Transcript:TWIS.ORG April 7, 2009


Justin: Disclaimer! Disclaimer! Disclaimer!

The future is rapidly approaching. This has always been the case, of course throughout the whole of human history. Tomorrow always seems to be on a hurry to reach the present. What may separate our presently encroaching future from future’s past?

The seemingly limitless landmarks that beacon this new age, from nano-engineering to synthetic-genetic manipulations; stem cell progenitors to microbial biofuels; from the nature of neural networks to a universe made of strings; the science that we are living in golden age of discoveries only clouded by the sheer volume of discoveries and the speed at which they are being made. Making the amazing a common place occurrence.

As human knowledge expands well beyond the familiar seemingly intuitive world we were born into, rerun the risk of falling behind in our time of being primitive thinkers in the modern world.

In all primitive thinking much like the hour of our programming does not necessarily represent the views or opinions of University of California at Davis, KDVS or its sponsors.

The speed that which the secrets of the universe are being revealed to us is increasing at such a rate that if we turn our attention away too long, if will allow ourselves to be mired in daily destruction, we may miss our chance to glimpse the world made naked by knowledge.

The universe as revealed by This Week in Science coming up next.

Good morning, Kirsten!

Kirsten: Good morning, Justin! How is it going today?

Justin: It’s early. It’s earlier than it normally feel. I don’t what’s going on today.

Kirsten: I don’t know it’s later for me. I kept thinking I was late today because where I am is 9:30.

Justin: Wow! You are late.

Kirsten: I am late.

Justin: The show is over. Let’s wrap it up.

Kirsten: (I haven’t been in) the show.

Justin: So, you obviously are not here because you just announced that you’re somewhere else. Where are you?

Kirsten: I am in Boulder, Colorado at the Conference on World Affairs. And it’s a conference that’s being going on. I think this is the beginning of their 70th decade of this conference.

Justin: Wait NO! It can’t be their 70th decade.

Kirsten: It is. This conference has been going on for…

Justin: Hey, it would not be like 700 years?

Kirsten: Sixty-one years.

Justin: No, it would be like 700 years if it’s a…

Kirsten: I mean 7th decade. Sorry.

Justin: Wow! Well, you know, they do have some the Naropa Institute over there. It’s some ancient Buddhist wisdom schools over there. But I don’t think they’ve been there for 700 years. I don’t know.

Kirsten: No. Yeah, that was my bad. Sixty-one years this year. And it is a really fascinating conference. There’s about people here from Pakistan, from Israel, from Washington D.C. We’ve got scientists, Seth Shostak is here, Alex Filippenko.

You know, there are people from all different disciplines and areas of expertise and they’re throwing them together in rooms on panels to talk about all sorts of topics.

Yesterday, I was on a panel talking about Pseudoscience in the movies. And we all agreed that you know, fiction is fiction as long as it’s a good story. You know, you can suspend disbelief, enough to like maybe accept some made up science.

Justin: Maybe. I don’t know. I have a hard time doing that myself.

Kirsten: Yeah.

Justin: I don’t suspend all disbelief even while dreaming. No, no. Like some people can fly when they dream.

Kirsten: Yeah.

Justin: I don’t. There’s still the laws of Physics they are applying largely to, you know…

Kirsten: There’s no way I could be flying.

Justin: No. And I do, I have a real problem sometimes with too much Pseudoscience in fiction or fantasy when they – just don’t this – they don’t explain stuff. I need a good excuse for the world being out of kilter in my science fiction.

Kirsten: Yeah. Let’s see, what am I doing today? Today, I’m doing a panel on brain corpse.

Justin: Huh?

Kirsten: Yeah. So, funky thing, funny things about the way the brain works.

Justin: Awesome!

Kirsten: Yeah. It will be fun. And then, there’s other panels. I went to Alex Filippenko’s talk yesterday on black holes. It’s just fascinating. There are, you know, I don’t know, I might go to a talk on science and religion later this week.

There’s some talks on evolution and Darwin. There’s some other stuff going on on – there’s a panel opposite me that’s really interesting on, you know, how we can bridge that divide between the Muslim world and the western world and you know, create better understanding. There’s just all sorts of wonderful topics.

Justin: And it sounds like a blast.

Kirsten: Yeah. And I just feel very honored to have been invited here. And everybody is so nice. Yeah. Everybody is just being nice to me. And I keep turning around going where’s the “Kick me” sign.

Justin: I don’t know. I’m telling you. This is what would happen if scientists took over the world.

Kirsten: Yeah.

Justin: You’d have this big conversations about things.

Kirsten: Yeah.

Justin: Mm hmm.

Kirsten: Big conversations. And it’s great. Everyone is so excited about discussing. I mean, I got in a conversation yesterday. And last night I’ve sat down at a table to eat a meal with people I’ve never met before.

And somebody turns to me and says, “Well, what do you do?” “I’m a neurophysiologist.” “Well, you know, I’m a lawyer and I work for nuclear disarmament. But do you think about consciousness? Do you think consciousness is just a chemical process? Or do you think the chemicals are moderated by your consciousness?”

Justin: Wow!

Kirsten: There’s just like wow!

Justin: That’s a good question.

Kirsten: I just sat down at a table and suddenly we’re in this deep conversation. Very cool place.

Justin: Wow! Well, thank you for taking time out of your cool day to come back to us…

Kirsten: Yes.

Justin: …here at little Davis.

Kirsten: And the science news because we have a whole bunch, don’t we?

Justin: I hope you do.

Kirsten: I have news about birds and beer.

Justin: Mm hmm.

Kirsten: Mm hmm. And World Robot Domination.

Justin: Yes.

Kirsten: That’s my big story for today, World Robot Domination. And then, I’ve got some space news and, you know, some other fun stuff.

Justin: I’ve kind of taken up your stem cells.

Kirsten: Cool.

Justin: I’ve got some blood, some nerve-y story, drugs. Well, that sorts of things. Yeah well, let’s get right into your big story.

Kirsten: Okay. So, World Robot Domination. Robots are now taking over the lab. They’re taking over science.

Justin: This is so cool.

Kirsten: This is such a great story. Some researchers at Aberystwyth University in the U.K. – and I have no idea if I pronounced that right because there are “Ys” where there should be other vowels in the name of the university.

So, they’ve created this robot that – they named it Adam. And what he does is – it doesn’t look like a person. But he can grow yeast cells in petri dishes. And Adam has a library of over 12,000 petri dishes inside of the box, that is Adam.

And Adam has been going through those petri dishes and selecting different dishes for different genetic mutations going, “Okay well, I’m going to analyze the DNA in this one. This one has this kind of a mutation. This one has this kind of a mutation. What is it doing?”

So, Adam has been observing the cells, analyzing the DNA and actually came up with 12 new gene functions.

Justin: What?

Kirsten: Yeah. Discovered independently through experiments that Adam designed and ran. I mean, Adam basically – like the process of elimination – basically, so, we’re going to do this, this, this and logically went through, was able to determine the functions of 12 new genes.

Some of the genes had actually previously been described. So Adam, confirmed those results that had come out from human ran labs independently, all by himself.

Justin: Wow!

Kirsten: Yes.

Justin: So, that’s why, you know, that’s entering into the realm of some sort of critical thinking human.

Kirsten: It’s getting there. And basically, they’ve given him – (I don’t care) I’m using the personal term “him” – and some advance artificial intelligence that lets Adam, make his own decisions, act on those decisions and not depend on the humans in the lab.

And the laboratory is – they’re creating another robot named Eve that – I mean, I love the biblical references to the first two robots that are taking over the laboratory and investigating knowledge. It’s kind of appropriate that Eve is going to be one of these knowledge, knowledge-gaining robots.

Justin: They are like playing with it.

Kirsten: Mm hmm, yeah. But so, you’re going to like this one though. Eve is actually is going to be investigating cures or treatments for Malaria, looking for ways that we can help get rid of Malaria, looking for drugs and other stuff.

So, that I think is going to be – Eve is going to have a very, very important function.

Justin: Love her.

Kirsten: We love Eve.

Justin: Yes.

Kirsten: Yes.

Justin: So, is there any – I mean, is there any threat? Do that need to scientists feel as though they are now being edged out by these robots?

Kirsten: No, I don’t think people feel like they’re being edged out yet. I mean, that the one part of it is the work that these robots do is repetitive, it’s the kind of work that if you were doing it, you might make mistakes because…

Justin: Oh, yeah.

Kirsten: …it’s gets kind of boring. You’re going (pipet, pipet, pipet). Then, you know…

Justin: Oh, no.

Kirsten: …it’s very repetitive. And humans kind of lose track of what they’re doing sometimes if they’re not incredibly careful. And doing repetitive experiments with the way our brains work, you know, mistakes do happen.

So, it’s maybe better that robots like Adam and Eve can do these very highly repetitive jobs to free up scientists to be able to do other work and come up with other ideas and be able to do different experiments that maybe aren’t so repetitive.

Justin: And I’ve retold the story too about the tour of the Public Health Lab in Santa Cruz County where…

Kirsten: Right.

Justin: Yeah. A machine now that can analyze and tells what’s in the petri dish, what’s growing in there.

Kirsten: Yeah.

Justin: And it’s a process that used to – it was a process of elimination and doing stains that would take, you know, he shared with me what it would take to have drill down and analyze just something as simple as E.coli.

And it took so many test tubes and, you know, it would be like 30, 40, 50, 60 of them. You’d have to keep doing. And every time that it came it negative, you’d have to go through and do more of these tests just to analyze one thing. Now, you put it into the computer and within 24 hours, it kicks out an answer for you.

Kirsten: Yeah. And, you know, there’s going to be a human to make sure that the robot, the computer is doing it’s job appropriately.

Justin: Right.

Kirsten: There will be some kind of quality control. And, you know, so, humans are not going to lose their jobs entirely to these robots.

Justin: Yeah, right.

Kirsten: The robots also are extremely expensive.

Justin: Humans have been losing jobs to robots for 50 years now.

Kirsten: Yeah.

Justin: We’ve got to be used to it.

Kirsten: Yeah. And these robots, I mean, they’re not going to like be in labs everywhere because they cost so much. You know, they’re still like 10 or 20 years from becoming cost-effective enough to actually be in a majority of labs.

So, I think there’s, you know, people don’t have to worry about it too much.

Justin: So, if robot makes a discovery, that’s a really, really critical discover…

Kirsten: Yeah, who gets Nobel prize, right?

Justin: Yeah, who gets credit? The roboticist? The lab operator who pushed the big green button to make it go? Who gets that?

Kirsten: That’s a good question.

Justin: But I guess, that’s just the vanity. And when is being too vein a good thing?

Kirsten: Oh, good segway.

Justin: Yeah, segway. But I’m on it. When you are suffering from peripheral artery disease, that’s when having more veins could come in handy.

Kirsten: Oh.

Justin: It’s a disease that has – it’s actually a side disease which has a number of causes that reduces blood flow, blood flow throughout the body. Diabetes causes certain, things that like smoking can do this in our lungs. It’s stroke can do this – well, you just have a reduce blood flow in some area of the body.

New research published in Scientific Journal Blood which is not to be confused with blood spectator, the nocturnal periodical for vampires. Researcher David Hess of the Robarts Research Institute University of Western Ontario has figured out how to use pro-angiogenic stem cells from bone marrow to grow new blood vessels. New blood vessels, science!

Kirsten: Yeah.

Justin: Wow! So, from human bone marrow – this is important distinction, they’re using human bone marrow on this already – has this isolated three different types of stem cells that when combined together, put together – coordinate to form the new blood vessels.

So, it’s no single – this is some serious, critical thinking going on here. Cells were then injected into the circulation of mice. Researchers showed how the stem cells have a natural ability to hone in on an area with ischemia, it’s a place where…

Kirsten: Ischemia?

Justin: Yeah.

Kirsten: Ischemia.

Justin: Ischemia.

Kirsten: Ischemia.

Justin: Where the blood flow, blood flow is too low to induce blood vessel repair. So, they actually figure out where they are needed.

Kirsten: Yeah.

Justin: That’s amazing. That’s very amazing. Hess says, the research is clinically applicable because they studied the function of human stem cells in the immune deficient mice. So, immune-deficient mice because that way, they don’t reject.

So, we can select the right stem cells from the patient’s own bone marrow, put them back in the area of the ischemia.

Kirsten: Ischemia. You’re right this time, yeah.

Justin: Oh, that’s right? Oh, okay. To allow – okay – to allow these cells to coordinate and form the new blood vessels. Says Hess, a professor in physiology and pharmacology at Western Schulich School of Medicine and Dentistry, “These principles could be applied not only to ischemia limbs, but to aid in the formation of new blood vessels and tissue anywhere in the body, for example after stroke, heart attack, that sort of thing.”

The pre-clinical data has received FDA approval for a multi-center clinical trial now on their way involving some 21 human patients who have end the stage peripheral artery disease.

So, it’s already moving into the human trials. And we’ll probably be one of those unaffordable pharmaceuticals that…

Kirsten: Yeah. I don’t know, it might not be that unaffordable.

Justin: No, no, no. That was a joke. It’s just – well, this is an issue that I was – oh, gosh and now, I’m going to sub-tangent without information properly to describe this. But I was listening to a description on a another public radio station about how, when scientific research is published, the journals own much of that information.

And so, dissemination of that information gets harder. And how it turns into the hands of say, a pharmaceutical company who then own rights to discoveries that, you know, were paid for largely by free – or the tax dollars by the taxpayers. But that’s a different conversation. That’s not what we should rant about later.

Kirsten: Yeah. But I don’t know necessarily that just publishing a result in a journal that’s owned by somebody outright would actually – that doesn’t mean they have rights to the discovery, that just means they have rights to your article.

Justin: Correct.

Kirsten: But in terms of, you know, it’s where the funding comes from. So, probably this, you know, if you get funding from a pharmaceutical company then, you know, that pharmaceutical company is going to have, you know, some rights. They’re going to take some rights for the discovery and how that discovery is going to be used. Anyway, we can talk about it all later.

So, who knew that birds are beers actually have something in common?

Justin: Birds and bees, you mean?

Kirsten: No, beers.

Justin: Beers and the birds and bees.

Kirsten: Birds and the birds.

Justin: No bees?

Kirsten: No bees.

Justin: Huh?

Kirsten: And as our loyal contributor (Ed Dyre) had to say, “What is there not to love about a story linking bird feathers and beer foam?” You have to love it.

Justin: That’s pretty wild.

Kirsten: It is totally wild. So, this story comes out of Yale University. Researchers looking at bird feathers and the colors in bird feathers have realized that the really bright colors that are in the feathers of bird are created by little tiny nanostructures that are very similar to beer foam.

So, the way that beer foam has, you know, has the bubbles or even like a sponge has holes in it in this bubble-shape formations, the light is going to be produced by these nanostructures. They look like air bubbles.

And this Yale engineers took a look at it and tried to figure out how the structures are formed to it to be able to actually create these colors that are in, you know, bright blue feathers like Bluebirds.

And they looked at these nanostructures. What they say is they looked at these nanostructure-material undergoing phase separations in which the different substances become unstable and they separate from each other.

So, it’s kind of like when you have a carbonated beverage like beer. And you pour it into a glass and these bubbles, the carbonation makes a phase separation that creates bubbles or foam on the top of the beer.

And the color, the structures, these nanostructures in the feathers that produce the bright-blue color actually appeared to assemble themselves in the same way that bubbles and foam are created in beer.

Justin: That’s pretty interesting.

Kirsten: It’s neat. So, what they’re looking at is this, the water bubbles actually forming in the protein of cells and then being replaced with air as the feather grows.

Justin: Huh?

Kirsten: And so, they get replace with air. And so, they have these bubble-like structures like a sponge. You know, how they have the solid framework but with where you can see that there were bubbles at one point inside of it. But maybe those water bubbles have disappeared.

And so, it’s just fascinating that the information – what Richard Prum, the chair of the Department of Ecology and Evolutionary Biology says, “Such information would have to be encoded in the feather as the bubbles grow.” Basically that information about quality that a bluer male is a better male.

And he says, “I think our hypothesis that phase separation is involved, provides less opportunity for encoding information about quality than most biologists thought. At the same time, it’s exciting to think about other ways that birds might be using phase separation.”

Justin: We have that story sometime last year about the birds that had the stripe on the wing.

Kirsten: Yeah.

Justin: And there was, you know, there was some that had the more distinct stripe, white stripe on the wing that tend to be the dominant males. They sing more. They got more attention. They mated more often.

Kirsten: Yeah.

Justin: And they were interested to see if this was a genetic trait that showed help, if it was something being encoded (right) into that wing that was illustrating this. And then, they went in painted some less dominant males. They painted their wings and suddenly they got the attention.

Kirsten: Yeah.

Justin: Suddenly, they were singing. Suddenly, they became more dominant and took over more territory and did more pitching of the woo.

Kirsten: Yeah. I mean the comments that, you know, the researcher makes about, you know, that maybe this phase separation process isn’t related to quality…

Justin: Mm hmm.

Kirsten: …as much as biologists thought. I mean, I don’t necessarily agree with him on that. I mean, this is now a physical process that could potentially be affected by processes inside the cell.

So, if you’ve got water bubbles forming in the proteins of the cell, maybe, the number of bubbles that are formed, the way that they’re formed, maybe that IS affected by your health, the metabolism of the cell. Whether or not you have a parasite load that’s going to affect how well, you know, how healthy your cells are and the way that your metabolism functions.

Justin: Mm hmm.

Kirsten: You know, so they’re could be now looking at this process maybe an even more direct link. You know, the link that researchers have been looking for.

Justin: Interesting.

Kirsten: Yeah.

Justin: Yeah. Maybe it could still be linked to health but then, you never know what else is going on. Like I – that’s the thing that I wish we could get to that point where we could really understand just animal psychology in general.

Kirsten: Yeah.

Justin: It maybe that they are healthier. But just genetically worse in a conversation.

Kirsten: Okay.

Justin: Yeah. I mean, it could be that also – like in that formation maybe there is, where there is less of the bubbles, less stuff going on there. Maybe their energies are being applied to the brain or to a different aspect of development that…

Kirsten: Right.

Justin: …that’s actually a benefit. So, no way to tell yet.

Kirsten: No way to tell. It’s very – I don’t know, just an interesting new piece of information that, you know, it will be neat to see what other researchers take from this and start doing to actually look into this link between behavior and the actual physiology of these animals.

Justin: Speaking of physiology – this has nothing has nothing to do with – well, sort of. General Session of the International Association for Dental Research has unveiled new studies connecting oral disease and systemic disease.

Kirsten: Yeah.

Justin: A reccurring theme that there’s relationship between, you know, gum disease and in this case, they were looking at infant prematurity.

Kirsten: Oh, really?

Justin: Yeah. Infant prematurity, they looked at diabetes. They looked at stroke. Stroke, I’d heard for diabetes and premature births, those are kind of new to me. I don’t know how this relate.

Kirsten: And heart disease definitely.

Justin: Heart disease, yeah.

Kirsten: There’s a definite link between gum disease or infections in your mouth that can be transferred to your heart.

Justin: Huh?

Kirsten: Yeah.

Justin: So, the studies reporting on the efficacy of treating a periodontal disease to lower the incidence of, in this case, they were looking at infant prematurity worldwide, maybe conflicting pregnant mothers with – okay, wait – maybe conflicting – pregnant mothers with periodontal disease are treated with scaling and root planning – I don’t know what those are – some sort of tooth cleaning.

Kirsten: Mm hmm.

Justin: So, basically what they did was they calculated the amount of non-treatment for 1600 pregnant women with all levels of severity of periodontal disease and they compared what it would cost to give them regular cleanings versus what it would cost to treat their premature infants in a hospital situation.

Kirsten: Yeah.

Justin: Just in 1600 women, they estimate the savings to be around $14 million.

Kirsten: Wow! That’s a lot.

Justin: They follow this trend over to a treatment of patients with diabetes and a history of stoke. In a single year, patients with medical and dental coverage from a private single carrier exhibited average savings in medical costs of $10,000 for those who had strokes and about $1400 for patients with diabetes.

So, basically they’re illustrating that prevention in the case of dental hygiene…

Kirsten: Yeah.

Justin: If we, you know, if we made this something that was widely available, that we would save considerably on the other end, on the other health care aspects. So, next week the Association for Dental Research is going to hold their Annual Panel of Five Convention where they will gather together by the thousands in attempt to make a unanimous recommendation.

Kirsten: Well, it would be interesting to see, you know, how the…

Justin: That was the (unintelligible).

Kirsten: …how the insurance companies end up responding to this research. You know, will – I don’t know. I really tend to think that preventive care is always going to be the best option.

Justin: Mm hmm.

Kirsten: So, I mean that so often, it’s not preventive, it’s as a result of. So, it’s when somebody get sick then you care for them instead of taking care of them beforehand. I don’t know. We’ll see. I think it’s fascinating.

Justin: We’re right here at the break. So, I’m going to zip us off into…

Kirsten: Okay.

Justin: …into announcements and what have you, messages from KDVS 90.3 in Davis. And we’ll be right back with more at This Week in Science.

Kirsten: Oh, see you.

Justin: Hang on, Kirsten.

Kirsten: Okay.

Justin: Last (time).

Kirsten: Right, this is the last phone call from New York City. I’ll be back in Little Davis, yet again, full of culture shock next Tuesday. In the meantime, I’ve got lots of New York science going on.

Justin: And we are back with more of This Week in Science.

Kirsten: Howdy. I’m still here. I (ain’t) gone nowhere.

Justin: Good, good. So, did you go to anything conferences during our break?

Kirsten: No. I just stayed where I am sitting at the – sitting, staring at the Flatiron of the eastern slope of the Rocky Mountain, beautiful view. It’s gorgeous here. There’s snow, you know.

Justin: Mm hmm.

Kirsten: Mm hmm.

Justin: Mm hmm. I’ve heard of that stuff.

Kirsten: What other science news do we have Justin?

Justin: Oh, my goodness. Well so, we were talking about veins.

Kirsten: Mm hmm.

Justin: Growing new veins earlier. They just did another one through of Avastin.

Kirsten: You want to stay about stay in the same vein here?

Justin: I want to stay in the same vein, so to speak. Although, this is slightly different take on the same basic idea. Avastin is being used to do the exact opposite of what that stem cell research is looking to do.

Kirsten: Huh?

Justin: The stem cell research is all about putting these combinations of stem cells in the areas and having them form new blood vessels. The way Avastin works, it’s a drug that’s used to PREVENT the forming of veins connecting to cancerous tumors.

Kirsten: Cool.

Justin: Yeah.

Kirsten: If you don’t feed the tumor then…

Justin: Yeah.

Kirsten: …the tumor doesn’t grow.

Justin: It doesn’t grow. And so – what is it called? This is oh, gosh, this is giant words. This looks like Greenlandic word combinations. Alkylator-refractory anaplastic oligondendroglioma, okay.

Kirsten: What?

Justin: Well, it’s AO for short, which I think is brilliant for all those words to be shorten to two letters. So, yeah anyway, they’ve been using it I guess for colon cancer up to recently because it doesn’t kill the tumors but it prevents them from getting access to more blood flow. And so, like you’re saying, it can’t grow.

They’ve now done a study and found that it’s working on brain tumors.

Kirsten: Neat.

Justin: Very neat, very neat. These brain tumors because the typical treatments tend to use a lot of steroids and things.

Kirsten: Yeah. Typically, you have to use things that can cross the blood brain barrier.

Justin: Mm hmm.

Kirsten: And that’s the big difficulty in treating brain tumors is how do you get a drug that pass the really tight control of the blood brain barrier and into the brain where you can actually do something about the tumor.

Justin: Yeah, yeah. And so, these are things that also have considerable side effects. And one of the side effects usage of steroids can even be things like blindness. I mean, it can be pretty severe.

So, there are no significant side effects for using Avastin in this – (like they were saying) in this brain tumor studies.

This is, you know, and this could add, you know, it doesn’t save the patient. The patients who have been involved in the study are all expected not to make it. But this is adding years of life WITHOUT side effects.

Kirsten: Yeah.

Justin: You know.

Kirsten: Which is fabulous. Anything that can extend somebody’s time here is just wonderful. Just wonderful. Did you want a new heart?

Justin: You know, mine has been broken so many times. I just keep patching it together with Duct Tape and Super Glue, I figure.

Kirsten: Well, you know, maybe you don’t really need that Duct Tape and Super Glue. It turns out that the heart actually replaces itself.

Justin: Mm hmm.

Kirsten: Yeah. So, researchers have been looking at the heart. It is the muscle, it just beats here your entire life, you know. It starts beating before you’re born and it continues until you die. And it is the strongest muscle on our bodies. The most never or the least tiring muscle in our body.

And how does it maintain this ability to continue pumping and working our entire life? It turns out that the heart muscle, there are actually stem cells within the heart. So, the heart muscle actually replaces itself. And this has been understood for several years.

The question though has been how much does it replace itself? How often are the cells replaced? One researcher, long time ago suggested that the heart muscle must replace itself at least four times during your lifetime.

Justin: Wow!

Kirsten: Yeah. So, at one point, it was thought that the heart, you know, during your lifetime, you’d have four different hearts. But other researchers like, “Well, that just seems a little bit extreme. Maybe it’s not quite that much. Maybe it doesn’t actually replace itself, not enough new cells are created during it’s lifetime.”

So, new researchers took a look using carbon-14. And carbon-14 – because of nuclear blasts during World War II, there has been a large amount of carbon-14 and also in nuclear weapons that were tested up until 1963.

Justin: Oh, yeah. So, the above ground test, they did this – they use this I think in the study of fat cells…

Kirsten: Yeah.

Justin: …to try to figure out how long they last in when new ones are formed. Because it – yeah, these above ground blasts, leave this carbon-14 imprint somewhere in the cell, right?

Kirsten: Yeah. And so, because there is a known amount of carbon-14 in the atmosphere and in our environment, we take that up into our bodies through our diet, you know, through eating plants and animals that were created on the planet and that just incorporated the carbon-14 and the diet gets incorporated into the DNA of our cells.

And because it is the special configuration of the carbon atom of the carbon molecule, we can actually take a look at how much carbon-14 is in ourselves. And so, new cells that are born will have a different amount of carbon-14 than cells ten years ago because the amount of carbon-14 has been decaying because it’s radioactive. It’s been decaying ever since 1963 at a known amount.

Justin: That’s awesome. So, all of our cells now have a clock in them.

Kirsten: Exactly.

Justin: They’re all datable.

Kirsten: Yeah.

Justin: Brilliant.

Kirsten: We have this clock in every single one of ourselves. And so, a researcher, Dr. Frisen from Sweden, the Karolinska Institute in Stockholm took a look at heart muscle cells and apply this carbon-14 dating method to heart muscle cells.

And he said, it was really complicated actually because these heart cells have two – many of the cells have two nuclei and within this double nuclei, the DNA would maybe duplicated again.

And so, they had to really use some rigorous methods to be able to determine how much carbon-14 was in these cells and to be able to date them. And so, what they found is that the rate of birth of cells is about 1% of the heart muscles being replaced every year up until about age 25.

Justin: Wow!

Kirsten: So, only 1% of your heart muscle cells get replaced every year. After 25…

Justin: That’s a tense for such a busy, busy, busy, busy organ.

Kirsten: Yeah, busy, busy. But you know, maybe one reason that were looking at deterioration of heart function as we age might relate to the fact that after 25, that rate goes down to less than 0.50% per year by the age of 75.

Justin: Oh.

Kirsten: So, our heart muscle cells gradually – they get reproduce a little more slowly as we get older. And maybe that had something to do with our heart’s ability and prevalence of cardiovascular disease as we age.

Justin: That’s pretty wild.

Kirsten: But maybe, if we can figure out how to keep those cells replacing themselves, maybe we won’t have a problem with cardiovascular disease. At least, you know, heart disease as much as we get older. Maybe we can fix that.

Justin: Fix it. Fix it.

Kirsten: Yeah.

Justin: Yes, yes. That’s what science is doing. Look at this, this is amazing. So far, we are at what? New heart, new veins?

Kirsten: Yes.

Justin: Stopping tumors, now, the nerve of science to discover new things, never ending. New research has also shown regeneration of critical nerve fibers…

Kirsten: Wow!

Justin: …that travel between the brain and the spinal cord.

Kirsten: That’s very, very significant.

Justin: Yes. This is – regeneration was accomplished in a brain injury site in rats by scientists of University of California, San Diego School of Medicine described on the on-line edition of the Proceedings of the National Academy of Scientists, PNAS.

And yeah, so this is – I guess it’s from the base of the skull to where it connects to the upper end of the spine. These nerve tissues where they go in and basically if you have a severe neck injury. This is what…

Kirsten: Yeah.

Justin: This is why people will have the – what do you call it? What’s the thing we can’t move…

Kirsten: Become a quadriplegic or…

Justin: Yeah, yeah, paralysis.

Kirsten: Paralysis.

Justin: That’s what I was thinking. But yeah, yeah. Let’s see, findings establish a method of regenerating a system and nerve fibers called corticospinal…

Kirsten: Corticospinal.

Justin: Corticospinal motor axons. “Restoring this axons is an essential step in one day enabling patients to regain voluntary movement after spinal cord injury,” says, Mark Tuszynski, MD, PhD, professor of neurosciences and director of the Center for Neural Repair at UC San Diego and a neurologist at the Veterans Affairs San Diego Health System. He’s got a big card, I bet, when he has to.

The coricospinal tract is a massive collection of nerve fibers called axons. They are these long, slender projections of neurons that travel between the cerebral cortex of the brain and spinal cord. And they carry the signals for movement from the brain to the body.

So, a voluntary movement occurs through the activation of the upper motor neuron that resides in the frontal lobe of the brain and extends its axon down to the spinal cord to the lower motor neuron.

The lower motor neuron, in turn, sends its axon out to the muscle cells. And in the case of the spinal cord injuries, the axons that run along the corticospinal tract are severed so that the lower motor neurons never know that they’re suppose to be doing something.

“Previous spinal cord injuries have shown regeneration of other nerve fiber systems that contribute to movement but have not convincingly shown regeneration of the corticospinal system,” says Tuszynski, theorizing that this was due to some sort of limited intrinsic ability of corticospinal neurons to turn on genes that allow regeneration after injury.

Without that regeneration, it’s questionable whether any sort of functional recovery could take place over all. This is – there’s also – he has previous study he did earlier this year – just earlier this year, back in February was looking at something called BDNF.

Kirsten: Yup. Brain-Derived Neurotrophic Factor.

Justin: Yeah. It’s a growth factor, right?

Kirsten: Mm hmm.

Justin: So, they’ve used this growth factor in helping to coax the regeneration here. And it also – previous finding has shown that there also has potentials as a therapy and reducing brain cell lost for Alzheimer’s disease. Very cool stuff.

Kirsten: Yeah.

Justin: So…

Kirsten: Yeah.

Justin: Bring me another disease, bring me a disease. Something that we can’t knockdown. Come on, on, on, on. Something that we’ll still work on. This is beautiful. This whole year so far has been, you know, if we have a theme this year, it’s definitely been curing all what ails us.

Kirsten: Yeah. I mean eventually, it really – once we understand how a lot of the signals in the body work, how the cells communicate with each other, you know, we will be able to develop treatments for all sorts of problems and be able to get over things, get neurons to grow, to replace neurons that have been damaged.

And within the spinal cord moving to areas outside of the spinal cord, that is one of the – I mean that is, seriously one of the most important things that nueroscience is looking at right now.

I mean, if we can understand how these neurons, the signals that get them connecting to each other and growing where we can solve the problems like paralysis. We’ll be able to get people to the point where they don’t, you know, they’re not going to have to spend their lives in wheelchairs or using other technical tools to be able to exist, they’ll be able to walk again. They’ll be, you know…

Justin: Yeah. We’ll lose the need for that mind-controlled experiment with the monkeys, moving with robotic arm.

Kirsten: Yeah. We’ll see which one comes first.

Justin: Which one gets there first.

Kirsten: I mean, I can see other uses for the mind-controlled robotic.

Justin: Oh, yeah…

Kirsten: Robotic arm.

Justin: It’s just too cool to ever give up there.

Kirsten: I want one.

Justin: We got a story left. I don’t have the story in front of me. But this is from minion (Glen) in Vancouver, British Canada – British Columbia at Canada.

“In my lifetime, I have a few sport injuries, fractured ankle, skiing; several broken fractured fingers, baseball; both wrists, baseball, hockey; collar bone, rugby; ligaments knee, jogging, hockey; ligaments shoulder, baseball, hockey, badminton” – how do you get injured playing badminton. Oh, come on now. Must been one aggressive game.

So, he throw us in this – sent us a story and says, So, I want this now. Yup, I do. I want this now. It’s a team that (kill) university testing injectable stem cells that they can control using magnets to take it to a certain location.

Kirsten: Mm hmm.

Justin: And once these immature cells can be guided for the right area, they can actually be – they can be encouraged to grow new cartilage and bone. And looks like it works on mice.

Kirsten: That’s excellent.

Justin: That’s awesome, yeah.

Kirsten: Yeah, cartilage is a big deal because we don’t have that many stem cells within cartilage. Bone will regrow. There are a lot of new osteo sites that are reproduced all the time. You know, lots of bone production.

But cartilage, not so much. And so, when you damage cartilage, it’s harder to replace. And so, if we can find ways to get cells to the area where there’s cartilage, like your knees, your wrist joints, these places that get damaged a lot because they undergo a lot of stress. Wow! That would be so neat. That would be neat.

I’m just saying a lot fabulous and neat today. I’m excited.

Justin: What? You know, at this point, that’s our job.

Kirsten: Yeah.

Justin: You know.

Kirsten: That’s right.

Justin: We just go, “Wow!”

Kirsten: (Unintelligible) like, wow!

Justin: Wow! Look, wow! Oh my – did they really – yes! Oh, wow! That’s incredible. That’s amazing.

Kirsten: Yeah. Something else this week? This week in saving humanity’s butts. This is another exciting story. It was sent to me. Thanks to (David Morgan), (Kalidasa) and (Ed Dyre) for the story.

Viruses can give you more than a cold. They can also power your car.

Justin: What?

Kirsten: Or at least they might, eventually. So, MIT research scientist, Angela Belcher has been working on viruses to create power for rechargeable batteries.

Justin: That seems so strange.

Kirsten: It does seem strange. But what they’ve done is they’ve genetically engineered viruses so that the viruses build the positive and negative, the cathode and the anode ends of a lithium-ion battery.

And so, they’ve been working on the anodes for several years. But they’ve had a really—the hard part for them has been getting the cathodes to create that end of the battery, to create a full circuit.

And so, what they finally did is they got the viruses to coat themselves with iron phosphate. And that iron phosphate grabs on to carbon nanotubes so that it creates a network through the tubes of carbon, this network of conductive material.

And so, each iron phosphate nanowire gets connected, wired in a sense because it’s a little nanowire. It gets wired to another carbon nanotube network. And electrons then, bounce along the network traveling through the carbon nanotube until they get to the iron phosphate and they transfer energy at that point.

Justin: That’s awesome.

Kirsten: Yeah. And the researcher say that they can get these batteries. The battery that they’ve created are very similar in the amount of power that comes from them to current car batteries, the rechargeable car batteries.

These virus-powered batteries, they say that they have as much power and energy capacity as the rechargeable batteries that are currently being considered for the plug-in hybrid vehicles.

Justin: Oh, wow!

Kirsten: So, I mean, virus-powered batteries. This is not like, you know, just something made of, you know, the harmful chemicals of viruses putting things together. It’s very fascinating.

And these batteries so far, they’re not going, you know, they don’t go on forever. But they’ve gotten them to a point where they can charge and discharge about a hundred times before they start losing their ability to hold charge.

Justin: Wow! And now, we’ve also, we’ve got new biofuels coming that are being developed by enzymes that are created in the (guttural) intestines of termites, you know, by microbes that live in termites and algae-based. You know, we can only really say, “Wow!” now.

You know, that’s I think, I’m looking back and like, yeah, we have been, you know, pretty amazed by those stuff. Pretty soon it’s going to be the next generation. It’s just going to be – yeah, of course. Like of course, electricity comes from viruses. Of course, my car runs on termite microflora. What else would you use?

Kirsten: What else would you use? I don’t understand. There’s no reason to use anything else.

Justin: That’s just going to be the normal thing.

Kirsten: Yeah. This bioengineering is just fascinating too. Like this current field of taking viruses or, you know, which are very simple structures that, you know, they have functions. They’re able to put pieces together to create proteins. To be able to use these structures to do what we want them to do, to genetically modify them, engineer them for certain functions.

I think it’s just so neat to be able to go, this microbe has this function. Let’s make it – let’s turn it up. Let’s give it some kind of an instruction to make it do more of that. Let’s get this virus to do this.

I mean, taking what they do naturally but also understanding the pieces that are inside of them well enough to be able to put them together whatever way we want. I mean, it’s just – the potentials for creating new technologies is huge.

Justin: Yeah. It is. It’s as though in the last ten years, it’s like we’ve witness with all their ability to do these things, to mess with the genetics of things. It’s like – it’s sort of like discovering Chemistry for the first time and learning that things have chemicals reactions that are different with each other and that there’s way to build compounds and that sort of thing.

It’s like we are definitely living in the golden age of science right now. There is no time in the history of the planet in which discoveries were coming out that were this big, this fast.

Kirsten: Yeah. But could you imagine? I mean, the doubling time for information, for technology is, you know, it’s exponential. And it’s going to get faster and faster. If we think now of that how much information is coming out, the information is just – there’s going to be more and more and more. It’s going to (unintelligible) our show.

Justin: Yeah. What is it on 50 years, 90% of what we know – how is it? How does it go? Fifty years form now, 90% of what we know would have been discovered in that next 50 years.

Kirsten: Right.

Justin: Yeah. And it something people are aware of when they looked their computer. How quickly the computer technology, the memory, the hard drive. How quickly these things have doubled over the years.

Really, that’s not just taking place on computers. It’s taking place in biotechnology and medical research. It’s taking place even in Physics. I mean, the discoveries that are being made, if you compare them to how much your computer has developed in just the last 10, 15 years, all of science is really following the same pattern right now.

Kirsten: Yeah. Quick headline before we end the show. (Paula) send in a story about Titan, one of the moons of Saturn. Cassini has found that even though Titan looks round from the outside, it’s not very round. It has a very bizarre shape. And it actually has flat spots that might explain some aspects of why water is at certain points and at the poles.

So, Titan is elongated and has a irregular shape. It suggest that it might be a sphere slightly flattened at the top and bottom. So, why is it oblate? We don’t know.

And also the big red spot on Jupiter is shrinking. It has lost about 15% of its diameter between 1996 and 2006 according to researchers at Berkeley.

Justin: Huh?

Kirsten: Yes. The spot is changing. The giant storm on the surface of Jupiter.

Justin: Well, I hope – I think we’re at the end here.

Kirsten: We are.

Justin: Hope everybody has enjoyed today’s show. Are we going to have you back next week, Kirsten?

Kirsten: I will be back next week. And in two weeks, our Fundraiser.

Justin: Yeah.

Kirsten: Yeah. So, in two week, we’ll be doing our Annual Fundraiser show. I hope everyone is excited about that. And this month, the TWIS Book Club is reading, “The Drunkard’s Walk: How Randomness Rules Our Lives” by Leonard Mlodinow.

Justin: Damn cool.

Kirsten: And I’m working on getting an interview with in him for maybe the beginning of May. That will be exciting. And so, big thanks to everyone who’s emailed with questions, comments and stories. Thank you so much.

Justin: Yeah. You can check out our website, www.twis.org. You can click on the Subscribe button if you’re not listening to the podcast already. You can also just Google us, look us up in the iTunes under This Week in Science.

Kirsten: That’s right. And for more information on anything you’ve heard here today, you can go to our website, twis.org for show notes with links to source articles and that will be available for you.

And we also want to hear from you, your stories, ideas. So, email us at kirsten@thisweekinscience.com or justin@thisweekinscience.com.

Justin: Be sure to put in there somewhere TWIS in the Subject, otherwise you automatically will be spam filtered.

Kirsten: Into oblivion. And we’ll be back here next Tuesday, like we said at 8:30 am, Pacific time or 9:30 am if you’re in Colorado. And we hope you’ll join us again for more great science news.

Justin: And if you have learned anything from today’s show remember…

Kirsten: It is all in your head.

Tags: KDVS, biology, biotechnology, cell biology, chemistry, end of the world, energy, engineering, medicine, molecular biology, physiology, planets, podcast, robots, science, space, stem cells, therapies, world robot domination

Podcast: http://www.twis.org/audio/2009/04/07/352/

One Reply to “Transcript:TWIS.ORG April 7, 2009”

Comments are closed.