chemical compound that's been discovered that may help preserve them, at least in laboratory mice. So, if you're a mouse, there's hope.

Stay with us. We'll be right back after this break.

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Friday, August 27, 2010

More Evidence Of A Wet Past On Mars

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Using data collected by the Mars Reconnaissance Orbiter, researchers say they’ve found evidence that more of Mars than previously thought was once covered by water. Science News astronomy writer Ron Cowen describes the research and other recent news about Mars and its watery past.

IRA FLATOW, host:

This is SCIENCE FRIDAY from NPR. I'm Ira Flatow. Evidence is mounting that Mars was a very, very wet planet billions of years ago. But how wet was it, oceans worth, lakes, rivers? And if it was wet, where did all that water go?

Those questions are getting more attention recently with the publication of new research analyzing the Red Planet's watery history. Joining me now to sort it out for us is Ron Cowen. He is an astronomy writer for Science News. You can find his articles on water and Mars at sciencenews.org. Welcome back, Ron.

Mr. RON COWEN (Astronomy Writer, Science News): Thanks, Ira, hi.

FLATOW: Lots of evidence for water. What's going on about the oceans here?

Mr. COWEN: There may be oceans, or there may be just shallow, localized patches of water. It's unclear. I mean, some of the people go back and forth, even in the new research. Some of the new work is saying that in the northern plains, which is really flat, people have looked at dried-up - what appear to be dried-up river deltas.

And they all seem to be at the same altitude, which is what you'd expect if there was an ocean there that kind of flattened everything. And these people in the June 13th Nature Geoscience say that there could be there could have been an ocean that formed this region like this, and it would've been I'm sorry I'm going to use meters - but it's a 550-meter-deep ocean if we spread across the entire planet.

But there's other people, however, who say that, you know, from the chemical evidence, if there was water, you ought to see a lot of minerals that were altered by water, clays, like the clays we have at the bottom of the ocean.

And there are some in the north and even more so, apparently, in the south of Mars, but not a lot. And then there so there are people who say, well, you know, there never was an ocean. Maybe there were brief wet periods, maybe up to say 10,000 years, and then it stopped.

And that may have been good for localized habitats for life, but it was not an ocean, and it may not have been global. So there's people sort of going back and forth or debating on both sides of the issue, really.

FLATOW: One other piece of evidence that they've published was the finding of some, what they think may be 40,000 dry riverbeds. That would carry a lot of water, would it...

Mr. COWEN: Right, and that would have been that's where they get the idea of a 550-meter-deep ocean. That's right. But then I know that there are other people like Phil Christensen, who's a scientist who's on many of the Mars missions, saying that, you know, such things like these dried-up riverbeds, well, you might have only needed water for, say, 10,000 years at most to form these, and then somehow it went away. And he just keeps saying that the mineral evidence, the clays and minerals are just they are there on Mars but not in large amounts.

And there's a mineral called olivine, which is very, very susceptible to being altered by water and changed into other compounds, but there is a lot of olivine on Mars, and that would indicate, well, maybe there wasn't water because there shouldn't be so much olivine there if there was an ocean.

So people agree that 3.5 billion years ago or so, there was some water, but it's not clear how much. What people are telling me, too, is that the Mars Science Laboratory, which is supposed to be launched in late 2011 and land on Mars in 2012, that they should pick a place where there is a little bit of this chemical evidence and, you know, look around there, dig around there, and maybe that may really help settle the question. Or go some of these places, again, where there was localized water, and look for life there.

FLATOW: So they're saying the only way you're going to really settle it is to send something there.

Mr. COWEN: That's right.

FLATOW: To dig a hole.

Mr. COWEN: To one of these interesting places where they have found these what they call phyllosilicates, which are really clays that have been formed in the presence of water. Go and take a look there because there's some new research where people have a lot of these places where there is chemical evidence for water, the reason they know that is that impactors have pummeled Mars and excavated through the lava that covers a lot of Mars, excavated deep down and found these chemical signatures of water-altered minerals.

And so people are saying, well, go and land there because that might be one of the most interesting places for life and to tell exactly how much water was there and when.

FLATOW: And of course, the question is if there was this much water there, where did it all go?

Mr. COWEN: Right, that's true, too. Now, some of it may have evaporated. Some of it may be now beneath the surface, maybe just beneath the surface, and some of it may have migrated or frozen at the poles. All of that is maybe true and, you know, people have suggested drilling into Mars, and some of these frozen deposits of water may not be that far beneath the surface. But that is also still a puzzle, yes.

FLATOW: Is there anything that looks like a shoreline that would be leftover...

Mr. COWEN: Yes. In, well, some people say in the northern parts of Mars, in the northern plains, there are what looks like shorelines. And other people are debating that and saying, well, maybe, and then saying okay, these may look like shorelines, but then why don't we see all these water-altered clays that should accompany that?

FLATOW: But wouldn't you if you just think it through a little bit about how the Earth got to be wet, right, and the theory now is that there were comets carrying water, things like that, to our surface, well, Mars is almost the same size as Earth. Wouldn't we think it would be bombarded with the same kind of comets creating oceans and water like that?

Mr. COWEN: Right, or right, or those, there was an early period when Earth and Mars and a lot of the inner solar system was bombarded by asteroids and comets. And what some people say is yes, that may have been when water was delivered, but it may have been just to localized places on Mars. And yes, Earth has these oceans, it may be that Mars never had oceans, that it was just small areas where maybe it melted the ice where these impactors came, and there was a wonderful habitat for a short time. And maybe it was, though short, long enough for life to have gotten a foothold, but then it got cold again after this period of intense bombardment, which we think happened about 3.9 ago billion ended.

So year, but yes, there could have been water delivered in the same way as Earth.

FLATOW: It just seems to be, you know, it seems to be illogical, but of course, science is not logical in many aspects.

Mr. COWEN: Right. No, no, it's just that people are I think there's this tension, as I said, between all these wonderful-looking, intriguing, dried-up riverbeds and deltas and things that look like much bigger than our Grand Canyon - that presumably were carved by water on Mars, and yet we don't see the chemical compounds pervasively that we think should be there.

Now, some people say that, you know, Mars was so much blanketed over by lava that we don't have a whole lot of windows deep down to where these water-altered minerals may be hiding, and maybe that's the answer. Maybe it is more widespread, and we just don't see it because we don't have that many places where more recently, asteroids gouged into the surface and exposed these regions.

But again, that's why they're saying, you know...

FLATOW: You've got to go there and...

Mr. COWEN: You've got to go there, and you've got pick a really great place for the lander.

FLATOW: The Mars Rovers that are there are not made to do that?

Mr. COWEN: That's right. They're not I mean, they are they're just more very much on the surface, and they don't, they can just sort of scratch the surface a bit.

They do go to places where there have been excavations, and they have found definitely some evidence of water sulfates, which are water-altered minerals. But we'd now like to go to a place where these phyllosilicates, as they call them, have really been exposed by big impact craters.

FLATOW: Would they be easily landable places, or would we be taking a chance?

Mr. COWEN: That might be somewhat of a challenge, but I think that there - but some of these places I think are on NASA's target list, or there are planetary scientists telling NASA that these would be interesting places to take a look, and it would be worth it to consider it as candidates, candidate landing sites, yes.

FLATOW: And we still have orbiters looking down?

Mr. COWEN: Sure, yeah.

FLATOW: The Europeans have had their missions we've heard about.

Mr. COWEN: Mars Express, and in fact, some of the recent evidence for, in fact, finding some chemical compounds like clays in the north for the first time were found by Mars Express, and I think the Mars NASA's Mars Reconnaissance Orbiter both.

And that was actually a paper in the June 25th Science, saying that no, you didn't need an ocean to do this, but shallow amounts of water were both in the south and the north.

So some of this all sounds a bit contradictory I realize, or a little confusing, but this story still is being played out, really, and what's exciting is, I mean, they're not just arguing. They're arguing with data, and more data is to come.

FLATOW: And we have to argue only from what we know about what we see here on Earth.

Mr. COWEN: That's true, and the point is there are places on Earth where we call them hydrothermal vents where there, you know, there is water, and actually high-temperature places in the sea that wouldn't seem to be hospitable for life but in fact are. And people are saying if there was an impact that struck Mars and melted some water for a short amount of time, hey, that might have been good enough for some sort of life to have begun.

FLATOW: Yeah. All right, Ron, fascinating.

Mr. COWEN: Okay.

FLATOW: Thanks for joining us.

Mr. COWEN: Thank you.

FLATOW: Thanks for taking off from your vacation.

Mr. COWEN: Thanks.

FLATOW: I know you're on vacation.

Mr. COWEN: I appreciate you saying that. Okay.

FLATOW: You're welcome. Bye-bye. Ron Cowen is astronomy writer for Science News. You can catch his articles at sciencenews.org. And we always thank folks who take off from vacation to be with us.

We're going to take a break, and we're not on vacation. We're talking we're going to switch gears and talk about a new kind of life. Remember Craig Venter and his Synthia? Well, the president has a panel that he'd like to have them discuss what to do about this new form of life. So stick with us. We'll be right back and talk about synthetic biology. Don't go away.

(Soundbite of music)

FLATOW: I'm Ira Flatow. This is SCIENCE FRIDAY from NPR.

Related NPR Stories Frosty Asteroid May Give Clues About Earth's Oceans April 29, 2010 NASA Lander Touches Ice on Mars June 20, 2008 Water May Still Flow on Mars, NASA Photo Suggests Dec. 6, 2006 E-mail Share Comments Print Facebook Stumble Upon Reddit Twitter Digg What is this?

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Where came the word ' genome ' from

Add to playlist download text size A A A July 9, 2010

1920 Merged a botanist explaining style with the name Hans Winkler the Greek words "Genesis" and "Soma" around a body of genes to beschreiben.Auf of this episode of science historian Howard Markel the word "Genome" and how it was the most popular way all our genetic material to describe.

IRA FLATOW, host:

Sound can only mean it's time for Science diction, our monthly history of scientific words.

Now, what are we word today get? genome.It is actively involved in our scientific vocabulary.It is defined as all are our genetic Informationen.vielleicht some of you think sell sequenziert.Wir spoke about this morning.

Howard Markel is Professor of history of medicine at the University of Michigan in Ann Arbor. Also, Director of the Center for the history of medicine, gibt.Willkommen back to Science Friday.

Professor HOWARD MARKEL: (History of medicine, University of Michigan; Director, Center for the history of Medicine) well, it of great to be back, IRA.

FLATOW: Coming Howard, where the word, genome, out?

Prof. MARKEL: Well, you know most of our genetic terminology comes from the Greek work Genesis, i.e. origin or creation. But when it comes to genome, we have to give a botanist at the University of Hamburg, his name was Hans Winkler all credit,. 1920 he was writing a textbook on botany and he collided the German root word for, the gene with the Greek suffix OME, is the body indicates.

Now this was a very common BREW. Know there BioM and Rhizome system of roots.And, of course, chromosomes, what actually colorful make means because an inclination to pick specific colours that are in use when you peering this cell through a microscope.But he used the word genome exactly how defines the entire chromosome set to specify the material basis of our species.

FLATOW: Mm-hmm.

Prof. MARKEL: And it really caught on especially after 1953, when Watson and Crick most famously the structure of DNA beschrieben.Und geneticist, a few years later States Department of energy and the National Institute began the genome several viruses and complex organisms to beschreiben.Und from the late 1980s and officially in 1990, United of health, to describe the 3.3 billion base pairs that include our human genome and its genetic repertoire.

FLATOW: And I think, a map is OM, meaning of the body, a better suffix as something important.

Prof. MARKEL: exactly. Because the map is a two-dimensional structure.It doesn't really tell you - it may tell you how far something from something else, but it will not inform the hills that can occur, the valleys or climatic conditions and so we really want to know, weiter.Und with the interaction of this chromosome set with the Protoplasma.Was is it - the proteins, the molecules and so on?

FLATOW: Mm-hmm.And the word OME habit is to set, was that - back 30 years ago was that often add suffix?

Prof. MARKEL: absolut.Sie know how I said all these wonderful words were hatched between 1900 or 1890 and 1930, BioM is the one that we use most.

FLATOW: Right.

Prof. MARKEL: And Zilome, a system of cavities and so weiter.So is very often.And now we see prodianomics(ph) and so weiter.Es is still on.

Now, what is very interesting for me as a historian, is, what the future of the genome, you know?It has come to everyone's vocabulary, and it has come to the Holy Grail of modern medicine darstellen.Sie know a tool that helps the cause, cure and even prevention of disease, but, of course, future evaluations reveal that where we will leave on the find scientific community's ability, such as closely secrets guarded.

FLATOW: Is there a different suffix like OME, that waiting in the wings?

Prof. MARKEL: I am sure, there are.And I'm sure, there are a number of words that are ready, effective werden.Aber thing about genome, scientists precise words of love.And if you know you genetic map - I actually asked a number of people who are so to speak, in the room if the human genome project has been developed.You said, there was no other word that we would ever to come because it nothing quite as precise.

The great is to comprise words that mean you can make, what you should mean.

FLATOW: And how long has take genome, know to be accepted?

Prof. MARKEL: Well, it started 1920, but it...

FLATOW: Right.

Prof. MARKEL:...by the 1950s, it was really catch auf.Und, certainly, once the structure of the double helix was understood and that different based couples respond differently with proteins and molecules and so on, you know that three had to predict dimensionality what would be the Repertoire of things are functional and not as functional for that matter - scientist it immediately adapted.

FLATOW: Mm hmm.Gut, thank you, Howard.

Prof. MARKEL: Thank you.

FLATOW: Have a good Wochenende.Howard Markel is Professor of history of medicine at the University of Michigan in Ann Arbor and Director of the Center for history of gibt.Wir said medicine about the word genome.

If you have a better word, insert into our Web site at sciencefriday.com and click us a Kommentar.Lassen comment what you think a better word than genome his could perhaps can we in Oxford English Dictionary somewhere could take a bit along the line to zwingen.Es, so please have patience.

That's about all the time that we composed haben.Greg Smith our theme music today, and we had help from NPR librarian Kee Malesky.

If you missed a part of our show, can it along with you nehmen.Sie our iPhone app for instant access to our Science Friday videos and our Science Friday audio podcast download can now also us on Twitter are all one-week twitting folgen.Wir:

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Spotting Summer Sickness In The Garden

Add to Playlist Download text size A A A July 9, 2010

It’s summertime but the living isn’t easy for everything. Plants are under attack by blight, wilt, rust and newcomer downy mildew, which kills basil. Plant pathologist Margaret McGrath runs through symptoms of plant sickness and shares tips for preserving pesto prospects.

IRA FLATOW, host:

This is SCIENCE FRIDAY from NPR. I'm Ira Flatow.

You may know that we're having a real big heat wave here in the East. Maybe you are also. And I was sure that I went outside yesterday and put a lot of water on my pot of pesto that's growing on my deck. Of course, it's not pesto yet. It's just a nice basil plant. But I've got big plans for it and I don't want the summer heat to do it in because while it is summertime and the living is easy, it's not easy for everything or everybody, especially plants.

Not only does heat stress the plants, but they're under a lot of attack. Think about it. There's wilt. There's rot, light, rust, and now, the newcomer that worries me the most, the basil downy mildew. Oh, my plant is in trouble.

This is a fungus that was first spotted way back in 2007 in the United States, and it's been spreading across the country ever since. So how do you identify the disease and what can you do to preserve your pesto prospects? And what about the other sicknesses that are going around your garden?

My next guest is going to run through some of the signs and symptoms of plant diseases you might encounter this season. Margaret McGrath is a plant pathologist at Cornell University. She's based at the Long Island Horticultural Research and Extension Center in Riverhead, New York.

Welcome to SCIENCE FRIDAY.

Professor MARGARET McGRATH (Plant Pathology, Cornell University): Thank you very much.

FLATOW: What does basil downy mildew look like? What should I watch out for?

Prof. McGRATH: It's a rather non-descript yellowing of the top side of the leaves is the first symptom. If you're lucky, you might see it in bands of yellowing. But not much - not a distinctive spot like you get with some other diseases. And then, really, the way to know is to turn the leaf over and that's where you will see the fungus producing its spores and getting ready to multiply and head off to another garden.

FLATOW: Mm-hmm. And so, is it very widespread around the country at this point?

Prof. McGRATH: We're starting to get a number of reports in. So it is starting to appear in a lot of different areas.

FLATOW: And so what can we basil lovers do to protect our plants?

Prof. McGRATH: There's not a lot you as a gardener can do. There's - in fact, even for commercial growers, there's few fungicides at this point that are registered for this problem. I think one of the best bets is just to be alert and know where the disease is occurring. I've got a monitoring spreadsheet up on the Web now and just be aware of when conditions could be favorable in your garden.

FLATOW: Mm-hmm.

Prof. McGRATH: Monitor if you can spot it early...

FLATOW: Right.

Prof. McGRATH: ...harvest it.

FLATOW: Yeah. Turn it into pesto. I imagine that this must be scaring a lot of commercial basil farmers.

Prof. McGRATH: It absolutely is. That's a very good point. Basil growers had not many diseases they've had to deal with. They haven't had a need to apply many, if any, fungicides, so this very much changes production for them, greatly increases their costs. Some growers have had complete losses. I know I talked to one greenhouse grower who'd lost two crops last year valued at $250,000 apiece.

FLATOW: Wow.

Prof. McGRATH: That's a lot of money. Yeah.

FLATOW: Wow.

Prof. McGRATH: Yeah.

FLATOW: 1-800-989-8255. Talking with Meg McGrath. If you have a question about gardening and seeing some diseases in your garden this summer and you want to ask her about it, we - the folks over there at the Cornell Extension all know everything about gardening. So I've been dealing with them for years.

When was it first sighted? I said 2007, but it goes way back further than that, doesn't it?

Prof. McGRATH: It goes back but it was just a non-known disease. So there's a report from 1933 in Uganda, and then nothing until we get into 2000s and a lot of reports out of Europe. To me, as a scientist, it's fascinating. What happened? Did the pathogen somehow find a way to get out of Africa or did it evolve and it's now a more aggressive critter out there? A lot of interesting questions.

FLATOW: Mm-hmm. Well, let's move on to another fear in your garden and that is late blight. Tell us what that is.

Prof. McGRATH: Late blight, that's - that pathogen, that's the one that's responsible for the disease that lead to the Irish potato famine.

FLATOW: Right.

Prof. McGRATH: Very deadly disease. I think it is probably, arguably our most nastiest plant disease in how quickly it can kill plants. I think a lot of gardeners experienced that last summer.

FLATOW: Yeah, we talked about that one last summer. Yeah.

Prof. McGRATH: Another situation that's changed. The pathogen has changed. The situation...

FLATOW: Oh, really?

Prof. McGRATH: ...in the U.S. - yes. We now believe that we have strains of the pathogen that can tolerate warmer temperature.

FLATOW: Oh, no.

Prof. McGRATH: Yes. So we're seeing it later into the spring in Florida than we have in the past. We're starting to see it in the fall, up in the north more frequently than we have. I've been here working as a vegetable pathologist since 1988 here on Long Island

First time I saw late blight was in 2002, and I've now seen it - last year was the fifth - well, I've seen it this year. I take that back. So I've now seen it six times on Long Island.

FLATOW: Wow.

Prof. McGRATH: Things have changed.

FLATOW: They outwit us, don't they?

Prof. McGRATH: Yeah, they do. The other is the interconnection, which I think is very interesting, with some of these diseases, between farmers and gardeners. A lot of the diseases we deal with don't move very far. But the late blight pathogen, the downy mildew in basil, downy mildew in cucurbit is another big disease that's increased recently. The pathogens produce spores. It could be moved by air - distances.

And now, we have this interconnection. If a gardener doesn't control one of those diseases, they can impact the farmer and vice versa. When farmers are having trouble controlling these diseases...

FLATOW: Mm-hmm.

Prof. McGRATH: ...gardeners are going to be impacted.

FLATOW: Well, the fact...

Prof. McGRATH: We're all interconnected.

FLATOW: Yeah. I know the fact that you're having the same weather we're having, the fact that so far this summer has been very hot and very dry.

Prof. McGRATH: Is fabulous.

(Soundbite of laughter)

Prof. McGRATH: Particularly the sunny days.

FLATOW: Yeah.

Prof. McGRATH: Because any spores that get taken up into the air, the UV radiation is going to kill them.

FLATOW: Mm-hmm. Let's see if we can get some calls in here. Let's go to Francis(ph) in Mount Shasta, California. Hi, Francis.

FRANCIS (Caller): Good evening, gentlemen. Ira, good morning.

FLATOW: Well, good afternoon to you. Are you there?

FRANCIS: Yes. What I do to take care of the basil problem, is I have a lot of trouble with basil myself, so I grow a German or French tarragon, which is a superhot basil-like flavor, and that's the way I get around the problem with the basil.

FLATOW: Wow. I'll have to try that. Thanks for calling.

Prof. McGRATH: Another way is the spice type basils. They are definitely less susceptible. We started doing some variety evaluations, and they've turned out as being much less susceptible, not the same flavor of the basil.

FLATOW: Mm-hmm.

Prof. McGRATH: What we're hoping to able to do is secure some funding that we can figure out why those basils are less susceptible and create a true basil that's resistant.

FLATOW: What would be a couple of names?

Prof. McGRATH: Oh, there is all kinds. There's a lemons, the limes, the Thais, some of the red basils.

FLATOW: Mm-hmm.

Prof. McGRATH: Many, many, many.

FLATOW: Mm-hmm. Let's get some more free advice. Tracy(ph) in Fair Oaks, California. Hi, Tracy. Tracy, are you there? Last chance, Tracy.

TRACY (Caller): Oh, hi. Sorry, I had a CHP officer behind me. I had to put my earphone on.

(Soundbite of laughter)

FLATOW: Oh, we don't want to do that.

TRACY: No, not again. I have some wine grape vines out in the backyard. They're in their third year. And I just noticed this morning and haven't had a chance to look it up that some of the vines - the leaves are showing some dimpled marks, like little wrinkles. Those (unintelligible) that is, if that's a pathogen.

FLATOW: Tracy, again. Are you a wine expert, right?

TRACY: I am a sommelier, yes. Now, I'm getting...

FLATOW: Yeah.

TRACY: ...into the oenology and viticulture part of it.

FLATOW: Ah. Well, you may know more than Meg does about grapes. There's only a little bit of grape growing out on North Fork there, right, Meg?

Prof. McGRATH: We've got a fair amount.

FLATOW: Yeah?

Prof. McGRATH: Actually, it's completely out of my area of expertise, I'm afraid.

FLATOW: Yeah, you're right in between the forks there. So, how about...

TRACY: Well, maybe I'll just pick the leaves off and make some Greek dolmades out of them.

(Soundbite of laughter)

FLATOW: There you go. Make lemonade.

TRACY: I'm a chef too.

FLATOW: Good luck to you.

TRACY: I can find something to do with them. Thank you.

FLATOW: Thanks. 1-800-989-8255. Is fungus really, sort of, the biggest thing of all kinds during the summer, it's hot and humid, that sort of weather?

Prof. McGRATH: Most of our plant diseases are caused by fungi.

FLATOW: Mm-hmm.

Prof. McGRATH: There are a number of bacteria that also cause diseases. They're going to be much more of an issue in the rainy time period.

FLATOW: Mm-hmm.

Prof. McGRATH: And that's because the bacteria - most of them are moved by splashing water.

FLATOW: Mm-hmm. Let's go to...

Prof. McGRATH: Some are moved by insects.

FLATOW: Anne(ph) in Avon, New York. Hi, Anne.

ANNE (Caller): Hi. I live in western New York State. We love Cornell University all over the place up here. And I have a question for Meg, regarding transmission of the blight. I happened to plant a couple of basil plants that look healthy so far and I'm watching them carefully next to, because it was just a good place when the dirt was dug up, a new baby rose bush. And I'm just wondering if the basil starts to show evidence of illness, is the rose bush in jeopardy at all?

FLATOW: Because they like - they get that mildew too, don't they?

ANNE: Well, they can, but I guess that's a separate thing. But what should I watch for?

Prof. McGRATH: They are all very different pathogens, different diseases. Number of different downy mildews, but they're pretty much all caused by different pathogens. In fact, there is one now on coleus, very similar but enough difference that the pathogen can't go between the two.

TRACY: So if the basil started to look...

Prof. McGRATH: So, you don't need to worry about the downy mildew on basil going to anything else. It's a very specific pathogen.

FLATOW: There you go.

TRACY: Okay. Great.

FLATOW: All right. Good luck to you. Are we seeing more and more of these for -or this - for any special reasons, seasonal, climatic or is it just - this is how things work?

Prof. McGRATH: I think we're just in a phase where pathogens have been doing some evolving on us. And we've moved them. Clearly, the basil downy mildew pathogen snuck in through our guard and got in to the U.S. We've got a fabulous system to try and prevent new pests from getting into the U.S., but it does happen, and here is a case where it snuck in - probably on seed, contaminated seed.

FLATOW: Hmm. Interesting. Let's go to the phones. Matt(ph) in Buffalo, New York. Hi, Matt.

MATT (Caller): Hi, how are you?

FLATOW: Hi there.

MATT: Good, thank you. I'm just calling as a comment. I do a lot of restoration work, and I'm a student of ecology. And a lot of what I'm hearing is kind of bringing about a point I like to drive home to a lot of people, is using native plants, especially native plants that can provide some sort of edible value as a good way to keep from introducing new pathogens, new blights that tend to come in with the ornamental trade that are...

FLATOW: Hmm.

MATT: ...having, you know, bad affects on our environment, kind of like the Chinese chestnut bringing in chestnut blight.

FLATOW: Hmm. Good point, Meg?

Prof. McGRATH: Yes.

FLATOW: So we should try to stick to native plants, and they've been around for a while.

Prof. McGRATH: Unfortunately, we make a lot of those imports.

(Soundbite of laughter)

FLATOW: I know what you mean. Meg, I want to thank you for taking time to be with us today.

Prof. McGRATH: You are welcome.

FLATOW: Meg McGrath is a plant pathologist at Cornell University, based at the Long Island Horticultural Research and Extension Center out there in Riverhead, New York.

I'm Ira Flatow. This is SCIENCE FRIDAY from NPR.

Related NPR Stories Basil Blight Threatens Pesto Lovers June 23, 2010 Tomato Gardeners, Plant On! Late Blight Is Gone March 30, 2010 Potato Famine Pathogen's DNA Deciphered Sep. 18, 2009 E-mail Share Comments Print Facebook Stumble Upon Reddit Twitter Digg What is this?

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Thursday, August 26, 2010

Swimming Pool Chemistry ... Not Pretty

Add to Playlist Download text size A A A July 9, 2010

With a heat wave scorching the Northeast, a dip in the pool may sound like just what the doctor ordered. But before diving in, consider the chemistry. Engineer Ernest Blatchley reveals many things you didn't want to know about swimming pools and the chemical reactions occurring in them.

IRA FLATOW, host:

It's hot, really hot. The temperature has topped 100 degrees. It's like a furnace outside. But there is some relief: the swimming pool just down the block, the refreshing oasis in that blacktop jungle.

So you don your swimsuit, and you ooh-ah your way across the hot pavement and jump into that chlorinated, cooling comfort. Oh, life is good - or is it? Have you considered what you're diving into?

(Soundbite of music)

FLATOW: My next guest studies the chemical reactions that occur in swimming pools, and it's worse than you thought. Ernest Blatchley is a professor of engineering at Purdue University, and he joins us by phone from West Lafayette, Indiana. Welcome to SCIENCE FRIDAY.

Professor ERNEST BLATCHLEY (Engineering, Purdue University): Well, welcome, thank you.

FLATOW: You know, we put we were having fun with the swimming pool, put a little "Jaws" music in there, but your research shows that there are chemicals in swimming pools that we should be worried about. There's like a chemical soup going on in there.

Prof. BLATCHLEY: Yes. And I think we're largely responsible for it.

FLATOW: We? You mean we as individuals going in there?

Prof. BLATCHLEY: Sure, the people who use pools.

FLATOW: Tell us about why that is.

Prof. BLATCHLEY: Well, people's, let's say, social habits have evolved such that a lot of people don't worry about perhaps using the pool as a urinal as opposed to what we might ordinarily use as a urinal or a toilet. And also, people don't remove things from their skin that perhaps they should just by taking a shower. So when those things end up in pools, they end up reacting with, among other things, chlorine to produce some interesting chemicals.

FLATOW: What kinds of chemicals are we talking about?

Prof. BLATCHLEY: Well, there's a group of chemicals called the chloramines that are generated by pretty much any chemical in water that contains nitrogen. That's a bit of a generalization. But there are some other disinfection byproducts that are generated, for example, cyanogen chloride, dichloroacetonitrile, the halo forms. These are things that show up in drinking water as a result of very similar reactions. But not surprisingly, they end up in swimming pools as well.

FLATOW: And is it because of the chlorination in the pool?

Prof. BLATCHLEY: Yes. You could say that. I think without chlorine these chemicals wouldn't be generated.

FLATOW: Mm-hmm. Is there something, a sickness that we might not suspect we have but, you know, can affect us if we're in a swimming pool?

Prof. BLATCHLEY: Well, there are - there have been - first of all, the CDC has developed a division that looks into what they refer to as recreational water illnesses. They - so they developed that term, recreational water illness, to describe these things. And these are conditions that are attributable to exposure to microorganisms or chemicals in pools or sometimes combinations of these things. And they range from, you know, skin rashes to eye and skin irritation, to respiratory problems. And there have been suggestions, although they haven't necessarily been proven, that there is possibly a link between some of these chemicals and the promotion of asthma in some people.

FLATOW: Hmm. And so, there are microbial diseases in the water also?

Prof. BLATCHLEY: Sure. Microorganisms like warm water so - and sometimes we leave them behind for various reasons.

FLATOW: And so, when they say to you, and you see this at the pool all the time, take a shower before you come in here, they really mean it?

Prof. BLATCHLEY: I think it's a good idea. I think, yes, they do really mean it. I don't know that they always understand why. But we're hoping to take some of the work that we've done in the lab and in swimming pools and translate it so that the public can understand why it's important to do this.

I think most people take it for granted that, you know, swimming pools are going to be clean. And that, you know, if they jump in without taking a shower, it probably won't make any difference.

FLATOW: Mm-hmm. Talking about swimming pool hygiene this hour on SCIENCE FRIDAY from NPR. I'm Ira Flatow talking with Ernest Chip Blatchley.

So what do you say to somebody who wants to, you know, go to the swimming pool? Should they be fearful of getting some sort of illness from the pool?

Prof. BLATCHLEY: I'm glad you brought that up. I mean, in a general sense, I think, no, they should not. I think most pools most of the time are really pretty clean and the benefits associated with swimming in most circumstances, you know, outweigh the risks. But I think people can do some just basic things that could improve swimming pool chemistry and air chemistry, especially in indoor swimming pools, that would benefit not only themselves but the other people who use the pool and the people who work in those pools.

FLATOW: Mm-hmm. Such as?

Prof. BLATCHLEY: Well, taking a shower is a good idea. I mean, it really does make a difference in terms of removing some of the chemicals from your skin that ordinarily would be just removed when you dive in...

FLATOW: Right.

Prof. BLATCHLEY: ...or jump in. And, you know, a really important one, although it may surprise a lot of people, maybe it won't surprise a lot of people, is that, you know, people should urinate not in the pool. Use the bathroom. There's a remarkable amount of urine that ends up in pools, most of it voluntarily, let's say, introduced...

FLATOW: Hmm.

Prof. BLATCHLEY: ...because nobody is going to know.

FLATOW: A lot of people with baby diapers, too.

Prof. BLATCHLEY: Yeah. There's not much you can do about that. And, you know, even if people displayed what I would consider to be ideal hygiene practices in swimming pools, there's still going to be some of these compounds that are going to end up in pools. But we could do a much better job of limiting the amount of these chemicals that go into pools.

FLATOW: Of course, if some of these chemicals, the soup, the result of what's going on in the pool gets sprayed up into the air, you breathe that stuff in too, I would imagine.

Prof. BLATCHLEY: Sure. So swimming, I mean, is kind of an interesting, let's say, pathway for exposure to chemicals that are in water because, you know, when go swimming, you're, first of all, you're immersed in the water, but you're also probably breathing air right above the air-water interface.

FLATOW: Mm-hmm.

Prof. BLATHLEY: And probably you're going to ingest some water while you're there. So there's opportunities for exposure from at least three different pathways. And the one that you mentioned about, you know, release to gas phase, is particularly important with respect to the respiratory ailments that have been linked one way or another to swimming, especially in indoor swimming pools.

FLATOW: Let me get a quick call from Melissa(ph) in Denver. Hi, Melissa.

MELISSA (Caller): Hi. Thanks for taking my call. A freaky topic. Two questions for your guest. One, I - in my condo complex where I live, they switched over from the chlorine-based chemicals to clean the pool to a saltwater system. And my first question was, is that any better or is it any worse?

Prof. BLATCHLEY: It's hard to say at this point. It's not really a lot different because what they're doing there is they're generating the chlorine by a process called electrolysis. So they've added the salt to the pool and then they re-circulate that water through an electrolytic cell and they generate the chlorine that way. So, really, a lot of the same chemistry is going to be taking place. It's a little bit different just because of the salt that's present in the pool, but not a lot.

FLATOW: But what if you had a saltwater pool instead of freshwater?

Prof. BLATCHLEY: Well, I think that's actually what she's referring to.

FLATOW: That's what that is.

Prof. BLATCHLEY: Yes.

FLATOW: So no one is just getting seawater being pumped into their swimming pool.

Prof. BLATCHLEY: Not that I'm aware of, but I haven't done a complete survey so I don't know that so...

(Soundbite of laughter)

FLATOW: Someone writes: Does potassium peroxide monomer sulfate fix what's going on in there?

Prof. BLATCHLEY: So there are peroxide chemicals that are used in addition to chlorine, and that's usually how they're added. And I'm not sure, honestly, how much difference there is between a pool that uses chlorine alone and a pool that uses chlorine plus a peroxide chemical. So I don't really know the gory details of how the chemistry plays out under those.

FLATOW: All right. We won't - and we won't ask you to talk about something you don't know about. But I want to thank you for taking time to be with us today.

Prof. BLATCHLEY: You're welcome.

FLATOW: Ernest Blatchley, professor for engineering at Purdue. He joined us from West Lafayette, Indiana.

We're going to take a break. Come back. We're going to talk about, well, stuff that's lurking in the garden. Forget the pool. We're now moving to the garden. And, oh, my pesto preparation is in trouble so maybe yours is too. Stay with us. We'll tell you why after this break.

I'm Ira Flatow. This is SCIENCE FRIDAY from NPR.

Related NPR Stories New Take On Dumpster Diving: Just Add Water! Aug. 19, 2009 Racial History of American Swimming Pools May 6, 2008 Have a Stagnant Pool? Call the Mosquito Guy May 31, 2007 E-mail Share Comments Print Facebook Stumble Upon Reddit Twitter Digg What is this?

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Amygdaloids mix neuroscience and rock ' n ' roll

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A group of New York University neuroscientist takes an unlikely Doppelleben--as rocker.The songs on your new album, theory of my mind, based on the members Forschung.Die musicians play selection from the album and talk about the science behind the text.

IRA FLATOW, host:

This is Science Friday from NPR.I am Ira Flatow.

When you got home from school, her mother to be that you your homework before swings and roles in the garage or basement with your friends?In class, you have the music instead of playing dream math and wish you could be in your own band?Now, some people do not have between the band and Brain Science wählen.Sie are bright and talented enough to do both.

Join me now, is a group of unlikely rocker, a band of NYU have called a new album out, scientist named the Amygdaloids.Sie "Theory of My Mind", and you can see a video of the Amygdaloids at castaways cabaret in - it is in the village here in New York.Es is on the talkingscience.org Website.Und a live stream of the band here in the Studio you can also see when you go out on our website at sciencefriday.com.

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A Chemical Nurtures New Brain Cells In Rodents

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Scientists screened nearly 1,000 chemicals and found one that nurtures new neurons in rat and mice brains. University of Texas Southwestern Medical Center biochemist Steven McKnight describes the work and explains what has to happen before the chemical can be tried in humans.

IRA FLATOW, host:

You're listening to SCIENCE FRIDAY from NPR. I'm Ira Flatow.

Up next, the latest in the quest to replenish our ever-diminishing brain cells. What if you could take a drug, a shot or a pill that would nurture new neurons in your brain, neurons that actually worked and made your brain work better? Scientists at the University of Texas Southwestern have found a chemical that might do the job some day.

In what must have been a long and tedious effort, the researchers screened 1,000 chemicals to see whether one of them might stimulate the brains of mice to grow more brain cells, and they were actually laughed at by their colleagues who thought, ha, what kind of approach is this in this age of genetics, huh? But they said that we're going to go ahead. And they found a - they found that needle in a haystack, a chemical that worked in mice and in rats. And, of course, the obvious question is: Would it work in humans?

Joining me to tell us about that is Steven McKnight. He's professor of biochemistry and the chairman of the department at the University of Texas Southwestern Medical Center in Dallas. He's talking to us today from Montana.

Thanks for taking time out. Everybody's on their vacation today. Thanks for taking time to be with us.

Dr. STEVEN McKNIGHT (Biochemistry, University of Texas Southwestern Medical Center): No problem, Ira.

FLATOW: So why, you know - here you take a chemical approach when here we are in the age of biology and the rock stars are all these biologists and synthetic biology, is that why people were laughing at you?

Dr. McKNIGHT: No. I think they laughed at us because of the fact that the chances were pretty slim that this approach, this in vivo screening approach with chemicals injected right into the brain tissue of mice would work. So the likelihood of it working was pretty small.

FLATOW: So it was like a needle in a haystack.

Dr. McKNIGHT: I think that's a good description.

FLATOW: And what did the drug or the compound actually do?

Dr. McKNIGHT: Well, we - there were assays that are fairly straightforward to monitor the birth of new neurons in the brain of a mouse. And we're not the ones who developed that assay, but we're following the literature and knew that there was an assay. And so my associate, my postdoctoral fellow at the time, Andrew Pieper, took the risk of saying let's conduct the screen...

FLATOW: Mm-hmm.

Dr. McKNIGHT: ...and inject those compounds directly into the brain and see if we could find compounds that would enhance the formation of new neurons.

FLATOW: Now we were all taught - I certain was in biology class early on - that the brain doesn't make any new nerve cells. But that doesn't seem to be the state of the knowledge. We find out that they do, right?

Dr. McKNIGHT: No, you're exactly right. And I was the same way when I was in college 30 years ago. I was taught that you're born with all the brain cells that you have and you're never going to make any new ones, so be careful with them.

FLATOW: Mm-hmm.

Dr. McKNIGHT: And yet terrific inspirational work, primarily from a scientist by the name of Fernando Nottebohm at the Rockefeller Institute, gave evidence clear as a bell that in birds, when they need to learn a new song during their mating season, they actually make entirely new neurons in order to learn that song. So I think that was the first concrete evidence that the vertebrate brain could actually make new brain cells. In the ensuing years, over the past decade or so, it's become clear that that happens not only in birds but also in mice and rodents and even also in humans.

FLATOW: So when you injected and fed this compound into mice and rodents, you found that they - it helped preserved their brain cells, the ones that - their newborn brain cells, so to speak?

Dr. McKNIGHT: That's right. In essence, our compound - we call it - we dub it P7C3, it actually doesn't force new cells to be born. Instead, the ones that are born and are being made are protected from death.

FLATOW: Hmm.

Dr. McKNIGHT: Normally, many of them die along the pathway to become wired neurons in the brain. For reasons we don't understand, most of them don't make it. And the older an animal gets, the more of them don't make it. And for some reason, our compound, P7C3, helps preserve the livelihood - the life of these newborn cells so that they can become incorporated and actually function as neurons.

FLATOW: And so as these rodents age, they age better and their brains, too, then?

Dr. McKNIGHT: Well, you know, the one behavioral study we've done was with very old rats.

FLATOW: Right.

Dr. McKNIGHT: And when a rat is 18 or 20 months old, it begins to lose its cognitive capacity. It has a harder and harder time learning. And so we just followed the paradigm that many other scientists have used and asked the question, would our P7C3 compound, if administered the last two or three months of life, preserve cognitive capacity in these aged rats? And sure enough, it appeared to do so.

FLATOW: Wow. And did you have to inject them into the brains or could you actually feed this compound to the rats?

Dr. McKNIGHT: Well, the initial assays when we're chasing after the compound, we did have to inject them right into the brain. But this particular compound, P7C3, actually can be fed to the animals orally. It gets across their gut into the blood system and crosses the blood brain barrier. And so it ends up being a rather easy compound to use, and so we - now we don't have to any longer inject it directly into the brain.

FLATOW: Now, I'm sure everybody has asked you, how do I get my hands on this?

(Soundbite of laughter)

Dr. McKNIGHT: Well, listen. Ira, this is at least a year or two off before it would qualify for human testing. We've done this all in animals. And it's a good bit more work to know whether it is a viable approach to use in humans. And like I say, that's at least a year or two away.

FLATOW: Mm-hmm. Does it migrate to one part of the brain over another part of the brain?

Dr. McKNIGHT: We don't know the answer to that. Today, we simply measured its absorbance into the entire brain tissue of these animals. We haven't looked specifically whether it reaches some part of the brain and not others. So that's ongoing experimentation.

FLATOW: Mm-hmm. And the fact that it keeps new brain cells alive and viable, would you think that it would work in all parts of the brain where new brain cells are being produced?

Dr. McKNIGHT: That would be my guess, but we really have to dig in carefully to test that. There - we studied a region of the brain called the hippocampus that's known to produce new brain cells. So that was our focal point.

There is another part of the rat brain and the mouse brain called the subventricular zone. It also makes new neurons. And we have indications that the compound also works in that region of the brain, but we haven't carried out conclusive studies.

FLATOW: Mm-hmm. Are there any other compounds like it already out there?

Dr. McKNIGHT: Well, there are a couple of compounds that are somewhat similar in chemical nature. One of the more interesting ones is a compound that was used in Russia for decades and decades as an antihistamine. And completely by accident, Russian physicians anecdotally noticed that patients suffering from Alzheimer's disease were improving. And they traced it down to the fact that these patients were taking the antihistamine that's now called Dimebon.

So about six years ago, or five years ago, a biotechnology company in the Bay Area began performing clinical trials on this antihistamine Dimebon to ask whether it really might work to help treat Alzheimer's patients. So, that compound, Dimebon, has structural similarities to the compound that we call P7C3.

FLATOW: Mm-hmm.

Dr. McKNIGHT: And so, there's some chance that they might be working via a similar pathway.

FLATOW: Mm-hmm. And do you think yours works better?

Dr. McKNIGHT: Well, it's really hard to say until they're compared in human trials. In the mouse experiments and the rat experiments, the one that we stumbled over is considerably more potent and effective than Dimebon by maybe tenfold or 30-fold. But whether that would translate to humans is an entirely different matter.

FLATOW: How many more compounds are left for you to work your way through. You went through 1,000. How many potential more are they?

Dr. McKNIGHT: Well, Ira, there's limitations. Now that we've kind of got one, I don't think we're going to go back to the well and do another thousand or two.

FLATOW: Well, but you may have some graduate students listening today. I could do that. Right? And it would be - and what would be wrong with that?

Dr. McKNIGHT: Well, you know, I think what people are surprised by is the approach of actually doing this in living animals. It's arduous and slow, and yet if you're lucky enough to find a compound that actually works in the animal, you know, that's the ultimate goal. You want something that actually can treat a disease in a living animal. And I think that was the inspiration that Andrew Pieper brought to the project. He decided, let's see if we could get something that really worked in a living animal.

FLATOW: Mm-hmm. And with all these - and you talked about all the compounds -with so many of them, how did you screen out the ones that you were going to test and leave the other ones back in the medicine cabinet?

Dr. McKNIGHT: Okay. Well, you know, this is fairly simple, Ira. We have a compound file at the University of Texas Southwestern with maybe 200,000 compounds. So we knew we couldn't screen nearly that many.

FLATOW: Right.

Dr. McKNIGHT: So we asked our chemistry colleagues to pare down the 200,000 to 1,000 that would be representative of the chemical diversity of the entire library. So we didn't have any bias. We didn't think, oh, this one would be the one that would work in the brain or this one wouldn't. We simply preserved the chemical diversity in paring it down from 200,000 to 1,000. And then, we just blindly tested them.

FLATOW: Wow. Where did you get the money for this?

Dr. McKNIGHT: Most all the money has been provided by the National Institutes of Health via federal research grants to Andrew and to me and to others who work with us. But we have had philanthropic support from wonderful people in the Dallas community who support our research for 10 or more years.

FLATOW: Mm-hmm. So they have confidence in you, in other words.

(Soundbite of laughter)

Dr. McKNIGHT: I guess the answer to that is yes. Why that would be the case, I don't know. But we really simply got lucky this time.

FLATOW: Well, yeah. So let's say you want to continue this roll of good luck, where do you go from here now? You have a compound. You know it preserves the life of these baby neuron cells developing in the brain. Are you the one that goes on to try it out in humans or do you find a partner to try that out?

Dr. McKNIGHT: Well, we reached the point, Ira - we've made many derivatives of the P7C3 compound. We've improved it. We polished it to some measure. But the next level of actually, you know, perfecting it and getting it optimized for human trials is normally best done in the for-profit world, in a biotechnology company or in a pharmaceutical company.

FLATOW: Mm-hmm.

Dr. McKNIGHT: So I would think that over the next six months or 12 months, at some point we want to hand the baton off to the appropriately skilled professionals in that domain. It's not something that's typically done in academia. It's not that we couldn't do it. But in all likelihood, we would prefer to move it into the for-profit world for a drug company or a biotechnology company to take it into human trials.

FLATOW: This is SCIENCE FRIDAY from NPR.

I'm Ira Flatow talking with Steven McKnight of University of Texas Southwestern Medical Center in Dallas, talking about the compound that works in mice and rodents to prevent the death of brain cells. Could there be side effects to something like this that you might not - you know, unintended consequences?

Dr. McKNIGHT: Oh, that's always the case. You know, we've studied this carefully in mice for - perhaps administering it for months at a time. But unintended side effects could crop up at any time. So that's the boogeyman that always gets you as you're trying to develop a drug, discover a drug.

FLATOW: Mm-hmm.

Dr. McKNIGHT: You know, there are many pitfalls ahead of us.

FLATOW: Well, I'm asking, you know, this is just a basic question about basic research. Mice don't live very long, right? And could something crop up in the human lifetime that's, let's say, 75, 80 years, that might not show up in a mouse's life.

Dr. McKNIGHT: Absolutely. Absolutely. That's entirely possible.

FLATOW: And - but this is the standard that people - that researchers use every time they do research.

Dr. McKNIGHT: Well, you got to start somewhere, Ira.

(Soundbite of laughter)

FLATOW: So you're looking for basically a business partner at this point.

Dr. McKNIGHT: Well, that's, you know, probably in the cards, that's something we'd like to do. But, you know, in the meantime, there's lots of science for Andrew and our team to do ourselves. So there's...

FLATOW: Such as? Such as? Give us an example.

Dr. McKNIGHT: We don't know for - a really important shortcoming, Ira. We don't know what protein, what molecular target in the brain this compound P7C3 touches. We have an inkling that it's perhaps working in the energy factory of cells, mitochondria. But we don't know exactly what protein target it's tickling. And as scientists, that's what we got to nail. We've really got to understand mechanistically how is this compound working. And right now, we don't have the answer.

FLATOW: So you know it works, but you don't know how it works.

Dr. McKNIGHT: That's right. And...

FLATOW: Wow.

Dr. McKNIGHT: ...we would love to be ones to make that discovery. But now that the paper is published, I think as of today the cat's out of the bag and so other scientists are going to be able to chase after, you know, that discovery...

FLATOW: Right

Dr. McKNIGHT: ...to find out how P7C3 works and...

FLATOW: Because this compound is available to anybody...

Dr. McKNIGHT: Oh, sure.

FLATOW: ...who wants to use it. You go into the little book, open it up and order some.

Dr. McKNIGHT: Absolutely. So, you know, if we don't - if we're not the ones that make that discovery of exactly how it works, shame on us.

FLATOW: Well, that's because you got a few months lead on everybody else.

Dr. McKNIGHT: Well, we've got a bit of a lead. But, you know, the wonderful thing about science is it's a worldwide community, and if we're not the ones to discover how it works, the person or the group that does will be contributing just like we have.

FLATOW: Well, we want to thank you very much for taking time to talk with us and tell us about your discovery today. Of course, wish you good luck.

Dr. McKNIGHT: Well, thank you, Ira.

FLATOW: Because when we help you, you're going to help everybody else.

Dr. McKNIGHT: Well, we can all hope so.

FLATOW: We can all. Thank you, Dr. McKnight.

Dr. McKNIGHT: Bye-bye.

FLATOW: Steven McKnight is professor of biochemistry and chairman of the department at University of Texas Southwestern Medical Center in Dallas. And he was taking time, as other people do on this vacation period, to talk to us from his vacationing spot in Montana.

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Mess up weekend may turning point in golf.

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Human-Animal Hybrids In 'Lucy,' A Look To The Future?

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Science-fiction novels have often foreshadowed very real scientific debates. Laurence Gonzales' new novel Lucy, about the trials of a human-animal hybrid, may be one of these books. The author speaks with host Scott Simon about his new thriller and the real-life scientific discoveries that inspired it.

SCOTT SIMON, host:

This is WEEKEND EDITION from NPR News. I'm Scott Simon.

The new novel "Lucy" opens as an American primatologist named Jenny Lowe flees from a marauding group of Congolese rebels, comes upon the camp of a British primate researcher. Rebels have gotten there first. She finds the primatologist's young daughter in the ashes of her camp, shuddering on the body of a dead Bonobo.

Jenny Lowe is touched. She takes the girl into her arms, whisks her back to her home in Chicago. She finds that the girl who'd been raised in the jungle by her scientist father is bright, lively and sensitive. She speaks French and Dutch. She quotes Kipling and Shakespeare. She can smell the rain from a long ways off.

One night, Jenny Lowe returns home and finds the young girl that she's taken into her life racked by fever and asleep in the limbs of a tree. You see, there's something else about beautiful and gifted young Lucy. She's part homosapien, part Bonobo chimp.

"Lucy" is the first novel that Laurence Gonzales, probably best-known for his book "Deep Survival," has written in 25 years. And it's being acclaimed as a Crichton-like thriller. He joins us from member station WBEZ in Chicago. Thanks so much for being with us.

LAURENCE GONZALES (Author Lucy): Thanks for asking me.

SIMON: First thing I've got to ask, is this remotely scientifically possible?

Mr. GONZALES: Yes. Arizona just passed a law, which goes into effect on July 29th, that makes it illegal to make Lucy in real life, because the science has gotten to the point where you could actually do it. And so they passed a law in Arizona that says it's a felony to create a human-animal hybrid.

SIMON: Mercy. Now, Bonobo, we should explain, these are the chimps that are, what, I guess chromosomally closest to homosapiens.

Mr. GONZALES: Bonobos look very much like chimpanzees if you're not used to making the distinction. They're smaller. They used to be called pygmy chimpanzees but are now recognized as a separate species. Some people refer to them as the hippie chimps, make love not war, because they use sex to settle social disputes and things like that, whereas chimpanzees tend to fight a lot more.

SIMON: We should explain that the dead Bonobo in the encampment was Lucy's mother.

Mr. GONZALES: Correct.

SIMON: Jenny Lowe begins to read the notebooks of Lucy's father.

Mr. GONZALES: Yes.

SIMON: And that's how she finds out that this charming and borderline brilliant young girl she's taken into her life - how she began life.

Mr. GONZALES: Yes.

SIMON: Why would somebody try an experiment like what you outline?

Mr. GONZALES: Well, you'd have to be a bit of a mad scientist to start with. But this guy, in particular, explains himself. He was in love with the Bonobos and they're going extinct just as fast as people can arrange it. And he wanted to save some part of them.

And in addition, he looked at the world around him, as any of us can do by watching the news, and decided that people needed a change as a species. And by infusing people with a hint of Bonobo genes he would create a new species that would, you know, be better than people, be somehow less likely to wipe themselves out off the face of the Earth.

SIMON: And there have been experiments along these lines in the past, I gather, from reading your book.

Mr. GONZALES: Yes. There actually are - in the book I detail some of the experiments that were tried. Specifically in the early 1900s, the Russians were trying to breed people with chimpanzees. And they were - everybody seemed to think it was okay to try this somehow. The French were supporting them. They had a site in Africa where they had chimpanzees. And they went there with scientists and tried it and it didn't work. But, of course, that was before genetic engineering.

SIMON: You know, you put down the book and among the many questions that you're left with in your mind is, should Bonobos be in cages anywhere?

Mr. GONZALES: No. They shouldn't. It's a terrible problem. See, the Bonobos in the jungle in Congo right now are being killed off. There's a war going on there. And there are bushmeat hunters that kill them to eat them. And their habitat is being rapidly destroyed by various kinds of industries - logging and so forth. So they are really endangered in the wild.

The ones that are in captivity, you know, once a Bonobo is in captivity they can't readapt to the jungle. So you can't just go let them go. So it's a very, very difficult and kind of heartbreaking problem. And the only thing that I can - I've talked to the people who, you know, keep them in zoos and stuff - the only thing that I know of that can be done is to expand their captive habitat to the point that it's as comfortable as you can make it.

SIMON: That deprives them of something, too, doesn't it?

Mr. GONZALES: Yes. Yes, it does. And you have to remember, these creatures are extremely smart. They're extremely smart. They're really almost human. And so you have to remember that because of their social nature, I mean, you just put a bunch of random Bonobos in the same habitat together, that doesn't make any evolutionary sense. They don't know each other. They don't like each other. You know, it's very difficult.

SIMON: It does make you wonder though, is there always a neat and clear chromosomal distinction as to what is human?

Mr. GONZALES: Well, that point is raised in the book. There is a point at which a senator gets a bill passed that essentially makes - defines Lucy as an animal and therefore having no human rights. It defines being human as having the genome that was decoded, you know, when the genome was decoded for humans. And so, by definition she has no human rights.

But it's interesting because this very point was raised by the congressman who passed that bill in Arizona making it illegal to create a hybrid human. She said, well, you know, we can't be doing this because then who will decide whether this creature has rights or not? So, these issues are being raised in real life right now.

I mean, obviously, one of the things I took into consideration when writing it is I think we're so close to this technology, the ability to do things like this, that's it's useful for people to become aware of this - whatever their beliefs, whatever their political position or moral position, to become aware that this is real or could be real. And, of course, I do this in the form of an entertaining novel, but it can certainly spark conversations that I think need to go on before we get there.

SIMON: Does the name Lucy mean what a lot of people will think it does, referring to what's often identified as the first human Lucy?

Mr. GONZALES: Yeah. Actually, recently there was an older - 4.4 million, I believe, year-old skeleton found. So, Lucy's been kicked off her throne. But the answer is twofold. One is in the book Lucy's father says, I didn't name you for that. I named you because Lucy means light. And so, that's his reason.

My reason for choosing the name, however, is the ostritalpythecene(ph) that you're referring to.

SIMON: Laurence Gonzales, thanks so much.

Mr. GONZALES: Thank you for having me on.

SIMON: The new novel, "Lucy."

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