Synopsis: How To Say Kiki, Decade of Data, This Week in The End of The World, Fighting The Good Fight, Lots of Health, Saving Humanity, and a Competition For God
Justin: Disclaimer! Disclaimer! Disclaimer!
The following hour of our programming much like the human genome is full of endless possibilities, yet comprised of a few relatively simple base arrangements in a specific manner.
From these endless possibilities, it is virtually guaranteed that the host will be led on tangent spinning the show out of control. As their ideas and inquiries twirl about an endless spiral. It is comparable only to the coiling double-helical form of Deoxyribonucleic acid more commonly known as the abbreviated form DNA.
And while these twirling ideas and spinning inquiries do not necessarily represent the views or opinions of the University of California at Davis, KDVS or its sponsors, it is these such ponderings that have allowed scientist to methodically discover the countless breakthroughs and advancements which led ultimately to the creation of This Week in Science, coming up next.
Good morning, Kirsten!
Kirsten: Good morning, Justin!
Justin: It’s another Tuesday, February the 24th, 2009?
Kirsten: Another. It is.
Justin: How did that happen?
Kirsten: Wait. What?
Justin: Yeah. No, really.
Kirsten: What are you talking about?
Justin: Isn’t that what today is.
Kirsten: No.
Justin: It’s not the 24th of February, 2009?
Kirsten: Oh, the 24th. I thought you said the 4th. I was like, no, it’s not the 4th. We’re not repeating.
Justin: Oh, you need more coffee too.
Kirsten: I do need more coffee. What’s wrong with me?
Justin: Good morning, TWIS minions.
Kirsten: Good morning, everyone. Welcome to the show.
Justin: The disclaimer today was courtesy of a different Kirsten, who spells her name Kirsten, except apparently it’s pronounced Kirsten. So, I don’t know which one of you is pronouncing your name wrong. But it seems like you should rock paper, scissors and go with the winner.
Kirsten: Yeah. Well, you know, there’s a little story behind the pronunciation of my name, little history behind the Kirsten.
Justin: Is that?
Kirsten: Yeah. Well, okay. So, in Norway, the name (Kiersten).
Justin: (Kiersten).
Kirsten: (Kiersten). And – but, you know, coming here and the family – my family gave me name Kirsten.
Justin: Mm hmm. Oh, because what is…
Kirsten: It was Kirsten. But then, you know, and everything was fine. Everything was fine until I got to college.
Justin: Mm hmm.
Kirsten: And for some reason, people don’t pay any attention in college. And so, I would introduce myself to people. And people would go, “Kirsten who?” And they wouldn’t hear it. And they’d say, “Oh, Kristen?” And so, everybody called me Kristen. And I couldn’t deal with it. So, I started pronouncing it Kirsten. And if I pronounce it Kirsten, people at least got Kirsten.
Justin: You know what?
Kirsten: And then after college, people started paying attention again.
Justin: Yeah.
Kirsten: And so, now it’s formed a lot of confusion. So, you know.
Justin: I’m a little irritated for all the kicks I got into the shin for not saying Kirsten properly over the years.
Kirsten: Just call me Kiki.
Justin: Okay.
Kirsten: Just call me Kiki. It’s easier. It makes everybody happy.
Justin: I like (Kiersten).
Kirsten: (Kiersten).
Justin: (Kiersten). So, (Kiersten), you got any science-y news for us this morning?
Kirsten: I do have science-y news. I have stories about health – saving humanity and a competition to find God.
Justin: God?
Kirsten: Yeah. What do you have?
Justin: Could have waged down there. Let’s see. I’ve got – I have some interesting climate-y change news. I’ve got – actually, I’ve got one that – I got a couple of stories that are good for human health, a couple of things from the – not the pharmaceutical but from the medical field today.
Kirsten: The medical field.
Justin: The medical genre.
Kirsten: It sounds like we’re getting medical up here today.
Justin: Yeah.
Kirsten: Healthy medical.
Justin: Yeah. What happen? How did that happen?
Kirsten: What’s going on?
Justin: My favorite story is one that we kind of are lagging in covering. But we’ve been covering this story all along that – this is from earlier this month. Special court was set up by the US Court of Federal Claims. And it ruled earlier this month that a decade of scientific data is a legitimate way of knowing things. Yehey!
Also, some of that ruling was some mention of a preservative used in vaccines, and vaccines themselves not being link to autism. So there was this lawyer group representing like well over 5,000 parents of kids who have autism brought this case against the…
Kirsten: Vaccines, right?
Justin: Yeah. There’s a separate part of the government that handles claims against vaccines. And the idea behind this, you’re not going to sue an individual company.
Kirsten: You can’t sue the government.
Justin: Right because these are mandatory. You need these vaccines to travel. You know, you need to get them into school a lot of time. So, because it’s such a big thing, it is sort of suing the government. But they have a special court that’s designed to take a look at these issues.
And the idea was a preservative — what is it — thimerosal which contains…
Kirsten: Thimerosal.
Justin: Thimerosal which contains mercury, they were afraid was causing this damage that was leading to autism. Also though, they were saying that MMR vaccine which doesn’t contain that could cause autism by provoking a dangerous immune response.
Kirsten: Mm hmm.
Justin: So, there were two different angles there were going on.
Kirsten: Yup.
Justin: Government experts citing dozen of very large studies over the last decade. They found legally that there is no connection between vaccines and autism. The thing is there’s a lot of people who aren’t in advance toward thinking that this is an attempt to avoid the lawsuit, this, that and the other. I keep wondering where are the original belief came from? How it form? How this idea forge so strongly that…
Kirsten: It was an association that was made and there was one paper that was published by a researcher who had a vested interest. And I’m blanking on his name and I don’t have the references right here in front of me. But there was basically one paper that the researcher had done a study – and he actually came from a biased position.
And people looking at and reviewing his work now or even a few years back have realized that his work, his study is not a well-balanced study that he did have biased.
And a lot of the patients, the children that he was looking at, that what he was figuring out like he just basically came up with these ideas and just put them out there.
Justin: Right. So, then if you’re a parent and your child has autism and you read this or hear about this, come into contact with it, it reaffirms an excuse for something that just seems ungodly, unforeseeable.
Kirsten: And unfair.
Justin: Yeah.
Kirsten: And you want to find – I mean your child is going through a developmental difficulty. And it’s causing difficulty in your family. And you want to find a reason. You want to find a cause.
Justin: Right.
Kirsten: And so, the MMR vaccine became great. It’s a cause. Let’s get rid of it, you know. And people jumped on that van wagon because you have hope that you can get, you know, you can solve this for either your own child or other children down the road.
And, you know, unfortunately, this evidence has shown over and over again a number of studies. It’s not just the one study that the story came from.
Justin: Right, right.
Kirsten: That the idea came from. A number of studies have rejected the link between the MMR vaccine and autism.
Justin: What’s the statistical evidence? Because the autism has risen ever since we pulled the mercury out.
Kirsten: Yeah.
Justin: I’m still saying, maybe the mercury was limiting cases of autism and we should put more of it in the vaccine.
Kirsten: Stick it all back in there. Great!
Justin: Hey, we took it out. The autism rates went up higher, you know, maybe we put it in we drop them down a little bit.
Kirsten: Right. Well, you know, the mercury, it’s not – it was a very, very small amount in these vaccines.
Justin: Yeah.
Kirsten: But mercury is a toxic substance. So it’s not something that maybe (unintelligible) take it out.
Justin: I still – it’s one of my favorite things just watching the kids from the 50’s going to the science lab, dipping their whole arms in baths of mercury and watching it beat off and rolls off their arm.
Kirsten: Those were the days. I tell you. I tell you.
Justin: Oh, it’s just cringing.
Kirsten: In other big, big, big vaccine news, this is the big, big story.
So, some researchers working for the National Institute of Allergy and Infectious Diseases out of the National Institute of Health, as well as the Centers for Disease Control and Prevention have published a study in Nature Structural and Molecular Biology saying that they have found some antibodies to the flu virus…
Justin: What?
Kirsten: …that stop the virus from infecting cells. So, when your body has an immune response, basically what happens is you have a virus or some kind of external agent that gets into the body.
The body has certain cells that come in and kind of break up that virus into little pieces and create the body, uses these little pieces to create antibodies. And the antibodies – and the little pieces of the virus or the bacteria or whatever the infecting agent is, they’re called antigens.
And so, the antibody goes and sticks to the antigens. And that’s how it identifies these infectious things for your body to attack and destroy. It’s like putting a flag on it saying, “Hey, get your butt over here and attack!” you know.
And so, what they did is they’ve scanned millions or tens of billions actually of these antibodies that get produced in bacterial viruses or bacterial phages. So they use bacterial viruses to create a whole bunch of different antibodies, a number of them to the flu virus because there are several different strains of the flu virus.
Justin: Many, many, many kinds.
Kirsten: There are two groups. I think the HA or group 1 and group 2. There are two groups.
Justin: Just call it that.
Kirsten: Yeah. We will just call it that. And so, but within those groups there are a number of different strains. And so, there are a bunch of different possibilities, different – and within each of the different strains there are all sorts of different pieces of their genetic material – the viral material that could create different antibodies that the body would use.
Justin: Right. And so, your body though – your body finds one of these and it comes up with a counter too and it’s going to keep beating it going forward.
Kirsten: Right. But sometimes it doesn’t…
Justin: But because there are so many of them…
Kirsten: Yeah.
Justin: That’s why we don’t get the same cold twice, for instance.
Kirsten: Right, because these viruses have areas that mutate constantly, they’re constantly changing, the body goes, “Oh, I’ll get that one. I’ll make an antibody to that.” And so, it can attack that strain but then the virus goes and mutate some place else. And when it comes back as a mutated strain, your body goes, “Oh, I have to do it again.” And it creates a new one.
And so, it makes it very difficult to – for a body, an organism to be able to keep fighting it off and to create immunity to the flu.
So, what they did is they scanned billions of antibodies. And they ended up finding, I think they ended up finding ten different — out of billions — ten antibodies that instead of going after that rapidly mutating part of the virus, they found a part – if you can imagine the virus as looking like a lollipop.
Justin: Oh, okay.
Kirsten: There’s the head of the lollipop that mutates all the time. And then where the stick goes in to the pop, that – you can call that the neck. And that part is crucial for the virus to change its shape and get access into the cells and infect cells.
And that’s the part that does not mutate because it’s so specialized to the purpose of the virus that if it changes the virus, if it mutates the virus may not be able to get into cells and infect like it wants to.
So, they found these antibodies that seem to work against the viruses. They pinpoint that neck portion. And what they do is they get in there and they create – it’s like taking a piece of bubble gum and wrapping it around the lollipop. And you look at your lollipop and you like, “Eew, it’s time to be put chewed bubble gum on the lollipop.” You’re not going to put that in your mouth, right?
Justin: Well, I don’t know. Did it – are they actually touching the lollipop or is it just on the stick? Well, okay.
Kirsten: And so basically, these antibodies they keep – and they’ve only found antibodies that work against group 1, not group 2 flu virus. But at the same time, group 1 contains the 1918 Influenza virus…
Justin: Wow.
Kirsten: …which is the Spanish flu.
Justin: Yeah.
Kirsten: The H5N1 avian virus.
Justin: Bird flu, really?
Kirsten: Bird flue. A number of Influenza A viruses which is what we’re infected with on a regular basis.
And so, this is really a great potential. And so, now they’re at the point where they need to take it out of cells, take it out of mice and start actually looking to see how these antibodies will work and if we can create a vaccine for the flu.
Justin: Wow.
Kirsten: And they think that the way – looking at the way this works, they think that in about two years we’re going to have a vaccine…
Justin: Wow.
Kirsten: …for the flu.
Justin: That can just be the wet floor for a moment because that would be so awesome if that’s correct. If that’s right, then that would be something – to knock out things like bird flu that getting rid of a huge section of the pandemic possibilities of disease on the planet would be awesome.
Kirsten: Right.
Justin: What (Flouricide) of me though is already thinking like, well, if this was taken out things before they get in, before our bodies creating antibodies to it that means we don’t get all these looks to flu. That means our immune system doesn’t have to work as much as it does. That means our immune system is sitting ideally by while something else out there is building up and becomes – is that you…
Kirsten: I don’t think our immune system is going to be sitting – is not sitting ideally by.
Justin: If we – I mean does this mean though that – oh gosh, while I guess if it’s getting it before, everybody better have that vaccine then.
Kirsten: What?
Justin: No, it’s just I’m thinking like if the…
Kirsten: You’re jumping to conclusion.
Justin: I am. I’m jumping to conclusion that if we – because there have been links – for instance like kids who don’t go out and play with dogs and go to school and catch all this disease from other kids.
Kids are very isolated from these flu illnesses as children do end up developing higher rates of diabetes and other things. And they do think there maybe a link between how active your immune system is when you’re young and later health issues in life.
Kirsten: Right. But this is not going to be stopping the active – like stopping the activity of your immune system. Your immune system is still going to be identifying infiltrating viruses.
Justin: But if this is killing them before they infiltrate, that’s what I’m thinking.
Kirsten: But your body will still produce a low, you know – if a virus comes in, if it’s in any kind of a high – if it is a high infiltration, you know what, your body will produce a small amount of a low grade immune response.
You know, you’ll probably have – it has to get all those cells going that are going to it, attack the invaders. And there will be a certain amount of, you know, maybe you’ll get a little tired or something. But you’re not going to get sick. No, you’re not going to get the flu.
Justin: I don’t know. I still feel like we’re firing the coach on the team. But it means that – maybe you should test it on mice. Can they do a couple of animal studies first?
Kirsten: That’s what they’re going to do.
Justin: Well, good.
Kirsten: That’s what I said.
Justin: Well, good. They should.
Kirsten: Why don’t you listen to me?
Justin: Because I got other things on my mind.
Kirsten: Anyway…
Justin: I’m a busy guy.
Kirsten: Yeah, yeah. And the neat thing about this is that these are not from any – these antibodies that they’re using, they’re not any other animal. They’re not like monkey. They’re not pig. They’re not chicken. These antibodies are human. And so, they’re not – the antibodies themselves aren’t going to create any kind of strange reaction with it.
Justin: No, oh actually not. No. That’s brilliant though that they’ve been able to isolate the ones that are actually the most effective. You share them.
Kirsten: And you know?
Justin: What, bacteria sharing our DNA with (species)?
Kirsten: Along with this, the flu – seasonal flu kills more than 250,000 people worldwide each year.
Justin: Let’s put it on the market tomorrow. Go for it.
Kirsten: Yeah. So, I mean I’ll deal with a little bit of asthma if we’re going to save that many lives.
Justin: Wow. Yikes!
This is some interesting news coming out of NASA’s Goddard Institute for Space Studies. They have found that 2008 was the coolest year since 2000. Yehey! Global warming is over. We have nothing to fear…
Kirsten: Yeah.
Justin: Why are looking at me funny? Yeah. Well, there is of lower temperature than we’ve had in eight years. This is true. Unfortunately, we’re also – our planet is in a cycle. We’ve got the – what is that – the La Niña factor going on the Pacific which is lowering ocean temperatures which is a big factor there.
Kirsten: Right. And El Niño is expected to pick back up either this year or beginning of next…
Justin: It’s usually a year or two behind it picks up.
Kirsten: Yeah.
Justin: And the sun right now is passing through its solar minimum, which means that that’s the lowest point in a 10-12 year cycle where there is less electromagnetic activity, transmits less – lower amounts of radiation towards the Earth.
So, there are a lot of other factors that are contributing to this being the lowest. And just the last eight years, you know. At the solar minimum, we’re still in an average temperature for going back further.
Kirsten: It’s the coolest temperature in the last eight years, but I mean…
Justin: The last eight years have been records, yeah.
Kirsten: Yeah.
Justin: Yeah, that each one has been a record. I think it ranks as ninth out of it.
Kirsten: It’s still hotter than the average for, you know, the last 50 years.
Justin: Yeah. I think it ranks ninth overall since we’ve been making these measurements.
Kirsten: Yeah.
Justin: But this is just a word of warning because there maybe – I’m predicting a little bit of hucksterism around this report that you may be hearing from some of those, you know, places out there that like to debunk global warming as an industry.
Kirsten: Mm hmm.
Justin: That you maybe hearing some of these. So, keeping you out for that and be prepared to tell them, “No, it’s the lowest and the hottest decade but it’s at the solar minimum. We’re getting less heat from the sun. And as a result, we’re getting a little bit lower temperature this year by like less than a degree.”
Kirsten: Yeah.
Justin: And we’ll bounce back in the next couple of years.
Kirsten: Yeah. And it’s – I mean, beyond that, it’s also – the thing that is the problem with reporting things like a yearly temperature. Say, “Oh, this is the temperature of the Earth for this year.”
Justin: Mm hmm.
Kirsten: Is that any one year on its own is not necessarily going to undergo the amount of change. An amount of change that is greater than the error for the overall average of the number of years that we’re looking at. I mean, what is important is the trend.
Justin: Right.
Kirsten: And which way is the line going over time not just one instant in time. So, if we take one year as one time point, you know, that’s not a lot. And it’s the same thing with any kind of weather, any extreme weather event or even looking at the amount of sea ice up North, you know. It’s just.
Justin: And that’s a good point too because actually even though globally the temperature is a little lower, right. The Arctic and the Antarctic peninsulas were exceptionally warm in the over – I mean they were actually warmer than they would have expected.
Kirsten: Yeah.
Justin: So, there – it’s a mixed bag of – but yeah. If you hear any hype – if you can hear any hype on this, let us know. I want to get on the hype, the anti-hype wagon.
Kirsten: There’s going to be a lot of hype. All right, everybody. Advise for a longer life.
Justin: Don’t eat ice cream?
Kirsten: Be naked.
Justin: What?
Kirsten: A naked mole-rat.
Justin: Oh, a mole-rat.
Kirsten: Yeah.
Justin: I don’t know that it’s already.
Kirsten: Yeah, sorry.
Justin: I’m ready to go there.
Kirsten: Sorry to get your hopes up there. It turns out – okay, the naked mole-rat, it’s called naked because it doesn’t have any hair.
Justin: Furless.
Kirsten: It’s furless – hairless, furless.
Justin: Remember to shave.
Kirsten: Mice normally live about 3.5 years whereas the naked mole-rat can live up to 30, to 35 even.
Justin: What?
Kirsten: Yeah. The naked mole-rat…
Justin: Holy cow.
Kirsten: …just goes on and on and on and on but it’s, you know, not that different from the rest of Rodentia.
Justin: So, what is going on?
Kirsten: So, what is going on?
Well, some researchers have been checking this out. And Rochelle Buffenstein of the University of Texas Health Science Center in San Antonio looked at liver tissue from mice and from the naked mole-rat and then checked out the proteins in the liver tissue. They found twice as many undamaged proteins in the naked mole-rat as in the mice.
So, what’s happening is that mice who don’t live as long, their proteins are breaking down over time. There’s damage occurring to the proteins that take care of all the body processes within the metabolism of the animals. And the naked mole-rat, the damage isn’t there.
So, the question is, how are the mole-rats maintaining the quality of the proteins in their tissues? And that’s something that has to be investigated.
What they have looked at and published in the proceedings of the National Academy of Sciences is that they have a less accrual of oxidation damage to thiol groups up regulation of homeostatitc radiolytic activity. And so, these are mechanisms that help to keep proteins protected.
Justin: Can I get that in a pill form yet?
Kirsten: Yeah. And that’s the question. Is there something that we can do? Basically, these mole-rats have more stable proteins. And the mechanisms that protect them are up regulated and are maintaining the stability of those proteins and allowing them – and the hypothesis is that it’s this protein structural integrity that is allowing them to age so much longer. You know, ten times longer than mice.
Justin: That would be a, you know, average life span of a 700-year human if we got to advance.
Kirsten: Yeah.
Justin: Wow.
Kirsten: If we could figure it out, you know, and we get that kind of multiplication factor on our life span.
Justin: Number one, we better make birth control a top priority once we figure that out especially. Okay, so we lose the flu, we live ten times longer.
Kirsten: But maybe even if it’s not allowing us to live ten times longer, maybe the ability to treat age-related diseases that are involved, that are related to metabolic or protein structural issues — Alzheimer’s disease, Parkinson’s disease, maybe even diabetes.
You know, so many things that occur as individual’s age and become a problem with old age, maybe we’ll be able to get rid of those.
Justin: Oh, that’s the other thing. Yeah, if I’m living 700 years, they better cure all the diseases because by 73 you have all of them.
Kirsten: I don’t want to live to 700 years and be sick.
Justin: You’ll have every single thing possibly wrong with you.
Kirsten: That’s right.
Justin: But the biggest issue I think, if we live that long is going to be gray hair.
Kirsten: Gray hair, but…
Justin: There’s a European scientist have found that the fashionable follicular frosting of aging humans is the fault of hydrogen peroxide.
Kirsten: Excuse me, yeah, hydrogen peroxide I do use that to make the hair blonde occasionally.
Justin: Forming – no, no, that naturally forming in the hair follicle itself. That’s something I didn’t know was possible or even existed.
Kirsten: All that brushing, all the ponytails.
Justin: Yeah. I guess it’s, you know, damage to the hair creates build ups in – which doesn’t make sense to me because I thought that hair was dead anyway and that it was…
Kirsten: The hair itself is dead but the follicle is not. And that’s where the hair proteins are created.
Justin: Interesting.
Kirsten: The collagen and everything else.
Justin: So yeah, they found that this is build up of hydrogen peroxide caused by reduction of an enzyme that is normally in the follicle that breaks down the hydrogen peroxide. It turns it into, I guess, water and oxygen than having it turns break it down more than that.
Kirsten: Yeah.
Justin: So, they’ve discovered that the hair follicle can’t reproduce this enzyme any longer. And the hydrogen peroxide is there. And when the hydrogen peroxide there, it creates even lower levels of another enzyme that can’t form in the presence of the hydrogen peroxide. And that enzyme is responsible for the melanin, for the color stuff.
Kirsten: Which makes a color – allows the color to have it in your hair.
Justin: Right.
Kirsten: So, the hydrogen peroxide eventually — you have hydrogen peroxide, you don’t have color.
Justin: Yeah.
Kirsten: And there you go.
Justin: Yeah.
Kirsten: White, gray hair.
Justin: The two combined for one of the best, you know, bleach jobs you could ever possibly get.
Kirsten: I really want white hair someday. I think that that’s just pretty cool.
Justin: I think that would be pretty cool too. But there’s some mention here that it also may lead to a difficulty for some people, you know, picture the little lady going to get her hair done and the color doesn’t quite stick, right, it comes out faded.
Kirsten: Right.
Justin: And I’m picturing my grandmother who had bright orange hair and I swear she always went for red. But her hair always ended up this just incredibly bright orange color.
And she rolled with it, you know, it became her color. But I guess, you know, maybe that’s part of the thing. Maybe dyes have a harder time sticking when you’ve got all these hydrogen peroxide build up in there.
Kirsten: Yeah. Well, there is a difference with the hair follicle and the hair shaft itself. So, that’s part of the issue was, part of the issue definitely. But the idea too is now that we know what’s causing the lack of melanin, could you imagine having some kind of a hair wash that gets into your scalp, maybe gets into the follicle somehow and reduces the amount of hydrogen peroxide.
Justin: Yeah.
Kirsten: So, you just wash your hair and reduce the hydrogen peroxide allowing the follicle to do its normal job with pretty some melanin.
Justin: And then you have dark roots.
Kirsten: Then you have dark roots. Right. Right you are. Oh, okay.
So, eggs, other healthy news, you know, people say, “Okay, as you’re aging watch your cholesterol levels. Don’t eat too many eggs.” And this kind of an adage, this kind of information it comes from the FDA because, you know, eggs are very high in cholesterol and that cholesterol can get – when you ingested it can – they believe that it can end up within your arteries causing blood pressure problems and further on down the line chronic pulmonary disorders.
But a few years back, I remember a study that said that, “Well, even though eggs have all these cholesterol, they took a look at the different amounts of enzymes and different proteins within the parts of the egg.” And they said that, “Hey, there are these enzymes in the egg that actually break down cholesterol.”
So, even though you’re getting cholesterol in the yolk, the enzymes in the white actually might reduce the amount of cholesterol that you’re actually getting.
And I was like, “Oh, hey, that’s kind of cool.” And now there’s another study that was just published in the Journal of Agriculture and Food Chemistry where they took different kinds of cooked eggs and subjected them to simulated digestive processes. So they basically threw them into a little vat with pepsin and hydrochloric acid.
Justin: Fake stomach.
Kirsten: Yeah, a fake stomach to see what was left and what the eggs were broken down into just to say, “Okay, well, this is what we think about eggs.” But what is actually happening?
It turns out that there is a group of proteins within the egg that seem to act like a group of prescription medications that lower blood pressure.
Justin: Wow, that’s awesome.
Kirsten: Right. So, if in the human – in any actuality of the human digestive tract, if in a stomach they do get broken down into these blood pressure lowering compounds and then get taken up into the blood stream, that’s good news for us and maybe we should eat more eggs.
However, because this is still just in a dish, this was a simulation. This wasn’t actually something, you know, looking at a person eating eggs. This is just in a laboratory simulation. We don’t know for sure whether or not this peptides actually end up getting – will end up having an effect on heart disease risk.
They found that it was fried eggs that seem to have the best peptide levels.
Justin: Really?
Kirsten: Yeah. You would think of all of them, why fried eggs? I was thinking that maybe because of the level of cooking. So, fried eggs are usually like really – the proteins in the eggs are probably get tightly bound together. And so, maybe it’s harder for them to be broken up by the stomach’s digestive juices.
Justin: Interesting.
Kirsten: And so, maybe there are more complete peptides that are left over by the time the egg is taken up by the time it’s put into the other parts of the digestive tract that soak up stuff in the bloodstream. It’s just an idea.
Justin: Well, it’s good news for me. I eat a lot of eggs because I’m all for it. I can now eat my eggs and not be worried about my high blood pressure…
Kirsten: Eat your eggs, eggs!
Justin: …hypertension or any of the rest. Plus it helps regulate your blood sugar throughout the day which is why it’s such a good breakfast.
Kirsten: Right. But still the US Department of Health and Human Services in its nutrition guidelines suggests no more than four eggs per week and until…
Justin: I thought four eggs per day.
Kirsten: No.
Justin: Really?
Kirsten: Per week.
Justin: Oh boy!
Kirsten: And according to the American Heart Association, one egg contains 213 mg. of dietary cholesterol, and a limit per day is less than 300 mg…
Justin: Wow.
Kirsten: …for people with normal bad cholesterol levels.
Justin: I think they will drop dead by now. I should be long since gone from the planet.
Kirsten: So, until the more information comes in, this is the standard and, you know, this is what is recommended. Don’t over due the egg intake.
Justin: I really love the idea of the study with the…
Kirsten: But it’s interesting to know.
Justin: Yeah. I really the idea of the studying things with the fake stomach and seeing what actually ends in the body as opposed to what you put into it. I think that I want to play that to every food and see what happens now.
Kirsten: Yeah.
Justin: It’s just – that’s a great way of doing it.
Kirsten: Yeah.
Justin: We’re at the top of the hour, which is the middle of the show.
Kirsten: Which is the middle of the show.
Justin: And we’ll be back with the second half after this message of things.
[Music]
We’re back with more This Week in Science.
Kirsten: Welcome back to the show. We’ve got more great science news for you. Where was I? Oh, what the flowers and anthrax have in common?
Justin: Nothing?
Kirsten: Not true.
Justin: Oh, there’s something wrong.
Kirsten: Researchers at the University of Warwick have been looking at the African Violet – very pretty flower. And a bacterial pathogen that attacks the Violet called Pectobacterium chrysanthemi.
Justin: That was cute name of this.
Kirsten: Yeah. It afflicts plants. It harvests iron from the plants using an enzyme catalyst. It has its chemical structure allows it to take advantage of a catalyst that binds iron to – or a citric acid which then binds iron to the entire structure and makes it happy, allows it grow, do things that it relies on iron for. You know, otherwise without the iron it will starve and it will die. So, this is very essential to this bacterium.
Interesting thing that was found as they researching this plant pathogen. The plant pathogens iron-binding siderophore is really similar to the enzyme that’s used to incorporate citric acid and thus iron by anthrax.
Yeah, anthrax when it infects and when it starts to try and survive within an organismic environment, it uses and enzyme that incorporate citric acid which binds iron to allow it to harvest iron and be able to survive. This citric acid dependent process is – I mean, by looking at the African Violet plant, they’ve been able to see how they could potentially block the process from occurring and kill off or get rid of — treat an anthrax infection.
Justin: That’s awesome.
Kirsten: Yeah, by looking at a flower. Yes. It’s very exciting. I thought it was a fascinating study. And they found that there other. Aside from anthrax, there are really similar enzymes that are involved in this – what’s called the citric acid derived siderophore in E. coli and MRSA. So this is something that could potentially help with treating MRSA.
Justin: Wow.
Kirsten: Multidrug-resistant Staphylococcus aureus or in E. coli infections, all sorts of bacteria who rely on this citric acid enzyme to work.
Justin: That’s really cool.
Kirsten: All from looking at a pretty flower. Hey, I love Science.
Justin: You know, looking very closely.
Kirsten: I love the connections.
Justin: So, I may have to – I either have to stop eating less eggs as we learned in the first part of this hour.
Kirsten: More eggs, yummy.
Justin: Or according to a study published in the online edition of Stroke, which just reading…
Kirsten: Stroke.
Justin: …because it raises my blood pressure a little. I couldn’t cut out eggs. I could be drinking at least three cups of green or black tea a day.
Kirsten: Three cups.
Justin: Three cups to your day significantly reduces the risk of stroke according to a new study published of UCLA. So, researchers conducting evidence-based review for all human observational studies on stroke and tea consumptions. So it’s another one of these studies where they’re looking at all the other studies that they can find.
Kirsten: Mm hmm.
Justin: They found nine studies that described 4,378 strokes among nearly 195,000 individuals because basically you have, yeah, test group 200,000 with 4,378 having the stroke. And in this group is also they have records on how much tea these people are drinking.
What they saw was that there was a consistency of effect of presumable magnitude that three cups of tea a day, the risk of stroke was reduced by 21%. Whoa! That’s a very significant.
Kirsten: Significant.
Justin: And it didn’t matter if it was green or black tea. So, the antioxidants doing something in there, working out something, maybe it’s caffeine. I don’t know something in there. Well, now because they don’t…
Kirsten: They didn’t say anything about coffee.
Justin: This wasn’t that they weren’t in a coffee.
Kirsten: I mean could you have two cups of black tea and a cup of coffee?
Justin: Coffee has got – you know, actually I think coffee is supposedly has…
Kirsten: It’s a lot of fluids.
Justin: …more antioxidants anyway than tea. The study was focused on tea. So, they didn’t – I guess, they didn’t do – they didn’t throw a coffee into the microwave.
Kirsten: Yeah. Sometimes, when you look at all of these studies, you have four cups of these, and two cups of that, and this amount of this. If you were to add it all up and how much would each compound would make us healthy. Oh my goodness, I would be so full all the time.
Justin: You could – I know. You could just knee to your plate of vitamins and have very little fiber in your diet.
Kirsten: Very little fiber. Well, let’s get back to The End of the World.
Justin: Yehey!
Kirsten: Yehey! Right. Well…
Justin: All right, which one is – I forget what made this…
Kirsten: It’s not so much the end of the world. It’s just taking a look at the end of the world and trying to be proactive about it.
Justin: Yeah. Purchase real estate on higher ground, people, rising sea levels.
Kirsten: Researchers have created a map, an interactive map that’s funded – this is funded by NASA and the US Department of Energy through the joint North American Carbon Program. They’ve taken a map and stuck it on Google Earth.
Using the Google Earth platform, you can now see United States Carbon Dioxide Emissions and it goes on a county by county basis so you can take a look at how – say San Francisco County is doing, Monterey County, Yolo County, New York County. I don’t know if there’s a New York County.
But across the United States, you can now actually see where carbon is coming from in your area. Is it coming from traffic? Is it coming from industry? Is it coming from agricultural uses? Is it unknown where it’s coming from? You know, you can now see where different sources of carbon dioxide are coming from and maybe this will allow what they’re hoping.
Says Peter Griffith, Director of the Carbon Cycle and Ecosystems Office at NASA Goddard Space Flight Center, and he’s the coordinator of this North American Carbon Program, “One of the goals of the US Climate Change Science Program is to assist with scientifically-based formulation of policy and decision-making by allowing non-specialists to see changes in carbon dioxide emissions in time and across broad areas.”
“We’re helping them to understand critical information for climate change policy decisions. So, maybe this will allow people who are affecting policy to have a better idea of the information that’s coming in to play and how to use that information.”
“Additionally, it might help people who, you know, parents with their children who want to take a look and know more about this broad area, this kind of vague idea of carbon dioxide emissions what exactly is it and where do these things come from and maybe start conversations in families’ homes talking about this important compound.”
This is kind of interesting. It’s a neat viewing tool. I will put the link to this Vulcan carbon dioxide map, all at Vulcan.
Justin: I don’t know how they collected the data.
Kirsten: The Vulcan project.
Justin: I’m thinking like San Francisco is going to have a nice, little oceanic breeze. And then you have like these are very little carbon and then the next county over. It was like – gosh, you have a really – yeah, there like no population but a ton of carbon.
Kirsten: Right. And they will – well, there are estimates on where these things are coming from and how they’re coming in. So, you know, this is something that they’ve looked at – they’re looking at seven primary data sets, according to the story here that include imagery of the Earth’s surface built by the NASA – captured by the NASA built Landsat 5 satellite, fossil fuel, carbon dioxide emission’s data from the US Environmental Protection Agency and population data from the US Census Bureau.
Justin: Mm hmm.
Kirsten: So that’s three of the different data sets. And they have constructed an inventory of the carbon dioxide that results from the burning of 48 different types of fossil fuel. And it shows estimates for the hourly carbon dioxide outputs of factories, power plants, vehicle traffic, residential and commercial areas.
I think it’s pretty neat. I took a look at it yesterday. It’s rather interesting. And they’re starting to look at or create similar maps for Canada and Mexico so that, you know, we can see where the United States stands in relation to our neighbors.
Justin: I still say they need to be GIS mapper out there that just goes with the sea level changes and puts out the real estate guy throughout the county by county. You will be able to see, okay, if I’m Florida, you know, I’m like, “Oh, well look. Over here is some territory. It’s a little world. It’s not worth much. But it’s going to be a nice tropical island one day.”
Kirsten: It’s proactive. And in that vane, the UK’s Institution of Mechanical Engineers are calling next month. They’re going to be putting out of call for the world’s governments to accept that climate change is inevitable. Not necessarily that, you know, humans are at fault. That’s not that part of the argument.
But yes, climate change is occurring. It is inevitable and that we need to start planning ahead for the changes that are going to occur, try and take a look at new scientific information to estimate what is going to be happening in your area. Do you expect to become a drought area? Do you expect to have – are you coastal? Are you going to loss land to oceans? And infrastructure needs to be protected.
And some of the recommendations they are putting out there include underground reservoirs to combat increased evaporation during drought, subterranean water distribution systems, electricity being produced from renewable resources which is something that many people are talking about these days, and reducing the urban heat island effect by designing new cities to disperse heat in different manners away from buildings.
Justin: Wow. We are already at Plan B.
Kirsten: We’re already at Plan B. That’s basically what’s going on. We’re at Plan B. And there’s a paper that just came out in the ecologists. A couple of ecologists — John Vucetich and Michael Nelson, they’re both from Michigan.
They have put out a paper and challenging the widespread belief that hope can motivate people to solve overwhelming social, environmental problems. The paper is titled – wait, where is it, where is it, where is it? I’ve totally lost it in here. It’s called “Abandon Hope”.
They say that people are getting mixed messages. They are hearing that the environment is inevitable, disaster is coming. But then you hear people like Jane Goodall and Al Gore say, “Oh, we have hope. We can still do something. We can fix something.”
So, it’s the environmentalists versus the scientists. And is it inevitable? Do we have hope? What is the reality? We need to get rid of this mixed message that’s going out to the public.
And that, we need to actually just say, “Hey, we need to give reasons to live sustainably that are rationale and effective and need to be based…” They say they need to be based on virtues rather than consequences and equate sustainable living not with hope for a better future but with basic virtues such as sharing and caring.
Justin: Oh, that’s too Nancy Fancy. You see like, here’s the thing. Like, yeah, March, you know, getting nations to acknowledge that there’s heating going on without attributing it to human – you know, like why? Why break that rule? We won’t say it’s humans. Like no, I mean that’s part of the problem too is the mixed message. You’re absolutely right.
Kirsten: Right.
Justin: They are absolutely right.
Kirsten: It’s been too muddled.
Justin: It’s going to – we’re ruining the planet. That’s why I’m telling you climydia. That’s what we have to start calling it. If we’re not calling it climydia…
Kirsten: And you can treat climydia.
Justin: It’s treatable, you know, and it’s avoidable. You wear your Carbon Jimmy hat and suddenly you’re fine.
Kirsten: And the answer, I think, I think the answer though, what we – where we really to put all of our…
Justin: Silver bullet – here it comes.
Kirsten: …the silver bullet, hamsters.
Justin: What? No. We got a call. Hang on.
Kirsten: Hamsters, I’ll explain in a minute, all right? Here we go.
Justin: Good morning, Minion. You’re on This Week in Science.
Man: Well, yeah. I was hoping that you can’t really expect much when you use all your resources and blowing up other countries and stuff like that. I heard that with a monthly budget that they use in Iraq, they could have like a lot of these – like that, alternative energies and clean and environmental production facilities in America, probably like a month’s worth of what we spend in Iraq. (Unintelligible) hope and change isn’t going to get you that far if you don’t want to make actual serious like structural changes, it seems like.
Kirsten: Yeah.
Justin: Absolutely. No…
Kirsten: There needs to be compromise.
Man: Yes, exactly.
Justin: I’m still boggled that the town’s people haven’t grabbed a pitch for. It’s a long time ago, you know. The Frankenstein has been terrorizing the village for quite some time now.
And we’re like, “Oh gee, here we lost another one last night.” “Really?” “Oh, another one of us disappeared.” “Gosh, that’s awful. Somebody should do something about that at some point.” “Yeah me, too.” “What are you doing today?” “Oh, nothing.”
Kirsten: I know. You will get better.
Man: Yeah. (Unintelligible) it will be all right for me. Leave San Francisco. I never liked that place anyway.
Kirsten: All those liberals.
Man: I (unintelligible) but you never talk about the ocean acidity as far as carbon dioxide levels go. It’s all about like the land getting encroached by the sea. But it’s like, well, we’re not making the sea any better for this poor fish and coral reefs around that either.
Kirsten: And I think that’s a really good point to bring up. There’s actually a paper coming out. And I can’t remember exactly the reference on it. But there are a couple of researchers who have brought up the fact that the pH level of the acidity of the oceans is increasing.
And it has increased within the time that we’ve been monitoring it. And it is expected to increase substantially more. And one of the things to remember, if you have a change from like 8.4 to 8.1 in the pH, even though it doesn’t sound like a lot it’s a log scale.
Man: Yes.
Kirsten: You know, so we’re looking at powers of ten, you know, different in changing the amount of carbon dioxide, the amount of acid that’s in the oceans.
Justin: Wow.
Kirsten: And that’s the kind of thing that can affect the coral. But not just the coral, it will affect the basic parts of the food chain. And it could affect the properties of the water itself changed at different acid use.
And people have even suggested that it will change the way in which sound travels through water. And so, it could affect the communication of different species of animals under water.
Man: Yeah.
Kirsten: It just mind-boggling me the number of – the affects that it could have down the line.
Man: Yeah. But I’ve heard studies. And I think that noise level of the sea and it sounds like a New York like subway line how noisy it gets. It was like all the different industrial work they do down there. I feel bad for all the poor whales.
Kirsten: Oh yeah.
Man: But yeah, the people didn’t realize that that global warming, they have a variety of issues involved in it. But that’s something like that acidity level of the ocean has changed and it’s a little bit different and especially, they don’t want to come to like no (tag) issues and things like that though. But the sea changes, definitely a big issue.
Kirsten: It’s a big issue. It is.
Man: Yes. But you guys keep up the great work.
Kirsten: Thanks for calling in.
Justin: Thank you very much for checking in.
Man: Bye-bye. Thank you.
Kirsten: Bye.
So, like I said hamsters could solve the world’s problem.
Justin: I still don’t know where this is going.
Kirsten: Yeah, I know. I love to surprise you every once in a while. Researchers at Georgia University’s Nano Research Group have been investigating self-power, so creating nano generators that produce power when basically these wires are bent and stretch.
So, they’ve creative – and it’s not just the hamsters running in the wheel, and then the wheel powering a generator. The hamster is wearing a little jacket with these little wires in it that bend every time the little hamster runs in the wheel and power a little generator.
To date though, the amount of power is very small, about 120th of the output of the double-A battery. So, you would have to – from this telegraph article, it would take 1,000 hamsters to generate enough energy to power a mobile phone.
But over time if this technology is made a little bit more efficient, you could imagine that these nano wires would be in place in any article of your clothing. You could wear a gloves that power – create power as you’re working at a computer from every keystroke that you make. There are many ways that this could be implemented and it’s not just hamsters. But it could – I mean, we create all sorts of work-producing energy all the time.
Justin: Maybe, maybe. I just, you know, I come – I was a big believe in that.
Kirsten: I say the next step after the hamster is the children. Put the children in the jackets.
Justin: Right. Put the children in the treadmills with the jackets. The thing that I didn’t realize is how much power there is in electricity. You know, you can get there on your mobile bike, you know, and try to do the Gilligan’s Island thing where you ride the stationary bike to get a light bulb to light up. It takes that incredible amount of effort to get…
Kirsten: Yeah, a lot of effort.
Justin: …any light to go into a light bulb even. So you can get 80 watt bulb to be shining. I don’t know. I think it was really good enough.
Kirsten: Yeah, we’ll see. People are working on these problems.
Justin: Unless we had millions of hamsters creating energy, billions of hamsters.
Kirsten: An army of hamsters. Yes. Yes! Fermilab is – they’re stepping out and they’re saying the competition is on to find the God particle.
Justin: Oh yeah.
Kirsten: The so-called God particle which is otherwise known as Higgs boson or something like that. That’s what they think the Higgs might be the God particle. But the God particle is the one that can brings everything together and explains everything, gives us gravity and all that kind of stuff.
It would explain why matter has mass. And that is one of the goals of CERN’s Large Hadron Collider. The Hadron Collider is offline.
Justin: Mm hmm.
Kirsten: And while that’s offline, it allows Fermilab…
Justin: Fermilab will be hard at work.
Kirsten: Fermilab is hard at work. And they’re expecting that they’re going to have some data before the LHC gets its data out. Yeah. So, there’s this competition. I’m just pretty excited about this, you know.
Justin: Yeah.
Kirsten: First, it was like the whole drama of the LHC and the struggle to bring it to life. And now, it’s a competition between these two great locations. However, people at the LHC, they’re like, “Yeah, you know, Tevatron, you’re just a little baby collider. You might think that you’re going to get some time on the work here. And you might think you’re going to have a chance of the particle. But really, you’re so jaded. You’re so deluded.”
Yes, it’s interesting. I love the competition. I love the competition. We have about one minute left.
Justin: I still – we have one minute left. Oh, this was sent in from Minion (Dylan). US space agency’s Fermi — here we go — telescope has detected a massive explosion in space. Scientists say it is the biggest gamma ray burst ever detected.
Kirsten: It could change Physics forever.
Justin: Yeah. It isn’t a spectral range which — producing energies that range from 3,000 to 5 billion times that of visible light.
Kirsten: Wow!
Justin: Wow, right. Okay.
Kirsten: That’s huge.
Justin: Yeah. So, these are things that have – I mean, penetrating through deep, deep space going just zipping through anything that gets in a way. This is not really even such high energy that they’re not bothered by any. But they’ve worked out from the distance where this is – that this would – this blast is stronger than 9,000 super nova.
Kirsten: Whoa!
Justin: What?
Kirsten: That’s huge.
Justin: That is – yeah, it’s about – luckily it took place at about 12 billion light years from us.
Kirsten: Not in the neighborhood.
Justin: Not in our direct neighborhood, thank goodness.
Kirsten: Ouch!
Justin: Yeah. So that was just a pretty incredible burst thing. Do you know what they kind of picture it? It sort of like a giant ripple in the pond, like you just realize there’s something bigger in the swamp than just me because that wave was kind of big.
Kirsten: That’s a very good point. And I’d like to give shout outs. It’s the end of our show. Shout outs to everyone who wrote in. Chris Bilinsky, writing in about music, (Kalidasa), (Shannon Sanders), (Amanda Sharbonough), (Judy Heights) – I’ll get to your email next week, (Jay Michael Pinns), (David Eckerd), (Rick Shepherd), (John Sudeep), (Glenn) in Vancouver, (Ed Dyer) — who else was there — and (Neil), (Shirley), (Barbara) and (Dexter). (Dexter), thanks so much for writing in.
If you’re looking for a book to read, consider the TWIS Book Club’s Book of the Month. We’re digging into “Your Inner Fish” by Neil Shubin right now. And we’ll be discussing that very soon. Hopefully, I’ll be able to get Neil into the discussion as well. That would be fun.
And also, think about sending in your music submission for our compilation album, the 2009 Music Compilation Album is going to be awesome. And you all, songs in deadline is March 1st. Email me, kirsten@thisweekinscience.com if you have any questions or just send me your files. You don’t have to wait until March 1st to send them to me. Now, I like music now.
And check out the forums if you have the time to look at the Question of the Month and give it a try. Answer the question of the month. It’s a pretty interesting question.
Justin: Yeah.
Kirsten: We want to hear your answers. So, thanks a lot.
Justin: We hope you enjoyed the show. We are also available via podcast. Go to our website, www.twis.org. Click on subscribe to the TWIS Science podcast for information on how to subscribe or just go look for us in the iTunes directory.
Kirsten: For any information on anything you’ve heard here today, Show Notes with links to the source articles will be available on our website, twis.org. And we want to hear from you so email us, kirsten or justin@thisweekinscience.com.
Justin: Put TWIS in the subject or you will be spam filtered. Thank you for emailing, comments, stories, we love your feedback. Whoa!
Kirsten: Whoa! We’ll be back here on KDVS next Tuesday at 8:30am Pacific Time. And we hope you’ll join us again for more great science news.
Justin: And if you learned anything from today’s show, remember…
Kirsten: It’s all in your head.
Tags: KDVS, NASA, animals, astrophysics, avian flu, biology, botany, cell biology, chemistry, conservationism, ecology, end of the world, engineering, evolution, genetics, global warming, infectious diseases, medicine, microbiology, molecular biology, nanotechnology, pharmacology, podcast, science, science and politics |
Podcast: http://www.twis.org/audio/2009/02/25/346/
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